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Neurosurgery Fundamentals
Nitin Agarwal, MD
Neurosurgery Resident
Enfolded Spine Surgery Fellow
Department of Neurological Surgery
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania
301 illustrations
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To my family for the unconditional support.
To my fellow residents for helping me carry the message.
To my mentors for educating me in the art of neurosurgery.
To my patients for teaching me on a daily basis.
Contents
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii
Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv
1 Roadmap to a Career in Neurosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Ahmed Kashkoush, David T Fernandes Cabral, Robert M Friedlander
1.1 Introduction. . . . . . . . . . . . . . . . . . . . . 1 1.3 Profiles . . . . . . . . . . . . . . . . . . . . . . . . . 7
1.2 Applications. . . . . . . . . . . . . . . . . . . . . 1
2 History of Neurological Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Edward G Andrews, Chandranath Sen
2.1 Introduction. . . . . . . . . . . . . . . . . . . . . 13 2.4 Spinal Neurosurgery . . . . . . . . . . . . . . 17
2.2 The Pre-Cushing Era. . . . . . . . . . . . . . 14 2.5 Instrumentation . . . . . . . . . . . . . . . . . 17
2.3 The Cushing Era. . . . . . . . . . . . . . . . . . 15
3 Neurological Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
Prateek Agarwal, Daniel Y Zhang, M Sean Grady
3.1 Introduction. . . . . . . . . . . . . . . . . . . . . 23 3.6 Sensory Examination . . . . . . . . . . . . . 32
3.2 Mental Status. . . . . . . . . . . . . . . . . . . . 23 3.7 Gait and Coordination . . . . . . . . . . . . 32
3.3 Cranial Nerves . . . . . . . . . . . . . . . . . . 23 3.8 Special Tests . . . . . . . . . . . . . . . . . . . . 34
3.4 Motor Examination . . . . . . . . . . . . . . . 28 3.9 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 37
3.5 Reflex Examination . . . . . . . . . . . . . . . 31
4 Neuroanatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40
David T Fernandes Cabral, Sandip S Panesar, Joao T Alves Belo, Juan C Fernandez-Miranda
4.1 Introduction. . . . . . . . . . . . . . . . . . . . . 40 4.6 Spinal Cord. . . . . . . . . . . . . . . . . . . . . . 57
4.2 Bones of the Skull . . . . . . . . . . . . . . . . 40 4.7 Vertebral Column . . . . . . . . . . . . . . . . 60
4.3 Cerebrum. . . . . . . . . . . . . . . . . . . . . . . 42 4.8 Vascular Anatomy. . . . . . . . . . . . . . . . 69
4.4 Brainstem. . . . . . . . . . . . . . . . . . . . . . . 50 4.9 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 78
4.5 Cisterns . . . . . . . . . . . . . . . . . . . . . . . . 57
5 Neuroradiology for the Neurosurgeon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81

David R Hansberry, Kofi-Buaku Atsina, Mougnyan Cox, Adam E Flanders
5.1 Introduction. . . . . . . . . . . . . . . . . . . . . 81 5.4 Clinical Scenarios . . . . . . . . . . . . . . . . 85
5.2 Computed Tomography. . . . . . . . . . . 81 5.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 95
5.3 Magnetic Resonance . . . . . . . . . . . . . 82
vii
Contents
6 Operating Room . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
Hanna Algattas, Kristopher Kimmell, G Edward Vates
6.1 Introduction. . . . . . . . . . . . . . . . . . . . . 97 6.7 Bedside Procedures . . . . . . . . . . . . . . 101
6.2 Operating Room . . . . . . . . . . . . . . . . . 97 6.8 Cranial Approaches . . . . . . . . . . . . . . 104
6.3 Cranial Positioning . . . . . . . . . . . . . . . 97 6.9 Spinal Approaches. . . . . . . . . . . . . . . . 112
6.4 Spinal Positioning . . . . . . . . . . . . . . . . 98 6.10 Pediatric. . . . . . . . . . . . . . . . . . . . . . . . 115
6.5 Positioning-Related Complications. . 100 6.11 Functional . . . . . . . . . . . . . . . . . . . . . . 117
6.6 Cerebral Relaxation . . . . . . . . . . . . . . 101 6.12 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 118
7 Neurocritical Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121

Xiaoran Zhang, Lori Shutter
7.1 Introduction. . . . . . . . . . . . . . . . . . . . . 121 7.5 Cerebral Metabolism and
Perfusion . . . . . . . . . . . . . . . . . . . . . . . 125
7.2 Respiratory Physiology . . . . . . . . . . . . 121
7.6 Hematology and Coagulation. . . . . . 126
7.3 Shock . . . . . . . . . . . . . . . . . . . . . . . . . . 123
7.7 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 128
7.4 Fluid and Electrolytes . . . . . . . . . . . . . 124
8 Traumatic Brain Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130

Christine Mau, Shelly Timmons
8.1 Introduction. . . . . . . . . . . . . . . . . . . . . 130 8.5 Anticoagulation. . . . . . . . . . . . . . . . . . 140
8.2 Classification of Head Injury. . . . . . . . 130 8.6 Penetrating Trauma . . . . . . . . . . . . . . 143
8.3 Monitoring. . . . . . . . . . . . . . . . . . . . . . 138 8.7 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 144
8.4 ICP Treatment . . . . . . . . . . . . . . . . . . . 138
9 Spinal Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150

Katherine E Wagner, Jamie Ullman
9.1 Introduction. . . . . . . . . . . . . . . . . . . . . 150 9.10 Cervical Injuries. . . . . . . . . . . . . . . . . . 155
9.2 Examination. . . . . . . . . . . . . . . . . . . . . 150 9.11 C1 Fractures . . . . . . . . . . . . . . . . . . . . 157
9.3 Imaging . . . . . . . . . . . . . . . . . . . . . . . . 150 9.12 Additional Principles for Cervical

Trauma. . . . . . . . . . . . . . . . . . . . . . . . . 162
9.4 Shock . . . . . . . . . . . . . . . . . . . . . . . . . . 151
9.13 Thoracic Injuries . . . . . . . . . . . . . . . . . 163
9.5 Steroids . . . . . . . . . . . . . . . . . . . . . . . . 151
9.14 Thoracolumbar and Lumbar Spine
9.6 Immobilization . . . . . . . . . . . . . . . . . . 151 Injuries . . . . . . . . . . . . . . . . . . . . . . . . . 163
9.7 Spinal Cord Syndromes . . . . . . . . . . . 152 9.15 Sacral Fractures. . . . . . . . . . . . . . . . . . 165
9.8 Spinal Column Model . . . . . . . . . . . . . 153 9.16 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 165
9.9 Cervical Spine . . . . . . . . . . . . . . . . . . . 155
viii
Contents
10 Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168
Robert F Heary, Raghav Gupta, Georgios A Maragkos, Justin M Moore
10.1 Introduction . . . . . . . . . . . . . . . . . . . . 168 10.7 Spinal Vascular Disorders. . . . . . . . . . 178
10.2 Cervical Spine Degenerative 10.8 Spinal Deformity. . . . . . . . . . . . . . . . . 180

Disease. . . . . . . . . . . . . . . . . . . . . . . . . 168
10.9 Inflammatory
10.3 Degenerative Cervical Spondyloarthropathies. . . . . . . . . . . . 184
Myelopathy . . . . . . . . . . . . . . . . . . . . . 168
10.10 Spinal Infections . . . . . . . . . . . . . . . . . 185
10.4 Thoracic Spine Degenerative
Disease . . . . . . . . . . . . . . . . . . . . . . . . 174 10.11 Cauda Equina Syndrome . . . . . . . . . . 186
10.5 Lumbar Back Pain . . . . . . . . . . . . . . . . 176 10.12 Other Spinal Syndromes . . . . . . . . . . 186
10.6 Spinal Neoplasms . . . . . . . . . . . . . . . . 176 10.13 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 187
11 Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 194
James Mooney, Charles Munyon
11.1 Pathway Anatomy . . . . . . . . . . . . . . . 194 11.4 Procedures for Pain. . . . . . . . . . . . . . . 204
11.2 Major Types of Pain . . . . . . . . . . . . . . 197 11.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 209
11.3 Craniofacial Pain Syndromes . . . . . . . 197
12 Cerebrovascular . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
Kamil W Nowicki, Brian L Hoh
12.1 Stroke. . . . . . . . . . . . . . . . . . . . . . . . . . 216 12.4 Vascular Malformations . . . . . . . . . . . 234
12.2 Subarachnoid Hemorrhage . . . . . . . . 225 12.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 240
12.3 Aneurysms. . . . . . . . . . . . . . . . . . . . . . 228
13 Neurosurgical Oncology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245

Desmond A Brown, Hirokazu Takami, William Gibson, Abhijeet Singh Barath,
Michael W Ruff, Terrence C Burns, Ian F Parney
13.1 Lymphomas and Hematopoietic 13.6 Embryonal/PNETs . . . . . . . . . . . . . . . . 257
Tumors . . . . . . . . . . . . . . . . . . . . . . . . 245
13.7 Tumors of Cranial and Paraspinal
13.2 Mesenchymal Tumors . . . . . . . . . . . . 246 Nerves . . . . . . . . . . . . . . . . . . . . . . . . . 260
13.3 Neuroepithelial Brain Tumors . . . . . . 251 13.8 Sellar Tumors. . . . . . . . . . . . . . . . . . . . 261
13.4 Ependymoma and 13.9 Cysts and Tumor-Like

Subependymoma . . . . . . . . . . . . . . . . 256 Lesions. . . . . . . . . . . . . . . . . . . . . . . . . 264
13.5 Pineal Region Tumors. . . . . . . . . . . . . 256 13.10 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 264
14 Pediatric Neurosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 268

Alexandra A Sansosti, Michael M McDowell, Krystal L Tomei
14.1 Examination. . . . . . . . . . . . . . . . . . . . . 268 14.4 Pediatric Trauma. . . . . . . . . . . . . . . . . 285
14.2 Developmental Anomalies. . . . . . . . . 273 14.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 286
14.3 Pediatric Tumors. . . . . . . . . . . . . . . . . 284
ix
Contents
15 Movement Disorders and Epilepsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291

Pablo A Valdes, Garth Rees Cosgrove
15.1 Movement Disorders . . . . . . . . . . . . . 291 15.3 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 310
15.2 Epilepsy . . . . . . . . . . . . . . . . . . . . . . . . 300
16 Stereotactic Radiosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315

Rachel Jacobs, Daniel Tonetti, L Dade Lunsford
16.1 Introduction . . . . . . . . . . . . . . . . . . . . 315 16.9 Treatment Procedure . . . . . . . . . . . . . 325
16.2 Radiation Background . . . . . . . . . . . . 315 16.10 Clinical Outcomes. . . . . . . . . . . . . . . . 327
16.3 Types of Radiation. . . . . . . . . . . . . . . . 315 16.11 Radiation-Induced Changes. . . . . . . . 327
16.4 Main SRS Modalities . . . . . . . . . . . . . . 316 16.12 Vasculopathy. . . . . . . . . . . . . . . . . . . . 327
16.5 Dosing . . . . . . . . . . . . . . . . . . . . . . . . . 317 16.13 Cranial Nerve Deficits. . . . . . . . . . . . . 327
16.6 Occupational Exposure. . . . . . . . . . . . 318 16.14 Radiation-Induced Tumors. . . . . . . . . 327
16.7 Adverse Reactions. . . . . . . . . . . . . . . . 318 16.15 Future Directions . . . . . . . . . . . . . . . . 327
16.8 Indications. . . . . . . . . . . . . . . . . . . . . . 319 16.16 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 328
17 Neurological Infectious Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332

Divyansh Agarwal, Harvey Rubin, Ali Naji
17.1 Introduction. . . . . . . . . . . . . . . . . . . . . 332 17.7 Postsurgical Infections. . . . . . . . . . . . 337
17.2 Microbiological Diagnosis. . . . . . . . . . 332 17.8 Additional Neurological

Infections . . . . . . . . . . . . . . . . . . . . . . . 338
17.3 Flavivirus-Mediated Neurological
Disease. . . . . . . . . . . . . . . . . . . . . . . . . 332 17.9 Empiric Treatment . . . . . . . . . . . . . . . 341
17.4 Meningococcal Disease. . . . . . . . . . . . 334 17.10 Big Data . . . . . . . . . . . . . . . . . . . . . . . . 342
17.5 Neurocysticercosis . . . . . . . . . . . . . . . 335 17.11 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 343
17.6 Primary Amoebic

Meningoencephalitis. . . . . . . . . . . . . . 336
18 Interdisciplinary Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349

Logan Pyle, Joshua Smith, Jeffrey Esper
18.1 Neurology . . . . . . . . . . . . . . . . . . . . . . 349 18.4 Neurotology. . . . . . . . . . . . . . . . . . . . . 367
18.2 Neuroanesthesia. . . . . . . . . . . . . . . . . 359 18.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 370
18.3 Neuro-Ophthalmology. . . . . . . . . . . . 362
19 Socioeconomics in Neurosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374

Catherine Miller, Deborah L Benzil, Ann R Stroink
19.1 Training. . . . . . . . . . . . . . . . . . . . . . . . . 374 19.4 Personal Finance. . . . . . . . . . . . . . . . . 378
19.2 Patient Care. . . . . . . . . . . . . . . . . . . . . 375 19.5 Job Satisfaction . . . . . . . . . . . . . . . . . . 379
19.3 Medical Economics. . . . . . . . . . . . . . . 376
Contents
20 Advice from the Masters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380

Michael D White, Michael P D’Angelo, Ahmed Kashkoush, Edward A Monaco III
20.1 Introduction . . . . . . . . . . . . . . . . . . . . 380 20.5 Journals. . . . . . . . . . . . . . . . . . . . . . . . . 388
20.2 Additional Reading . . . . . . . . . . . . . . . 380 20.6 Leadership. . . . . . . . . . . . . . . . . . . . . . 390
20.3 Conferences. . . . . . . . . . . . . . . . . . . . . 384 20.7 Board Review. . . . . . . . . . . . . . . . . . . . 390
20.4 Grants and Awards . . . . . . . . . . . . . . . 386 20.8 The Masters. . . . . . . . . . . . . . . . . . . . . 392

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 396
xi
Foreword
When Nitin Agarwal asked me to write this succeeding in neurosurgery is invaluable
foreword, I was happy to learn that he put and rarely done, and this book captures the
together his experiences, reflections, and advice of key leaders. I congratulate the edi-
advice in this Neurosurgery Fundamentals. tors and authors of this handbook. I expect
The process of collecting
important bits that it will soon become a classic for aspi-
of knowledge and insight is so critical and ring neurosurgeons who want to get off on
I am happy to see a young writer already the right foot, and that we will be seeing
making his contributions. I know from my this handbook in the coat pockets of many
own w
ritings that brevity is essential to be neurosurgical subinterns and residents on
relevant for medical students and residents, the wards.
and this handbook distills the basics of his-
tory, neurological examination, anatomy, Michael T. Lawton, MD
radiology, and the operating room. This
Professor of Neurosurgery
handbook also summarizes key concepts in President and Chief Executive Officer
trauma, vascular, tumor, spine, functional, Barrow Neurological Institute;
and pediatric neurosurgery, which are the Chairman
clinical problems most likely to be encoun- Department of Neurosurgery
tered in patients in the early stages of the Chief of Vascular and Skull Base
aspiring neurosurgeon’s career or when on Neurosurgery Programs
call in the middle of the night. The accompa- Robert F. Spetzler Endowed Chair
nying figures and illustrations are well done in Neurosciences
and complement the text. I particularly St. Joseph′s Hospital and Medical Center;
enjoyed the roadmaps to academic careers Phoenix, Arizona
and the advice from masters. Getting leaders
in our specialty to share their insights on
xii
Preface
Neurological surgery is a complex and highly a roadmap for matching into residency as
selective specialty. As such, excellent texts well as advice from prominent academic
are available to educate medical students, neurosurgeons. Lastly, this handbook features
advanced practice providers, and residents a comprehensive collection of resources
engaged in the field. Given the magnitude including textbooks, electronic resources,
of neurosurgical information to absorb, conferences, grants and awards, select peer-
many of the existing references may be reviewed journals, organized neurosurgical
overwhelming. Neurosurgery Fundamentals membership, and board review references.
offers a portable reference for neurosurgical High yield resources are highlighted to help
providers in training to quickly digest the in reader identification. Overall, this text is
essentials of neurosurgical care. Its content a unique and succinct guide for any aspiring
enables quick preparation for medical neurosurgical provider.
student sub-
internships or neurosurgical
residency. Chapters include questions to aid Nitin Agarwal, MD
retention of k
nowledge. The text also features
xiii
Acknowledgements
I would like to say thanks to all my E. Landis, for guiding me through this
colleagues who contributed to this hand-
opportunity to enhance medical student,

book to
augment the training of future advanced practice provider, and resident
neurosurgical providers. I am very grateful education in Neurological Surgery.
to all the Thieme editors, especially Timothy
Y. Hiscock, Gaurav Prabhuzantye, and S
arah
xiv
Contributors
Divyansh Agarwal, MS Joao T Alves Belo, MD
Perelman School of Medicine Research Fellow
University of Pennsylvania Department of Neurosurgery
Philadelphia, Pennsylvania University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania;
Prateek Agarwal, AB Attending Neurosurgeon
Perelman School of Medicine Hospital Felício Rocho
University of Pennsylvania Belo Horizonte, Brazil
Philadelphia, Pennsylvania
Deborah L Benzil, MD, FAANS, FACS
Hanna Algattas, MD Vice Chair
Resident Department of Neurosurgery
Department of Neurosurgery Cleveland Clinic
University of Pittsburgh Medical Center Cleveland, Ohio
Desmond A Brown, MD, PhD
Edward G Andrews, MD Neurosurgery Resident
Resident Enfolded Fellow, Neurosurgical
Department of Neurosurgery Oncology
University of Pittsburgh Medical Center Mayo Clinic
Pittsburgh, Pennsylvania Rochester, Minnesota
Kofi-Buaku Atsina, MD Terrence C Burns, MD, PhD

Resident Senior Associate Consultant
Department of Radiology Department of Neurosurgery
Thomas Jefferson University Hospitals Mayo Clinic
Philadelphia, Pennsylvania Rochester, Minnesota
Abhijeet Singh Barath, MBBS David T Fernandes Cabral, MD

Resident Resident
Department of Trauma and Emergency Department of Neurosurgery
Medicine University of Pittsburgh Medical Center
All India Institute of Medical Sciences Pittsburgh, Pennsylvania
Jodhpur, India
xv
Contributors
Garth Rees Cosgrove, MD, FRCS(C) Department of Radiology

Director of Epilepsy and Functional Thomas Jefferson University Hospitals
Neurosurgery Philadelphia, Pennsylvania
Brigham and Women’s Hospital
Harvard Medical School Robert M Friedlander, MD, MA
Boston, Massachusetts Chairman and Professor
Walter E Dandy Chair
Mougnyan Cox, MD Head of Cerebrovascular Neurosurgery
Neuroradiology Fellow University of Pittsburgh School of
Department of Radiology Medicine
Hospital of the University of Pittsburgh, Pennsylvania
Pennsylvania
Philadelphia, Pennsylvania William Gibson, MD, PhD
Resident
Michael P D’Angelo, BS Department of Neurosurgery
University of Pittsburgh School of Medicine Mayo Clinic
Pittsburgh, Pennsylvania Rochester, Minnesota
Jeffrey Esper, DO, MHSA, MS (Med Ed), M Sean Grady, MD

FACN, FAANEM Charles Harrison Frazier Professor of
Residency Program Director Neurosurgery
Department of Neurology Chairman, Department of Neurosurgery
UPMC Hamot Perelman School of Medicine
Erie, Pennsylvania University of Pennsylvania
Juan C Fernandez-Miranda, MD
Professor of Neurosurgery and (By Raghav Gupta, BS
Courtesy) of Otolaryngology—Head Rutgers New Jersey Medical School
and Neck Surgery Newark, New Jersey
Stanford University Medical Center
Stanford, California David R Hansberry, MD, PhD
Resident
Adam E Flanders, MD Department of Radiology
Professor of Radiology and Rehabilitation Thomas Jefferson University
Medicine Hospitals
Co-division Director, Neuroradiology Philadelphia, Pennsylvania
Vice-chair Imaging Informatics
xvi
Contributors
Robert F Heary, MD, FAANS Director, Neurosurgery Residency Program

Professor Chair, Technology and Innovative Practice
Department of Neurological Surgery Committee
Director University of Pittsburgh
Center for Spine Surgery and Pittsburgh, Pennsylvania
Mobility
Rutgers New Jersey Medical School Georgios A Maragkos, MD
Newark, New Jersey Postdoctoral Research Fellow
Neurosurgery Service
Brian L Hoh, MD, FACS, FAANS Beth Israel Deaconess Medical Center
James and Brigitte Marino Family Harvard Medical School
Professor and Chair Boston, Massachusetts
Lillian S. Wells Department of Neurosurgery
University of Florida Christine Mau, MD
Gainesville, Florida Neurosurgery Resident
Department of Neurosurgery
Rachel Jacobs, BS Penn State Health Milton S. Hershey
University of Pittsburgh School of Medical Center
Medicine Hershey, Pennsylvania
Michael M McDowell, MD
Ahmed Kashkoush, BS Resident
University of Pittsburgh School of Department of Neurosurgery
Medicine University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania Pittsburgh, Pennsylvania
Kristopher Kimmell, MD Catherine Miller, MD

Adjunct Clinical Assistant Professor Assistant Professor
Department of Neurosurgery Department of Neurosurgery
University of Rochester Medical Center University of California, San Francisco
Rochester, New York San Francisco, California
L Dade Lunsford, MD, FACS Edward A Monaco III, MD, PhD

Lars Leksell Distinguished Professor Assistant Professor
Department of Neurosurgery Department of Neurological Surgery
Director, Center for Image Guided University of Pittsburgh School of Medicine
Neurosurgery Pittsburgh, Pennsylvania
xvii
Contributors
James Mooney, MD Sandip S Panesar, MD, MSc

Neurosurgery Resident Postdoctoral Research Fellow
University of Alabama at Birmingham Stanford University
Birmingham, Alabama Stanford, California
Justin M Moore, MD, PhD Ian F Parney, MD, PhD

Assistant Professor Professor and Vice-Chair (Research)
Beth Israel Deaconess Medical Center Consultant
Harvard Medical School; Department of Immunology
Department of Neurosurgery Mayo Clinic
Boston Medical Center Rochester, Minnesota
Boston University
Boston, Massachusetts Logan Pyle, DO
Resident
Charles Munyon, MD Department of Neurology
Director, Functional and Restorative UPMC Hamot
Neurosurgery Erie, Pennsylvania
Lewis Katz School of Medicine at
Temple University Harvey Rubin, MD, PhD
Philadelphia, Pennsylvania Professor
Department of Medicine
Ali Naji, MD, PhD University of Pennsylvania
Professor Philadelphia, Pennsylvania
Department of Surgery
University of Pennsylvania Michael W Ruff, MD
Philadelphia, Pennsylvania Senior Associate Consultant
Department of Neurology
Kamil W Nowicki, MD, PhD Department of Medical Oncology
Resident Mayo Clinic
Department of Neurosurgery Rochester, Minnesota
Pittsburgh, Pennsylvania Alexandra A Sansosti, BS
University of Pittsburgh School of Medicine
xviii
Contributors
Chandranath Sen, MD Shelly D Timmons, MD, PhD, FACS,

Professor FAANS
Department of Neurosurgery Professor of Neurosurgery
New York University Langone Vice Chair for Administration
Medical Center Director of Neurotrauma
New York, New York Department of Neurosurgery
Penn State Health Milton S. Hershey
Lori Shutter, MD Medical Center
Professor Hershey, Pennsylvania
Departments of Critical Care Medicine,
Neurology, and Neurosurgery; Krystal L Tomei, MD, MPH
Vice Chair of Education Assistant Professor
Department of Critical Care Medicine; Department of Neurosurgery
Director Rainbow Babies & Children’s Hospital
Division of Neurocritical Care; University Hospitals Cleveland
Pittsburgh, Pennsylvania Cleveland, Ohio
Joshua Smith, DO Daniel A Tonetti, MD, MS

Resident Resident
Department of Neurology Department of Neurosurgery
UPMC Hamot University of Pittsburgh Medical Center
Erie, Pennsylvania Pittsburgh, Pennsylvania
Ann R Stroink, MD, CPE, FAANS Jamie Ullman, MD

Faculty Neurosurgeon Director of Neurotrauma
Central Illinois Neuro Health Sciences; North Shore University Hospital
Advocate System Medical Director Manhasset, New York;
Neurosciences Quality & Educational Department of Neurosurgery
Development; The Donald and Barbara Zucker School of
Bloomington, Illinois Medicine at Hofstra/Northwell
Hempstead, New York
Hirokazu Takami, BM
Neurosurgery Fellow Pablo A Valdes, MD, PhD
Department of Neurosurgery Neurosurgery Resident
Mayo Clinic Brigham and Women’s Hospital
Rochester, Minnesota Harvard Medical School
Boston, Massachusetts
xix
Contributors
G Edward Vates, MD, PhD, FACS Michael D White, BS

Professor University of Pittsburgh School of
Department of Neurosurgery; Medicine
Director Pittsburgh, Pennsylvania
Rochester Early Medical Scholars
Program; Daniel Y Zhang, SB
University of Rochester Medical Center Perelman School of Medicine
Rochester, New York University of Pennsylvania
Katherine E Wagner, MD
Resident Xiaoran Zhang, MD, MS
Department of Neurosurgery Resident
Donald and Barbara Zucker School of Department of Neurosurgery
Medicine at Hofstra/Northwell University of Pittsburgh
Hempstead, New York; Medical Center
Department of Neurosurgery Pittsburgh, Pennsylvania
Northwell Health
North Shore University Hospital
Manhasset, New York
xx
1 Roadmap to a Career in Neurosurgery
Ahmed Kashkoush, David T Fernandes Cabral, Robert M Friedlander
1.1 Introduction Neurosurgery was 86%; for comparison,

the match rate for all specialties combined
Neurological surgery is the field of medi- was approximately 94%. For 43 total inter-
cine dedicated to surgical treatment of national medical graduate (IMG) appli-
nervous system pathology within the cants in 2018, the match rate was 23%.5
brain, spine, and in the periphery. The
American Board of Neurological Surgery
(ABNS) is responsible for selecting the Given the limited spots open for incom-
training requirements for Neurosurgery ing residents, it is important to prepare
residents.1 Neurosurgery residency is early in medical school for the application
7 years (84 months) in duration, which process in order to have the best chance
consists of 54 months of core clinical neu- for success.
rosurgery and 30 months of electives. The
aim of this chapter is to lay down a frame-
work for preparing for the neurosurgery In a survey of 28 out of 104 residency di-
residency application. rectors (27% response rate) for Neurologi-
cal Surgery conducted in March 2018,
responders were asked to cite factors in
1.2 Applications interviewing and ranking applicants. Of all
factors, most program directors cited the
1.2.1 Match Data following as important factors for selecting
applicants to interview6:
For the 2017–2018 academic year, there
were 110 Neurosurgery residency pro-
• Letters of recommendation (100%).
grams accredited by the Accreditation
• United States Medical Licensing Exam-
ination (USMLE) Step 1/Comprehensive
Council for Graduate Medical Educa- Osteopathic Medic al Licensing Exam-
tion (ACGME).2 Generally, Neurosurgery ination (COMLEX) Level 1 scores (100%).
programs accept 1 to 3 incoming residents
every year, with the larger programs
• Performing a neurosurgery rotation in
that department (88%).
accepting 4 residents per year. Neurologi-
cal surgery was among the most competi-
• Alpha Omega Alpha membership (88%).
tive specialties in the 2018 Match.
• Evidence of professionalism and ethics
(84%).
According to the National Resident Match-
ing Program (NRMP), there were a total of When asked about important factors in
310 applicants who preferred the specialty ranking applicants, residency directors
for 225 positions (1.38 applicants/posi- most frequently cited6:
tions).3 Note: All NRMP statistics in this • Interactions with faculty during inter-
chapter are calculated for applicants that view and visit (96%).
preferred Neurological Surgery (n = 310) • Interpersonal skills (88%).
and not those that ranked Neurological • Interactions with house staff (88%).
Surgery programs (n = 325).3,4 The match • Letters of recommendation (84%).
rate for U.S. allopathic seniors into • USMLE/COMLEX Step 1 Score (84%).
Roadmap to a Career in Neurosurgery
Results from the NRMP suggest that aca- data (▶Table 1.1).3 For those 28 US seniors
demic achievements are most important in who preferred Neurosurgery but did not
selecting applicants to interview, but person- match in the specialty, the mean score was
ality and interactions with others are most 234. Utilizing probabilities calculated with
influential in ranking applicants. It is import- 2016–2018 data, the likelihood of matching
ant to note that the relative importance of in Neurosurgery as their preferred specialty
each of these factors vary with program. with a score of 250 or higher is approxi-
mately 85 to 95%. For scores within the
ranges of 220 to 230, 230 to 240, and 240 to
1.2.2 Qualifications
250, the probabilities of matching are
USMLE Step 1 scores are important screen- approximately 50 to 60%, 70 to 80%, and
ing factors to assess ot one’s candidacy for 80 to 85%, respectively (▶Fig. 1.1). For
neurosurgical residency programs. As IMGs, the mean scores for matched and
noted earlier, 100% of residency directors unmatched applicants are similar to those
utilize Step 1 scores to select applicants for of US allopathic seniors.5 However, a nota-
an interview.6 For those who matched in ble difference is that even with an extremely
Neurosurgery as their preferred specialty, high score (> 260), the probability of match-
the mean Step 1 score for 2018 was 245 ing in Neurosurgery as a preferred specialty
among 188 matched United States (US) for IMGs is still about 45% according to
allopathic seniors according to 2018 NRMP 2016–2018 NRMP data (▶Fig. 1.2). As such,
Table 1.1 Summary statistics on United States allopathic seniors that preferred neuro-
logical surgery*
Measure Matched Unmatched
(n = 188) (n = 28)
Mean number of contiguous ranks 16.4 8.5
Mean number of distinct specialties ranked 1 1.3
Mean USMLE Step 1 score 245 234
Mean USMLE Step 2 score 249 238
Mean number of research experiences 5.2 4.4
Mean number of abstracts, presentations, and publications 18.4 8.9
Mean number of work experiences 3.2 2.5
Mean number of volunteer experiences 7 6.9
Percentage who are AOA members 31.9 21.4
Percentage who graduated from one of the 40 US medical
43.6 10.7
schools with the highest NIH funding**
Percentage who have PhD degree 13.6 3.8
Percentage who have another graduate degree 20 28
*Used with permissions from NRMP.3
**Top 40 US medical schools with the highest NIH funding is from the NIH website.
Abbreviations: AOA, Alpha Omega Alpha; NIH, National Institutes of Health; US, United
States; USMLE, United States Medical Licensing Examination.
1.2 Applications
Fig. 1.1 Probability of United

States allopathic seniors
matching into neurological
surgery by United States
Medical Licensing Examina-
tion (USMLE) Step 1 score.
(Reproduced with permis-
sion from National Resident
Matching Program [NRMP].)3
Fig. 1.2 Probability of inter-

national medical graduates
matching into neurological
surgery by United States
Medical Licensing Examina-
tion (USMLE) Step 1 score.
(Reproduced with permis-
sion from National Resident
Matching Program [NRMP].)5
IMG applicants may benefit from getting 1.2.3 Research

involved in research at a Neurosurgery
department and building relationships
with the faculty at that institution. Research is very important part of the
While Alpha Omega Alpha (AOA) mem- Neurosurgery application as producing
bership is not necessary for Neurosurgery peer-reviewed publications demonstrates
residency, top-tier programs may have a an ability to bring tasks to a conclusion.
preference for selecting AOA members.7
Performance during clinical rotations is
evaluated with grades, which are based on In the 2018 Match, the mean number of
performance on shelf examinations, enthu- abstracts, presentations, and publications
siasm for the subject matter, and ability to for US allopathic seniors who matched was
assist other members of the healthcare 18.4 whereas that for unmatched appli-
team. Performance on clinical rotations is cants was 8.9.3 The importance of research
largely subjective and if residents or pre- is especially true for candidates targeting
ceptors detect arrogance or disinterest, it highly ranked academic centers and for
may be reflected as a low grade for the IMG applicants. One study suggested that
course. Given the competition for Neuro- student h-index was an independent
surgery residency positions, applicants predictor of matriculation into top-tier

should strive for high grades in all of their research institutions,8 thus emphasizing
rotations (High pass to Honors).7 the role of actively contributing impactful
papers to the neurosurgical literature. Rec- 1.2.4 Research for IMGs

ognizing faculty that have a proven track
record of working with students is a key The importance of research for IMG appli-
aspect to identifying potential mentors in cants cannot be stressed enough. In 2018,
the field. Looking at past years’ match lists the mean number of abstracts, presenta-
may help to evaluate which prior students tions, and publications for IMG applicants
of the group were successful in matriculat- who preferred and matched in Neurosur-
ing into programs of interest. Other very gery was 46.6.5 For those who have already
important factors to consider in a faculty finished medical school and do not have
mentor are seniority, personality, pro- research experience, the best next step is
jected timeline of the project, funding to find a research position in a US aca-
availability for conferences, impact of the demic Neurosurgery department. In this
research produced, and availability. Also case, doximity.com is a very useful website
remember, pairing up with residents who for assessing the research output of differ-
are active in research may open up connec- ent programs. Institutional websites can
tions with other more senior faculty mem- be utilized to assess research options
bers of the institution. Additionally, getting within the department and contact infor-
involved with the institution’s student in- mation for lab directors. Students should
terest group can open up networking op- contact various labs and not feel frustrated
portunities, and has also been shown to if emails go unanswered. Faculty members
increase publication count and institu- are extremely busy and often involuntarily
tional match rate into Neurosurgery.9 forget to reply to emails. Persistence is key.
Given the short time frame for complet- Applying to several laboratories as well as
ing publications, prospective Neurosurgery making an effort (if feasible) to meet
candidates should begin early, preferably in in-person will increase the chances of
their first or second year of medical school. success.
Early involvement in research is important IMGs must take into consideration the
because students are expected to attend to diverse types of research positions offered
a higher load of clinical duties during rota- by the lab. For instance, some laboratories
tions. there are many funding opportunities are very open to receive people for volun-
available specifically for medical students teer or unpaid research, which could dra-
during the summer after first year (see sec- matically impact entry into the US.
tion 20.4 Grants and Awards).10,11,12 Oppor- Students who are not US citizens or green
tunities to augment one’s research portfolio card holders will need to apply for a visa to
exist via dedicating a year to protected start the research job.
research time during medical school with
graduation in 5 years instead of 4 years.
However, delaying graduation for dedicated
research time is not necessary. Additionally, Please be aware that tourist visas are not
an individual must be highly productive allowed for research positions.
must strive to complete several publications
to account for this extra time. Again, there
are many funding opportunities that are Most labs will offer a J1 visa, which
available specifically for medical students, in most cases has a 2-year rule and a limit of
such as the Howard Hughes Medical Insti- 7 years. Visit the Department of State
tute Medical Research Fellowship and the website for details regarding 2-year home-
National Institutes of Health (NIH) Medical country physical presence requirements
Research Scholars Program.13,14 and eligibility for a waiver.15 In order to
1.2 Applications
apply for a J1 visa for a volunteer research During this time, students will spend a
position, the student will need to prove to month with the Neurosurgery service and
the US Government that the student or a develop the basic foundations of neurosur-
sponsor (most likely your family) has the gical knowledge and techniques. Here, both
equivalent of $30,000 or more. Another fac- the faculty and house staff will have the
tor to consider is that volunteering posi- opportunity to evaluate if a student has
tions will not come with health insurance. the caliber for the field of Neurosurgery. By
The bottom line is that IMG students will the end of the rotation, candidates should
need a significant amount of funds to apply be in a position to request a letter of recom-
for volunteering positions, which unfortu- mendation from the residency director or
nately are the most common. chairman of the department. To stand out
The second option, which would be the as a valuable member of the team during
best-case scenario, is to get a postdoctoral the Neurosurgery clerkship, students will
research fellow position. This case offers need to build on and utilize many of the
employment at the university, which comes skills learned in their prior rotations.
with a salary, health insurance, and in some
cases, different benefits offered by the uni-
versity. Again, a visa is required, which in
The 3 A’s (Affability, Availability, and Ac-
this case could be a J1 or an H1B. Please
countability) and “How to Swim with
refer to the Department of State for detailed
Sharks” have been frequently cited as
explanation regarding visa issues.15
guidelines for medical students.16
1.2.5 Away Rotations Many others cite “Message to Garcia” as a

guide for an exceptional performance on
As a candidate chooses where to do away the neurosurgery sub-internship:
rotations, it is important to define what the
student’s priorities are. It is critical to evalu- “The world bestows its big prizes,
ate the culture and training available at each both in money and in honors, for but
program. From a clinical stand, it is import- one thing. And that is Initiative. What is
ant to evaluate the case volume. A useful Initiative? I’ll tell you: it is doing the
metric is to compare the ratio of total case right thing without being told. But next
volume divided by the number of residents to doing the thing without being told is
in the program. Low volume translates into to do it when you are told once. That is to
lower operative exposure throughout resi- say, carry the Message to Garcia: those
dency. On the research side, perform a liter- who can carry a message get high hon-
ature search on the entire faculty to ors, but their pay is not always in pro-
understand the true academic commitment portion. Next, there are those who never
and faculty accomplishments. If the appli- do a thing until they are told twice; such
cant is interested in research, search to get no honors and small pay. Next, there
determine the number of clinical neurosur- are those who do the right thing only
geons who are principal investigators of NIH when necessity kicks them from behind,
or Department of Defense-funded projects. and these get indifference instead of
This will provide a measure of the role mod- honors, and a pittance for pay. This kind
els available at the specific program. spends most of its time polishing a
Performance on a sub-internship is per- bench with a hard-luck story. Then, still
haps the most important aspect of a candi- lower down in the scale than this, we
date’s profile at that particular institution. have fellow who will not do the right
thing even when someone goes along to 1.2.7 Interviewing

show him how and stays to see that he
does it; he is always out of job, and Interview season is an expensive and
receives the contempt he deserves, stressful process. One study reported that
unless he happens to have a rich Pa, in the average cost incurred during Neurosur-
which case Destiny patiently awaits gery residency interviews was approxi-
around a corner with a stuffed club. To mately $7,180 ± 3,880 (mean ± standard
which class do you belong?”17 deviation).18 Despite these costs, in-person
interviews are important for learning
about the culture of each institution, tour-
1.2.6 Recommendations ing the facilities, and meeting potential col-
leagues and mentors. Know that once an
Three letters of recommendation are
interview has been obtained, the applicant
required to apply for Neurosurgery. The
pool has become significantly narrowed
Electronic Residency Application Ser-
down. Most successful applicants aim to
vice (ERAS®) allows up to four letters to be
attend 10 or more interviews to optimize
submitted. One of these letters should be
their chances given that a greater number
from the department chair and/or the pro-
of contiguous ranks yields a higher proba-
gram director at the home institution. While
bility of matching.7 The interview day itself
on away rotations, try to obtain a strong let-
will be hectic. Most applicants will have an
ter from the chairman or program directors
introduction by the chairman, a walking
at those institutions. These letters will
tour of the hospital, and some time to
largely be based on input from residents and
spend with the residents. Arrive at the
other faculty observing your performance.
interview with a handful of prepared ques-
tions. Ask about key faculty projections and
transitions, operating room experience,
program for team building and social activ-
Letters from non-neurosurgeons are not
ities, variety of clinical experience from
encouraged as these may have a lower im-
hospitals within the healthcare system,
pact, given individuals outside of the field
enfolded fellowships, research opportuni-
may have limited ability to comment on
ties and support, resident matriculation
the qualities necessary for Neurosurgery.7
into academic centers, any other areas of
interest. During interview sessions, candi-
dates should strive for a bidirectional
The seniority of the letter-writer may also conversation. Be a good story-teller and

affect the impact of the letter. Neurosur- emphasize key strengths of the application.
geon research mentors may have a unique Candidates will likely be asked about their
ability to comment on candidate qualifica- specific interests and long-term goals in
tions as they have likely overseen their neurosurgery as well as their research.
work and long-term maturation. Students Conveying background knowledge, roles,
should also keep in mind that they can and key findings of research projects will
submit different letters to different probe expected of interviewees. After the
grams. For instance, if a student knows interview, consider sending thank you
that a certain letter-writer has connections notes to each program. Generic communi-
at a program of interest, that letter may be cations sound like generic c ommunications.
more strategic than others. In addition to Write about something specific and mean-
letters, mentors may offer to call programs ingful about the program and visit. Email
to advocate for the student. is an acceptable form of post-interview
1.3 Profiles
communication and follow-up inquiries. If things. Sometimes, we were breaking

an applicant is still undecided about how to things, but hopefully not too many times.
rank programs, a second look is always an The problems with surgery, however, were
opportunity to re-evaluate a program and several in my mind. I did not think it was a
demonstrate interest. In some cases, pro- field that was conducive to laboratory
grams may offer the applicant another research. Residents were on-call every
interview with key faculty and residents at other night for 5 years, which to me at that
the second look. point felt like too much. I then remember
talking to the Surgery clerkship director
about the dilemma that I was in. I liked
1.2.8 Ranking surgery but it seemed really hard and a lot
Much of ranking is based on the applicant’s of work. He said ‘Robert, you can be a der-
feeling for the program on interview day. matologist or a surgeon. If you like derma-
There are many aspects of a program that tology, then God bless you. In dermatology,
an applicant should consider when rank- residency is going to be much shorter,
ing and these vary based on personal pref- there will be fewer hours, your career will
erence. If an applicant genuinely disliked a be more or less 9 to 5, and you will not
program and would not be happy working have weekend emergencies. But if you dis-
there for 7 years, then it might be best not like what you do, you are going to wake up
to rank it highly regardless of perceived miserable, go to work miserable, go home
prestige. It is vital that applicants build an miserable, and not be happy. Surgery, sure,
intimate understanding of the matching you wake up early, you work hard, you may
algorithm. In brief, the match algorithm is have to take call every other night, but its
“applicant proposing,” which means that 5 years. It’s a long time, but it's a limited
preference is given to applicant over pro- amount of time, and you have the next
gram rank.19 The algorithm thus encour- 30 years to practice something that you
ages students to rank programs in order of love. You are going to love waking up, you
preference rather than in order of candi- are going to be excited to go to work,
dacy at each program. In essence, the order you are going to love doing surgery, you are
of the rank list does not influence the going to go home and be happy with your
chance of matching into Neurosurgery. family. But it really depends if you like it or
Applicants should not rank lower-tier pro- not.’ So that conversation at least opened
grams higher because they believe it will my eyes to a surgical career and was a very
increase their chances of matching. On the transitional conversation for me. It was my
contrary, it only increases the chances of good friend in medical school who put the
matching at a less preferable institution. neurosurgical bug in my head. He was
doing research and always so excited about
neurosurgery that I decided to do a rota-
1.3 Profiles tion in neurosurgery. And I loved it. I
remember the first time that I saw a neu-
Robert M Friedlander, MD, MA
rosurgical operation. It was a cerebellar
Chairman and Professor
met. I remember just seeing the cerebel-
Walter E Dandy Chair
lum pulsate and to me it was really cool
Head of Cerebrovascular Neurosurgery
and exciting, just seeing the brain, opening
the fissure, and seeing the blood vessels. To
me, it was just phenomenal. So, at that
“On my surgery rotation, I really liked point, I decided to do neurosurgery, about
taking care of an acute patient and fixing midway through third year of medical
school. To me, having the privilege of focused on epilepsy, before my first year of
opening someone’s head and fixing it, medical school. Over the course of time, my
being able to use my hands, and being able clinical interests in neuroscience centered
to teach residents—to me, it is too fulfilling. on neurosurgery. I spent time on the neu-
To have the ability to do research, which I rosurgical service at Columbia Presbyterian
love; surgery, which I love; and teaching, Hospital and did rotations at a couple other
which I love; and now, to be able to admin- places during my third and fourth years. I
ister and have a vision, to not only impact decided to go back to University of Virginia
what I do but to mentor a large number of to do my internship for a year, but after a
faculty and residents, and to establish a year, I decided I wanted to go to Pittsburgh
neurosurgical legacy in a leading neuro- to do my neurosurgical training. I came
surgical department, to me is a privilege, here in 1975. At the time that I came, the
an honor, and a great responsibility.” first major breakthrough in brain imaging
came with the development of the com-
L Dade Lunsford, MD, FACS
puted tomography (CT) scan, which
Lars Leksell Distinguished Professor
showed up on the same day I started my
residency. It became clear to me immedi-
Director, Center for Image Guided
ately that the world was going to change in
Neurosurgery
a big way. So I worked on combining imag-
Director, Neurosurgery Residency
ing with guiding technology. At the time,
Program
that was not actually done in brain surgery
Chair, Technology and Innovative
since movement disorder surgery had died
Practice Committee
during that era after the development of
University of Pittsburgh
L-dopa. To precisely reach areas in the
brain, I developed, as a resident here, a ste-
Path to neurosurgery reotactic guiding device that was CT-com-
“My interests in neuroscience probably patible. I became further interested in deep
began in college. At the University of Vir- brain types of surgery. I had an opportu-
ginia, I got to participate in a master’s level nity to spend a few months in Europe in
undergraduate program, where I spent 1979, trying to decide where I wanted to
2 years working on neuroscience research. do a fellowship after I finished training in
At that time, we were working on the neurosurgery here. I applied for an Ameri-
transfer of learning information in a rat can Association of Neurological Sur-
model and doing things like corpus callo- geons (AANS) supported William P. Van
sum resections and using a technique Wagenen fellowship, which is given once a
called “spreading depression” to function- year. This allowed me to spend a year in
ally inactivate brain function and study Sweden doing training in stereotactic sur-
memory function in one hemisphere of the gery and functional neurosurgery. I came
rat. That stimulated my interests in neuro- back to Pittsburgh in 1981, and joined the
science. I already knew that I wanted to go faculty and, in essence, I have been here
to medical school, so during that same ever since. My interests have still remained
time, I completed my pre-med require- in minimally invasive surgical techniques
ments. I had lived in the state of Virginia for to be able to avoid the risks and complica-
21 years and made the decision that it was tions of more aggressive brain surgery,
probably a good idea to go somewhere else while finding ways to minimize collateral
for a period of time for medical school. So I damage in brain surgery. One of the tech-
ended up going to Columbia University and niques that we developed was the first
started working for a neurologist who was dedicated stereotactic operating room
1.3 Profiles
with a CT scanner, which was put in 1981 who go into neurosurgery should be rocket
here at UPMC. In 1987, we brought in the scientists in the sense of being 200-level
first 201 source gamma knife (fifth unit IQs. I think those people are brilliant theo-
ever built) for brain surgery. Over the last reticians but they cannot deal with the real-
30 years, we have updated the various ity of taking care of a patient sitting in the
gamma knife devices five times and now emergency room with a blood clot in their
radiosurgery has become a major compo- head. You have to be able to focus and apply
nent of what is done in neurosurgery, both yourself. Certainly when I decided to come
in the brain and spine. Currently in our pro- to Pittsburgh for training, Peter Jannetta,
gram, which is probably one of the busiest who was the first truly academic chair of
in the US, we do about 9,000 operations per this department, was a major influence on
year. Radiosurgery techniques, using things me because of his somewhat demanding
like gamma knife and spine radiosurgery nature, but also his requirement that you
devices, accounts for somewhere around provide skillful surgical care of patients.
12% of the total neurosurgery practice. It After that, I had experience working with
has become a major component of what two Swedish neurosurgeons Eric Olof
the field is and it is a major component of Backlund at the Karolinska institute, and
what current residents in training need to Lars Leksell, who was the originator of
learn while they are in training. My other Gamma Knife. He was no longer clinically
interests have been related to proving that active, but was very much active in terms of
new technology has value. One of the crazy his continued research interests and how to
things about US healthcare is that some- do this type of noninvasive surgery.”
times industry develops tools that are
expensive but are not always shown to Nathan Zwagerman, MD
have sustained value over the course of Assistant Professor
time. What we have done in working with Department of Neurosurgery
tools like gamma knife is to maintain com- Medical College of Wisconsin
prehensive patient databases that allow us
to do long-term outcomes research. We “I grew up on a small farm in Michigan.
have published somewhere around 650 My parents are hog farmers and I am the
peer-reviewed articles in the scientific lit- oldest of four boys. In rural west Michigan,
erature plus 12 books related to technol- the plan was that I would continue the
ogy, a large number of them related to farming line. However, early on, I realized
gamma knife. Patient care, teaching, and that I did not want to be on a farm. Farming
academic publishing in clinical research is just was not for me. I did not mind the
what I have been doing for 40 years or so work, but I just did not like it. So I was
that I have been in practice.” looking for every opportunity I could get to
leave. It was clear from an early age that I
Mentorship enjoyed learning about the biology of the
“When I was in childhood and through high hogs and when I was in high school, I took
school, I studied piano for many years, and I Advanced Placement biology.
had a 90-year-old piano teacher who was a During medical school, I enjoyed anat-
concert pianist. She had a significant omy and doing dissections in the cadaver
impact on me in terms of the need to study lab. I realized very quickly that I could not
and apply myself. I was a never a natural sit in class anymore. I was very tired of lec-
talent in piano, but I was someone who was tures and lecture halls and all the lectures
able to work hard to meet her demanding were available online at twice the speed.
nature. Similarly, I do not think that people To get me out of the house, I ended up
going to different grand rounds, depending about 16, I read an article about brain sur-
on what subject we were studying. During gery and from that moment on, there was
neuroanatomy, I interacted with a couple nothing else I ever wanted or planned to
of neurologists in the beginning of my do. The brain as the arbiter of our interac-
third year and they told me about neuro- tions with others and the world had always
surgery grand rounds. fascinated me, and the opportunity to
I was leaning towards surgery at that work with my hands (as is so prevalent
point. I went to neurosurgery grand rounds amongst surgeons) was a driving factor, as
midway through my third year. They were well as the chance to study and understand
presenting at Morbidity and mortal- the most complicated organ in existence!
ity (M&M), it was an aneurysm case, which That interest also led me to pursue my PhD
was initially nonruptured. The video was in neurophysiology when the opportunity
up and as they were about to clip the aneu- arose at the end of my residency training.”
rysm and the aneurysm ruptured. I
Robert F Heary, MD, FAANS
remember the intensity of the room
Professor
changed. The entire atmosphere was
Department of Neurological Surgery
something that I had never experienced
Director, Center for Spine Surgery and
before. I thought this is something I must
Mobility
know more about. As a result, during my
Rutgers New Jersey Medical School
third year, I learned more about it, spent
Newark, New Jersey
more time going to grand rounds, meeting
the residents, picking their brains, just
“I began my career as a general surgery
kind of hanging out around the depart-
resident. Midway through my third year of
ment, while doing my rotations. I did a
residency, I rotated on the neurosurgery ser-
month of research with Dr. Ding, who also
vice and had a great time. It became appar-
helped guide me further toward neurosur-
ent that neurosurgeons had the opportunity
gery. I did a couple of rotations at Wayne
to use their minds to think through complex
State, Northwestern, and the University of
decisions and help many people in the pro-
Vermont, and was totally secured that neu-
cess. The thrill of taking care of debilitated
rosurgery was where I wanted to be. That
and injured patients was fabulous. After my
is how I got into neurosurgery, I was a late
rotation on neurosurgery was completed,
bloomer, so to speak. Ten years ago, I would
the Chief of the Section of Neurological Sur-
have never pictured myself as a skull-
gery (part of the Department of Surgery in
based surgeon in Milwaukee, but it is
those days) asked me to leave General Sur-
funny how life takes you on a ride.”
gery and become a neurosurgery resident. It
took me less than an hour to realize that this
Shelly D Timmons, MD, PhD, FACS, FAANS
was the chance of a lifetime. Between the
Professor of Neurosurgery
various spine surgeries and brain operations
Vice Chair for Administration
that I had the good fortune of participating
Director of Neurotrauma
in, I was thoroughly convinced that the cor-
rect career path for me was being handed to
Penn State University Milton S. Hershey
me and I accepted the position. I then began
Medical Center
five more years of residency in neurological
Hershey, Pennsylvania
surgery and I have never regretted this deci-
“From the time I was a little girl, I had a sion for an instant. Later in my neurosurgical
keen interest in all things medical and ana- training, I decided to specialize in spinal sur-
tomical, and I knew that I wanted to be a gery and I took an offer at a prestigious
doctor at a very early age. When I was orthopaedic spine program to become a
10
1.3 Profiles
spine fellow. Once again, I was very fortu- much of what our trainees learn today will
nate to make an excellent decision. Having be abandoned for new approaches or whole
spent the past 2+ decades performing com- new areas will open for surgical interven-
plex surgery, and training a large number of tion. So, if you like continuous learning and
superb neurosurgery residents during this change, neurosurgery is the specialty for
time, has been the best decision I have ever you. Finally, what we do as neurosurgeons
made. I would not trade the career in neuro- has huge implications for our patients and
surgery for any other job in this world. I am their families, both positive and negative.
also completely confident that our wonder- There is no higher high nor lower low than
ful profession will continue to attract the the surgical results in Neurosurgery—a neu-
“best and brightest” to enter into the rapidly rosurgeon must possess equanimities.
expanding field of medicine that enables us Always remember: do no harm.”
to do more positive things for our patients
than any other field in medicine.”
Pearls
M Sean Grady, MD
Charles Harrison Frazier Professor of • It is important to prepare early during
Neurosurgery medical school to build a competitive
Chairman, Department of Neurosurgery neurosurgery residency application.
Perelman School of Medicine • IMG applicants should focus on
University of Pennsylvania expanding their research portfolio
Philadelphia, Pennsylvania and developing relationships with
senior neurosurgery faculty in order
“Entering medical school at George- to enhance their chances for
town, I was unsure of what specialty I might matching.
ultimately choose. I was fascinated by Anat- • Sub-interns should always exhibit
omy and challenged by Neurosciences so Affability, Availability, and Account-
felt, upon starting clinical rotations that ability towards patients and
somewhere in the field of surgery would lie colleagues.
my future. A 2-week rotation on the Neuro- • USMLE Step 1 scores, research
surgery service set my career for the next 35 accomplishments, and letters of
years. Unlike other services, I would enthu- recommendation will help to secure
siastically spend all day and night taking interviews.
care of the patients, being in the operating • Letters of recommendation and
room and reading and learning nonstop. It interpersonal skills influence
was phenomenally exciting and I now real- applicant rank order.
ize that level of commitment is the hallmark
for someone interested in a career in Neuro-
surgery. It is an enormously rewarding and
at the same time incredibly humbling career References
in which I thought then and know now that [1] The American Board of Neurological Surgeons.
I would be an eternal student. In my training 2017. [online] Available from: http://www.abns.
org/. Accessed April, 2017
at the University of Virginia from 1981 to
[2] Accreditation Council for Graduate Medical Educa-
1987, I never saw a MRI; there was no endo- tion. 2018. [online] Available from: https://www.
vascular neurosurgery, endoscopic neuro- acgme.org/. Accessed July, 2018
[3] National Resident Matching Program. Charting
surgery, major spine instrumentation, or
Outcomes in the Match for U.S. Allopathic Sen-
deep brain stimulation, to name just a few iors, 2018. National Resident Matching Program.
advances in the field. I am most certain that Washington, DC; 2018
11
[4] National Resident Matching Program. Results and [11] Student Research Fellowships. 2017. [online] Avail-
Data: 2018 Main Residency Match®. National Resi- able from: http://alphaomegaalpha.org/student_
dent Matching Program, Washington, DC; 2018 research.html. Accessed March, 2018
[5] National Resident Matching Program. Charting Out- [12] Fellowships & Awards. 2017. [online] Available
comes in the Match for International Medical Grad- from: http://www.csnsonline.org/fellowship_goals.
uates, 2018. National Resident Matching Program. php. Accessed March, 2017
Washington, DC; 2018 [13] Medical Research Scholars Program. 2017. [online]
[6] National Resident Matching Program, Data Release Available from:https://clinicalcenter.nih.gov/training/
and Research Committee. Results of the 2018 NRMP mrsp/. Accessed March, 2018
Program Director Survey. National Resident Match- [14] Medical Research Fellows Program. 2017. [online]
ing Program, Washington, DC; 2018 Available from: https://www.hhmi.org/developing-
[7] Neurosurgery Match. 2017. [online] Available from: scientists/medical-research-fellows-program.
http://www.neurosurgerymatch.org/. Accessed April, Accessed March, 2017
2017 [15] Visitor Visa. [online] Available from: https:
[8] Kashkoush A, Prabhu AV, Tonetti D, Agarwal N. The //travel.state.gov/content/visas/en/visit/visitor.
neurosurgery match: a bibliometric analysis of html. A
ccessed March, 2018
206 first-year residents. World Neurosurg. 2017; [16] Cousteau V. How to swim with sharks: a primer.
105:341–347 Perspect Biol Med. 1987; 30:486–489
[9] Agarwal N, Norrmén-Smith IO, Tomei KL, Prestig- [17] Hubbard E. A message to Garcia. 1899
iacomo CJ, Gandhi CD. Improving medical student [18] Agarwal N, Choi PA, Okonkwo DO, Barrow DL,
recruitment into neurological surgery: a single Friedlander RM. Financial burden associated with
institution’s experience. World Neurosurg. 2013; the residency match in neurological surgery. J Neu-
80(6):745–750 rosurg. 2017; 126(1):184–190
[10] Grants and Fellowships. 2017; http://www.aans. [19] How the Matching Algorithm Works. 2017. [online]
org/Grants and Fellowships.aspx. Accessed March, Available from: http://www.nrmp.org/match-process/
2018 match-algorithm/. Accessed March, 2017
12
2 History of Neurological Surgery
Edward G Andrews, Chandranath Sen
2.1 Introduction civilizations of the Inca and Egyptians to

the medical world of 19th-century
Before the dawn of the 20th century, the Europe and United States. It was not until
tools available to medical practitioners, the late 19th century with the advent of
in particular surgeons, made operating anesthesia, antisepsis, and the ability to
on the central nervous system virtually localize lesions in the brain successfully
impossible except in the most rudimen- that neurosurgery could blossom. This
tary of applications. Advances developed chapter provides a historical timeline of
slowly, with the techniques and instru- advancements in the field of neurological
ments changing little from the incipient surgery (▶Fig. 2.1).
Fig. 2.1 Neurosurgical timeline.
13
History of Neurological Surgery
2.2 The Pre-Cushing Era

2.2.1 Paleolithic
Neolithic skulls with round or ovoid perfora-
tions recovered from prehistoric settlements
in France date back as early as 8000 BC. These
perforations were initially thought to be a
product of trauma, but the lack of any classi-
cal signs of trauma, such as associated frac-
tures, argued that these they were in fact
intentional. There is proof that Neolithic
man, inspired by magical or religious beliefs,
made postmortem “diskettes” from cadaver
skulls to wear as amulets.1 Nevertheless,
there are also data that suggest some of these
openings were made while the patient was
still living. The scarred margins at the wound
edges indicate healing had occurred before
the death of the patient, and therefore, the Fig. 2.2 Surgeon’s trephining kit from
perforations could have indeed been practi- the mid-1700s. (Image has been provid-
cal attempts at surgical intervention. Regard- ed courtesy of Science Museum, London.)
less of his motivation, Neolithic man made
holes in the skull by tedious scraping with At this stage, the prehistoric technique of
flint or obsidian to create a gradual depres- shaving bone evolved into a technique that
sion or to carve intersecting lines that formed involved cutting a c ircular groove and lift-
a rudimentary rectangular bone flap.2 ing the bone flap off, which then metamor-
phosed into the more efficient circular
crown saw, or “trupanon” drill, referenced
2.2.2 Ancient by Hippocrates.1,2 This was the t rephining
Archaeologists have found skulls with drill in its simplest form (▶Fig. 2.2).
craniotomies similar to those of their pre-
historic predecessors in burial sites of the
2.2.3 Classical
ancient Incans and Egyptians as well. The
Egyptians in particular documented exten- While these ancient civilizations all even-
sively their medical practices, outlined best tually faded into the background, the
in the Edwin Smith papyrus, the world’s trephine remained as the prime fixture in
oldest known surgical treatise dating back the neurosurgical armamentarium. There
to the 17th century BC. Its author, Imhotep, were modifications made to this design
discusses treatments of cranial wounds and that allowed accessing the intracranial
fractures with a twist drill wrapped in a space quicker and more efficient, but little
bowstring, with the backward and for- progress beyond this tool occurred over
ward motion of the bow spinning the drill.3 the centuries as this surgical option was
It was not until the age of the Greeks and often avoided at all costs due to significant
the arrival of Hippocrates, however, that rates of infectious complications.1,4 This
craniotomy was first codified as a surgical changed in the mid-to-late 1800s with the
treatment in the H
ippocratic works Corpus advent of antisepsis and aseptic technique.
Hippocraticum and On Wounds in the Head. Trephination was suddenly back in vogue
14
2.3 The Cushing Era
and, as a result, rapid innovation in neuro- with Sir William Gowers, who himself was
logical surgery would ensue. known for the successful evacuation of an
intracerebral abscess in 1886. Horsley was
one of the primary early influences on the
The Pre-Cushing Generation
treatment of trigeminal n euralgia, for which
For neurological surgery to emerge as a he achieved pain relief by sectioning the
specialty in the 20th century, a handful of posterior root of the trigeminal nerve. Last
physicians needed to lay the foundation for but not least of his accomplishments, he
its arrival with three important medical was the first to operate on the pituitary
discoveries: general anesthesia, antisepsis, gland in 1889, although Schloffer was the
and cerebral localization. first to clearly document the successful
• Anesthesia: William T.G. Morton, a den- removal of a pituitary tumor in 1907.5,6
tist, introduced ether in 1842 and William Macewen was a contemporary of
James Y. Simpson, an obstetrician, intro- Horsley’s based in Glasgow. While he was a
duced chloroform in 1857. latecomer to neurosurgery with his first
• Antiseptic: Ignaz Semmelweiz, a case recorded in 1876, he was no less
Hungarian physician and obstetrician,
impactful as he is among the earliest to doc-
demonstrated that handwashing with ument successful removal of a brain
chlorinated lime before delivery reduced tumor (meningioma) in 1879.1,5,7,8 He was
postpartum fever in the mother. Joseph followed by Franceso Durante, who had
Lister, in 1867, designed an antiseptic striking success removing an orbital groove
treatment of wounds that involved car- meningioma in 1885. To wit, the patient
bolic acid.5 was still alive 10 years after s urgery unlike
• Cerebral localization: Gustav Fritsch Macewan’s patient who succumbed to his
and Eduard Hetzig used electrical stim- disease and surgical wounds shortly after
ulation on the precentral gyrus to de- his operation. Other notable surgeons of the
fine function in wounded soldiers with pre-Cushing era included the following:
traumatic brain injuries in 1870. Pierre • William Detmold: the first to open the
Paul Broca, who was one of the first to lateral ventricle to evacuate a cerebral
trephine for removal of a cerebral ab- abscess in 1850.
scess, identified the left pars opercularis • Richman Godlee and Hughes Bennett:
and pars triangularis in 1861 as the first resection of glial neoplasm in 1884.
source of expressive aphasia. Carl Wer- While considered a success, the patient
nicke mapped receptive aphasia to the died from intracranial infection 28 days
posterior aspect of the left superior after surgery.4
temporal gyrus almost a decade later in • William W. Keen: Philadelphia-based
1874. Additional notable contributions surgeon who was the first to success-
came from neurologists Hughlings Jack- fully resect a brain tumor in the United
son, David Ferrier, Gowers, and Charcot. States in 1891.
A new era of experimentation and inven- • Charles Ballance: performed one of the
tion dawned once neurosurgery could earliest reported cases of acoustic neu-
occur at the leisure of the surgeon with the roma removal.
above p erquisites in place. Quickly, the list
of “firsts” grew. Sir Victor Horsley was
among the preeminent neurosurgeons
2.3 The Cushing Era
prior to Cushing. One of his most notable Harvey Cushing is arguably the most influ-
achievements was the successful resection ential neurosurgeon to date, which has
of a spinal cord tumor in 1888 in association earned him the reverent moniker of the
15
“Father of Neurosurgery.” He was famous his temporal and suboccipital decompres-

for his rigorously perfected technique. One sion for relief of high intracranial pressure,
of his critical inventions was epoch making which he used for palliation in the event of a
by addressing the problem of hemorrhage. nonresectable tumor. After the First World
Cushing’s silver clip, which he introduced in War, he outlined the management of pene-
1911, made hemostasis possible (▶Fig. 2.3). trating head trauma based on his experi-
Similarly, his solution to increased intracra- ences as a surgeon for the army. In 1927,
nial pressure during surgery was ground- Cushing adapted Bovie’s electrocoagulator
breaking when he first described the use of to neurosurgery, initially using it for piece-
lumbar puncture to relax the brain intraop- meal removal of brain tumors (▶Fig. 2.4).10
eratively in 1908. Prior to his arrival, the He removed his first pituitary for a
cromegaly
mortality associated with neurosurgery
was estimated around 50% or higher despite
antisepsis.9 Cushing’s mortality rate, how-
ever, was unprecedented: 8.4% for brain
tumor surgeries and around 10% for pitu-
itary surgeries, at a time when mortality for
the latter was almost 75%.10
Some additional examples highlighting
his contributions to neurosurgery include
Fig. 2.4 Bovie electrocoagulator.

Fig. 2.3 Cushing’s silver clip with (Reproduced from Vender J, Effect of
applicator kit. (Reproduced, with per- hemostasis and electrosurgery on the
mission, from Horrax G, Some of Harvey development and evolution of brain
Cushing’s contributions to neurologi- tumor surgery in the late 19th and
cal surgery, J Neurosurg. 1981;54(4): early 20th centuries, Neurosurg Focus.
436–447.) 2005;18(4):1–7.)
16
2.5 Instrumentation
in 1909 using Schoffler’s transsphenoidal

approach. Oscar Hirsch, a Viennese otolar-
yngologist, subsequently modified this tech-
nique in 1910 to the classic and now
commonly used endonasal transsphenoidal
approach.5
Other significant members of the neu-
rosurgical field at this time included
Charles Frazier, known for his treatment of
trigeminal neuralgia by division of the sen-
sory root instead of entire extirpation of
the gasserian ganglion as Cushing pro-
Fig. 2.5 Harrington’s rod system.
posed, and Emil T. Kocher, a large figure in
the operative treatment of epilepsy as well
(Reproduced from Vialle L, Berven S,
as spinal and cranial trauma.11 Walter de Kleuver M, AOSpine Master Series,
Dandy, a prolific contemporary of Vol. 9: Pediatric Spinal Deformities,
Cushing’s, is credited with discovering the ©2017, Thieme Publishers, New York.)
function of choroid plexus in 1914, the
third ventriculostomy in 1920, and the to its myriad complications like dural com-
first cerebral aneurysm clipping in 1937.12 promise and need for an concomitant
external brace. Eduardo Luque modified
Harrington’s approach in 1976 with his
2.4 Spinal Neurosurgery own Luque rod system, which used long
contoured rods affixed with sublaminar
Similar to its cranial counterpart, spinal wires.15 This signaled the arrival of
surgery was hamstrung by infection until three-column fixation with the transpe-
the advent of antisepsis in the closing dicular screw, a significant step toward
decades of the 1800s. With effective anti- modern techniques. Michele and Krueger
sepsis, the neurosurgeons of the pre- first described pedicle screw fixation in
Cushing and Cushing eras developed 1949, but it was not until the 1960s that
durable solutions to spine pathologies that this fixation technique established its
had been difficult to address previously. dominance as the main approach for pos-
Macewen performed the first recorded terior fixation.15 The surgeons responsible
laminectomy in 1886 and Menard per- for its rise in popularity and codification
formed the first costotransversectomy in were Roy- Camille in 1970, followed by
the opening years of the 20th century.13 Arthur D. Steffee in the United States with
Fritz Lang was the first to fix the spine pos- the development of his variable plating
teriorly in 1909 by tethering celluloid rods system and the Steffee screw (▶Fig. 2.6 and
with silk thread and steel wires adjacent to ▶Fig. 2.7).16,17
the spinous processes. Spinal fixation,
however, did not further progress until
Paul Harrington developed his eponymous
rod system in 1953, which became a means
2.5 Instrumentation
to stabilize the spine in multiple patho- The accomplishments of the above s urgeons
logic contexts such as traumatic injury, would not have been possible without the
degenerative disease, and deterioration long history of invention not only from
from neoplastic processes (▶Fig. 2.5).14,15 It their compatriots, but also from the innova-
was ultimately short-lived, however, due tive thinking of other pioneers of surgery
17
and even visionaries outside of medicine. A

summary of these remarkable achieve-
ments is catalogued chronologically below.
• 1851: Hermann von Helmholtz invented
the ophthalmoscope, introducing the fun-
doscopic examination and a helpful tool
in diagnosing intracranial mass lesions.
• 1876: Saemisch, a German surgeon, was
the first to wear loupes while operating.
• 1885: James L. Corning performed the
first lumbar puncture, but it was not used
in practice as a diagnostic and therapeu-
tic tool until 1891 by Heinrich Quincke.
• 1892: Sir Victor Horsley introduced an
Fig. 2.6 Pedicle screw plate fixation antiseptic wax in 1892 to control diploic
system designed by Roy-Camille made bleeding and to achieve hemostasis, al-
from cobalt-chromium. (Repro- though there is evidence that Henri
duced from Kabins MB, Weinstein JN, Dolbeau, a Parisian surgeon, first used
The history of vertebral screw and bone wax in 1864 during extirpation of
pedicle screw fixation, Iowa Orthop J. a frontal osteoma.18
1991;11:127–136.) • 1895: Wilhelm Röentgen invented X-ray-
based radiography, which subsequently
bears his name (roentgenography).
Craniography and spondylography were
created once Röentgen’s idea was adapted
to the needs of neurological surgery.
• 1898: Leonardo Gigli adapted his famous
saw for cranial surgery by creating a
curved wire that would not damage the
dura during formation of the bone flap.19
• 1908: The electric drill replaced
hand-powered trephining after Thierry
de Martel’s improvement upon the de-
sign of the foot-powered drills that den-
tists were using. That same year, German
neurosurgeon Fedor Krause introduced
an electrical suction for use in surgery,
which Cushing improved upon in 1920.20
• 1911: Cushing introduces silver clips for
hemostatic control (▶Fig. 2.3).
• 1918: Walter Dandy invented pneu-
moventriculography, and pneumoen-
cephalography the following year in
1919. In these studies, he injected air into
the patient’s cerebrospinal fluid (CSF)
spaces before shooting a craniograph,
Fig. 2.7 Steffee, or variable screw
outlining the ventricular system and
placement, system.
subarachnoid territories (▶Fig. 2.8).
18
2.5 Instrumentation
• 1920: William T. Bovie, a plant physiolo- • 1921: Jean-Athanase Sicard injected a

gist, invented his famous electrocoagu- contrast dye, lipiodol, into the CSF areas as
lator, which used electric current to Dandy had done with air, which was then
produce focused intense heat. Cushing followed by an X-ray. His experiments
applied this invention to his surgical produced the first m yelogram (▶Fig. 2.9).
practice in 1927 (▶Fig. 2.4).21,22 Carl Nylén also designed and built the
Fig. 2.8 Pneumoencephalog-

raphy and pneumoventricu-
lography pioneered by Walter
Dandy. (Reproduced, with
permission, from Rover RL,
et al, Progressive ventricular
dilation following pneumoen-
cephalography: a radiological
sign of occult hydrocephalus,
JNS. 1972;36(1):50-59.)
Fig. 2.9 X-ray myelography as engineered by Sicard. (Reproduced, with permission

from Mason MF, Raaf J, Complications of pantopaque myelography, J Neurosurg.
1962;19:302–311.)
19
world’s first surgical microscope in this • 1947: Speigel and Wycis report the first
year, which he used for the first time for a human use of a stereotactic apparatus to
case of chronic otitis media. It was up- target intracranial lesions, laying the
graded from monocular to binocular in foundation for frame-based stereotactic
1922 by Gunnar Holmgren, a Swedish brain biopsies.27
otolaryngologist.23 • 1951: Lars Leksell coins the term
• 1924: Hans Berger develops the electro- “stereotactic radiosurgery”28 and there-
encephalogram (EEG), building on the after develops the first Gamma Knife in
work of Fritsch and Hetzig. He first used 1967 for the treatment of trigeminal
his EEG during a neurosurgical operation neuralgia.
on a 17-year-old boy by Nikolai Guleke.24 • 1953: Paul Harrington develops his rod
• 1927: A. Egas Moniz adapted the previ- system for posterior spinal fixation and
ous two techniques from Dandy and fusion.
Sicard to intracranial vasculature, thus • 1955: Leonard Malis develops bipolar
inventing cerebral arteriography coagulation by using fine-tip jeweler’s
(▶Fig. 2.10). forceps.29
• 1944: Franc Ingraham and Orville Bailey • 1957: Theodore Kurze became the first
discover the hemostatic utility of fibrin neurosurgeon to use a microscope
foam, a product prepared by fraction- during surgery.
ation of human plasma, and the duralike • 1960s: A revolution was underway in
nature of fibrin film. Cohn and col- neurosurgery with the microscope at its
leagues were simultaneously working center. Contributors to its development
on a similar product made from frac- included R.M.P. Donaghy, Julius
tionated plasma called Gelfoam.25,26 Jacobson, Ernesto Suarez, M.G. Yasargil,
and Harold Buncke, a plastic surgeon.
Jacobson was also the leader in early

microsurgical instrumentation, credited
with creating the original microneedle
holder and microscissors.
• 1970s–1980s: The advent of computed
tomography (CT) in the early 1970s and
the emergence of magnetic resonance
imaging (MRI) in the later 1970s
provided the ability to visualize the

brain and gave neurosurgeons the op-
portunity to target tumors or perform
functional lesions to restore function.
The first CT and first MRI applied to pa-
tients were in 1971 and 1977
Fig. 2.10 Moniz’s cerebral arteriogra-
respectively.30
phy adapted from Dandy and Sicard’s
techniques for visualization of cranial • 1988: L. Dade Lunsford installs the first
Gamma Knife in the United States.31
and spinal cerebrospinal fluid spaces.
Gamma Knife offers noninvasive
(Reproduced, with permission, from
alternative treatment for a variety of in-
Lobo Antunes, J. Egas Moniz and
tracranial targets.
cerebral angiography, J Neurosurg.
1974;40:427–32.) • 1990s: Ken Winston and Wendell Lutz
adapt radiosurgery to linear accelera-
20
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tions to neurological surgery. J Neurosurg. 1981;
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intensity modulation, allowing for three odor Kocher: valve surgery for epilepsy. Epilepsia.
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dimensional shaping of radiation.33 [12] Greenblatt SH, Dagi TF, Epstein MH. A history of
• 2000s: The rod-lens endoscope is re- neurosurgery in its scientific and professional con-
fined and coupled to minimally invasive texts. Park Ridge, IL: American Association of Neu-
rological Surgeons; 1997
image-guided approaches to the [13] Knoeller SM, Seifried C. Historical perspective: his-
parasellar region, lowering morbidity tory of spinal surgery. Spine. 2000; 25(21):2838–
and length of hospital stay for tumors 2843
[14] Mohan AL, Das K. History of surgery for the correc-
previously requiring lengthy transcra-
tion of spinal deformity. Neurosurg Focus. 2003;
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significant postoperative morbidities [15] Singh H, Rahimi SY, Yeh DJ, Floyd D. History of pos-
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[16] Vaccaro AR. Fractures of the cervical, lumbar, and
Pearls
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[17] Kabins MB, Weinstein JN. The history of vertebral
screw and pedicle screw fixation. Iowa Orthop J.
• Among the titans of neurosurgery 1991; 11:127–136
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contributors to remember. [19] Goodrich JT. A millennium review of skull base sur-
• Prior to the late 1800s, neurosurgery gery. Childs Nerv Syst. 2000; 16(10–11):669–685
[20] Lichterman B. The factors of emergence of neu-
advanced little and was limited to the rosurgery as a clinical specialty. Hist Med. 2014;
simple technique of trephining for 2(2):37–51
cranial access. Spine surgery was [21] de Divitiis E. Development of instrumentation in
neurosurgery. World Neurosurg. 2011; 75(1):12–13
almost out of the question, given the [22] O’Connor JL, Bloom DA. William T. Bovie and elec-
rates of infection. trosurgery. Surgery. 1996; 119(4):390–396
[23] Kriss TC, Kriss VM. History of the operating
microscope: from magnifying glass to microneu-
rosurgery. Neurosurgery. 1998; 42(4):899–907
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Otorhinolaryngol Ital. 2007; 27(3):151–156 [25] Ingraham F, Bailey O, Nulsen F. Studies on fibrin
[2] Gross C. A hole in the head. Neuroscientist. 1999; foam as a hemostatic agent in neurosurgery, with
5(4):263–269 special reference to its comparison with muscle.
[3] El Gindi S. Neurosurgery in Egypt: past, present, J Neurosurg. 1944; 3:171–181
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[4] Calvert CA. The development of neurosurgery. Lan- 28(3–4):444–450
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[5] Maroon JC. Skull base surgery: past, present, and ic apparatus for operations on the human brain.
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[6] Pascual JM, Prieto R, Mazzarello P. Sir Victor Hors- [28] Leksell L. The stereotaxic method and radiosurgery
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[7] Macmillan M. William Macewen [1848–1924]. [29] Yaşargil MG. Personal considerations on the his-
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21
[31] Lunsford LD, Flickinger J, Lindner G, Maitz A. Ste- [33] Carol M, Grant WH, III, Pavord D, et al. Initial
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[32] Winston KR, Lutz W. Linear accelerator as a 66(1–3):30–34
neurosurgical tool for stereotactic radiosurgery.

Neurosurgery. 1988; 22(3):454–464
22
3 Neurological Examination
Prateek Agarwal, Daniel Y Zhang, M Sean Grady
3.1 Introduction 3.3 Cranial Nerves

Historically, the neurological examination The integrity of a cranial nerve (CN) can be
was the primary method by which neuro- determined by quickly assessing its respec-
surgeons evaluated a patient’s neurologic tive function (▶Table 3.4).
status, determined anatomic sites of dys-
function, and deduced the underlying
pathology. Today, however, outpatients 3.3.1 CN I
often arrive at the clinic with laboratory
CN I is rarely tested in clinical practice, but
testing, electrophysiological studies, imag-
can be tested by having the patient identify
ing, prior evaluation by a neurologist or
common odors in one nostril at a time (e.g.,
primary care provider, and even an estab-
coffee, vanilla).
lished diagnosis. Thus, in practice, neuro-
surgeons use a focused and selective
neurological examination to corroborate 3.3.2 CNs II and III
pathology identified by other diagnostic
modalities and assess the functional status The examiner should have the patient
of the patient. Similarly, for inpatients, the cover one eye at a time while covering his
neurological examination is a rapid and or her own contralateral eye. The exam-
cost-effective first-line assessment for iner should then hold up some fingers in
tracking patient progress and assessing the most peripheral areas of the visual
acute changes. This chapter summarizes fields and ask the patient to identify how
key elements of the neurological many fingers are held up. Monocular
examination. vision loss localizes anterior to the chi-
asm, bitemporal hemianopia localizes to
the crossing fibers of the chiasm, and
3.2 Mental Status homonymous hemianopia/quadrantano-
pia localizes posterior to the chiasm (see
This chapter offers a brief overview of the
▶Fig. 18.1). Acuity can be tested using a
mental status examination (MSE), which is
hand-held visual acuity card one eye at a
an important tool in assessing functional
time.
and cognitive deficits (▶Table 3.1). This
can be important in evaluating a patient
with dementia; and from a neurosurgical
Funduscopic Examination
perspective, the MSE may help localize a
lesion to cortical regions of the cerebral The funduscopic examination is performed
cortex (frontal, parietal, temporal, and using an ophthalmoscope in darkness and
occipital lobes), which are regions of ideally with the patient’s pupil dilated. One
higher cognitive function. Importantly, if should generally observe a red reflex
level of consciousness (▶Table 3.2) and (reddish-orange reflection off retina), the
language (▶Table 3.3) are not intact, other margins and size of the optic disc, retinal
elements of the MSE cannot be accurately vessel abnormalities, and retinal lesions
assessed. (e.g., hemorrhages, exudates).
23
Neurological Examination
Table 3.1 Mental status examination for neurosurgeons

Elements Assessment Descriptors
Level of GCS, FOUR score Alert, attentive, vigilant, drowsy,
consciousness lethargic, fluctuating, confused,
unresponsive, asleep
Orientation “What is your full name?” Oriented to person, place, and time
“Where are we?”
“What is todays' date?”
Attention Subtracting serial 7s from Intact/impaired
100, spell “world” backwards
Language Fluency, repetition, naming, Fluency: Quantity, rate, rhythm
comprehension, reading/ Repetition: Able to repeat phrases
writing
Naming/comprehension: able to name
high/low frequency objects, able to
follow simple/complex commands
Reading/writing: Intact/impaired
Perceptual Perceptions of environment, Hallucinations, illusions, depersonali-
disturbances perceptions of self zation, derealization
Memory and Immediate, recent, and Intact/impaired
cognition remote memory (5-min
delayed recall of 3 items)
MMSE, Mini-Cog, MoCA,
clock-drawing test
Abbreviations: FOUR, Full Outline of Un Responsiveness; GCS, Glasgow Coma Scale;
MMSE, mini mental state examination; MoCA, Montreal Cognitive Assessment.
Table 3.2 Glasgow Coma Scale grading scale

Glasgow Coma Scale Response Score
Eye opening Spontaneous 4
Response to verbal command 3
Response to pain 2
No eye opening 1
Verbal response Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
No verbal response 1
Motor response Obeys commands 6
Localize to pain 5
Withdraw to pain 4
Flexion to pain 3
Extension to pain 2
No motor response 1
24
3.3 Cranial Nerves
Table 3.3 Aphasia syndromes and the associated locations of pathology

Syndrome Fluency Repetition Compre- Reading Writing Localization
hension
Broca's - - + + - Broca's area
Wernicke's + - - - - Wernicke's area
Anomic + + + +/- +/- Temporal,
parietal, and
occipital regions
of the cortex
outside of clas-
sical language
areas
Conduction + - + + +/- Arcuate fasciculus
Transcorti- - + + + - Left mesial fron-
cal motor tal, supplemen-
tary motor area
Transcorti- + + - - - Left posterior
cal sensory watershed
zone between
MCA and PCA
territories
Transcorti- - + - - - Anterior and
cal mixed posterior water-
shed zones
Global - - - - - Vast region of
the left hemi-
sphere
Pure word + + - + + Left or bilateral
deafness superior tempo-
ral gyrus lesion
Pure alexia + + + - + Left occipital
lobe with
involvement
of splenium of
corpus callosum
Aphemia - + + + + Motor cortex
outflow to
articulars
Pure + + + + - Left inferior
agraphia frontal region
Abbreviations: MCA, middle cerebral artery; PCA, posterior cerebral artery.
25
Table 3.4 Cranial nerves and their functions

Cranial Nerve Function
I (Olfactory) Sensory: Olfaction
II (Optic) Sensory: Vision
III (Oculomotor) Motor: Extraocular muscles, levator palpebrae superioris
Parasympathetic: Pupillary constrictor, ciliary muscles
IV (Trochlear) Motor: Extraocular muscle (superior oblique)
V (Trigeminal) Sensory: Sensation of the face, cornea, nasal and oral cavities,
anterior 2/3 of the tongue
Motor: Muscles of mastication, tensor tympani
VI (Abducens) Motor: Extraocular muscle (lateral rectus)
VII (Facial) Sensory: Taste of anterior 2/3 of tongue
Motor: Muscles of facial expression, stapedius
Parasympathetic: Salivary and lacrimal glands
VIII (Vestibulocochlear) Sensory: Hearing, vestibular system
IX (Glossopharyngeal) Sensory: Sensory and taste of the posterior 1/3 of tongue,
pharynx
Motor: Stylopharyngeous
Parasympathetic: Salivary glands
X (Vagus) Sensory: Pharynx, larynx, thoracic, and abdominal viscera
Motor: Soft palate, pharynx, larynx
Parasympathetic: Cardiovascular, respiratory, gastrointestinal
XI (Accessory) Motor: Sternocleidomastoid, trapezius
XII (Hypoglossal) Motor: Tongue muscles
Pupillary Light Reflex suggests an afferent pupillary defect

(APD) whereby CN II of the eye with the
The pupillary light reflex simultaneously larger pupil is not intact.
tests CNs II and III, as CN II senses incom-
ing light and parasympathetic fibers run-
ning along the outside of CN III stimulates
3.3.3 CNs III, IV, and VI
the pupillary constriction both in the
ipsilateral eye (direct reflex) and in
Eye Movements
the contralateral eye (consensual reflex). The examiner should first observe for any
The examiner should shine light directly ptosis, eye deviation, and nystagmus
onto one eye and observe whether both (involuntary eye movements) at baseline.
pupils constrict equally, and then test the Then, the examiner should have the
other eye in the same manner. If the patient follow his or her finger to make an
examiner swings the penlight back and “H” in space and observe if either eye is
forth between eyes, and one pupil is unable to fully move in a particular direc-
consistently larger than the other, this
tion or if any nystagmus is elicited.
26
3.3 Cranial Nerves
Classic nerve palsies include CN III patient’s forehead (V1 ophthalmic divi-

palsy (“down and out”) in which the sion), cheeks (V2 maxillary division), and
affected eye cannot be raised or adducted, chin (V3 mandibular division). The exam-
CN VI palsy in which the affected eye iner should have the patient close both
cannot be abducted, and CN IV palsy in eyes and ask if light touch or pinprick feels
which the affected eye cannot look “in the same on both sides and probe for any
and down” (e.g., going down stairs, read- pain, paresthesias, or numbness in each of
ing a book). Another classic finding is an the three divisions.
internuclear ophthalmoplegia (INO) as a
result of medial longitudinal fascicu-
lus (MLF) damage in which the affected Muscles of Mastication
ipsilateral eye cannot adduct when it
To test the muscles of mastication, the
attempts to gaze contralateral relative to
examiner should have the patient open the
the affected eye.
jaw and close the jaw against resistance as
well as move the chin laterally on both
sides.
Vestibulo-ocular Reflex
The vestibulo-ocular reflex (VOR)
assesses the integrity of both CN VIII and 3.3.5 CN VII
two nerves that control extraocular mus-
cles (CNs III and VI) simultaneously Facial Strength
because activation of the vestibular sys-
Facial strength can easily be assessed by
tem through head movement in one
having the patient shut the eyes tightly,
direction produces eye movement in the
smile, and puff out the cheeks. The exam-
other direction, thereby enabling the
iner can also observe more subtle signs of
eyes to remain fixed on a target. The VOR
facial weakness such as mild facial droop,
can also be elicited via cold-caloric test-
nasolabial fold flattening, drooling, or
ing, especially during a brain death
dysarthria. With regards to CN VII, a cen-
examination, which mimics head move-
tral lesion will affect the contralateral
ment away from the ear in which cold
lower half of the face but spare the fore-
water is infused. Intact brainstem func-
head, whereas a peripheral lesion will
tion is indicated by eyes moving toward
affect the entire ipsilateral face.
the ipsilateral ear, while intact cortical
function is indicated by contralateral
horizontal nystagmus. It should be noted Blink-to-Threat
that if voluntary eye movement is
impaired, but the VOR is intact, this Blink-to-threat is generally reserved for
points to a supranuclear gaze palsy stem- the patient with depressed consciousness
ming from a lesion above the brainstem. or aphasia. It simultaneously tests CNs II
and VII, as CN II transmits visual informa-
tion from a threat, whereas CN VII controls
3.3.4 CN V blinking. The examiner should flick his or
her fingers near the lateral edge of each eye
Facial Sensation and observe for blinking, being careful not
to stimulate the corneal reflex (CNs V and
Facial sensation can initially be tested VII) with excessive air movement or actu-
using light touch or pinprick testing on the ally touching the cornea.
27
3.3.6 CN VIII response to stimulating the oropharynx

with a cotton swab on either side is
Vestibular Function compared.
The VOR via head movement and cold-

caloric testing can be assessed to evaluate Tongue Movement
the integrity of CN VIII. The presence of
nystagmus that suppresses with visual fix- The patient should protrude the tongue
ation and is not direction-changing also and move it laterally in both directions as
suggests a peripheral CN VIII lesion that is well as superiorly and inferiorly. In addi-
affecting vestibular function. tion, the examiner should have the patient
push the tongue against the inside of the
cheek on both sides with resistance from
Hearing Function the examiner pushing on the outside of the
cheek. A CN XII lesion may result in ipsilat-
The examiner can grossly assess hearing by eral tongue deviation.
rubbing his or her fingers together close to
the patient’s ear while the patient’s eyes are
closed. The Weber and Rinne tests using a Dysarthria
512 Hz tuning fork may provide a more
detailed assessment to distinguish between Lesions of these nerves may result in dys-
sensorineural and conductive hearing loss. arthria, which is a disorder of speech pro-
duction rather than language. Verbal
articulation may be tested with the follow-
3.3.7 CN XI ing phrases: “no ifs, ands, or buts”, “base-
ball player”, and “fifty-fifty.”
Strength of the sternocleidomastoid is tested
by asking the patient to rotate the head
against resistance (hand pushing on chin).
Strength of the trapezius is tested by asking
3.4 Motor Examination
the patient to shrug the shoulders against
resistance (hands pushing on shoulders).
3.4.1 Bulk
The motor examination should begin with
an inspection of muscle bulk, looking for
3.3.8 CNs IX, X, and XII symmetry, atrophy, and fasciculations,
which are random, spontaneous, and
Palatal Movement involuntary muscle twitches.
The examiner should instruct the patient
to open the mouth and say “ahhh”, observ-
ing for symmetric upward movement of 3.4.2 Tone
the palate as well as the absence of uvula
Muscle tone refers to residual tension in a
deviation. A CN X lesion may result in con-
relaxed muscle, which often manifests as
tralateral uvula deviation.
the resistance to passive stretch in a
relaxed muscle. In order to accurately
Gag Reflex assess tone, the patient must relax the
muscles and allow the examiner to move
If the examiner requires more information, them passively.
a gag reflex can be performed to simulta- Hypertonia is further described as
neously assess CNs IX and X, whereby the spastic or rigid. Spasticity is seen when a
28
3.4 Motor Examination
limb is moved quickly, the tone increases each movement is performed with the
and more force is required to move the relevant joint stabilized, such that muscles
limb further. This is often tested with pas- and the nerves that innervate them are
sive foot dorsiflexion. In contrast, increased tested in isolation (▶Table 3.5). If a patient
tone in rigidity does not depend on how is unable to overcome any resistance, the
fast the muscle is moved. Cogwheel rigid- examiner should have the patient perform
ity is characterized by rhythmic, jerky the movements without resistance both
increased tone during passive motion, against gravity and in a plane that
whereas lead-pipe rigidity is characterized eliminates the effect of gravity in order to
by continuous increased tone during pas- appropriate grade strength (▶Table 3.6).
sive motion.
Subtle Weakness
3.4.3 Strength
Drift
When testing muscle movements, the
examiner should have the patient resist In clinical practice, drift can refer to either
the examiner as he or she attempts to simple extremity drift or pronator drift.
move a certain limb. It is important that Extremity drift refers to an extremity
Table 3.5 Major muscles and their associated movements and innervation
Spinal Peripheral nerve Movement Major muscle(s)
cord level
Upper C5 Axillary nerve Shoulder Deltoid
extremities abduction
C5–C6 Musculocutaneous Elbow flexion Biceps
nerve
C7 Radial nerve Elbow extension Triceps
C7–C8 Median and ulnar Wrist flexion Flexor carpi radialis,
nerves flexor carpi ulnaris
C7 Radial nerve Wrist extension Extensor carpi radi-
alis brevis, extensor
carpi radialis longus,
extensor carpi ulnaris
C7 Radial nerve Finger extension Extensor digitorum
C8–T1 Median and ulnar Finger flexion Flexor digitorum
nerve profundus, flexor
digitorum superficialis
C8–T1 Median nerve Thumb opposi- Opponens pollicis,
tion, abduction, abductor pollicis brevis,
flexion flexor pollicis brevis
C8–T1 Ulnar nerve Finger abduction Dorsal interosseus
muscles
(Continued)
29
Table3.5
Table 3.5 Major
(Continued)
musclesMajor muscles
and their and their
associated associatedand
movements movements and innervation
innervation
Spinal Peripheral nerve Movement Major muscle(s)
cord level
Lower L1–L3 Nerve to iliopsoas Hip flexion Iliopsoas
extremities
L3 Obturator Hip adduction Adductor brevis,
adductor longus,
adductor magnus,
adductor minimus
L3–L4 Femoral Knee extension Quadriceps
L4–L5 Peroneal Ankle dorsiflexion Tibialis anterior
L5 Superior gluteal Hip abduction Gluteus medius,
gluteus minimus
L5 Peroneal Big toe extension Extensor hallucis
longus
L5–S1 Sciatic Knee flexion Biceps femoris
S1 Inferior gluteal Hip extension Gluteus maximus
S1 Peroneal Foot eversion Fibularis peroneus
revis, fibularis
b
peroneus longus
S1 Tibial Ankle Gastrocnemius
lantarflexion
p
S1 Tibial Big toe flexion Flexor hallucis longus
the head for approximately 10 seconds. Arm

Table 3.6 Strength grading scale
pronating and downward drift are signs of
Score Criteria an upper motor neuron lesion.
5 Full strength
4 Overcome some resistance
Satelliting
3 Overcome gravity Satelliting is another sign of subtle weak-
ness and is assessed by having the patient
2 Cannot overcome gravity rotate the arms around each other. If one
1 Muscle twitching arm becomes more stationary after several
seconds with the other arm “satelliting”
0 No muscle contraction
around it, this suggests some degree of
weakness in the stationary arm.
gradually drifting downward after 5–10 sec-
onds when voluntarily raised against grav-
3.4.4 Involuntary
ity. P
ronator drift is assessed by having the
patient fully extend the arms at shoulder There are several involuntary motor move-
level with the palms facing upwards. The ments that the examiner should also note
patient should then close the eyes and shake should they be present (▶Table 3.7).
30
3.5 Reflex Examination
3.5 Reflex Examination as myoclonus. As this scale is relatively

subjective, comparing right-sided and left-
sided reflexes is often more valuable than
3.5.1 Reflex Grading
the grading itself.
There are several deep tendon reflexes that
the examiner should assess (▶Table 3.8).
Deep tendon reflexes are graded on a scale 3.5.2 Babinski’s Sign
from 0 to 4, where 0 is absent, 1 is reduced,
Babinski’s sign is a primitive reflex that
2 is normal, 3 is increased, and 4 is defined
occurs in infants and normally disappears
by 12 months of age. The examiner assesses
Table 3.7 Involuntary movements
for Babinski’s sign by stroking the sole of
Movement Features the patient’s foot with a blunt instrument
Tremor Note frequency, ampli- along the lateral aspect starting at the heel
tude, resting vs. intention and then moving in a curve just below the
toes. In adults, the normal response is a
Myoclonus Brief, twitching muscle flexor plantar response (i.e., down-going
jerk big toe), whereas the abnormal Babinski’s
Chorea Brief, irregular, jerky sign is an extensor plantar response
movements that flow (i.e. up-going big toe).
from muscle to muscle
Athetosis Slow writhing of the Hoffman’s sign
extremities
Hoffman’s sign is not a true primitive
Ballismus Large amplitude flinging reflex and can be present in normal adults.
Tics Abrupt repetitive motor The examiner assesses for Hoffman’s sign
movements or vocaliza- by flicking distal aspect of the middle fin-
tions ger and observing for any flexion of the
thumb. The presence of Babinski’s and/or
Dystonia Sustained or repetitive
Hoffman’s sign can suggest an upper motor
muscle contraction
neuron (UMN) lesion.
leading to abnormal fixed
A careful motor and reflex examination
posture
can often distinguish between UMN and
Table 3.8 Deep tendon reflexes

Reflex Spinal cord level Location to elicit
Biceps C5–6 Anterior aspect of the elbow, insertion of biceps
tendon on the forearm
Brachioradialis C5–6 Radial aspect of forearm, either proximally or
distally
Triceps C7 Posterior aspect of the elbow, just proximal to the
olecranon
Knee jerk L3–L4 Anterior knee, just distal to the patella
Ankle jerk S1 Posterior aspect of the ankle, on the Achilles tendon
31
the examiner can feel the tuning fork

Table 3.9 Features of upper motor
vibrating after the patient can no longer
neuron versus lower motor neuron
feel vibration, vibration sense may be par-
dysfunction
tially impaired.
Upper motor Lower motor
neuron neuron
Spasticity Muscle atrophy
3.6.4 Proprioception
Proprioception refers to a sense of body
Hyperreflexia Hyporeflexia
position in space and can be assessed by
Myoclonus Fasciculations having the patient close the eyes and state
Babinski's sign the direction of movement as the exam-
iner moves a body part. Second, the exam-
Hoffman's sign iner can perform the Romberg test, in
which the patient stands up with the eyes
lower motor neuron (LMN) lesions, as both closed and the examiner observes whether
will present with weakness, but UMN the patient loses balance without visual
lesions lack inhibitory modulation via sensory information.
descending pathways (▶Table 3.9).
3.6.5 Sensory Localization

3.6 Sensory Examination
Findings from the sensory examination
3.6.1 Light Touch can be used for localization of lesions
given the presence of dermatomes, which
To assess light touch, the examiner should
correspond to areas of sensory innerva-
ask the patient to close the eyes and indi-
tion arising from a single spinal nerve
cate whether he or she feels touch in vari-
ganglion (▶Fig. 3.1). It is worth remem-
ous regions of all extremities and the
bering that the median nerve transmits
trunk. It is reasonable to begin more dis-
sensation from the thumb, index finger,
tally and then progress proximally.
middle finger, and half of the fourth fin-
ger, while the ulnar nerve transmits sen-
3.6.2 Pain and Temperature sation from the fifth finger and the other
half of the fourth finger. In the leg, the
Pain is assessed in a similar manner to light
common peroneal nerve transmits sensa-
touch, but with a sharp pin and asking the
tion from the lateral aspect of the lower
patient if it feels sharp or dull while the
leg and dorsum of the foot, while the tib-
eyes are closed. Temperature sense is car-
ial nerve transmits sensation from the
ried by the same afferent small fibers as
posterior aspect of the lower leg and sole
pain, and can be assessed with a cold
of the foot.
object (e.g., tuning fork).
3.6.3 Vibration 3.7 Gait and Coordination

Vibration is assessed by placing a vibrat- Gait and coordination are critical aspects
ing 128 Hz tuning fork against the of the neurological examination because
patient’s joints while the eyes are closed they can inform the examiner about the
and asking if the patient feels vibration. If presence of a lesion in the cerebellum.
32
3.7 Gait and Coordination
Fig. 3.1 Sketch of human dermatome map with (a) anterior and (b) posterior views.
(Reproduced from Khanna A, MRI Essentials for the Spine Specialist, ©2014, Thieme
Publishers, New York.)
3.7.1 Gait 3.7.2 Coordination
The examiner should begin by observing The simplest coordination test is finger tap-
the patient’s spontaneous gait. Following ping, in which the patient taps the thumb to
this, the examiner should have the patient the index finger repeatedly as fast as possi-
walk on the heels and tiptoes. The exam- ble. The examiner can also have the patient
iner should also instruct the patient to per- tap the thumb to each of the other fingers
form tandem gait, where one foot is placed sequentially as fast as possible. Speed, accu-
in front of the other for each step. racy, and rhythm should be assessed.
33
Rapid alternating movements can be accuracy with either of these tests is

tested by having the patient flip one hand termed dysmetria.
back and forth as fast as possible against a
flat surface or the other hand. Dysdiado- 3.8 Special Tests
chokinesis describes abnormal rapid
alternating movements. 3.8.1 Straight Leg Raise
Finger-to-nose is performed by having The straight leg raise can be used to deter-
the patient alternate touching the index mine whether a patient may be suffering
finger to the examiner’s index finger and from lumbar radiculopathy, particularly of
then patient’s own nose as the examiner the L5 nerve root. The test is performed by
moves his or her index finger to various having the patient lie supine and passively
positions. Heel-to-shin is performed by lifting the patient’s straight leg. The exam-
having the patient place the heel on the iner asks the patient whether this maneu-
contralateral knee and move the heel ver reproduces radiating sciatic pain down
down the shin. An abnormality in the leg (▶Fig. 3.2).
Fig. 3.2 Illustration of straight leg raise to evaluate for lumbar radiculopathy.
(Reproduced from Albert T, Vaccaro A, Physical Examination of the Spine, 2nd edition,
©2016, Thieme Publishers, New York.)
34
3.8 Special Tests
Fig. 3.3 Illustration of FABER

test to evaluate for hip and
sacroiliac joint pathology.
(Reproduced from Vialle
L, AOSpine Masters Se-
ries, Volume 8: Back Pain.
1st Edition, ©2016, Thieme
3.8.2 FABER/FADIR Tests 3.8.4 Lhermitte’s Sign

The FABER (Flexion, ABduction, and Exter- Lhermitte’s sign suggests an upper cervical
nal Rotation) test is used to evaluate hip spinal cord lesion and is often described as
and sacroiliac joint (SI) pathology, which an electrical shock sensation that passes
may be important to distinguish from spi- down the neck and back and into the
nal pathology in evaluating a complaint of extremities. The examiner assesses for this
low back pain. The patient’s leg is flexed, sign by flexing the neck (i.e., bending the
and the thigh is then abducted and exter- neck forward).
nally rotated (▶Fig. 3.3). A related test if the
FADIR (Flexion, ADduction, and Internal
Rotation) test where the patient’s leg is 3.8.5 Tinel’s Sign
flexed, and the thigh is then adducted and
Tinel’s sign suggests irritated or damaged
internally rotated. Each specific pain
nerves and is performed by tapping
response guides decision-making regard-
directly over the nerve, resulting in pares-
ing a corresponding pathology. Other tests
thesias (i.e., tingling) within the sensory
to evaluate for sacroiliac joint pathology
distribution of the nerve. Tinel’s sign is
include distraction, compression, thigh
commonly checked when evaluating for
trust, sacral trust, and Gaenslen’s test.
carpal tunnel syndrome from median
nerve entrapment.
3.8.3 Spurling Test
The Spurling test can be used to determine
Phalen’s maneuver
whether a patient may be suffering from cer-
vical radiculopathy. The examiner performs Phalen’s maneuver is specific to carpal tun-
the test by passively rotating the patient’s nel syndrome and is performed by having
head to the side while simultaneously apply- the patient fully flex both wrists and then
ing downward and extending force on top of push the dorsal surfaces of the hands
the patient’s head. The examiner asks the together for 60 seconds. Paresthesias within
patient whether this maneuver reproduces the sensory distribution of the median
radiating pain from the neck on the same nerve during this maneuver suggests the
side of head rotation (▶Fig. 3.4). presence of carpal tunnel syndrome.
35
Fig. 3.4 Illustration of Spurling test to evaluate for cervical radiculopathy. (Reproduced
from Albert T, Vaccaro A, Physical Examination of the Spine, 2nd edition, ©2016,
Thieme Publishers, New York.)
3.8.6 Bulbocavernosus 3.9 Top Hits

The bulbocavernosus reflex involves
S2–S4, and is a useful test for spinal shock or
3.9.1 Questions
spinal cord injuries. The test is performed by
monitoring internal or external anal sphinc- 1. A 26-year-old man with no relevant
ter contraction in response to squeezing the past medical history is brought into
penis or clitoris, or tugging on an indwelling the ED following a motor vehicle colli-
Foley’s catheter (▶Fig. 3.5). sion. The patient’s eyes are open and
he was conversing with you appropri-
ately. CT spine shows complete tran-
Pearls section of cervical spinal cord. Patient
is not moving any extremities. What is
• Use the neurological examination to
corroborate pathology identified by the GCS for this patient?
other diagnostic modalities. a) 9
b) 15
• Use the neurological examination to
assess daily clinical status in the c) 14
inpatient setting. d) 8
• Tailor the neurological examination to 2. You ask a patient to name items in
your own unique style as well as each
your white coat such as “pen” and
patient and clinical situation.
“stethoscope”, but the patient is unable
36
3.9 Top Hits
Fig. 3.5 Illustration of

eliciting the bulbocavernosus
reflex (S2–S4) to evaluate for
spinal shock after spinal cord
injury. (Reproduced from
Albert T, Vaccaro A, Physical
Examination of the Spine,
2nd edition, ©2016, Thieme
to do so. The patient is also unable to missing!” Where does the lesion
follow simple commands such as localize?
“stick out your tongue”. Otherwise, a) Left optic nerve
the patient speaks fluently, but the b) Bilateral occipital lobes
content is nonsensical. Where is the c) Right thalamus
lesion? d) Optic chiasm
a) Broca’s area
b) Arcuate fasciculus 5. A patient presents to the clinic with
c) Transcortical motor area chief complaint of frequent tripping.
d) Wernicke’s area When you ask the patient to walk up
and down the hallway, the gait ap-
3. You are called to evaluate a patient pears normal. When you ask the pa-
with a newfound facial droop. On ex- tient to walk on tippy-toes, you notice
amination, the corner of the patient’s that the right heel barely lifts above
left mouth is drooping, there is nasola- the floor. To which spinal cord root
bial fold flattening, and the patient does this motor deficit localize?
cannot close the left eye tightly. Where a) S1-S2
does the lesion localize? b) C8-T1
a) Right-sided central CN VII c) L4-L5
b) Right-sided peripheral CN VII d) L2-L3
c) Left-sided central CN VII
d) Left-sided peripheral CN VII 6. On a patient’s MRI, you notice a lesion
in the cortical region anterior to the
4. On visual field examination, you ask central sulcus. What motor findings
the patient to cover up the right eye. might you expect to see on neurologi-
The patient exclaims “Doc! The right cal examination?
side of your face is missing!” In- a) Pronator drift
trigued, you ask the patient to cover b) Fasciculations
up the left eye. The patient exclaims c) Diplopia
“Doc! Now the left side of your face is d) Positive Romberg sign
37
7. A 21-year-old college student was straight leg test is negative. What

brought to ER for acute alcohol intoxica- dditional test would be helpful to
a
tion on Sunday morning after a night of localize the lesion?
festivities. On reflex examination, you
a) Bulbocavernosus reflex
notice that the biceps and brachioradia-
b) Babinski’s sign
lis reflexes are intact but the triceps re-
c) Tandem gait
flex is diminished. To which spinal cord
d) FABER/FADIR
root does this deficit localize?
a) C5
b) C6
c) C7
d) C8 3.9.2 Answers
8. A patient comes into the clinic com- 1. b. The patient has spontaneous eye
plaining of back pain with radiation opening (eye opening = 4) and ori-
down the lateral aspect of the thigh ented spontaneous speech (verbal = 5).
and anterior aspect of the leg to the Although he cannot move lower ex-
dorsum of the foot. On sensory exam- tremities, he is speaking appropriately
ination, you also notice diminished which is indicative of full motor move-
pinprick sensation in the web space ment with his tongue (motor = 6).
between the big toe and second toe. To
which spinal cord root does this sen- 2. d. The patient has deficits in compre-
sory deficit localize? hension, as manifested by impaired
a) L3 naming and an inability to follow com-
b) L4 mands. However, the patient speaks
c) L5 fluently though the content is nonsen-
d) S1 sical, which fits with a fluent aphasia
from a lesion in Wernicke’s area.
9. A patient presents with a long history
3. d. Central CN VII lesions result in con-
of pain in the right hand and wrist. On
tralateral facial weakness that spares
careful examination, you elicit tingling
the forehead, whereas peripheral CN
of the thumb, index, and middle finger
VII lesions result in ipsilateral facial
by tapping the anterior aspect of the
weakness that includes the forehead.
distal forearm. What other physical ex-
amination finding might you observe? 4. d. The clinical vignette describes bi-
a) Tingling in fifth finger temporal hemianopia, meaning loss of
b) Atrophy of the thenar eminence temporal visual fields in both eyes.
c) Weakness on wrist flexion This usually results from compression
d) Positive Hoffman’s sign of the optic chiasm, which contains
crossing nasal retinal fibers.
10. An 80-year-old patient presents to the
clinic with a chief complain of low 5. c. The clinical vignette describes a
back pain that gets worse after walk- case of foot drop, which is due to
ing for 5 minutes and radiates along weakness in ankle dorsiflexion. This
the lateral aspect of the right hip and localizes to the L4–L5 spinal cord root,
thigh. On neurological examination, which contributes to the peroneal
lower extremity strength is 5/5, re- nerve and innervates the tibialis ante-
flexes are normal and symmetric, and rior muscle.
38
3.9 Top Hits
6. a. The cortical region anterior to the 10. d. The clinical vignette describes low
central sulcus corresponds to primary back pain that might initially suggest
motor cortex. Thus, a lesion in this re- radiculopathy with neurogenic claudi-
gion may result in UMN findings, one cation due to degenerative disc dis-
of which is pronator drift. Fascicula- ease. However, given an unremarkable
tions are a LMN finding. neurological examination with a nega-
tive straight leg test, it would be pru-
7. c. The clinical vignette describes a
dent to perform FABER/FADIR to
case of radial neuropathy, colloquially
evaluate for SI pathology, which can
known as “Saturday night palsy”, due
mimic lumbar spinal pathology. Addi-
to compression of the radial nerve in
tional tests for SI joint pathology in-
the axilla. The radial nerve is respon-
clude: compression, thigh thrust,
sible for the triceps reflex and arises
distraction, and Gaenslen.
from the C7 spinal cord root. The
biceps and brachioradialis reflexes

correspond to the C5–C6 spinal cord
root. Suggested Readings
[1] Drislane F, Acosta J, Caplan L, Chang B, Tarulli A.
8. c. The distribution of the sensory Blueprints neurology. 4th ed. Philadelphia, PA:
deficit described in the clinical vi-
Lippincott Williams & Wilkins; 2013
gnette corresponds to the L5 spinal [2] Gelb DJ. The detailed neurologic examination in
adults. 2012. [online] Available from: https://www.
cord root, which is particularly nota- uptodate.com/contents/the-detailed-neurologic-
ble for carrying sensation from the examination-in-adults. Accessed June, 2017
web space between the big toe and the [3] Gelb DJ. Introduction to clinical neurology. 5th
edition. Oxford: Oxford University Press; 2016
second toe. [4] Greenberg MS. Handbook of neurosurgery. 8th
edition. New York, NY: Thieme; 2016
9. b. The clinical vignette describes [5] Po-Haong L. The mental status examination in
long-standing carpal tunnel syndrome adults. 2014. [online] Available from: https://
www.uptodate.com/contents/the-mental-status-
that is confirmed on exam with Tinel’s
examination-in-adults. Accessed June, 2017
sign. As compression of the median [6] Roundy N. Neurosurgery Survival Guide. 2011.
nerve underlies this syndrome, one [
online] Available from: http://neurosurgerysur-
vivalguide.com/. Accessed June, 2017
would also expect atrophy of the mus-
[7] Strub RL, Black FW. The mental status examination
cles (thenar muscles) supplied by the in neurology. 2nd ed. Philadelphia, PA: F.A. Davis;
median nerve over time. 1985
39
Neuroanatomy
4 Neuroanatomy
David T Fernandes Cabral, Sandip S Panesar, Joao T Alves Belo, Juan C Fernandez-Miranda
4.1 Introduction frontal, parietal and squamous

ortion of the temporal bone meet.
p
Neurosurgery as a surgical field relies on • Asterion: Located posterolaterally.
anatomical knowledge to successfully and The point where the parietomastoid,
safely perform a wide variety of procedures. occipitomastoid, and lamboid sutures
These might be as simple as a lumbar punc- meet.
ture to the most complex skull base tumor • Opisthion: The name given to the
resection. As such, this chapter reviews the posterior border of the foramen
most high-yield neuroanatomy topics. magnum at the midline.
• Inion: Also known as external
occipital protuberance, correlates
4.2 Bones of the Skull with the confluence of the venous
sinuses on the internal surface.
The human skull is divided into two Routinely used as a surgical
regions: the face and cranium. The face is landmark.
composed of 14 bones; while the cranium
is composed of 8 bones. Here, we focus on
cranial bones (▶Table 4.1).
The cranial bones are joined via fibrous 4.2.1 Cranium
joints. Articulations between two adjacent The cranium is an ovoid bony box which
bones are called sutures, and places where functions to protect the encephalon. For ana-
two or more sutures meet are named tomical and clinical purposes, the cranium is
according to their location (▶Fig. 4.1). divided into two segments—superolateral or
• Nasion: Suture between the frontal vault, and inferior or skull base.
and nasal bones.
• Bregma: Located at the vertex of the
skull vault at the point where the Skull Vault
sagittal suture meets the coronal
suture. Comprised anteriorly by the vertical seg-
• Pterion: Located at the lateral aspect ment of the frontal bone; at its middle
of the skull vault. The point where aspect by the parietal bones superiorly and
the greater wing of the sphenoid, the the squamous portion of the temporal
bones inferiorly; and posteriorly by the
superior portion of the occipital bone.
Table 4.1 Bones of the cranium (8 bones)
Medial bones Bilateral bones
Skull Base
Frontal Parietal
The internal surface of the skull base con-
Ethmoid Temporal sists of three fossae, each with associated
Sphenoid foramina which transmit efferent and
afferent neurovascular structures (▶Fig. 4.2
Occipital
and ▶Fig. 4.3).
40
4.2 Bones of the Skull
Fig. 4.1 Anatomic landmarks of the (a) lateral and (b) posterior skull. Frontal bone
(yellow), parietal bone (blue), sphenoid bone (purple), temporal bone (green), occipital
bone (red). (Modified from Di Ieva A, Lee J, Cusimano M, Handbook of Skull Base
Surgery, 1st edition, ©2016, Thieme Publishers, New York.)
41
Neuroanatomy
Fig. 4.2 Axial view diagram of the anterior, central (middle), and posterior portions of
the skull base. (Modified from Meyers S, Differential Diagnosis in Neuroimaging: Head
and Neck, 1st edition, ©2016, Thieme Publishers, New York.)
4.2.2 Clinical Applications 4.3 Cerebrum

Kocher’s point (▶Fig. 4.4), Frazier’s point.
Please refer to chapter on Operating Room
4.3.1 Surface Anatomy
(▶Table 6.2). The brain is comprised of two hemi
spheres separated by an interhemispheric
fissure (IHF), also known as longitudinal
Sinus Landmarks
fissure of cerebrum. This fissure runs
A horizontal line across the inion delin anteroposteriorly in the midline and it is
eates the trajectory of the transverse sinus. occupied by an extension of the dura
A vertical line going from the tip of mastoid mater, known as the falx cerebri. Both
and passing through the mastoid (digas hemispheres are joined together by the
tric) groove delineates the sigmoid sinus. interhemispheric commissures: Corpus
These landmarks are commonly used to callosum, fornix, and the anterior com
plan craniotomies for retrosigmoid missure (▶Fig. 4.6).
approaches (▶Fig. 4.5).1
42
4.3 Cerebrum
Fig. 4.3 Skull base anatomy. (Reproduced from Choudhri A, Pediatric Neuroradiol-
ogy: Clinical Practice Essentials, 1st edition, ©2016, Thieme Publishers, New York,
Illustration by Karl Wesker.)
Each brain hemisphere is divided into lobule has its own circumvolutions delin-
five lobules. The divisions are centered eated by secondary and tertiary sulci, the
around main sulci, which are deep and latter demonstrating greatest intersubject
generally constant across subjects. Each variability (▶Fig. 4.7).
43
Neuroanatomy
Fig. 4.4 Kocher’s point: (a)

11 cm posterior to the nasion
and 3 cm lateral to midline,
(b) 11 cm anterior to coronal
suture and 3 cm lateral to
midline. (Reproduced from
Ullman J, Raksin P, Atlas of
Emergency Neurosurgery,
1st edition, ©2015, Thieme
Fig. 4.5 Transverse and sigmoid sinuses: Anatomic landmarks on the surface of the
skull. (Reproduced from Di Ieva A, Lee J, Cusimano M, Handbook of Skull Base Surgery,
1st Edition, ©2016, Thieme Publishers, New York.)
Frontal Lobe Central Sulcus

This is the largest cerebral lobe. When the Central sulcus separates the frontal and
brain is viewed from a lateral perspective, parietal lobes, following an oblique trajec-
the frontal lobe is limited posteriorly by tory from superior to inferior, and posterior
the central sulcus and inferiorly by the lat- to anterior. It starts at the IHF and ends
eral sulcus (Sylvian fissure). above the lateral sulcus, leaving a small
44
4.3 Cerebrum
Fig. 4.6 Brain surface anatomy,

superior view. 1. Longitudinal fissure of
cerebrum. 2. Superior margin of
cerebrum. 3. Frontal pole. 4. Superior
frontal sulcus. 5. Inferior frontal
sulcus. 6. Precentral sulcus. 7. Central
sulcus. 8. Postcentral sulcus.
9. Intraparietal sulcus. 10. Parietooc-
cipital sulcus. 11. Transverse occipital
sulcus. 12. Occipital pole. 13. Superior
parietal lobule. 14. Inferior parietal
lobule. 15. Postcentral gyrus.
16. Paracentral lobule. 17. Precentral
gyrus. 18. Inferior frontal gyrus.
19. Middle frontal gyrus. 20. Superior
frontal gyrus. (Reproduced from Von
Frick H, Leonhardt H, Starck D, Human
Anatomy, ©2016, Thieme Publishers,
New York.)
Fig. 4.7 Brain surface anatomy, right lateral view. 1. Central sulcus. 2. Precentral gyrus.
3. Precentral sulcus. 4. Superior frontal gyrus. 5. Superior frontal sulcus. 6. Middle fron-
tal gyrus. 7. Middle frontal sulcus. 8. Frontal pole. 9. Orbital gyri. 10. Olfactory bulb.
11. Olfactory tract. 12–14. Lateral sulcus. 12. Anterior ramus. 13. Ascending ramus.
14. Posterior ramus. 15. Frontal operculum. 16. Frontoparietal operculum. 17. Superior
temporal gyrus. 18. Middle temporal gyrus. 19. Superior temporal sulcus. 20. Inferior
temporal sulcus. 21. Inferior temporal gyrus. 22. Preoccipital notch. 23. Occipital pole.
24. Transverse occipital sulcus. 25. Inferior parietal lobule. 26. Intraparietal sulcus.
27. Superior parietal lobule. 28. Postcentral sulcus. 29. Postcentral gyrus. 30. Supramarginal
gyrus. 31. Angular gyrus. 32. Pons. 33. Pyramid (medulla oblongata). 34. Olive.
35. Flocculus. 36. Cerebellar hemisphere. (Reproduced from Von Frick H, Leonhardt H,
Starck D, Human Anatomy, ©2016, Thieme Publishers, New York.)
45
Neuroanatomy
communication between the frontal and • Precentral sulcus: Runs parallel to the
parietal lobes, called the subcentral gyrus. central sulcus and delineates anteriorly
the precentral gyrus or motor
Lateral Sulcus (Sylvian Fissure) strip (Brodmann area 4, primary motor
cortex).
Lateral sulcus separates the frontal lobe
from the temporal lobe. It is the deepest
sulcus in the frontal lobe and covers the
Inferior Surface
insula and branches of the middle cerebral The inferior surface of the frontal lobe is
artery (MCA). Two divisions—the a nterior/ limited posteriorly by the medial projec-
horizontal, and the posterior/ascending— tion of the Sylvian fissure (▶Fig. 4.8). Medi-
divide the inferior frontal gyrus into three ally, next to the IHF runs the gyrus
segments, resembling the letter M. rectus (straight gyrus), which is limited
laterally by the olfactory sulcus with the
olfactory nerve and bulb. This segment lies
The three segments of the inferior frontal over the cribriform plate of the ethmoid
gyrus are from anterior to posterior: pars bone. Lateral to the olfactory sulcus is the
orbitalis, pars triangularis, and pars oper- orbital segment of the frontal lobe, which
cularis (the latter two otherwise known is divided into four orbital gyri (anterior,
as Broca’s area within the dominant posterior, lateral, and medial) by the
hemisphere). orbital sulci which has an H shape.
Secondary Sulci Parietal Lobe

Secondary sulci divide the lateral surface The parietal lobe is limited anteriorly by
of the frontal lobe into four gyri. the central sulcus, posteriorly by the
• Superior frontal sulcus: Divides the parieto-occipital sulcus, inferiorly by the
superior frontal gyrus (SFG) from the Sylvian fissure, and over the medial
middle frontal gyrus (MFG). hemispheric surface by the subparietal

• Inferior frontal sulcus: Divides the sulcus. Two main sulci (i.e., the postcen-
MFG from the inferior frontal tral and intraparietal) divide this lobule
gyrus (IFG). into three main gyri.
Fig. 4.8 The orbital surface of

the right frontal lobe. (Repro-
duced from Yasargil M, Smith
R, Young P et al, Microneuro-
surgery, Volume I, 1st edition,
©1984, Thieme Publishers,
New York.)
46
4.3 Cerebrum
Postcentral Sulcus located laterally on the inferior surface of

the temporal lobe. The collateral sulcus,
This is the posterior limit of the postcentral located medially, divides the fusiform
gyrus or primary sensory cortex (Brodmann gyrus and the parahippocampal gyrus,
areas 3, 1, and 2). Its anterior limit is the cen- which continues posteriorly in the
tral sulcus. occipital lobe within the lingual gyrus.

(▶Fig. 4.9).
Intraparietal Sulcus
Originates perpendicular to the postcen- Occipital Lobe
tral sulcus, dividing the remainder of the
Located at the posterior aspect of the
lateral surface of this lobule into the
hemispheres, the occipital lobe assumes a
superior parietal lobule (SPL) and inferior
pyramidal shape, limited dorsally by the
parietal lobule (IPL). The SPL continues
parietooccipital sulcus. Ventrally, its
within the medial surface of the hemi-
boundary with the temporal lobule is not
sphere as the precuneus. The IPL contains
well-defined, as previously mentioned.
the supramarginal gyrus (SMG), also
Its lateral surface has three gyri. The
known as Wernicke’s area, and the angu-
superior gyrus continues anteriorly as the
lar gyrus (AG). Localizing the SMG
SPL; the middle gyrus continues as the
involves following the Sylvian fissure
AG, and the inferior occipital gyrus con-
until its termination within the parietal
tinues as the MTG and ITG. The inferior
lobe. The AG can be located by following
surface has two gyri, the lateral gyrus is
the superior temporal sulcus instead.
continuous with the fusiform gyrus. The
medial gyrus forms the lingual gyrus
Temporal Lobe which continues anteriorly within the
temporal lobe.
Considered as the most epileptogenic The medial surface of the occipital lobe
lobule, it is limited superiorly by the Syl- is known as the cuneus and is limited by
vian fissure. Posteriorly, its limit is the parieto-occipital sulcus anteriorly and
poorly defined although in some cases, it superiorly, and the calcarine sulcus inferi-
is possible to visualize a temporo-occipi- orly. The primary visual area (Brodmann
tal sulcus. Two main sulci divide the lat- area 17) surrounds the calcarine sulcus.
eral surface of temporal lobe into three
gyri. The superior temporal sulcus sepa-
rates the superior temporal gyrus (STG)
from the middle temporal gyrus (MTG).
Medial Surface
The inferior temporal sulcus separates The cingulate gyrus is limited superiorly by
the MTG from the inferior temporal the cingulate and subparietal sulci, and infe-
gyrus (ITG). The STG contains the pri- riorly by the sulcus of the corpus callosum.
mary auditory area, also known as trans- The cingulate sulcus separates the cingulum
verse gyri of Heschl or Brodmann areas from the SFG and continues posteriorly and
41 and 42. superiorly to form the posterior limit of the
The inferior surface of the temporal paracentral lobule. The paracentral lobule is
lobe contains two main sulci. The occipi- a continuation of the precentral and post-
totemporal sulcus, located laterally, central gyri within the medial surface of the
divides the ITG and the fusiform gyrus hemisphere (▶Fig. 4.10).
47
Neuroanatomy
Fig. 4.9 Cerebrum, inferior view. (Reproduced from Peris-Celda M, Martinez-Soriano

F, Rhoton A, Rhoton’s Atlas of Head, Neck, and Brain, 1st edition, ©2017, Thieme
4.3.2 Subcortical Structures • Claustrum: Thin layer of gray matter

separated from the insula by a thin
Basal Ganglia layer of white matter (extreme
capsule) and separated from the
The basal ganglia are gray matter nuclei lentiform nucleus and the striatum
located deep within the cerebral hemi- by the white matter of the external
spheres (▶Fig. 4.11). From medial to lateral capsule.
these are:
• Thalamus.
• Striatum: Internal Capsule
◦ Caudate nucleus, divided into
head (lateral to the frontal horns Thick layer of white matter running between
of the ventricle and medial to the the caudate nucleus and thalamus medially
anterior limb of the internal capsule), and the striatum laterally. It has five seg-
body, and tail. ments running from anterior to posterior2:
◦ Lentiform nucleus, lateral to the • Anterior limb:
internal capsule, it has a medial ◦ Frontopontine fibers.
segment or globus pallidus (with its ◦ Thalamocortical fibers.
internal and external segments), and ◦ Corticothalamic fibers.
a lateral segment or putamen. ◦ Caudatoputamenal fibers.
48
4.3 Cerebrum
Fig. 4.10 Brain surface anatomy, view of medial surface of right hemisphere. 1. Frontal
pole of frontal lobe. 2. Medial frontal gyrus. 3. Cingulate sulcus. 4. Sulcus of corpus
callosum. 5. Cingulate gyrus. 6. Paracentral lobule. 7. Precuneus. 8. Subparietal sulcus.
9. Parietooccipital sulcus. 10. Cuneus. 11. Calcarine fissure. 12. Occipital pole of
occipital lobe. 13–16. Corpus callosum (cut surface). 13. Rostrum. 14. Genu. 15. Body.
16. Splenium. 17. Lamina terminalis (cut surface). 18. Anterior commissure (cut
surface). 19. Septum pellucidum. 20. Fornix. 21. Tela choroidea of third ventricle.
22. Choroid plexus of third ventricle (cut edge). 23. Transverse cerebral fissure.
24. Thalamus. 25. Interthalamic adhesion (cut surface). 26. Interventricular foramen of
Monro. 27. Hypothalamus. 28. Suprapineal recess and pineal body (cut surface).
29. Vermis of cerebellum (cut surface). 30. Cerebellar hemisphere. 31. Choroid plexus
of fourth ventricle. 32. Medulla oblongata (cut surface). 33. Fourth ventricle.
34. Pons (cut surface). 35. Tectal lamina (cut surface) and mesencephalic aqueduct of
Sylvius. 36. Mamillary body. 37. Oculomotor nerve. 38. Infundibular recess.
39. Temporal lobe lateral occipitotemporal gyrus. 40. Rhinal fissure. 41. Hypophysis
(cut surface) with adenohypophysis (anterior lobe) and neurohypophysis (posterior
lobe) of pituitary gland. 42. Optic chiasm (cut surface). 43. Optic nerve. 44. Olfactory
bulb and tract. (Reproduced from Von Frick H, Leonhardt H, Starck D, Human Anatomy,
49
Neuroanatomy
Fig. 4.11 Subcortical
structures of the brain.
a, Thalamus. b, head of the
caudate nucleus. c, internal
globus pallidus. d, external
globus pallidus. e, putamen.
f, claustrum. Rectangle shows
internal capsule: anterior
limb (yellow), genu (blue),
posterior limb (red),
sublenticular part (gray),
retrolenticular part (green).
(Illustration by Joao T Alves
Belo, MD.)
• Genu: or horns, into the frontal, occipital, and

◦ Corticobulbar fibers. temporal lobes. Their point of meeting is
◦ Corticoreticulobulbar fibers. known as atrium or trigone. The lateral
• Posterior limb: ventricles are connected to the 3rd ventri-
◦ Corticospinal fibers. cle through the interventricular foramen
◦ Corticorubral fibers. or foramen of Monro (one for each lateral
◦ Corticothalamic fibers. ventricle).
◦ Thalamocortical fibers. The 3rd ventricle is located between
• Sublenticular segment: the medial surface of both thalami and is
◦ Auditory radiations. connected to the 4th ventricle through the
◦ Corticopontine fibers. cerebral aqueduct, also known as the Syl-
◦ Optic radiations. vian aqueduct. From the 4th ventricle, CSF
• Retrolenticular segment: leaves the ventricular system and enters
◦ Optic radiations. the subarachnoid space through three
◦ Corticotectal fibers. foramina—two Lateral (foramen of Lus-
◦ Corticonigral fibers. chka) and one Medial (foramen Magendie)
◦ Corticotegmental fibers. (▶Fig. 4.12).
Ventricles of the Brain 4.4 Brainstem

The ventricles of the brain are cavities con-
4.4.1 Surface Anatomy
taining the cerebrospinal fluid (CSF) cov-
ered by ependymal cells. There are four The brainstem contains all major motor
ventricles (two lateral, 3rd and 4th and sensory pathways traveling to and
ventricles). from the brain, cerebellum, and spinal
The lateral ventricles surround the cau- cord. Furthermore, cranial nerves (CNs)
date nucleus and the thalamus in each II–XII also originate from nuclei within
hemisphere. They present three extensions, the brainstem. Topographically, it is
50
4.4 Brainstem
Fig. 4.12 Overview of the ventricular system and important neighboring structures.
Left lateral view. The ventricular system is an expanded and convoluted tube that is the
upper extension of the central spinal canal into the brain. (Reproduced from Schuenke,
Schulte, and Schumacher, Atlas of Anatomy, 2nd edition, ©2014, Thieme Publishers,
New York. Illustration by Markus Voll.)
divided into three segments from superior two superior (connected to the lateral
to inferior: midbrain, pons, and medulla geniculate nucleus of the thalamus) related
(▶Fig. 4.13, ▶Fig. 4.14, and ▶Fig. 4.15). to vision, and two inferior (connected to the
medial geniculate nucleus of the thalamus)
related to the auditory pathway. Immedi-
Midbrain ately below the inferior colliculi and on each
The midbrain is limited superiorly by an side of the midline, CN IV (trochlear nerve)
imaginary line between the mammillary exits the brainstem.
body and the pineal gland; limited inferi-
orly by the pontomesencephalic sulcus
which separates it from the pons. The ante-
rior surface is denoted by two columns of The trochlear nerve is the only CN that
white matter called cerebral peduncles. The exits the brainstem via its posterior
peduncles are separated by the interpedun- surface. Moreover, it is the only CN
cular fossa where CN III (oculomotor nerve) that decussates, resulting in contralat-
exits, to reach the orbit. The posterior sur- eral motor innervation (▶Fig. 4.16 and
face of the midbrain or tectum has four ▶Fig. 4.17).
spherical structures, known as colliculi:
51
Neuroanatomy
Fig. 4.13 Ventral view of brainstem. 1. Corpus callosum in depths of anterior interhemi-
spheric or longitudinal cerebral fissure. 2. Olfactory bulb. 3. Olfactory tract. 4. Olfactory
trigone. 5. Medial olfactory stria. 6. Lateral olfactory stria. 7. Anterior perforated sub-
stance. 8. Diagonal band of Broca. 9. Optic tract. 10. Cut surface of left temporal lobe.
11. Infundibulum with hypophyseal stalk. 12. Mamillary body. 13. Interpeduncular fossa
with interpeduncular perforated substance. 14. Ventral part of cerebral peduncle.
15. Pons. 16. Basilar sulcus. 17. Middle cerebellar peduncle. 18. Pyramid (medulla oblon-
gata). 19. Olive. 20. Ventrolateral sulcus. 21. Ventral root of first cervical nerve.
22. Ventral median fissure. 23. Spinal roots of accessory nerve. 24. Decussation of pyra-
mids. 25. Accessory nerve and cranial roots. 26. Hypoglossal nerve. 27. Glossopharyngeal
and vagus nerve. 28. Facial nerve with nervus intermedius and vestibulocochlear nerve.
29. Abducens nerve. 30. Motor and sensory roots of trigeminal nerve. 31. Trochlear
nerve. 32. Oculomotor nerve. 33. Optic chiasm. (Reproduced from Von Frick H, Leonhardt
H, Starck D, Human Anatomy, ©2016, Thieme Publishers, New York.)
52
4.4 Brainstem
Fig. 4.14 Lateral view of the brainstem. 1. Medial geniculate body. 2. Lateral geniculate
body. 3. Optic tract. 4. Hypophysis. 5. Infundibulum. 6. Mamillary body. 7, 8. Cerebral
peduncle. 7. Ventral part (crus cerebri). 8. Dorsal part (mesencephalic tegmentum).
9. Trigeminal nerve. 10. Pons. 11. Abducens nerve. 12. Pyramid (medulla oblongata).
13. Olive. 14. Hypoglossal nerve. 15. Ventrolateral sulcus. 16. Ventral root of the first
cervical nerve. 17. Spinal roots of accessory nerve. 18. Dorsal root of first cervical
nerve (retracted). 19. Dorsolateral sulcus (medulla oblongata). 20. Cranial roots of
accessory and vagus nerve. 21. Tenia of fourth ventricle. 22. Glossopharyngeal and
vagus nerves. 23. Facial nerve with nervus intermedius and vestibulocochlear nerve.
24. Middle cerebellar peduncle. 25. Inferior cerebellar peduncle. 26. Superior cerebellar
peduncle. 27. Trochlear nerve. 28. Inferior colliculus and brachium of inferior colliculus.
29. Superior colliculus. 30. Pulvinar. (Reproduced from Von Frick H, Leonhardt H, Starck
D, Human Anatomy, ©2016, Thieme Publishers, New York.)
53
Neuroanatomy
Fig. 4.15 Dorsal view of brainstem with cerebellum removed. 1. Caudate nucleus.

2. Lamina affixa. 3. Terminal stria and superior thalamostriate vein in terminal sulcus.
4. Tenia choroidea. 5. Pulvinar. 6. Habenular trigone. 7. Pineal body. 8–11. Mesenceph-
alon. 8. Brachium of superior colliculus. 9. Brachium of inferior colliculus. 10, 11.
Tectum. 10. Superior colliculus. 11. Inferior colliculus. 12. Superior medullary velum.
13. Trochlear nerve. 14. Superior cerebellar peduncle. 15. Middle cerebellar peduncle.
16. Inferior cerebellar peduncle, 17. Stria medullares (fourth ventricle) and lateral recess
of fourth ventricle. 18. Median eminence. 19. Facial colliculus. 20. Tenia of fourth
ventricle. 21. Trigone of hypoglossal nerve. 22. Trigone of vagus nerve (ala cinerea).
23. Obex. 24. Dorsal intermediate sulcus. 25. Dorsolateral sulcus. 26. Dorsal median
sulcus. 27. Lateral funiculus. 28. Fasciculus gracilis. 29. Fasciculus cuneatus.
30. Tuberculum gracile. 31. Tuberculum cuneatum. 32. Vestibular area. 33. Median
sulcus. 34. Sulcus limitans. 35. Cerebral peduncle. 36. Lateral geniculate body.
37. Medial geniculate body. (Reproduced from Von Frick H, Leonhardt H, Starck D,
Human Anatomy, ©2016, Thieme Publishers, New York.)
54
4.4 Brainstem
Optic nerve Perioculomotor

(CN II) safe entry zones
Corticospinal
tract
Oculomotor
nerve (CN III)
Interpeduncular Interpeduncular
a fossa safe entry zone
Medial Substantia
lemniscus nigra
Corticospinal Corticospinal
tract tract
Oculomotor nerves (CN III)
b
Fig. 4.16 Ventral surface, safe entry zones, and internal structures of the midbrain.
(a) The corticospinal tract is situated in the middle three-fifths of the crus cerebri.
The anterior mesencephalic (perioculomotor) safe entry zone is directed through the
frontopontine fibers and between the exit point of the oculomotor nucleus and the me-
dial edge of the corticospinal tract. Alternatively, a second ventral safe entry zone, the
interpeduncular safe entry zone, is located medial to the exit point of the oculomotor
nerves (CN III) and directed through the interpeduncular fossa. (b) The removal of the
frontopontine fibers exposes the medial lemniscus and substantia nigra. (Reproduced
from Spetzler R, Kalani M, Nakaji P et al, Color Atlas of Brainstem Surgery, 1st edition,
55
Neuroanatomy
Medial geniculate
body
Pineal
Optic tract gland
Superior
colliculus
Cerebral
Lateral
peduncle
mesencephalic
sulcus
Inferior
colliculus
Oculomotor nerve
(CN III)
Trochlear nerve
Pontomesencephalic
(CN IV)
sulcus
Fig. 4.17 Cadaveric dissection showing the lateral surface of the midbrain. The lateral
mesencephalic sulcus extends from the pontomesencephalic sulcus inferiorly to the
medial geniculate body superiorly, and it forms the border between the cerebral pe-
duncle and the tectum of the midbrain. The tectum contains the superior and inferior
colliculi. (Reproduced from Spetzler R, Kalani M, Nakaji P et al, Color Atlas of Brainstem
Surgery, 1st edition, ©2017, Thieme Publishers, New York.)
Pons pontomedullary sulcus and inferiorly by

The pons is separated from the midbrain an imaginary plane running below the
superiorly by the pontomesencephalic sul- motor decussation and above the roots of
cus, and inferiorly from the medulla by the the first cervical nerves. The anterior sur-
pontomedullary sulcus. From the ponto- face has a vertically oriented fissure on its
medullary sulcus and on each side of the midline known as the anterior median fis-
midline, the CNs VI (abducens), VII (facial), sure, representing the medial limit of the
and VIII (vestibulocochlear) exit the brain- pyramids. The lateral limit of the pyra-
stem. CN VI exits right above the pyramids mids is the anterolateral sulcus. The ante-
of the medulla, CN VII above the olivary rior median fissure and anterolateral
nucleus, and the CN VIII from the outer- sulcus continue inferiorly to the spinal
most portion of the pontomedullary cord, except for the anterior median fis-
sulcus, a region known also as the ponto- sure on the lower third of the medulla
cerebellar angle. The anterior surface of the where the motor decussation takes place
pons has an impression over its midline and momentarily efface it. On the supe-
known as the basilar sulcus. Laterally, the rior portion of the anterolateral sulcus, CN
anterior surface is limited on each side by XII (hypoglossal nerve) exits the brain-
CN V (trigeminal nerve). The posterior sur- stem anterior to the olives, on each side.
face of the pons will be described along The lateral surface of the medulla its lim-
with the posterior surface of the upper ited anteriorly by the anterolateral sulcus
medulla, as both form the rhomboid fossa. and posteriorly by the posterolateral sul-
cus. From superior to inferior, the CNs IX,
X, and XI exit the brainstem via the pos-
Medulla
terolateral sulcus. The posterior surface of
The medulla is the most caudal brainstem the medulla is divided into a superior and
segment, limited superiorly by the an inferior segment. The inferior segment
56
4.4 Brainstem
has on its midline the posterior median Rhomboid Fossa

fissure separating the gracile fasciculi on
either side. These fasciculi are laterally The superior segment of the posterior
limited by the posterior intermedius sulci surface of the medulla, forms with the
which separate the gracile and cuneate posterior surface of the pons the so-called
fasciculi. The latter are limited laterally by rhomboid fossa or floor of the 4th ventri-
the posterolateral sulcus (▶Fig. 4.18 and cle. For didactic purposes, the pontomed-
▶Fig. 4.19). ullary sulcus is employed as a reference to
Glossopharyngeal
nerve (CN IX) Pyramid
Vagus nerve
(CN X)
Olive
Hypoglossal nerve Anterior
(CN XII) median
fissure
Accessory
nerve (CN XI)
Pyramidal
decussation
Glossopharyngeal
nerve (CN IX)
Supraolivary
fossette
Olive Vagus nerve
(CN X)
Postolivary
sulcus
Preolivary
sulcus Hypoglossal nerve
(CN XII)
Accessory
nerve (CN XI)
Fig. 4.18 (a) The medulla contains the glossopharyngeal (CN IX), vagus (CN X),
accessory (CN XI), and hypoglossal (CN XII) nerves. The medulla is divided in the
midline by the anterior median fissure. The corticospinal tract runs within the
pyramid. (b) Lateral view of the medulla. The preolivary sulcus is located between
the pyramid and olive, and the postolivary sulcus is located behind the olive. The
hypoglossal nerve exits from the preolivary sulcus, and the accessory nerve exits
from the postolivary sulcus. The depression rostral to the olive, the supraolivary
fossette, is just below the junction of the facial nerve (CN VII) and the vestibulo-
cochlear nerve (CN VIII) with the brainstem. The glossopharyngeal, vagus, and
accessory nerves exit the medulla just dorsal to the postolivary sulcus, which is
located between the olive and the inferior cerebellar peduncle. (Reproduced from
Spetzler R, Kalani M, Nakaji P et al, Color Atlas of Brainstem Surgery, 1st edition,
57
Neuroanatomy
Obvvex Cuneate
Gracile tubercle
tubercles Lateral
medullary
safe entry
zone
Posterior median
sulcus and safe
entry zone
Posterior lateral
sulcus and safe Posterior
entry zone intermediate
sulcus and
safe entry
zone
Fig. 4.19 The surface anatomy and safe entry zones of the dorsal medulla. There are
three dorsal medullary sulci, which have been used to gain entry to the dorsal medulla
and have been described as safe entry zones. These include the posterior median sulcus
below the obex in the midline, the posterior intermediate sulcus between the gracile
tubercle and the cuneate tubercle, and the posterior lateral sulcus along the lateral
margin of the cuneate tubercle. An additional safe entry zone, the lateral medullary
(inferior cerebellar peduncle) safe entry zone, has been proposed. (Reproduced from
Spetzler R, Kalani M, Nakaji P et al, Color Atlas of Brainstem Surgery, 1st edition,
divide the rhomboid fossa into an inferior Superior or Pontine Triangle

or medullary triangle and a superior or
pontine triangle. At each side of the midline and just above
an imaginary plane from the pontomedul-
lary sulcus, the facial colliculi are
Inferior or Medullary Triangle located (▶Fig. 4.20). The abducens nucleus
The medullary triangle is limited laterally and the fibers of the CN VII make an inden-
by the inferior cerebellar peduncles tation in the white matter as they loop
(▶Fig. 4.20). Three important structures around this nucleus.
occupying this area from medial to lateral In the superolateral segment, the
include: motor nucleus of the trigeminal nerve
makes an impression. Lateral to the tri-
• Hypoglossal trigone, related to the geminal impression lies the locus coeruleus
nucleus of the CN XII.
which is the main source of noradrenaline
• Vagal trigone, related to the motor in the central nervous system (CNS).3
nucleus of the CN X. On the inferolateral
aspect of the trigone is the area
postrema which controls vomiting.
A lesion of the pons at the level of the abdu-
• Vestibular trigone, related to the cens nucleus may cause Millard-Gluber syn-
vestibular and dorsal cochlear nuclei.
drome characterized by CNs VI and VII
palsies and contralateral body hemiplegia.
58
4.6 Spinal Cord
Fig. 4.20 The infrafacial collicular safe entry zone (shaded area inside green dashed
lines) is limited medially by the medial longitudinal fasciculus, laterally by the nucleus
ambiguus, superiorly by the facial colliculus, and inferiorly by the hypoglossal trigone.
Thus, the lateral border of the infrafacial collicular safe entry zone corresponds to the
most medial point of attachment of the tela choroidea along the lower margin of the
lateral recess, whereas the rostral and caudal borders are the same as the upper and
lower edges of the lateral recess. (Reproduced from Spetzler R, Kalani M, Nakaji P et al,
Color Atlas of Brainstem Surgery, 1st edition, ©2017, Thieme Publishers, New York.)
4.5 Cisterns cervical portion and one in the lumbar

portion, representing areas where the bra-
The cisterns are areas where the pia matter chial and lumbar plexi are respectively
and arachnoid are separated and filled with located.
CSF. Additionally, these spaces are also Generally, there are 31 spinal cord seg-
occupied by blood vessels and cranial ments, each of which give off a pair of spi-
nerves. ▶Fig. 4.21 summarizes the different nal nerves:
cisterns and their relationship with the ana-
• Eight pairs of cervical spinal nerves,
tomical structures in the posterior fossa. the first spinal nerve (C1) exits
between the occipital bone and the
4.6 Spinal Cord atlas or first cervical vertebra. For this
reason, there are eight cervical pairs,
4.6.1 Surface Anatomy the last being located between C7
and T1.
The spinal cord is the most caudal segment • Twelve thoracic spinal nerves. The first
of the CNS. It is located in the superior thoracic nerve pairs (T1) start below the
two-third of the spinal canal, ending at the first thoracic vertebrae, this order
level of L2 (second lumbar vertebrae). continues for the remaining segments.
Along its length, the spinal cord has two • Five lumbar pairs.
regions where its maximal diameter • Five sacral pairs.
increases. One of these regions lies in its • One coccygeal pair.
59
Neuroanatomy
Posterior cerebral artery Interpeduncular

cistern
Oculomotor nerve (CN III) Crural cistern
Superior cerebellar artery Ambient cistern
Basilar artery
Prepontine cistern
Trochlear nerve (CN IV)
Trigeminal nerve (CN V) Cerebellopontine
cistern
Anterior inferior
cerebellar artery Abducens nerve
(CN VI)
Facial and
vestibulocochlear Cerebellomedullary
nerves (CN VII & VIII) cistern
Glossopharyngeal
and vagus nerves Posterior inferior
cerebellar artery
(CN IX & X) Hypoglossal nerve Vertebral
(CN XII) artery
Accessory Premedullary
a nerve (CN XI) cistern
Posterior cerebral
artery
Crural cistern Ambient cistern Trochlear nerve (CN IV)
Interpeduncular cistern Quadrigeminal cistern

Oculomotor nerve
(CN III) Cerebellopontine
Superior cerebellar cistern
artery
Prepontine cistern
Trigeminal nerve
(CN V)
Basilar artery
Facial and
vestibulocochlear
nerves (CN VII & VIII)
Anterior inferior Glossopharyngeal
cerebellar artery and vagus nerves
(CN IX & X)
Abducens nerve (CN VI)
Cisterna magna
Premedullary cistern
Posterior inferior
Hypoglossal nerve (CN XII) cerebellar artery
Accessory nerve (CN XI) Cerebellomedullary cistern
b Vertebral artery
Fig. 4.21 The brainstem and the cisterns that are associated with the cranial nerves.
(a) Ventral view and (b) lateral view. (Reproduced from Spetzler R, Kalani M,
Nakaji P et al, Color Atlas of Brainstem Surgery, 1st edition, ©2017, Thieme Publishers,
New York.)
60
4.7 Vertebral Column
These are extensions of the pia matter

and arachnoid towards the dura mater.
Above C7, the spinal nerves exit above
the vertebra with the same name,
except for C8, which exits below C7 and 4.6.2 Internal Configuration
above T1. From T1 and below, the spi-
nal nerves exit below the vertebra with Understanding the anatomical arrange-
the same name. ment and physiology of the spinal cord is
essential for determination of different
pathological syndromes that may affect it.
Topographically, the spinal cord its divided Opposite to the brain, white matter sur-
into three columns on each side: rounds the gray matter in the spinal cord.
• Anterior column, between the anterior Spinal gray matter lies centrally around
median fissure and anterolateral sulcus. the central canal, assuming the shape of an
• Lateral column, between the anterolat- “H.” ▶Fig. 4.22 and ▶Fig. 4.23 show anaxial
eral and posterolateral sulci. These sulci cut of a spinal cord segment, the Rexed
represent the exit of the ventral (motor) laminae configuration and the ascending
and the entry of the dorsal (sensory) and descending white matter tracts
nerve roots that forms the spinal nerve. (▶Table 4.2). ▶Fig. 4.24 shows the myo-
• Posterior column, between the tomes and dermatomes.
posterolateral sulcus and posterior
median fissure. From T6 and above, the
posterior column is further divided into 4.7 Vertebral Column
two tracts by the posterior intermediate
sulcus. A medial tract (fasciculus gracile), The spine is composed of 33–35 vertebrae
limited medially by the posterior median in the following distributions:
fissure and laterally by the posterior • 7 cervical.
intermediate sulcus, and a lateral • 12 thoracic.
tract (fasciculus cuneate) limited medially • 5 lumbar.
by the posterior intermediate sulcus and • 3–5 coccygeal.
laterally by the posterolateral sulcus.
4.7.1 Vertebrae Constitution
Fixation of the Spinal Cord Except for the first (C1 or atlas) and sec-
ond (C2 or axis) vertebrae, six segments
The spinal cord is maintained in its posi-
can be identified in a standard vertebra
tion via the following structures:
(▶Fig. 4.25):
• Superiorly, its continuation with the
brainstem. 1. Vertebral body: Forms the anterior
• Laterally, spinal nerves exiting through portion of the vertebra and has two
the intervertebral foramens. horizontal portions (superior and in-
• Dura mater, two attachments: Filum ferior) in which the intervertebral disc
terminalis with the anterior coccyx and sits. The posterior wall forms the ante-
sacrum, and the periosteum of the rior arch of the vertebral canal.
skull. 2. Pedicles: There are two pedicles (left
• Dentate ligaments, located between the and right) extending from the postero-
ventral and dorsal nerve roots. lateral aspect of the vertebral body.
61
Neuroanatomy
Fig. 4.22 Cross-sectional cut of the cervical spinal cord. Blue descending fibers, red
ascending fibers. (Illustration by Joao T. Alves Belo, MD.)
Fig. 4.23 Cross-sectional cut of the spinal cord with a close-up view of the anatomical
classification of the gray matter. For a description, please see ▶Table 4.2. (Illustration by
Joao T. Alves Belo, MD.)
body. They serve as attachments for foramina (spaces where the nerve

the transverse processes, the laminae, roots exit the spinal canal).
and the facets (articular processes). 3. Laminae: Extend from the pedicles in a
The superior and inferior borders of posteromedial direction relative to the
the pedicles form the inferior and spinous processes. They form the
superior borders of the intervertebral posterior arch of the spinal canal. The
62
Table 4.2 Configuration of the gray matter in the spinal cord

Rexed laminae Classical terminology Function
I Posteromarginal nucleus Exteroceptive sensations
II Substantia gelatinosa
III Nucleus proprius
IV
V Neck of the posterior Proprioceptive sensations
horn
VI Base of the posterior
horn
VII Two groups: 1. Medial, thoracic nucleus: from
1. Medial, thoracic nucleus C8–L3 receive information from
2. Lateral, divided in two the muscle spindle and Golgi
other nuclei: tendon organ
a) Intermediomedial 2. Lateral:
zone a) Intermediomedial zone: γ mo-
b) Intermediolateral tor neurons involved in motor
zone reflexes
b) Intermediolateral zone: motor
visceral function. From C8–
L2–3 sympathetic thoracolum-
bar column. S2–S4 parasympa-
thetic sacral nuclei
VIII Commissural nucleus Regulates skeletal muscle
contraction
IX Ventral horn Main motor area composed by α
motor neurons
X Grisea centralis/substantia Contains motor nuclei from the auto-
gelatinosa centralis nomic nervous system
internal surface of the laminae serves as and inferior) which articulate with
an attachment for the yellow ligament. their superior and inferior vertebral
4. Spinous process: Starts from the counterparts.
point where laminae join in the mid- 6. Transverse process: Attached to the
line and follows a posterior trajectory. pedicles on either side. Their shape
The inferior and superior edges of the varies according to the segment of the
spinous processes serve as an attach- spine they originate from.
ment for the interspinous ligament.
The supraspinous ligament runs over
the tip or free edge of the spinous pro- Intervertebral Foramen
cess in the midline.
As previously mentioned, this is the space
5. Facet or articular process: There are
where the spinal nerves exit the spinal
four facets, two on each side (superior
63
Neuroanatomy
Fig. 4.24 Dermatomes and sensory distributions of peripheral nerves. (Reproduced

from Baaj A, Mummaneni P, Uribe J et al, Handbook of Spine Surgery, 2nd edition,
canal. Its limits are important from a surgi- Cervical Vertebrae

cal standpoint (▶Fig. 4.26):
• Superior: Inferior border of the The vertebrae of the cervical spine have
overlying vertebral pedicle. unique characteristics differentiating them
• Inferior: Superior border of the from the thoracic and lumbar vertebrae
underlying vertebral pedicle. (▶Fig. 4.27). The first and second vertebras
• Anterior: Posterolateral aspect of the possess unique morphology including
intervertebral disc. presence of the transverse foramina on the
• Posterior: The capsule of the facets and transverse processes.
the yellow ligament.
64
Fig. 4.25 (a) Anatomic drawing of a typical cervical vertebra from a superior projection.
(b) Anatomic drawing of a typical cervical vertebra from a lateral projection.
(c) Anatomic drawing of a typical thoracic vertebra from a superior projection.
(d) Anatomic drawing of a typical thoracic vertebra from a lateral projection.
(e) Anatomic drawing of a typical lumbar vertebra from a superior projection.
(f) Anatomic drawing of a typical lumbar vertebra from a lateral projection.
(Reproduced from Schuenke, Schulte, and Schumacher, Atlas of Anatomy, 2nd edition,
©2014, Thieme Publishers, New York. Illustration by Karl Wesker.)
lateral masses that articulate with the

The vertebral arteries and veins run within occipital condyles superiorly, and
the transverse foramina of C6 to C1 and C2 (axis) inferiorly. From these lateral
C7 to C1 respectively, entering the cranial masses, two arches (one anterior and
vault via the foramen magnum. one posterior) enclose anteriorly and
posteriorly the spinal canal at this level.
In the midline, the interior surface of the
Some of these special features are summa-
anterior arch of C1 articulates with the
rized here:
anterior segment of the odontoid
• C1 (Atlas): The first cervical vertebra process of C2 (axis). The anterior surface
lacks a body. Instead, it possesses two
65
Neuroanatomy
Fig. 4.26 Lateral view of

two adjacent vertebral
segments showing the
boundaries of the interver
tebral foramen. (Illustration by
Joao T. Alves Belo, MD.)
of the anterior arch also possesses an spinous process is prominent and its
anterior tubercle, which serves as the transverse foramen is smaller or absent,
insertion point for the longus colli and is occupied by the vertebral vein.
muscle. The posterior arch possesses a
posterior tubercle on its exterior surface,
in the midline, which serves as an
insertion for the rectus capitis posterior
Thoracic Vertebrae
minor muscle. The medial aspect of the The most distinguishing feature of the
lateral masses has tuberculae where the thoracic vertebrae is the presence of trans-
transverse ligament originates and runs verse costal facets, which articulate with
posteriorly to the odontoid process the ribs.
before attaching to C1. The transverse
process and foramen of C1 are located
on the lateral surface of the C1 masses. Lumbar Vertebrae
• C2 (Axis): This vertebra is characterized The lumbar vertebral bodies are larger than
by its odontoid process (dens). The dens
those of other segments; this is function-
articulates with the anterior arch of the
ally related with their weight-bearing role.
atlas. The left and right occipitoodon-
toid ligaments (alar ligaments) attach
firmly to either side of the dens. The 4.7.2 Ligaments of the
spinous process of the axis serves as an
attachment for the rectus capitis Occipitoatlantoaxial
posterior major muscle and the Junction
obliquus capitis inferior muscle.
• C6: Unique to this vertebra is the Transverse and Cruciate
presence of a tubercle at the anterior Ligaments
aspect of its transverse process. This
tubercle is called carotid tubercle or The transverse ligament is a short ligament
Chassaignac tubercle. It denotes the attached laterally to the transverse tuber-
entry of the vertebral artery into the cle, at the medial aspect of the lateral mass
transverse foramen. of C1 (▶Fig. 4.28). It runs posteriorly to the
• C7: This vertebra possesses features dens of the axis and for this reason it has
similar to the thoracic vertebrae. Its an anterior concave trajectory. At the
66
Fig. 4.27 (a) Superior and (b) anterior view of the first, second, fourth, and seventh
cervical vertebrae. (Reproduced from Schuenke, Schulte, and Schumacher, Atlas of
Anatomy, 2nd edition, ©2014, Thieme Publishers, New York. Illustration by Karl
Wesker.)
67
Neuroanatomy
a b
c d
Fig. 4.28 Craniocervical ligaments. Views of the upper part of the vertebral canal with
the spinous processes and parts of the vertebral arches removed to expose the liga-
ments on the posterior vertebral bodies viewed posteriorly (a) before and (b) and (c)
after removal of the posterior longitudinal and transverse atlas ligaments. (d) The
ligaments of the median atlantoaxial joint are shown from a superior view. (Reproduced
from Schuenke, Schulte, and Schumacher, Atlas of Anatomy, 2nd edition, ©2014,
Thieme Publishers, New York. Illustration by Karl Wesker.)
midline are two more bands of vertically Alar Ligaments

oriented ligaments: The superior and infe-
rior longitudinal bands constitute the These are two short and strong ligaments
transverse and cruciate ligaments. The (left and right) connecting the superolat-
superior band ends at the anterior edge of eral segments of the dens of the axis to
the foramen magnum, whereas the inferior the medial segment of the occipital
extension ends attach to the body of C2. condyles.
68
4.8 Vascular Anatomy
Apical Ligament Posterior Longitudinal

The apical ligament is a short ligament, Like its anterior counterpart, this ligament
attaching the vertex of the dens to the runs over the posterior surface of the
anterior edge of the foramen magnum. vertebral bodies from the internal aspect
of the basilar segment of the occipital bone
to the coccyx.
Tectorial Membrane
This membrane lies posteriorly to the alar
and apical ligaments. It is divided into a
Supraspinous Ligament
medial segment and two lateral segments. This is a thick fibrous band attached to the
The medial segment runs from the vertex of the spinous processes throughout
anterior edge of the foramen magnum to the entire length of the spine. At the cervi-
the body of C2 where it continues to the cal segment, this ligament turns into the
posterior longitudinal ligament of the spine. ligamentum nuchae.
The lateral segments (left and right),
connect C2 with the occipital condyles.
Interspinous Ligament
Atlanto-Occipital Membrane Differing from the previously described
ligaments, the interspinous ligament has a
This membrane is composed of two segmental distribution, joining the space
segments: between spinous processes. It attaches
• Anterior segment: Connects the superiorly at the inferior border of the
anterior arch of C1 with the anterior edge overlying spinous process and inferiorly at
of the foramen magnum. Considered to the underlying spinous process. Posteriorly
be an extension of the anterior it attaches to the supraspinous ligament,
longitudinal ligament of the spine. whereas anteriorly it attaches to the liga-
• Posterior segment: Connects the mentum flavum.
posterior arch of C1 to the posterior
edge of the foramen magnum. The
posterior atlantooccipital membrane is Ligamentum Flavum
traversed by the vertebral arteries after
This ligament has two segments (left and
they exit the transverse foramen to
right). Each are thick, short, strong, and
enter the cranium via the foramen
elastic. They attach superiorly at the ante-
magnum. It is also the equivalent of the
rior segment of the lamina and inferiorly
ligamentum flavum for the remaining
over the superior border of the underlying
segments of the spine.
lamina.
4.7.3 Common Ligaments

Anterior Longitudinal
4.8.1 Arterial Anatomy
This ligament runs anteriorly to the verte-
bral bodies of the spine from the basilar The vascular supply of the intracranial CNS
portion of the occipital bone, to the ante- components is from branches and anasto-
rior segment of the second vertebra of the moses of the carotid and vertebral
sacrum. (▶Fig. 4.29) arteries (▶Fig. 4.30).
69
Neuroanatomy
Fig. 4.29 (a) Artist’s drawing of a midsagittal section of the bones and ligaments of the
skull base, craniocervical junction, and cervical spine. Diagrams showing the differenc-
es in sagittal alignment of the vertebral column in (b) infancy and (c) in adulthood.
(Reproduced from Schuenke, Schulte, and Schumacher, Atlas of Anatomy, 2nd edition,
©2014, Thieme Publishers, New York. (Illustration by Karl Wesker.)
Common Carotid Artery • Lingual artery.

• Ascending pharyngeal artery.
The common carotid arteries (CCAs) differ • Facial artery.
in their origin. On the right side, the bra- • Occipital artery.
chiocephalic trunk bifurcates into the right • Posterior auricular artery.
CCA and the right subclavian artery; on the • Parotid arteries.
left, it arises directly from the aortic arch.
Terminal branches: The ECA bifurcates
into two terminal branches approximately
Generally, both CCAs bifurcate into the 4 cm superior to the mandibular angle.
external carotid artery (ECA) and internal These two terminal branches are:
carotid artery (ICA) 1 cm superior to the 1. Superficial temporal artery.
thyroid cartilage corresponding to the 2. Maxillary artery: This artery gives off
level of the 4th cervical vertebra (C4).4 approximately 14 different branches
(variable). Relevant are:
◦◦ Middle meningeal artery: Enters
External Carotid Artery
the skull via the foramen spinosum.
Collateral branches: These follow an Its trajectory along the internal sur-
ascending order of bifurcation (▶Fig. 4.31): face of the squamous portion of the
• Superior thyroid artery. temporal bone makes it highly
70
Fig. 4.30 Coronal view of

the arteries from the aortic
arch, which supply the brain.
(Reproduced from Meyers
S, Differential Diagnosis
in Neuroimaging: Brain
and Meninges, 1st edition,
New York.)
susceptible to bleeding after pteri- • C3 or lacerum segment: Small segment

onal trauma, which may result in where the ICA passes over the foramen
epidural hematoma. lacerum.
◦◦ Accessory meningeal artery: This • C4 or cavernous segment: From the
artery is inconstant, entering the foramen lacerum to the anterior clinoid
skull via the foramen ovale. process. Multiple branches originate
◦◦ Anterior and posterior deep tempo- from this segment:
ral arteries supply the anterior and ◦ Meningohypophyseal trunk: A
posterior portions of the temporal surgically important branch giving off
muscle. three arteries:
– Tentorial artery or Bernasconi and
Internal Carotid Artery Cassinari artery.
– Dorsal meningeal artery.
From the carotid bifurcation, the ICA trav- – Inferior hypophyseal artery.
els directly into the cranial cavity via the ◦ Inferolateral trunk.
carotid foramen before ending at the level ◦ Medial trunk or McConnell’s artery,
of the optic nerve3(▶Fig. 4.32). For ana- goes to the capsule of the pituitary
tomical purposes, the ICA has been divided gland.
into seven segments: • C5 or clinoid segment: Between the
• C1 or cervical segment: From the proximal and distal dural rings.
carotid bifurcation to the carotid • C6, ophthalmic segment: From the
foramen at the skull base, no branches distal dural ring to the posterior
originate from this segment. communicating artery (P-Comm). Two
• C2 or petrous segment: From the carotid important branches from this segment:
foramen to the posterior edge of the ◦ Ophthalmic artery.
foramen lacerum. The segment of the ◦ Superior hypophyseal artery.
petrous bone where the ICA runs is known • C7 or communicating segment: From
as the carotid canal. In this segment, it the P-Comm artery to the bifurcation of
gives off the caroticotympanic artery. the ICA into anterior and middle
71
Neuroanatomy
Angular artery
Superficial temporal
artery
Posterior auricular artery
Superio labial arteryr
Maxillary artery
Occipital artery
Inferior labial artery Facial artery Ascending pharyngeal artery
Facial artery
Internal carotid artery
Lingual artery Carotid bifurcation with
Superior thyroid artery carotid body
External carotid artery Vertebral artery
Common carotid artery
Thyrocervical trunk
Subclavian artery
Fig. 4.31 Overview of arteries of the head. Left lateral view. The common carotid
artery divides into internal and external carotid arteries at the carotid bifurcation, which
is usually at the level of the fourth cervical vertebra. There are eight branches of the
external and none of the cervical internal carotid artery. (Reproduced from Schuenke,
Schulte, and Schumacher, Atlas of Anatomy, 2nd edition, ©2014, Thieme Publishers,
New York. Illustration by Karl Wesker.)
cerebral artery. The branches of this • A1 or precommunicating segment:

segment are: From the ICA bifurcation to the ACoA.
◦ P-Comm. • A2: From the ACoA to the junction of the
◦ Anterior choroidal artery (ACh). rostrum and genu of the corpus
callosum. The recurrent artery of
Heubner may arise either from A1, A2, or
Anterior Cerebral Artery
at the A1/A2 junction. The A2 segment
The anterior cerebral artery (ACA) arises commonly gives off the infraorbital
from the ICA lateral to the optic chiasm, it artery and the frontopolar artery.6
supplies the medial surface of the cerebral • This artery travels around the genu
A3:
hemisphere except for the medial occipital of the corpus callosum and continues to
lobes (▶Fig. 4.33). Grossly, the ACA can be the A4 segment after turning sharply,
divided into precommunicating and post- posterior to the genu. The branches of
communicating segments based upon the A3 segment are highly variable and
their proximal and distal location to ante- include the callosomarginal artery
rior communicating artery (ACoA). Another which may give off three further
classification dividing the ACA into five arteries including anterior internal
segments follows5: frontal artery, middle internal frontal
72
Fig. 4.32 Microsurgical
anatomy of the internal
carotid artery and ophthalmic
artery. (a) Superior and
(b) left lateral view of the
internal carotid artery showing
its segmental anatomy:
C1, cervical segment; C2,
petrous segment; C3, lacerum
segment; C4, cavernous
segment; C5, clinoidal
segment; C6, ophthalmic
segment; and C7, communi-
cating segment. Dolenc's
loops of cavernous ICA are
also shown: anterior loop,
medial loop, lateral loop, and
posterior loop. AChA, anterior
choroidal artery; ACP, anterior
clinoid process; OphA,
ophthalmic artery; PCoA,
posterior communicating
artery; SHA, superior
hypophyseal artery; Tent,
tentorium. (Reproduced from
Lawton M, Seven Aneurysms:
Tenets and Techniques for
Clipping, 1st edition, ©2011,
Thieme Publishers, New York.)
artery, and the posterior internal frontal • A4 and A5: Segments run over the
artery.6 In some cases, these three body of the corpus callosum. These
arteries may arise directly from the segments are themselves separated
A3 segment. Additionally, the from each other by a vertical line
pericallosal artery may arise from the running posterior to the coronal suture.
A3 segment or it could be a direct The A4 segment gives off the paracen-
continuation of the ACA. tral lobular artery, whereas the A5
73
Neuroanatomy
Fig. 4.33 Schematic rep-

resentation of the relevant
anatomy of the distal anterior
cerebral artery and its sur-
rounding structures. The most
common sites for traumatic
aneurysms are denoted (*).
a., artery. (Reproduced from
Spetzler R, Kalani M, Nakaji
P, Neurovascular Surgery,
segment gives off the superior internal travel to the cortical surfaces of the
parietal artery and the inferior internal hemispheres.
parietal artery.6
Vertebral Artery
Middle Cerebral Artery
The vertebral artery (VA) arises directly
The middle cerebral artery (MCA) arises from the subclavian artery on each side
from the ICA (▶Fig. 4.34). Its branches ter- from where it runs superiorly to enter the
minate at the lateral surface of the cerebral transverse foramen of C6 on its way to the
hemispheres. For anatomical purposes, the posterior cranial cavity. The VA is divided
MCA its divided into four segments7: into four segments:
• M1 or sphenoidal, horizontal • V1 or prevertebral: Goes from its origin
segment: From the origin of the MCA to at the subclavian artery to C6.
the bifurcation of the MCA into a • V2 or vertebral segment: Runs within
superior and inferior trunk. The lateral the transverse foramen from C6 to C2.
lenticulostriate arteries arise from this • V3 or extradural segment: From C2 to
segment. the foramen magnum.
• M2 or insular segment: Runs in the • V4 or intradural: From its entry to the
depth of the Sylvian fissure from its dura of the foramen magnum until its
bifurcation. junction at the contralateral VA forming
• M3 or opercular segment: From the the basilar artery (BA).
depth of the Sylvian fissure on its
posterior segment to the surface of the
Collateral Branches
Sylvian fissure.
• M4 or cortical segment: Starts at the • Anterior meningeal artery.
surface of the Sylvian fissure posteriorly • Posterior meningeal artery.
and gives multiple branches which • Posterior spinal artery.
74
Fig. 4.34 Vascular anatomy. (a) Diagram of the arterial supply to the brain, including
the circle of Willis formed by anastomoses between the anterior circulation (i.e., the
anterior and middle cerebral arteries, arising from the internal carotid artery) and
the posterior circulation (the basilar artery and posterior cerebral arteries, supplied
by the vertebral arteries). (b) Midsagittal venous anatomy showing the major venous
sinuses and the contributing veins. (c) Surface venous anatomy depicted from a lateral
projection. (Reproduced from Schuenke, Schulte, and Schumacher, Atlas of Anatomy,
2nd edition, ©2014, Thieme Publishers, New York. Illustration by Karl Wesker.)
• Anterior spinal artery, formed from two Basilar Artery

branches (left and right) originating
from each of the VAs prior to their The BA originates from the unison of the
continuation as the single BA. This two VAs over the anterior brainstem sur-
artery runs in the surface of the face (▶Fig. 4.34). It runs over the anterior
anterior median fissure. surface of the pons giving off numerous
• Posterior inferior cerebellar artery
(PICA), supplies the posterolateral
medulla, the 4th ventricle, and the CN III travels on either side of the SCA and
posteroinferior cerebellar posterior cerebral arteries.
hemispheres.
75
Neuroanatomy
collateral branches. It terminates at the fossa, mammillary bodies, infundibulum

level of the interpeduncular cistern, where and optic chiasm (▶Fig. 4.35). This arterial
it contributes to the posterior cerebral polygon (which is complete in approxi-
arteries. The branches of the BA are: mately 20% of the population)2 is formed
• Anterior inferior cerebellar artery. by the anastomoses of the tip of the BA,
• Labyrinthine artery. PCA (P1), and P-Comm posterolaterally,
• Pontine arteries. and the ICA, ACA (A1), and ACoA anterolat-
• Superior cerebellar artery (SCA). erally. The circle of Willis gives off multiple
penetrating arteries to anatomical struc-
tures within its vicinity.
Posterior Cerebellar Artery
The posterior cerebellar artery (PCA)
arises from the bifurcation of the BA at the
4.8.2 Venous Anatomy
interpeduncular cistern (▶Fig. 4.34). It

terminates at the medial surface of the
Dural Sinuses
occipital lobe. It is divided into four • Superior sagittal sinus (SSS): From the
segments7: foramen cecum at the cribriform laminae
• P1 or precommunicating segment: of the ethmoid bone to the internal
From the bifurcation of the BA to the occipital protuberance, where the
junction of the P-Comm. This segment confluence of the sinuses is lo-
gives off multiple perforators to the cated (▶Fig. 4.36) . Trauma to the vertex
thalamus, hypothalamus, subthalamus, of the skull may cause rupture of the SSS,
and the anterolateral segment of the resulting in vertex epidural hematoma.8
midbrain. • Inferior sagittal sinus (ISS): Runs
• P2 or ambient segment: From the within the inferior edge of the falx
junction of the P-Comm to the posterior cerebri and is formed by smaller cortical
edge of the midbrain. Some of the PCA veins from medial hemispheric surfaces.
branches at this segment are the lateral • Straight sinus: Formed by the Vein of
posterior choroidal artery and Galen (deep vein of the brain) and the ISS.
thalamogeniculate arteries. Also ends at the sinusoidal confluence.
• P3 or quadrigeminal segment: From • Transverse sinuses: One per side,
the posterior edge of the midbrain to originating from the confluence of the
the anterior limit of the calcarine sinuses. Runs laterally and continues
fissure. The branches of this segment drains into the sigmoid sinus. Receives
supply the posteroinferior temporal drainage from the vein of Labbé.
lobe (posterior temporal artery), • Sigmoid sinus: Continuation of the
occipital lobe (parieto-occipital artery transverse sinus and the point at which
and calcarine artery) and the posterior transverse sinuses meet. Receives an
segment of the corpus callosum (poste- anastomosis from the superior petrosal
rior pericallosal artery). vein which drains the cavernous sinus.
The sigmoid sinus ends at the jugular
foramen, where it receives an
Circle of Willis
anastomosis from the inferior petrosal
The ICA and vertebrobasilar arterial sys- sinus. It continues as the internal
tem are connected through a polygon jugular vein following its exit from the
located between the interpeduncular jugular foramen.
76
Fig. 4.35 Subarachnoid

cisterns around the circle of
Willis, as viewed from above
the brain, which has been
sliced axially. The relationship
between aneurysms in the
circle of Willis and their asso-
ciated cisterns is shown.
(Reproduced from Lawton
M, Seven Aneurysms: Tenets
and Techniques for Clipping,
Fig. 4.36 Dural sinus tributaries from the cerebral veins (after Rauber and Kopsch).
Right lateral view. Venous blood collected deep within the brain drains to the dural si-
nuses through superficial and deep cerebral veins. The red arrows in the diagram show
the principle directions of venous blood flow in the major sinuses. (Reproduced from
Schuenke, Schulte, and Schumacher, Atlas of Anatomy, 2nd edition, ©2014, Thieme
Publishers, New York. Illustration by Markus Voll.)
77
Neuroanatomy
Cerebral Veins Pearls

Superficial Veins • Knowing surface anatomy is key to
perform bedside procedures such
The superficial veins of the brain form
as lumbar punctures/drains and
multiple anastomoses which terminate
external ventricular drains.
within two main veins:
• Understand the different
• Vein of Trolard: Located superiorly, anatomical segments for the main
drains from the sylvian fissure to the SSS.
arteries supplying the brain: ICA,
• Vein of Labbé: Located inferiorly, drains MCA, ACA, PCA, and vertebral artery.
from the sylvian fissure to the
transverse sinus. • Recognize the main venous
structures such as dural sinuses as
well as Trolard and Labbé veins.
Deep Veins • A firm command of the various
dermatomes and myotomes is
• Internal cerebral vein: Receives the essential to ensure a proper
thalamostriate vein (caudate and neurological exam for patients
thalamus) at the foramen of Monro, and with spinal cord injury.
the septal vein (septum pellucidum,
anterior corpus callosum and head of
the caudate).2
b) Anterior choroidal artery—tentorial
• Basal vein of Rosenthal: This vein artery—anterior meningeal artery
drains the base of the brain (anterior
c) Tentorial artery—anterior meningeal
and medial temporal lobe) from the
artery—inferior hypophyseal artery
anterior perforated substance to join
d) Tentorial artery—dorsal meningeal
the internal cerebral vein and form the
artery—inferior hypophyseal artery
vein of Galen.
e) Tentorial artery—dorsal meningeal
• Vein of Galen or Great cerebral vein: artery—superior hypophyseal artery
Formed by the internal cerebral veins
and the veins of Rosenthal. The vein of 3. Which of the following options better
Galen then joins the ISS to form the describes the trajectory of the cortico-
straight sinus. spinal tract:
a) Primary motor cortex—internal
capsule—corona radiata—cerebel-
4.9 Top Hits lar peduncle—anterior pons—pyra-
mids—spinal cord
4.9.1 Questions b) Primary motor cortex—corona ra-
1. The middle meningeal artery enters diata—cerebral peduncle—anterior
the skull through: pons—pyramids—posterior column
a) Foramen lacerum of the spinal cord
b) Foramen ovale c) Primary motor cortex—corona ra-
c) Foramen rotundum diata—cerebellar peduncle—anterior
d) Foramen spinosum pons—pyramids—anterior and later-
al columns of the spinal cord
2. What are the branches of the mening- d) Primary motor cortex—corona ra-
ohypophyseal trunk? diata—cerebral peduncle—anterior
a) Anterior choroidal artery—posterior cho- pons—pyramids—anterior and lat-
roidal artery—dorsal meningeal artery eral columns of the spinal cord
78
4.9 Top Hits
e) Primary motor cortex—corona ra- c) C6

diata—internal capsule—cerebral pe- d) Clinoid segment of the ICA
duncle—anterior pons—pyramids— e) Common ophthalmic artery
spinal cord
9. The body of the α-motor neurons are
4. Which of the following is correct re- most commonly located in which of
garding the interventricular foramen, the followings:
also known as foramen of Monro? a) Dorsal root ganglia
a) Connects the 4th ventricle with the b) Rexed lamina IX
subarachnoid space c) Anterior spinal root
b) Connects the right lateral ventricle d) Rexed lamina II
with the left lateral ventricle
c) Connects each of the lateral ventri- 10. Which of the following statements is
cles with the 3rd ventricle true regarding the brainstem?
d) Connects the 3rd and 4th ventricles a) The only cranial nerve arising from
e) It is located at the atrium the posterior surface is the 4th cra-
nial nerve
5. Which of the following better de- b) The basilar artery provides blood
scribes the 3rd cranial nerve? supply to the entire anterior sur-
a) It crosses between the PCA and SCA face of the brainstem
b) It has sympathetic fibers coming c) The CN V exits through the pon-
from the Edinger-Westphal n ucleus tomedullary sulcus
c) It reaches the orbit through the op- d) The superior cerebellar peduncle
tic canal crosses between the corticospinal
d) It arises from the pontomedullary tracts in the anterior pons
sulcus
6. Please select the correct statement re-

4.9.2 Answers
garding the pterion:
a) Suture between the frontal-zygo- 1. d. The middle meningeal artery
matic-temporal-sphenoid bones (branch of the internal maxillary
b) Suture between the frontal-sphe- artery), enters the skull through the
noid-temporal-parietal bones foramen spinosum. The foramen lace-
c) Suture between the frontal-zygo- rum is occupied by fibrocartilage
matic-parietal-sphenoid bone resulting from the confluence of the
d) Suture between the frontal-zygo- petrous portion of the temporal bone
matic-parietal-temporal bones with the sphenoid and occipital bones.
The deep and greater petrosal nerves
7. The ambient cistern is located at the cross the lacerum. The foramen ovale
level of: is occupied by the mandibular nerve
a) Anterior midbrain (V3) and lesser petrosal nerve. The
b) Anterolateral midbrain maxillary nerve (V2) crosses the fora-
c) Posterolateral midbrain men rotundum.
d) Posterior midbrain 2. d. The meningohypophyseal trunk
e) None of the above arises from the cavernous segment of
the ICA. Three main branches from
8. The ophthalmic artery most com- this trunk have been described: Tento-
monly arises from: rial artery (Bernasconi and Cassinari
a) ACoA artery), dorsal meningeal artery, and
b) A1 the inferior hypophyseal artery.
79
Neuroanatomy
3. f. Following a craniocaudal order: The 8. c. The most common origin for the
body of the upper motor neuron is lo- ophthalmic artery is the C6 segment
cated at the primary motor cortex, the of the ICA, also known as ophthalmic
axons form the corona radiata which segment (from the distal dural ring to
travels through the posterior limb of the P-Comm). This segment also gives
the internal capsule to reach the mid- the superior hypophyseal artery.
dle three-fifth of the cerebral pedun- 9. b. The α-motor neuron in the spinal
cle, they continue down to the anterior cord are located on Rexed lamina IX.
pons. On the medulla, it forms the pyr- Dorsal root ganglia have the body for
amids decussating approximately 90% the sensory neurons. The anterior spi-
of the fibers in the lower one-third to nal root has the motor axons. Rexed
finally reach the spinal cord where it lamina II has the substantia gelatinosa
travels in two different bundles (ante- for exteroceptive neurons.
rior and lateral corticospinal tract). 10. a. The only CN arising from the poste-
4. c. There are two foramen of Monro. rior surface of the brainstem is the CN
Each of them connects the ipsilateral IV or trochlear nerve. It is also the only
lateral ventricle with the 3rd ventricle. CN which decussates. The BA provides
The 4th ventricle drains CSF to the irrigation mostly to the pons. The CN V
subarachnoid space through one me- exits at the anterolateral surface of the
dial foramen (Magendie) and two lat- pons. The superior cerebellar peduncle
eral foramen (Luschka). There are not crosses at the inferior midbrain.
normal connections between the right
and left lateral ventricles. The 3rd and
4th ventricles are connected through References
the cerebral aqueduct.
[1] Kempe LG. Operative Neurosurgery: Volume 1 Cra-
5. a. Once the CN III leaves the interpe-
nial, Cerebral, and Intracranial Vascular Disease.
duncular cistern, it crosses between Springer Science & Business Media; 2013
the PCA (superiorly) and SCA (inferi- [2] Adel KA, Ronald AB. Functional Neuroanatomy:
Text and Atlas. Functional Neuroanatomy: Text and
orly). The Edinger-Westphal nucleus
Atlas. 2005
provides parasympathetic fibers. The [3] Sara SJ. The locus coeruleus and noradrenergic
only CN occupying the optic canal is modulation of cognition. Nat Rev Neurosci. 2009;
10(3):211–223
the optic nerve (CN II). CN III reaches
[4] Rouviere H, Delmas A. Anatomía humana. Descrip-
the orbit through the superior orbital tiva, topográfica y funcional. 2005;1:336–414
fissure. The CNs at the pontomedul- [5] Perlmutter D, Rhoton AL, Jr. Microsurgical anatomy
lary sulcus are (from medial to lateral) of the distal anterior cerebral artery. J Neurosurg.
1978; 49(2):204–228
CNs VI, VII, and VIII. [6] Cilliers K, Page BJ. Description of the anterior cer-
6. b. The pterion is the suture between ebral artery and its cortical branches: variation in
the frontal-sphenoid-temporal-pari- presence, origin, and size. Clin Neurol Neurosurg.
2017; 152:78–83
etal bones. [7] Rhoton AL, Jr. The supratentorial arteries. Neuro-
7. c. The ambient cistern is located at the surgery. 2002; 51(4, Suppl):S53–S120
posterolateral midbrain. The interpe- [8] Fernandes-Cabral DT, Kooshkabadi A, Panesar SS, et
al. Surgical management of vertex epidural hemat-
duncular cistern is located anterior. oma: technical case report and literature review.
The quadrigeminal cistern is located World Neurosurg. 2017; 103:475–483.
posterior to the midbrain.
80
5 Neuroradiology for the Neurosurgeon
David R Hansberry, Kofi-Buaku Atsina, Mougnyan Cox, Adam E Flanders
5.1 Introduction studies performed during the course of

the typical neurological workup. Advanced
Timely and accurate performance and inter- imaging modalities such as magnetic reso-
pretation of neuroimaging are essential for nance (MR) perfusion, MR spectroscopy, and
the care of the acute neurological patient. diffusion tensor imaging are reserved for
While a detailed neurological examination special indications such as brain tumor
can provide a wealth of specific information imaging at specialized centers.
about the site of pathology in the neuroaxis,
the majority of the central nervous system
(CNS) is occult to the human eye, ear, and 5.2 Computed
touch. It is one of the few systems that can-
not be visually inspected, auscultated, or pal-
Tomography
pated noninvasively. As such, most patients CT is the workhorse for the acute neurologi-
with a neurological problem undergo some cal patient (▶Fig. 5.1, ▶Fig. 5.2); it is fast,
form of imaging, with the specific imaging widely available, and is able to exclude the
test determined by the patient's p
resentation majority of cranial and spinal emergencies
and the acuity of the symptoms. Computed that would require a trip to the o perating
tomography (CT), conventional magnetic room. Unlike MRI, there are no compatibility
resonance imaging (MRI), and ultrasound issues with CT for clinical monitoring devices
comprise the majority of neuroimaging in critically ill patients, and no metal
Fig. 5.1 Axial non-contrast CT of the brain; slice above the ventricles (left), and slice at the
ventricles (right). (Images are provided courtesy of Thomas Jefferson University Hospital.)
81
Neuroradiology for the Neurosurgeon
Fig. 5.2 Axial non-contrast CT of the brain; slice below the ventricles and at the mid-
brain (left), and slice slightly lower at the pons (right). (Images are provided courtesy of
Thomas Jefferson University Hospital.)
screening is required. In the trauma patient, Subtle skull fractures, paranasal sinus/
CT readily shows the presence of blood in the mastoid pathology, and temporal bone dis-
various intracranial compartments. Acute ease are better evaluated on CT than on
hemorrhage is hyperdense on non-contrast radiographs or MRI.
CT in comparison to brain and cerebrospi-
nal fluid (CSF), and is readily detected when
present even in small amounts. Other 5.3 Magnetic Resonance
pertinent information, such as the pres-

ence of midline shift, ventriculomegaly/ MRI provides exquisite soft tissue con-
hydrocephalus, herniation, depressed skull trast and detail of the intracranial
fractures, and radiopaque foreign bodies can (▶Fig. 5.3, ▶Fig. 5.4, ▶Fig. 5.5) and intra-
also be evaluated by CT. In the patient pre- spinal structures, and is therefore the
senting with an acute stroke syndrome, a imaging test of choice whenever direct
non-contrast CT can distinguish between parenchymal assessment of the brain,
hemorrhagic and ischemic strokes, enabling orbits, skull base, cranial nerves, or spi-
timely administration of intravenous tissue nal cord is required. Proper interpreta-
plasminogen activator (tPA) in the absence of tion of an MRI study requires familiarity
other contraindications. It can also help to with the various sequences, the informa-
differentiate conditions that might mimic tion they provide, and their pitfalls/
other neurologic diseases. associated artifacts. Some standard MR
sequences include T1-weighted images
(T1WI), T2-weighted images (T2WI), fluid-
In addition to the detection of acute attenuated inversion recovery (FLAIR),
hemorrhage, CT is also excellent for as- gradient-recalled echo (GRE), diffusion
sessing bony pathology and calcification. weighted imaging (DWI), and post-contrast
T1-weighted images.
82
5.3 Magnetic Resonance
Fig. 5.3 Axial T2-weighted image of the brain. (Image is provided courtesy of Thomas
Jefferson University Hospital.)
Fig. 5.4 Sagittal T1-weighted image of the brain; slice through the midline. (Image is
provided courtesy of Thomas Jefferson University Hospital.)
5.3.1 MRI Sequences

An important caveat is that MRI is not ade- T1WI are good for evaluating anatomy.
quate for the detection of fractures, there- Fat, blood, and proteinaceous products
fore, MRI may be used to supplement but can appear whiter in signal on T1WI.1
not replace CT in the setting of trauma. Application of fat-suppression on T1WI
can distinguish between fat and blood in
83
Fig. 5.5 Sagittal T1-weighted image of the brain; slice off the center (left) and slice
further off center (right). (Images are provided courtesy of Thomas Jefferson University
Hospital.)
cases of a T1 hyperintense mass.2 T2WI technique for the diagnosis of acute cere-
highlight many pathologic processes in bral infarction.3 Areas of acute infarction
the brain that produce either edema or will appear bright on the DWI sequence
areas of signal abnormality which tend to and dark on the corresponding apparent
be lighter in signal intensity on T2WI. diffusion coefficient maps.3 Post-contrast
FLAIR images are also T2WI, but with imaging increases the sensitivity of MRI
suppression of signal from bulk water for detecting pathologic changes in the
such as CSF in the subarachnoid space. brain. Areas of subtle T1 or T2 signal
This allows T2-bright pathologic pro- abnormality sometimes show striking
cesses in the brain or CSF space to be enhancement on the post-contrast
more conspicuous and easier to detect. images, increasing the likelihood that
GRE images are sensitive for the detec- they will be detected. Contrast enhance-
tion of subacute or chronic blood prod- ment can also distinguish between truly
ucts in the brain because of their cystic/nonenhancing lesions and cyst-like
magnetic properties yielding a dark, low, brain masses which will enhance along
or hypointense signal. Hypointensity on their periphery. In general, most patients
GRE is not specific for blood products with suspected intracranial infection or
however, and other substances like cal- tumor who undergo MRI should also have
cium or metal can also appear contrast-enhanced imaging, as this helps
hypointense to varying degrees. DWI is with detection and characterization of
the most sensitive and specific MR intracranial abnormalities.
84
5.4 Clinical Scenarios
5.4 Clinical Scenarios the tentorial leaflets for a similar reason.

The hematoma usually causes mass effect
on the underlying brain, and there may be
5.4.1 Epidural Hematoma
midline shift to the contralateral side. The
Imaging of epidural hematomas is primarily hematoma usually happens on the same
done with CT, as these patients may be side as the soft tissue swelling (i.e., the site
unstable or under consideration for emer- of the traumatic blow), and there is usually
gent decompression. The classic appearance an underlying skull fracture which leads to
of an acute epidural hematoma is a lenti- laceration of the middle meningeal artery.
form or convex hyperdense extra- axial In some instances, epidural hematomas
(external to the brain) mass that does not may also be venous in origin, particularly in
cross the lambdoid or coronal suture the posterior fossa.4
lines (▶Fig. 5.6). However, epidural hemato-
mas can cross the midline sagittal suture as
the periosteal layer of the calvarium forms
5.4.2 Subdural Hematoma
the outer layer of the dura, and extravasated Subdural hematomas are located in the
blood would be external or “epi”-dural to potential space between the dura mater
this layer. Epidural hematomas can cross and the pia-arachnoid mater. In older
Fig. 5.6 Left epidural hematoma. A 32-year-old male with witnessed fall from a ladder.
Axial nonenhanced CT scan was performed in the emergency room. (a) Soft tissue win-
dow shows lentiform-shaped hyperdense blood products along the left frontotemporal
convexity. The hematoma does not cross suture lines indicating that it is within the epi-
dural space. There is mild mass effect on the underlying brain tissue. Also note overlying
scalp welling adjacent to the extra-axial blood. (b) Bone window shows a nondisplaced
temporal bone fracture in the region of the hematoma. Findings are compatible with
acute epidural hematoma, and is most likely from injury to the left middle meningeal
artery. (Images are provided courtesy of Thomas Jefferson University Hospital.)
85
patients, these collections may occur after

minimal trauma as a result of brain atro-
phy and stretching of the cortical bridging
veins, which makes them vulnerable to
injury. In younger patients, these collec-
tions occur after substantial trauma, and
are usually located opposite to the side of
traumatic head impact. On CT, subdural
hematomas typically appear as hyper-
dense crescentic collections that cross
suture lines. In the region of the vertex or
falx cerebri, subdural hematomas layer
along the falx and tentorial leaflets w
ithout
crossing these structures. One important
pitfall on CT to be aware of are older hema-
tomas that have degraded and therefore
may appear of similar density to the adja-
cent brain (i.e., an isodense subdural col-
lection), and may be difficult to detect
without a high index of suspicion (▶Fig. 5.7). Fig. 5.7 Isodense left subdural hema-
In the absence of significant midline shift, toma. A 69-year-old female presents
abnormal thickening or blurring of the with chronic headache. Axial nonen-
gray matter on the side of the isodense hanced CT scan shows concave-shaped
subdural hematoma may be the only isodense blood products along the left
f inding on CT. hemispheric convexity. The hematoma
crosses suture lines indicating that it is
within the subdural space. There is mild
mass effect on the underlying parenchy-
Equivocal cases of suspected isodense or ma but no midline shift. These findings
thin subdural hematomas can be con- are compatible with subacute subdural
firmed on MRI, which can show extremely hematoma. (Image is provided courtesy
thin collections on FLAIR images. of Thomas Jefferson University Hospital.)
5.4.3 Subarachnoid The location of the greatest amount of SAH

can be a clue to the location of the ruptured
Hemorrhage aneurysm; focal clot in the anterior inter-
Subarachnoid hemorrhage (SAH) has a dis- hemispheric fissure is classic for a ruptured
tinctive appearance on CT, with hyperden- anterior communicating aneurysm, or a
sity conforming to the cisterns and sulci of focal clot or large SAH in the Sylvian cistern
the brain (▶Fig. 5.8). The most common is suggestive of a ruptured middle cerebral
cause of SAH is trauma, which usually pres- artery (MCA) aneurysm.5 A pertinent find-
ents with scattered areas of sulcal hyper- ing to include in every imaging evaluation
density on CT. This is in contradistinction of aneurysmal SAH is the presence or
to aneurysmal SAH, which usually presents absence of hydrocephalus. Ventricular dila-
with large or diffuse dissemination of tation, particularly of the temporal horn, is
hyperdense material in the sulci and cis- a key imaging feature of acute hydrocepha-
terns at the base of the brain (▶Fig. 5.8). lus on CT.6
86
Fig. 5.8 Diffuse subarachnoid hemorrhage. A 41-year-old male presents with a

thunderclap headache and syncope. Axial nonenhanced CT scan is performed in the
emergency room. (a) There is diffuse distribution of high density material, representing
acute blood products within the cerebral sulci of the temporal, insula, and frontal lobes,
as well as along the anterior interhemispheric fissure. (b) There are acute blood prod-
ucts within the cerebral sulci bilaterally, Sylvian fissures, as well as the interpeduncular,
crural, and ambient cisterns. There is an intraparenchymal component of hemorrhage
within the left medial frontal lobe. Findings are compatible with aneurysmal type SAH.
The accumulation of blood products within the region of the anterior communicating
artery suggests the possibility of anterior communicating artery aneurysm rupture as
the cause. (Images are provided courtesy of Thomas Jefferson University Hospital.)
5.4.4 Parenchymal
Abnormally low signal may be seen Hemorrhage
around the ventricles in cases of acute
Hypertension is the most common cause
hydrocephalus, which represents tran-
of nontraumatic parenchymal hematoma
sependymal CSF flow or flow that is im-
in older patients. In nonhypertensive
peded from the normal resorption
elderly patients, cerebral amyloid angi-
pathway at the convexity.
opathy is a leading cause. Hemorrhagic
conversion of a recent infarct or hemor-
rhage into an existing neoplasm should
On MRI, SAH can be seen as abnormally also be considered in older patients.
bright signal in the CSF spaces on FLAIR An intraparenchymal hematoma in a
imaging. Hypointense material in the young adult raises a different specter of
sulci may also be seen on the GRE diseases, with other etiologies like an
sequence. underlying vascular malformation or
87
illicit drug use being among the leading “dense cerebellum” sign).10 CT findings in
considerations.7 early cerebral edema can be easily missed,
Acute parenchymal hematomas appear particularly in young patients without
as hyperdense space-occupying masses much atrophy. However, the basal cisterns
on CT. If hemorrhage occurs close to the should always be visible on head CT in
ventricular surface, the hematoma may every patient.
dissect into the ventricle with secondary
intraventricular hemorrhage and possibly
hydrocephalus. The volume of parenchy-
mal hematoma has been correlated with 5.4.6 Ischemic Stroke
risk of morbidity and mortality.8 Other CT is insensitive for early acute infarction.
important imaging findings to note (or The main role of CT is to exclude intracra-
to ask the radiologist about) are the nial hemorrhage or large areas of com-
presence and degree of midline shift, and pleted infarction prior to intravenous tPA
evidence of herniation (manifested as infusion.
effacement/obliteration of the CSF spaces
surrounding the brain). As acute hemato-
mas evolve, the degree of surrounding
edema increases, peaks, and then gradu- Imaging findings in early acute ischemic
ally subsides. The hematoma eventually stroke are subtle, but include loss of gray-
fades and disappears from the outside in, white differentiation, blurring/indistinct-
reminiscent of a melting ice cube. ness of the basal ganglia, loss of the
insular cortex, and a hyperdense ves-
sel (from thrombus).11
5.4.5 Cerebral Edema
Diffuse cerebral edema can be seen after MRI is much more sensitive for the detec-
trauma or prolonged anoxia, and findings tion of acute stroke, and shows restricted
on CT can be subtle when imaging is per- diffusion conforming to the territory of the
formed early in the disease course. Typi- occluded artery (▶Fig. 5.9, ▶Fig. 5.10,
cal CT findings include loss of gray-white ▶Fig. 5.11, ▶Fig. 5.12, ▶Fig. 5.13 ).3 MRI can
differentiation, effacement of the basal also be used to detect subtle hemorrhagic
cisterns and cortical sulci (due to cerebral conversion of acute ischemic stroke, which
swelling), and increased attenuation of would be best visualized on the GRE
the falx, tentorium, and subarachnoid sequences.
spaces.
5.4.7 Aneurysms
The increased attenuation of the CSF
Familiarity with imaging, treatment, and
spaces in diffuse cerebral edema is multifac
surveillance of intracranial aneurysms is
torial, but can be mistaken for SAH (so-called
an important part of any neurosurgical
“pseudo-subarachnoid” pattern).9
practice. In general, the two main noninva-
sive methods for diagnosing intracranial
There may also be relatively low attenua- aneurysms are CT or MR angiography. CT
tion of the cerebral hemispheres compared has several advantages over MRI in the
with the cerebellum, causing the cerebel- acute setting. In addition to being more
lum to appear artifactually dense (so called widely available and quicker to perform,
88
Fig. 5.9 Acute right middle cerebral artery distribution infarct. A 55-year-old male
presents with left hemiparesis and confusion. (a) CT scan shows wedged-shaped area
of low attenuation involving both gray and white matter in the right MCA territory con-
sistent with cytotoxic edema. (b) Diffusion weighted imaging and (c) apparent diffusion
coefficient maps show corresponding areas of high signal and low signal respectively
consistent with restriction of diffusion. (d) T2 and (e) fluid-attenuated inversion
recovery maps show corresponding white matter signal abnormality. Findings are
compatible with an acute right MCA territory infarction. (Images are provided courtesy
of Thomas Jefferson University Hospital.)
virtually all invasive monitoring devices MRI is advantageous in younger pa-

for acutely ill patients are essentially CT tients undergoing surveillance for small
compatible. unruptured/untreated aneurysms as no
radiation is involved and contrast admin-
istration is not required. On both imaging
modalities, aneurysms appear as focal
The spatial resolution of CT is superior to dilatations or outpouchings in the vessel
MRI, however, even 1–2 mm aneurysms wall, usually at branching points or areas
are readily identified on with modern MR of stress. While all the vessels should be
angiography (MRA) techniques. inspected, common sites of occurrence
that should undergo additional scrutiny
89
Fig. 5.10 Subacute left anterior cerebral artery distribution infarct. A 59-year-old male
presents with right lower extremity weakness. (a) Non-contrast CT scan shows an area
of low attenuation involving both gray and white matter in the left anterior cerebral
artery territory consistent with cytotoxic edema. (b) Diffusion weighted imaging and
(c) apparent diffusion coefficient maps show corresponding patchy areas of high signal
respectively consistent with facilitated diffusion. (d) T2 and (e) FLAIR maps show corre-
sponding white matter signal abnormality. Findings are compatible with a subacute left
anterior cerebral artery territory infarction. (Images are provided courtesy of Thomas
include the anterior communicating 5.4.8 Arterial Dissection

(AComm) complex, MCA bifurcation,
basilar tip, and o rigins of the posterior Arterial dissections occur as a result of a tear
communicating (PComm) arteries. In in the intima of the vessel wall, with dissec-
general, angiography is better for sur- tion of blood into the media of the wall cre-
veillance of surgically clipped aneurysms ating a false lumen adjacent to the true
as the artifacts produced by the metal- lumen. On cross-sectional imaging, there is
lic clips prohibit a dequate assessment usually irregularity and narrowing of the
of the adjacent v asculature, while MRA true lumen, with eccentric thickening or
is superior for follow-up of coiled aneu- slight dilatation of the outer circumference
rysms.12,13 of the vessel wall by thrombus/subacute
90
Fig. 5.11 Acute left occipital lobe infarct. A 32-year-old male presents with syncope
and visual disturbance. (a) Non-contrast CT scan shows an area of low attenuation
involving both gray and white matter in the left posterior cerebral artery territory con-
sistent with cytotoxic edema. (b) Diffusion weighted imaging and (c) apparent diffusion
coefficient maps show corresponding areas of high signal and low signal respectively
consistent with restriction of diffusion. (d) T2 and (e) fluid-attenuated inversion recov-
ery maps show corresponding white matter signal abnormality. Findings are compati-
ble with an acute left posterior cerebral artery territory infarction. (Images are provided
courtesy of Thomas Jefferson University Hospital.)
blood in the media of the vessel wall. Con- resultant local or distal vascular occlusion
ventional MR images may show loss of the and infarction.
expected flow void in the compromised
vessel, or narrowing of the flow void with
5.4.9 Intracranial Infection
abnormal hyperintense signal in the vessel
wall on T2WI or fat-suppressed T1WI.14 Imaging for meningitis is usually per-
Arterial dissections may be complicated by formed to exclude any related process such
formation of a pseudo-aneurysm if the dis- as abscess. The main role of MRI is to
secting blood weakens the adventitial lining exclude complications of meningitis, and
of the vessel wall. Thromboembolic compli- contrast-enhanced MRI is the modality of
cations can also occur if the intramural choice. MR findings in meningitis include
hematoma re-enters the true lumen, with abnormal hyperintensity of the CSF spaces
91
Fig. 5.12 Acute right pontine

infarct. A 53-year-old female
with a history of basilar throm-
bosis who presents with new
right hemianopia and change
in mental status. (a) CT scan
shows an area of low atten-
uation involving right pons.
(b) Fluid-attenuated inversion
recovery image shows corre-
sponding signal hyperintensity
in the region in question.
(c) Diffusion weighted imaging
and (d) apparent diffusion
coefficient maps show corre-
sponding areas of high signal
and low signal respectively
consistent with restriction of
diffusion. Findings are compati-
ble with an acute right pontine
infarction. Also note additional
punctate areas of restricted
diffusion in the left cerebellar
hemisphere. (Images are
provided courtesy of Thomas
from exudate on FLAIR images, with with CT/MR showing a ring-enhancing col-
abnormal leptomeningeal enhancement lection in the parenchyma, with surround-
and/or enhancement of the basal cis- ing vasogenic edema. Restricted diffusion on
terns.15 However, the MRI may also be nor- DWI sequences may be seen within the cen-
mal in many cases of viral meningitis, and tral portion of the abscess reflecting puru-
all clinically suspected cases of meningitis lent material, a finding that is helpful in
should undergo lumbar puncture and CSF distinguishing abscesses from tumors on
analysis to exclude infection. Complica- MRI.16
tions of meningitis include hydrocephalus,
empyema formation, and vasculopathy
with cerebral infarction.
5.4.10 Brain Tumor
Requests to exclude cerebral abscesses The initial analysis of any brain tumor on
are a common reason for imaging patients imaging begins with an assessment of
with suspected CNS infections. Mature cere- whether the mass is intra-axial (within the
bral abscesses are focal parenchymal collec- substance of the brain) or extra-axial (intra-
tions of purulent material, surrounded by a cranial, but external to the substance of the
well-vascularized wall.15 These histologic brain). Intra-axial masses include primary
characteristics are reflected on imaging, brain tumors (of which glioblastoma
92
Fig. 5.13 Right posterior inferior cerebellar artery distribution infarct. A 59-year-old
female presents with dizziness and change in mental status. (a) CT scan shows an
area of low attenuation involving both gray and white matter in the right cerebellar
hemisphere within the region supplied by the right posterior inferior cerebellar artery.
(b) Diffusion weighted imaging and (c) apparent diffusion coefficient maps show corre-
sponding areas of high signal and low signal respectively consistent with restriction of
diffusion. (d) T2 and (e) fluid-attenuated inversion recovery maps show corresponding
white matter signal abnormality. Notice that there is right cerebellar edema, with mass
effect on the right dorsal upper medulla. Findings are compatible with an acute right
posterior inferior cerebellar artery territory infarction. (Images are provided courtesy of
Thomas Jefferson University Hospital.)
multiforme [GBM] is the most common) masses tend to arise from and expend the
and metastases. Extra-axial masses include brain parenchyma. There may also be a rim
tumors arising from the meninges (classi- or “claw” of brain tissue reaching around
cally the meningioma), calvarium, synchon- the mass, which is another clue that the
droses, and metastases. The distinction lesion is intra-axial in origin. In cases where
between intra-axial and extra-axial masses an extra-axial mass subsequently invades
is not always clear-cut, but in general, the adjacent brain parenchyma, or an
extra-axial masses have a well-demarcated intra-axial mass secondarily involves the
interface between the cortex/brain paren- meninges, it can be difficult to determine
chyma and the mass, while intra- zaxial the origin of the mass.
93
Extra-axial Masses the most common CNS malignancy in

adults. Metastases are frequently multi-
Meningiomas are the classic extra-axial ple, bilateral, of varying sizes, and cen-
mass, and probably the most common tered in the gray-white matter junction.
extra-axial masses encountered on imag- However, solitary brain metastases are
ing in any neurosurgical practice. Meningi- also common, can occasionally be diffi-
omas are usually dural based, with a broad cult to distinguish from primary brain
contact surface with the dura. There may malignancy.17
be an enhancing dural tail at the edge of
the mass, which is commonly associated
with (but not specific for) meningiomas. One helpful finding is that metastases
On non-contrast CT, meningiomas are tend to incite extensive vasogenic edema
hyperdense relative to the brain paren- in the surrounding brain parenchyma,
chyma and may also have calcification. best visualized on the FLAIR images.
There is usually hyperostosis (sclerosis and
thickening) of the bone adjacent to the
meningioma. On post-contrast CT and MR, Small cortical metastases may have little, if
meningiomas usually enhance homoge- any, vasogenic edema, and may only be
neously. Dural-based metastases can look conspicuous as enhancing masses on the
similar, so it is always important to ask post-contrast images. In unclear cases, im-
about a history of cancer when one aging the chest, abdomen, and pelvis to
encounters an enhancing extra-axial mass. look for an occult primary can provide
some guidance regarding the origin of a
solitary brain tumor.
Intra-axial Masses
GBM is the most common primarily malig- Pearls
nant brain tumor in adults, and is the
quintessential primary intra-axial mass. • Develop a systematic method
evaluating each imaging modality to
GBMs are usually centered in the supraten-
ensure no pathology is inadvertently
torial cerebral hemispheres and preferen-
missed.
tially infiltrate the brain widely through
white matter tracts, sometimes involving • Evaluate all imaging personally and
do not rely solely on radiologic
the contralateral hemisphere via the cor-
interpretation of imaging.
pus callosum and anterior commissure.
The enhancing component of a GBM is • Utilize 3D reconstructions to better
delineate fractures, extra-axial
usually just the most obvious (usually
hematomas, and the location of
necrotic) component of the tumor. Viable
intracranial pathology.
nonenhancing tumor is usually present in
the surrounding T2/FLAIR signal abnor- • Review all sequences when reviewing
an MRI as each can distinctly
mality in the region of the tumor. Other
highlight a variety of pathologies.
disease processes that tend to favor
involvement of or spread along white mat- • Compare changes over time utilizing
the same imaging modality. However,
ter tracts include lymphoma and demye-
be aware that the gantry angle of a
linating disease.
CT can change the appearance of a
The other major consideration for an
lesion.
intra-axial tumor is metastasis, which is
94
5.5 Top Hits
5.5 Top Hits 4. b. A negative MRI does not rule out

meningitis. Lumbar puncture and CSF
analysis should be performed.
5.5.1 Questions
1. What imaging modality is first re-
quired for the evaluation of neurologi-
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[10] Han BK, Towbin RB, De Courten-Myers G, McLau-
rin RL, Ball WS, Jr. Reversal sign on CT: effect of
anoxic/ischemic cerebral injury in children. AJR Am
5.5.2 Answers J Roentgenol. 1990; 154(2):361–368
[11] von Kummer R, Meyding-Lamadé U, Forsting M,
et al. Sensitivity and prognostic value of early CT in
1. c. This can expediently evaluate for in- occlusion of the middle cerebral artery trunk. AJNR
Am J Neuroradiol. 1994; 15(1):9–15, discussion
tracranial hemorrhage, contusions and 16–18
skull fractures in the acute setting. The [12] Wallace RC, Karis JP, Partovi S, Fiorella D. Noninva-
presence of contrast can confuse eval- sive imaging of treated cerebral aneurysms, part I:
MR angiographic follow-up of coiled aneurysms.
uation for hemorrhage as contrast is AJNR Am J Neuroradiol. 2007; 28(6):1001–1008
also hyperdense. [13] Wallace RC, Karis JP, Partovi S, Fiorella D. Non-
2. b. Acute infarctions show restricted invasive imaging of treated cerebral aneurysms,
Part II: CT angiographic follow-up of surgically
diffusion on diffusion maps. clipped aneurysms. AJNR Am J Neuroradiol. 2007;
3. b. To evaluate for complications of 28(7):1207–1212
meningitis such as abscess, empyema, [14] Rodallec MH, Marteau V, Gerber S, Desmottes L,
Zins M. Craniocervical arterial dissection: spectrum
thrombosis and infarction.
95
of imaging findings and differential diagnosis. Radi- [16] Chang SC, Lai PH, Chen WL, et al. Diffusion-
ographics. 2008; 28(6):1711–1728 weighted MRI features of brain abscess and cystic
[15] Foerster BR, Thurnher MM, Malani PN, Petrou M, or necrotic brain tumors: comparison with conven-
Carets-Zumelzu F, Sundgren PC. Intracranial in- tional MRI. Clin Imaging. 2002; 26(4):227–236
fections: clinical and imaging characteristics. Acta [17] DeAngelis LM. Brain tumors. N Engl J Med. 2001;
Radiol. 2007; 48(8):875–893 344(2):114–123
96
6 Operating Room
Hanna Algattas, Kristopher Kimmell, G Edward Vates
6.1 Introduction
The operating room may be a confusing Being prepared as a trainee is essential,
landscape for the trainee to navigate, espe- including reading regarding the case at
cially early in one’s training. While much hand, knowing the basic anatomy, instru-
focus is rightfully placed on the techniques ments, and basic suturing and knot tying.
and steps to a given operation there are a
multitude of additional workings, prepara-
tions, and members which are key to any
successful procedure. Familiarizing oneself
6.3 Cranial Positioning
with ancillary staff and appropriate posi-
tioning, in addition to technical maneu-
6.3.1 Pterional
vers, will both streamline and improve the The pterion is the region where the fron-
likelihood of a positive outcome for the tal, parietal, temporal, and sphenoid
operation. bones meet. Patients are placed supine
in Mayfield three-point fixation. If the
head is rotated more than 30°, an ipsilat-
6.2 Operating Room eral shoulder roll is placed to reduce
muscular tension and venous outflow
6.2.1 Etiquette obstruction. The thorax is elevated
Understanding the roles of operating room 10–15° to reduce venous distension and
staff members and the expectations of the the neck is extended 10–15° to aid in
trainee are essential to a promising opera- retracting frontal lobe so skull base is
tive learning experience. Ultimately, the more accessible; a good landmark is the
role of the student is at the discretion of maxillary eminence which will be the
the surgical staff. Politely asking the highest point of the field. The pterional
attending or resident surgeon to “scrub in” craniotomy is tremendously versatile
is a start. Regardless of being able to assist and the degree of head rotation is useful
with the procedure or not, students are in projecting the approach towards dif-
expected to assist with preoperative and ferent segments of the anterior and mid-
postoperative care. Assisting with inser- dle fossae (▶Table 6.1).1,2
tion of Foley’s catheters and lines, patient
positioning, Mayfield placement, and addi-
6.3.2 Frontal
tional adjunctive measures are helpful.
Transferring the patient to a bed and Patients are placed supine in Mayfield
assisting with transport postoperatively three-point fixation with the head rotated
are also helpful. Asking thoughtful ques- 20–30° towards the contralateral shoulder
tions is invited but should not be done depending on the side of the operation.
during critical portions of the case. If per- A shoulder roll may be placed beneath
mitted to assist with the procedure, the the ipsilateral shoulder. Similarly to the
trainee’s role is highly dependent on the pterional craniotomy, the thorax may be
wishes of the lead surgeon and residents. elevated.3
97
Operating Room
Table 6.1 Pterional craniotomy positioning

Head rotation Exposure Example
30 Posterior Posterior communicating/basilar aneurysms
45 Middle Middle cerebral artery aneurysms
60 Anterior Anterior communicating aneurysms
6.3.3 Temporal prep a portion of the abdomen for harvesting

of a fat graft used in closure of the defect.
Patients are placed supine in Mayfield Adjunctive measures utilized include an oro-
three-point fixation with the thorax ele- gastric tube and packing the nose with
vated 10–15°. Importantly, the head is pledgets soaked in oxymetazoline prior to
rotated nearly a full 90° towards the contra- surgery to prevent drainage of blood into the
lateral shoulder such that it is horizontal; esophagus and bleeding, respectively.6
an ipsilateral shoulder roll is essential to
achieve this degree of rotation without
injury, postoperative muscular rigidity, and 6.4 Spinal Positioning
blockage of venous outflow through the
jugular system whiczh prevents brain relax- 6.4.1 Anterior Cervical
ation (▶Fig. 6.1).1,4 Due to the significant
degree of head rotation required, many Anterior cervical approachs are commonly
surgeons prefer to actually position these used for anterior cervical discectomy and
patients in the lateral decubitus position. fusion (ACDF) and odontoid fractures but
also in cases of carotid endarterectomy.
Patients are positioned supine, in slight
6.3.4 Occipital extension, with the head supported on a
Multiple positions are used for the occipital soft gel pad or horseshoe. Interscapular
craniotomy, all in Mayfield three-point fixa- rolls to maximize extension are used based
tion. Positions include three-quarter prone, on surgeon’s preference. Depending on the
semi-sitting position, or lateral oblique.1,3 pathology, head rotation may be helpful
Variants will allow positioning for retro- in reaching high cervical lesions. The
mastoid, suboccipital, far lateral, and infra- approach is usually off of midline and
tentorial supracerebellar approaches. many prefer approaching from the left due
to relatively increased protection of the left
recurrent laryngeal nerve by the espoha-
6.3.5 Transsphenoidal gus and trachea compared to the right
Patients are placed supine in either Mayfield nerve.7 Incision is often made through a
three-point fixation or with their head placed pre-existing skin crease to enhance post-
on a gel donut or horseshoe. As in most crani- operative cosmesis.
otomies the head is extended approximately
15°. The head may be kept midline or angled
15–20° towards the neurosurgeon. Especially Typically the hyoid bone approximates the
in endoscopic procedures where ENT sur- C3–C4 vertebrae, thyroid cartilage approx-
geons are often present, proper positioning imates C4–C5, cricothyroid membrane
of surgeons around the patient is vital for approximates C5–C6, and C6–C7 is often
ease of instrumentation and visualization on two fingerbreadths above the clavicle.3
adjacent screens.5 The surgeon may opt to
98
6.4 Spinal Positioning
Fig. 6.1 Temporal craniotomy positioning. Right temporal craniotomy approach po-
sitioning. (a) Location of the temporalis and superficial temporal artery. The degree of
head rotation is near 90° and an ipsilateral shoulder roll is placed to achieve additional
rotation. (b) The incision and location of temporalis muscle detachment is noted with
a dotted lines. A cuff of muscle is often left for reattachment of the temporalis muscle
to prevent temporal wasting. Relationship of the superficial temporal artery and muscle
to the coronal suture, zygoma, and tragus can be seen. 1. Skin incision; 2. tempora-
lis muscle incision; 3. midline; 4. vertex; 5. superficial temporal artery; 6. zygoma.
(Reproduced from Nader R, Gragnanielllo C, Berta S et al, Neurosurgery Tricks of the
Trade: Cranial, 1st edition, ©2013, Thieme Publishers, New York.)
99
Operating Room
6.4.2 Posterior Cervical potentials (SSEPs), motor evoked poten-

tials (MEPs), and/or electromyography.6
Posterior cervical approaches are well- Many cases will use a C-arm or O-arm for
suited for a number of pathologies including intraoperative imaging. C-arm provides
radiculopathies, cervical spine fractures, intraoperative two-dimensional fluoroscopy
cervical spondylosis, and high cervical whereas the O-arm has three-dimensional
pathologies which are difficult to reach capabilities. The O-arm allows quicker
anteriorly. Patients are placed prone typi- placement of pedicle screws, less radiation
cally on a Jackson-frame table, in slight flex- to the surgeon staff, but more exposure to
ion, and in either Mayfield fixation or on a the patient when compared with standard
gel donut/horseshoe with adequate padding fluoroscopy.9
to avoid postoperative visual loss.3 Arms are
either abducted to a maximum of 90° to pre-
vent axillary nerve stretch injury and flexed 6.5 Positioning-Related
at the elbow or slung at the patient’s side in
a “ski-jump” position. Appropriate padding
Complications
of weight-bearing areas, including the chest
are necessary to prevent bruising. The sit-
6.5.1 Peripheral Nerve
ting position for posterior cervical proce- Injuries
dures has many appealing advantages
Perioperative peripheral nerve inju-
including more easily verified spinal align-
ries (PPNI) are most often caused by isch-
ment, reduced radiographic shoulder arti-
emia, stretch, or compression. The ulnar
fact, and a drier operative field. The major
nerve is the most commonly injured and
theoretical complication is air embolism in
may cause weakness of opposition and
this position however data suggests the
abduction in the 5th digit with reduced
occurrence of this event relative to the mul-
sensation of the 4th and 5th digits. Brachial
titude of benefits is rare.8
plexus injury is the second most common
PPNI and is often due to prolonged and
6.4.3 Posterior extensive stretch. The superman prone
position places multiple components of
Thoracolumbar the brachial plexus at risk of stretch-
Positioning and preparation of cases, related injury; tucking of arms at the side
especially for spine, begins early with
may reduce risk. Use of appropriate pad-
acquisition of preop imaging. Obtaining ding beneath elbows and care to avoid
flexion-extension films may allow detec- excessive neck extension, shoulder abduc-
tion of dynamic instability which impacts tion, and nonphysiologic positions help
surgical and positioning decision making. reduce risk of these injuries.10,11,12
The prone position on either a Jackson
table, Wilson frame, or Andrews frame is 6.5.2 Visual Loss
the typical setup for posterior thoracolum-
bar cases. Care is taken to pad the appro- Postoperative visual loss is a serious com-
priate pressure points to avoid injury. plication often occurring in prolonged
Depending on the procedure, a variety of prone cases such as spine surgery. Injury is
adjuncts are available to the surgeon. In primarily attributed to ischemic optic neu-
cases where manipulation of the spinal ropathy and/or central retinal artery occlu-
cord and nerve roots is expected, surgeons sion. Excessive blood loss, hypotension,
may opt to use somatosensory evoked and prolonged operative time are risk
100
6.7 Bedside Procedures
factors for postoperative visual loss. • Preoperative placement of external ven-

Appropriate padding and maintaining tricular or lumbar drain, especially in
mean arterial pressure and hemoglobin endoscopic endonasal approaches.5
levels close to preoperative values is espe- • Intraoperative burst suppression.
cially useful in high-risk patients.10
Air Embolism 6.7 Bedside Procedures

Air embolism is a complication encoun-
tered when air enters the venous system
6.7.1 Lumbar Puncture/
due to an opening in non-compressible Drain
veins. The reported incidence varies but is
Equipment: Lumbar puncture kit (spinal
much higher in surgical positions where
needle with plug, collection tubes, iodine
the head is elevated relative to the right
preparation sponges, sterile draping, lido-
atrium (e.g., sitting position). For instance,
caine with epinephrine, opening pressure
recent estimates of air embolism in the
barometer and connecting valve, sterile
semi-sitting position are 21%; however,
normal saline, syringe), marking pen, ster-
there were few direct effects on postopera-
ile gloves.
tive morbidity in that study.13 Entry of air
1. Properly set-up the work area and po-
with the head elevated blocks venous
sition patient in the lateral decubitus
return at the right atrium and leads to
position with hip and knee flexion.
hypotension. The earliest indicator may be
Ensure that patient’s shoulders are
a drop-in end-tidal pCO2. Treatment upon
squared.
identification includes occluding further
2. Mark appropriate entry zone. Anterior
air entry at site, lowering level of the head
superior iliac crests mark L4–L5 disc
below the right atrium, compressing jugu-
space. One space above or below will
lar veins to prevent further air entry, 100%
avoid risking spinal cord injury. Note,
oxygen ventilation, and aspirating air from
it will be easier to palpate midline at
the right atrium if a central venous pres-
the thoracic spine due to its kyphotic
sure (CVP) catheter was employed. If sit-
curvature and then extrapolate mid-
ting position must be used, there are useful
line into the lumbar spine assuming
adjuncts to reduce risk of air embolism
no scoliotic spine.
including elevating legs to level of right
3. After marking, set up your sterile lum-
atrium which reduces the pressure gradi-
bar access kit and don sterile gloves.
ent by which air embolism may occur.1,14
4. Widely prepare the region with beta-
dine and place sterile drapes over top.
6.6 Cerebral Relaxation 5. Inject lidocaine with epinephrine sub-
cutaneously and deeper along the
• Head rotation, flexion, and extension for track of the spinal needle.
gravity-based lobe retraction. 6. Repalpate and aim the needle to enter
• Maintain venous outflow. For example, with the spinal needle at a slightly ros-
avoid tight overly tight cervical collars tral angle in between two spinous
or over-rotating head. processes.
• Administration of hyperosmolar agents 7. Upon entry of spinal needle, you will
including mannitol. often feel bone which may be the spi-
• Knowledge of cisternal anatomy and se- nous process or lamina and will re-
lective cerebrospinal fluid (CSF) drainage. quire repositioning the needle towards
101
Operating Room
the inter-laminar space. Do not swing

the needle but rather draw back
slightly, re-angle, and move forward. A Caution: Avoid excessive loss of spinal
“pop” may be felt upon entry through fluid which may cause collapse of the
dura. thecal sac, thus making threading the

8. Remove the spinal needle stylet and catheter more difficult.
observe for CSF egress. When egress
is confirmed, take care to reduce
the amount of additional CSF that is 12. After ensuring continued CSF flow,
lost. carefully remove the spinal needle.
9. When entry into thecal sac is con- Grasp the catheter to prevent its mobi-
firmed, take care to avoid moving the lization further inside or outside the
spinal needle and attach the barome- canal.
ter for an opening pressure reading. An
opening pressure is most accurate
when patients straighten their legs Caution: Avoid rotating the spinal needle
from their flexion position. The flex- which may sever the proximal catheter in
ion position provides a slight overesti- the canal.
mate of opening pressure. *
10. After removing the barometer, fill col-
lection tubes with CSF (often 4–6 cc of 13. Pledget jackets can be used to secure
CSF per tube). Excessive drainage the catheter in place.
should be avoided with posterior fossa 14. Coil the excess catheter tubing in a
crowding or with suspected ruptured strain relief loop and secure at the
aneurysms. midline on the back using staples and/
11. When CSF is completely collected, the or suture. Take care to avoid punctur-
barometer may be connected for a ing the catheter.
closing pressure. 15. Lead the catheter over to the side of
12. Remove the barometer, replace spinal the patient’s lower back and secure
needle plug, and carefully remove the the drain system in place with multi-
needle apparatus. ple Tegaderm bandages.
13. Place a bandage or dressing over the 16. Set up the lumbar drain system to the
site and clean the area of betadine external collection system.
which is a skin irritant.
*The below steps diverge from the above if 6.7.2 External Ventricular
a lumbar drain is being placed. Drain
10. The lumbar drain spinal needle is
placed into the interspinous space Equipment: External ventricular drain
similarly to a lumbar puncture. The (EVD) catheter and cranial access kit, lido-
bevel should be facing up on insertion caine with epinephrine, sterile attire,
and should be rotated to face rostral nylon suture, sterile instruments (clamp,
prior to threading of the catheter. forceps, scissor), skin stapler, sterile nor-
11. The lumbar drain catheter will be rap- mal saline, razor/scissors for hair removal.
idly fed into the spinal needle so that Follow institution-specific protocols;
3–4 black dots are visualized on the some will require a single dose of antibiot-
outer segment. ics such as cefazolin (Ancef) prior to
102
6.7 Bedside Procedures
placement. EVDs will most often be placed from the drill tip and tighten the drill-
on the right side unless the clinical situa- bit into the chuck.
tion suggests otherwise.
1. Clear the appropriate work area and
position the patient to ensure your
comfort and access to instruments. Caution: Neglecting to use the drill stop-
2. Shave and clean the site. per increases risk of plunging through
3. Make preliminary markings based on dura and cerebral tissue.
measures and anatomical landmarks.
• Measure 11 cm posterior to the na-
sion (nasion: divot between nose 10. Measure out 6.5–7.0 cm on the cathe-
and glabella). ter either with a sterile marker or a
◦◦ If the anatomy is unusual (e.g., 2–0 silk tie. This will be the mark for
growth hormone-secreting ade- how deep the catheter should be
noma) then a rough approxima- passed. If 7.0 cm is used, the tied mark
tion may be 1 cm anterior to the is often left at the outer table of cra-
coronal suture, if palpable. nium, 6.5 cm at the inner table of
• Measure 3 cm to right of midline cranium (▶Fig. 6.2).
which is approximately at the mid-
pupillary line (drawing a sagittal
line and examining from a distance Caution: Passing a catheter further than
can ensure appropriate placement). 7.0 cm drastically increases risk of dam-
4. Place trajectory marks. Upon inser- aging sensitive structures including mid-
tion, EVD will be angled at ipsilateral brain and prominent vasculature.
medial canthus and 1 cm anterior to
ipsilateral tragus.
5. Inject lidocaine with epinephrine to 11. Carefully bend the tunneling trocar.
your site. Do not bend to an acute angle which
can make tunneling more difficult.
12. Carefully clean the procedural site and
place sterile drapes.
Caution: Excessive injection and swelling
13. Remeasure your site. Make an approx-
of tissue may slightly distort landmarks.
imately 2 cm incision to the bone at
your marked site. Use the blunt scalpel
6. While lidocaine takes effect, open your end to strip pericranium from the site.
sterile equipment, place at a nearby Place a retractor.
location, and ensure a trash receptacle 14. Quickly achieve a satisfactory degree
is nearby. Make sure all appropriate of hemostasis and remeasure your ap-
components of the kit are in place. propriate burr hole site. Mark the bone
Open sterile items and drop them onto if desired.
your field. 15. Drill burr hole with careful attention
7. Don sterile attire. to outer cortical, cancellous, and inner
8. Place the red cap on the plastic nipple cortical bone. Upon reaching the inner
to be able to cap the EVD after cortical table of bone, we recommend
placement. placing one's hand at the tip of the
9. Assemble the drill and ensure the stop- drill and manually rotating rather than
per’s placement at about 1.0–1.5 cm continuing to use the axle handle. An
103
Operating Room
Fig. 6.2 External ventricular

drain placement. Placement
of a right external ventricular
drain into the lateral ventricle
towards the foramen of Mon-
ro. The catheter is inserted
approximately 6.5 cm deep
from the surface. (Reproduced
from Ullman J, Raksin P, Atlas
of Emergency Neurosurgery,
Publishers, New York.)15
errant burr hole will deflect your cath- Medial tunneling is used so that if a
eter in inappropriate directions. hemicraniectomy is needed for refrac-
16. Clean and remove bone fragments tory ICP control, the catheter will not
after the burr hole is made. be in the way of the operative site.
17. Use the trocar to create a durotomy. 20. Cap the catheter with the nipple and
18. Pass the catheter through the incision, attached red cap.
aiming for the ipsilateral medial can- 21. Suture the catheter at the tunneled lo-
thus and 1 cm anterior to the ipsilat- cation to prevent inadvertent slipping.
eral tragus with care to avoid placing 22. Suture the incision site with running
the catheter deeper than 6.5 cm from 3–0 nylon taking care to avoid punc-
the inner table of the cranium. Remove turing the underlying catheter.
the stylet to check for flow. When flow 23. Coil the catheter externally in to a
is established, always ensure control strain relief loop from the posterior
of your catheter and its depth. A rough exit. Secure the coiled catheter with
estimate of intracranial pressure (ICP) suture and staples.
may be gauged by dropping and rais- 24. Remove the red cap and connect the
ing catheter above the external acous- EVD to the external drainage collec-
tic meatus. Take care to minimize the tion system. Using a 2–0 silk tie secure
early loss of CSF. the catheter to the distal drainage
tubing.
Caution: In aneurysmal subarachnoid

hemorrhage patients, draining off large 6.8 Cranial Approaches
volumes of CSF may increase risk of
rebleeding. 6.8.1 Pterional
The pterional (frontosphenotemporal) cra-
19. Attach trocar to catheter end and tun- niotomy is a versatile approach providing
nel posteriorly and medially. While corridors to anterior and posterior circula-
tunneling, it is helpful to grasp the tion aneurysms, lobar pathologies, and sel-
catheter at its cranial entry site with lar/suprasellar lesions. The incision is
the nontoothed portion of your f orceps. made anterior to the tragus and above the
104
6.8 Cranial Approaches
zygomatic arch in a curvilinear fashion 3. Upon anterior retraction of skin flap

staying behind the hairline. Critical struc- and temporalis, the supraorbital nerve
tures to avoid damaging are the frontal should be identified emanating from
branches of the facial nerve, superficial the supraorbital notch before vigorous
temporal artery (STA), and supraorbital stripping of pericranium ensues.
nerve. Below are techniques employed for
avoiding each structure: Classically, two burr holes are used for
1. Frontal branches of facial nerve often the pterional approach but anywhere
branch below the zygomatic arch. between one and four may be employed.
Starting the incision slightly above the One burr is placed at the intersection of the
arch avoids injury. Anterior elevation zygoma, superior temporal line, and supra-
of the fat pad overlying the deep por- orbital ridge. The second is placed at the
tion of the temporal fascia avoids in- posterior portion of the zygomatic arch in
jury as well since the nerve runs the squamosal temporal bone. On some
through this fat pad. occasions, a third burr is placed at the
2. STA injury is often prevented by keep- posterior portion of the superior tempo-
ing incision within 1 cm anterior to ral bone (▶Fig. 6.3).16 After connecting
tragus of ear. the burrs with a foot-plated tool and
Fig. 6.3 Burr hole placement

and craniotomy. Location of
burr holes placed in pterional
craniotomy. Number of burr
holes may range from two
to four depending on the
surgeon’s preference.
(Reproduced from Connolly E,
McKhann II G, Huang J et al,
Fundamentals of Operative
Techniques in Neurosurgery,
105
Operating Room
rongeuring off additional bone, the dura is orbit and maxillary buttress points of
incised and, depending on what the attachment; additional craniectomy of
pathology requires, the Sylvian fissure is additional bone with rongeurs is done to
sharply dissected.1,3,17 widen the viewing angle (▶Fig. 6.4).6,16
6.8.2 Orbitozygomatic 6.8.3 Temporal

The orbitozygomatic craniotomy is actu- The temporal craniotomy also serves as a
ally a modification of a frontotemporal versatile corridor for pathologies including
approach and is indicated for structures temporal lobectomy, hematoma evacua-
of lateral anterior cranial fossa or orbit tion, lobar tumors, and access to middle
and aneurysms of anterior communicat- cranial fossa floor. In cases requiring mini-
ing artery and basilar apex.16 Removal of mal exposure (i.e., chronic subdural hema-
portions of the orbit and zygomatic arch toma, biopsy) a linear skin incision and
allows for more inferior retraction of burr hole suffice. However, a larger expo-
temporalis muscle and gains increased sure is needed in most cases.
exposure to anterior and inferior struc- The skin incision is carried out as a
tures.6 The first phase is akin to a pteri- “question-mark” shaped incision. The inci-
onal craniotomy; the skin incision begins sion starts above the zygomatic arch and
at the level of the zygomatic arch, approximately 1 cm anterior to the tragus
approximately 1 cm anterior to the tra- and courses superiorly to avoid injuring
gus, and is carried posteriorly before frontalis branches of the facial nerve and
curving anteriorly towards the widow’s the STA. At the level of the pinna, the inci-
peak of the hairline. Careful retraction of sion curves posteriorly and then superiorly
the skin flap and underlying fat pad to the level of the superior temporal line
ensures protection of the facial nerve from which point it continues in an ante-
branches coursing anteriorly; the ret rior direction towards the hair line.1,6 The
racted flap may be dissected off the tem- size of the incision can be varied depend-
poralis muscle in a supra- or subfascial ing on the extent of exposure desired and
manner. Periorbital dissection of tempo- the depth of the pathology (▶Fig. 6.5).4
ralis off the lateral orbit and root of Number of burr holes used is at the dis-
zygoma may be necessary to ensure an cretion of the surgeon, often three to four.
inferior exposure for the McCarthy burr Burr hole placement is often done at poste-
hole. This burr hole is placed approxi- rior point of zygomatic arch, anterior junc-
mately 7 mm superior and 5 mm poste- tion of zygoma in proximity to the
rior to the frontozygomatic suture and frontozygomatic suture, and then along
should ideally visualize the floor of ante- the posterior aspect of the skin incision.1
rior cranial fossa and periorbita.18 Using Preparation of the flap and burr hole is
a foot-plate, the craniotomy can then be demonstrated in ▶Fig. 6.6.4 In cases aimed
fashioned around this burr hole prior to at attacking petrous apex and internal
the orbital osteotomy. Further dissection auditory canal lesions, a middle fossa
at the osteotomy site may be needed to approach is often employed via a similar
identify the supraorbital nerve. Next, the incision; however, a small temporal crani-
periorbita from the superior-lateral sur- otomy is made with two-third anterior to
face of the orbital rim is gently dissected external acoustic canal and one-third pos-
and carried inferiorly until the inferior terior to this landmark.3
orbital fissure if felt. A series of orbital When operating in the dominant
cuts are made to remove the superior hemisphere, one must caution the
106
Fig. 6.4 Orbitozygomat-

ic craniotomy. Burr hole
placement and series of bone
cuts made for orbitozygo-
matic craniotomy, including
orbitectomy. (Reproduced
from Connolly E, McKhann II
G, Huang J et al, Fundamen-
tals of Operative Techniques
in Neurosurgery, 2nd edition,
New York.)
superior temporal gyrus. The language one may plan the incision/approach to
centers in the dominant hemisphere are minimize such damage. The incision begins
farthest anterior at the superior temporal midline at the area of the inion, continues
gyrus. Safe margins are roughly estimated superiorly, and then curves inferiorly
as up to 2.5 cm posterior on superior tem- towards the area of the squamosal suture
poral gyrus and 4.5 cm posterior on the posterior to the ear; some allow the inci-
middle and inferior temporal gyri.16 In sion to extend across midline to allow
many cases, the incision is taken a shorter space for a burr hole which will not damage
distance posteriorly to the pinna when at the superior sagittal sinus while widening
the dominant hemisphere.6 the exposure.3 Typically four to five burrs
are placed with one approximately 1–2 cm
lateral to midline and another 2 cm below
the external occipital protuberance.6
6.8.4 Occipital
The occipital craniotomy serves as a corri-
dor not only to the occipital lobes but key 6.8.5 Endonasal
structures of the posterior fossa including
Transsphenoidal
the tentorium and sinuses. Care must be
taken to avoid damaging the sagittal, trans- The endonasal transsphenoidal approach
verse, or sigmoid sinuses. By carefully is a method of increasing utility as a tech-
marking midline and palpating the inion, nique for a variety of lesions involving the
107
Operating Room
Fig. 6.5 Craniotomy Incision

Planning. Frontotemporal
craniotomy incisions can
be made of various sizes
depending on pathology.
Incision 1. Notes a typical
pterional craniotomy incision,
2. Demonstrates a larger
frontotemporal exposure,
3. Is for larger orbitobasal
and middle fossa exposures.
In cases of decompressive
hemicraniectomies, the
incision is extended farther
posteriorly than incision 3.
(Reproduced from Nader R,
Gragnanielllo C, Berta S et al,
Neurosurgery Tricks of the
Trade: Cranial, 1st edition,
New York.)
sella, suprasellar space, sphenoid, and whereas the endoscope widens the sur-
even posterior structures including the cli- geon’s field of view.5 Overall, the approach
vus as far back as the upper cervical verte- allows minimal brain trauma due to a lack
brae. Classically, transsphenoidal access of brain retraction and no visible scars
was accomplished via anterior mucosal or (besides what may be harvested for a nasal
sublabial incisions; however, the direct mucosa fat graft).
endonasal corridor has gained favorability. After appropriate preparation with
Common lesions well-served by this oxymetazoline pledgets and sterilization
approach include pituitary adenomas, with betadine solution, the procedure
Rathke pouch cysts, craniopharyngiomas, begins. A speculum is used to visualize
and clival chordomas.1,6 In cases involv- the turbinates and nasal septum. Upon
ing anterior, posterior, or lateral exten- identification, an incision is made through
sion, transcranial or expanded endonasal the posterior portion of the nasal sep-
approaches may be considered. Impor- tum and the septum if fractured and
tantly, the expanded endonasal approach deviated. A diamond-tipped drill is used
is part of the armamentarium of a few and to remove bone of sphenoid ostia, por-
should only be considered by surgeons tions of dorsum sella, and sella turcica
with considerable expertise and exposure before encountering dura. Also used are
to such an approach.5 Kerrison rongeurs, and occasionally, the
The microscope and endoscope are two ultrasonic aspirator. The dura is incised in
tools which offer different benefits to the a cruciate fashion and the pituitary gland
surgeon in gaining access via the nasal cor- is encountered.
ridor. The microscope offers magnification Care must be taken during the entire
and additional three-dimensional viewing procedure to maintain proper orientation
108
Fig. 6.6 Craniotomy fascial exposure. Elevation of the temporalis muscle with a
periosteal is seen in (a). (b) Temporalis muscle and relation to temporalis fascia is seen.
1. Superficial temporal line, 2. Vascularized pericranial flap, 3. Temporal fascia, 4. Skin,
galea, and connective tissue, 5. Superficial temporal fat pad upper half, 6. Superficial
temporal artery, 7. Craniotomy outline, 8. Muscle cuff remnant. (Reproduced from
Nader R, Gragnanielllo C, Berta S et al, Neurosurgery Tricks of the Trade: Cranial, 1st
edition, ©2013, Thieme Publishers, New York.)
(▶Fig. 6.7).16 Identifying the opticocarotid tumor is also essential for a successful out-
recess provides a lateral landmark by which come. The normal pituitary gland strongly
you need to exhibit extreme caution. Carotid enhances on contrasted studies and should
injury mandates judicious packing with probe delineated from tumor. If the infundibu-
coagulant adjuncts, cotton pads, and gentle lum is deviated towards a side, the pituitary
pressure.6 Distinguishing normal gland from gland will often be mobilized with it.16
109
Operating Room
Fig. 6.7 Endonasal transsphenoidal approach. (a) Positioning of the patient with head
slightly flexed. (b) Axial view of structures traversed in reaching the sphenoid sinus.
(c) Endoscopic view of sphenoid and sella dura. Sagittal view noting entry into sella
with outlined floor; note the clivus posteriorly. (d) Axial view again demonstrating
structures traversed, including into ethmoidal sinus. (Reproduced from Connolly E,
McKhann II G, Huang J et al, Fundamentals of Operative Techniques in Neurosurgery,
2nd edition, ©2010, Thieme Publishers, New York.)
6.8.6 Decompressive secondary damages caused by malignant

edema post-ischemic stroke, or even pro-
Hemicraniectomy phylactically after evacuation of hemato-
Decompressive hemicraniectomy (DHC) is mas where postoperative elevated ICPs are
a last resort procedure for control of refrac- expected. The craniotomy is similar to that
tory ICPs. DHC may be done emergently in from frontotemporal approaches but is
traumatic cases, urgently for prevention of larger.
110
Patients are positioned supine with an position. Narrow-necked aneurysms are

ipsilateral shoulder roll and contralateral amenable to endovascular treatment; yet,
head rotation; care must be taken to pre- clipping remains an option for more diffi-
vent kinking or compression of jugular cult aneurysms. Lumbar drains or EVDs are
veins which will prevent venous drainage useful adjuncts for intraoperative fluid
and further increase ICP. Especially in trau- diversion control in these cases.
matic cases, manipulation of the head for A pterional craniotomy is carried out as
positioning should be done with cervical described in previous sections and a
spine precautions. Use of pins depends on C-shaped dural incision is made. For mid-
surgeon preference and whether concomi- dle cerebral artery (MCA) aneurysms, the
tant skull fractures are present. Sylvian fissure is split and depending on
A generous question mark skin incision the location splitting either occurs distal to
is taken from the zygomatic arch far posteri- proximal (lateral transsylvian) or proximal
orly and curving forward a few centimeters to distal (medial transsylvian). The lateral
lateral to the superior sagittal sinus (which transsylvian approach is most preferred for
is often slightly eccentric to the right rather MCA aneurysms; however, since exposure
than at a true midline) and coursing towards occurs distal to proximal, the aneurysm
the hairline (▶Fig. 6.8).16 The dissection is will first be realized before gaining proxi-
taken through the subcutaneous tissue and mal control and awareness of the internal
temporalis with anterior retraction and carotid and early branches. A distal MCA
Raney clips for hemostasis on the scalp branch is often identified and followed
edges. A large craniotomy is taken with down to its more proximal branches. In the
three burr holes and followed by a temporal medial transsylvian approach, early identi-
craniectomy using rongeurs to decompress fication of the internal carotid and optic
the middle fossa fxloor. nerve allows sharp dissection of arachnoid
Various techniques are used for dural membranes in optic and carotid cisterns
opening; in many cases, a stellate opening allowing relaxation of overlying brain. A
is used for maximum decompression. superior temporal gyrus approach is usu-
Dural substitutes are often placed over the ally reserved for cases of a ruptured MCA
opening with the dural flaps placed over. aneurysm with associated temporal hema-
This is followed by watertight galeal and tomas requiring evacuation for brain relax-
then skin closure due to relative exposure ation before clipping may occur.6 In any
of the underlying brain.6 case, clipping requires complete visualiza-
tion of the aneurysm neck and adjacent
structures to ensure no extra-aneurysmal
6.8.7 Craniotomy for vessels are clipped causing ischemia. Prior
Aneurysm to permanent clipping, temporary clips are
often place on feeding vessels for proximal
Many aneurysms are approached using a control while manipulating and examining
pterional craniotomy. The degree of head an aneurysm and its neck. Temporary clips
rotation provides a corridor to aneurysms, are removed after permanent clipping is
with larger degrees of rotation used for complete.6 Use of intraoperative indocy-
anterior communicating aneurysms and anine green angiography is a common
lesser rotation for posterior communicat- technique to confirm aneurysm closure
ing aneurysms. For any aneurysms, angi- and patency of adjacent vessels.19
ography utilizing the digital subtraction Increased head rotation when position-
technique is useful for preoperative under- ing allows a corridor to anterior communi-
standing of aneurysm morphology and cating aneurysm. Due to the midline nature
111
Operating Room
Fig. 6.8 Dural incision in

decompressive hemicraniec-
tomy. Stellate dural incision
is one method of opening
this outer membrane during
decompressive hemicraniec-
tomy. (Reproduced from
Connolly E, McKhann II G,
Huang J et al, Fundamentals
of Operative Techniques in
Neurosurgery, 2nd edition,
New York.)
of these lesions, it is preferred to approach S1 vertebra may give the appearance of six
from the patient’s nondominant hemi- lumbar vertebral levels whereas sacraliza-
sphere. On the other hand, posterior com- tion of L5 may give the appearance of four.
municating aneurysms are best approached The latter is more common but overall rates
with decreased head rotation. After eventu- of lumbosacral abnormalities range from
ally splitting the Sylvian fissure, the internal 2.3 to 14.6%.20,21
carotid is tracked deeper, towards the optic
chiasm, to visualize the origin of the poste-
rior communicating artery. 6.9.2 Anterior Cervical
Discectomy and Fusion
6.9 Spinal Approaches ACDF is a commonly performed proce-
dure for cervical radiculopathy second-
ary to disc compression. As mentioned
6.9.1 Level Localization
previously, patients are placed supine
Integral to any spinal procedure is confirm- and a transverse incision is made in a
ing the appropriate level. Localization is pre-existing neck crease to minimize vis-
confirmed in a variety of ways across insti- ibility of an unsightly scar. Anatomical
tutions and surgeons. Fluoroscopy is the landmarks facilitate proper placement of
primary method and may be used before or the incision; the angle of the mandible
after the incision is made. A number of approximates C2, hyoid bone approxi-
landmarks are used, including visualization mates C3-C4, thryoid cartilage approxi-
of the sacrum, counting ribs, and using the mates C4-C5, cricothyroid membrane
unique C2 vertebra. Care must be taken for approximates C5-C6, and C6-C7 is often
anatomical variations. Lumbarization of the two finger breadths above the clavicle.22
112
6.9 Spinal Approaches
The initial superficial fascial dissection After the disc space is exposed and
involves splitting the platysma, retract- localization is confirmed, the discectomy
ing trachea and esophagus medially, takes place. A number of different tech-
retracting sternocleidomastoid laterally, niques exist for disc removal. Often, the
and identifying the location of the annulus fibrosus is incised and disc compo-
carotid so that the sheath containing nents are removed with curettes and ron-
artery, jugular vein, and vagal nerve are geurs until the posterior longitudinal
retracted laterally. Care may also be ligament is identified. The ligament may be
taken to identify superior and inferior incised and proper inspection, including
thyroid vessels and ligate if necessary. foraminotomies, may be completed to
Once superficial dissection is complete, ensure adequate decompression. Appropri-
attention is paid to the deep dissection. ate graft or cage construct is inserted in the
The prevertebral fascia is incised and lon- disc space and an anterior plate is placed.
gus colli muscles are retracted (▶Fig. 6.9).4 Meticulous hemostasis prevents complica-
The anterior longitudinal ligament will be tions, including retropharyngeal hema-
exposed. Care must be taken at the deep toma, and the surgical site is closed. Patients
lateral margins since the sympathetic should be monitored closely postopera-
chain and also vertebral arteries lie in tively, especially for development of retro-
proximity. At this juncture, spinal levels pharyngeal edema which may compromise
are radiographically confirmed. the airway and require reintubation.
Fig. 6.9 Anterior cervical

discectomy and fusion.
Number of structures can
be seen after applying the
self-retaining tractor displac-
ing the longus colli muscle. 1.
Sternocleidomastoid muscle,
2. Carotid sheath, 3. Longus
colli, 4. Omohyoid muscle, 5.
Esophagus, 6. Trachea. Image
below notes completed ACDF
in coronal and sagittal planes.
(Reproduced from Nader R,
Berta S, Gragnanielllo C et al,
Neurosurgery Tricks of the
Trade: Spine and Peripheral
Nerves, 1st edition, ©2014,
Thieme Publishers, New
York.)
113
Operating Room
6.9.3 Laminectomy/ indication, the extent of the decompression

may vary to range from spinous process
Laminotomy preservation with laminotomy or hemilami-
Laminectomy is the core operative tech- nectomy to full laminectomies (▶Fig. 6.10).4
nique in the spinal neurosurgeon’s arsenal. Tight closure of the different tissue layers,
Indications range from posterior decom- including deep and superficial fascia, is vital.
pression to complex posterior spinal In cases where the dura is violated, a water-
approaches for discectomy, tumor, abscess, tight closure is necessary.6
and more. Specific details of positioning and
approach vary depending on the location of 6.9.4 Lumbar Interbody
the laminectomy. Cervical cases will have
the patient’s head secured in three-point
Fusion
fixation and many will obtain baseline MEPs There are a variety of types of lumbar inter-
and SSEPs prior for ease of intraoperative body fusion. Most common is the transfo-
monitoring; these measures are not rou- raminal lumbar interbody fusion (TLIF)
tinely taken in lumbar laminectomies. which is done for a range of pathologies and
Cervically, C2 (bifid) and C7 (vertebra new approaches continue to be developed
prominens) spinous processes are usually (▶Fig. 6.11).4 Lumbar instability, progres-
most prominent and serve as useful land- sive spondylolisthesis, scoliosis, and symp-
marks when planning the skin incision. tomatic spinal stenosis with significant
Care is taken to keep the exposure medial to back pain are among some indications.
the facet joints since their compromise may Preoperatively, flexion-extension radio-
produce instability. There are varying tech- graphs are helpful in determining the degree
niques for removal of lamina, including use of instability. As with other spinal proce-
of a small burr drill or Kerrison punches. dures SSEPs, MEPs, and fluoroscopy may be
Planning the incision in the lumbar useful adjuncts. TLIF may also be done mini-
region can be done with fluoroscopy or, mally invasively through a tubing system.
simply, with palpation for anterior supe- The procedure is carried out similarly
rior iliac crests which provide an approxi- to the initial steps of a laminectomy. After-
mation for the L4–L5 interspace. After wards, a facetectomy with removal of the
incision, subcutaneous fat will be met and pars is completed to expose the neural ele-
dissected away exposing thoracolumbar ments and the region of ultimate pedicle
fascia. Midline or paramedian (if desiring screw placement. Prior to pedicle screw
to preserve interspinous ligament) incision insertion, a small incision into the annulus
through the fascia is performed next. fibrosus is made, followed by a discectomy.
Fluoroscopic localization is done at this The annulectomy is made off the median
juncture. After dissection and exposure of which allows the TLIF to have the benefit of
the spinous process and medial aspect of the limited retraction of the neural elements.
facets, bone cutters and/or rongeurs are A graft for fusion is then inserted into the
used to remove the spinous process. Simi- disk space and pedicle screws with rods
larly to the cervical spine, a drilling burr or are placed.6
Kerrison can be used to thin out and remove Multiple variations exist. Posterior
the lamina and underlying ligamentum fla- lumbar interbody fusion (PLIF) is theoreti-
vum. The laminectomy can be widened and, cally similar to a TLIF; however, the
when complete, a ball-tipped probe is used approach extends through the midline and
to palpate neural foramina and ensure requires retraction of the thecal sac and
adequate decompression. Depending on nerve roots to gain access to the disc space.
114
6.10 Pediatric
Fig. 6.10 Laminectomy/laminotomy. Laminectomy for central disc herniation is seen

in (a) where preservation of the facets and pars interarticularis is essential. (b) Lami-
notomy bony removal for lateral disc herniation, seen in inset. (c) Medial facetectomy
is seen with associated laminotomy. Care is taken to minimize the amount of facet
removed to preserve joint stability. (Reproduced from Nader R, Berta S, Gragnanielllo C
et al, Neurosurgery Tricks of the Trade: Spine and Peripheral Nerves, 1st edition,
Other iterations include the anterior lum- by the pediatric neurosurgeon. VPS is indi-
bar interbody fusion (ALIF) and lateral cated for hydrocephalus cases of varying
lumbar interbody fusion (LLIF). The latter etiologies and often require revision. The
forgoes the need to retract musculature of patient is positioned supine with the head
the back or abdomen and starts with an turned left (for a right-sided shunt) and the
incision placed at the flank. scalp, neck, clavicle, and abdomen are ster-
ilely prepared. There are a wide variety of
shunt valves available, including fixed,
6.10 Pediatric adjustable, and anti-siphon; the decision is
based on the patient’s age, pathology, and
6.10.1 Ventriculoperitoneal the surgeon’s preference. The distal location
of the shunt also varies with options includ-
Shunt ing the pleural and atrial spaces as well.
Ventriculoperitoneal shunts (VPS) are one Proximal shunt catheters can be inserted
of the most common operations completed via a number of trajectories, including
115
Operating Room
Fig. 6.11 Transforaminal lumbar interbody fusion. (a) Bony removal for TLIF is shown
in image to left with removal of facet joint. The relationship to exiting and traversing
nerve roots is seen. (b) Axial view of working channel for TLIF. (Reproduced from Nader
R, Berta S, Gragnanielllo C et al, Neurosurgery Tricks of the Trade: Spine and Peripheral
Nerves, 1st edition, ©2014, Thieme Publishers, New York.)
frontal or occipital. There are a variety of valve is connected to the proximal end of
points based on bony landmarks for place- the distal catheter to ensure flow directed
ment of a shunt (▶Table 6.2). Kocher’s cranially to abdominal. Attention is then
point is most commonly used in adult redirected to the cranial burr where a
shunts; however in pediatrics, placement small dural incision is made and a catheter
may vary based on the surgeon’s judg- is passed into the ventricle. Care is taken to
ment. Frontal shunts are measured simi- secure the depth and position of the cathe-
larly to EVDs and require a second releasing ter, CSF flow is confirmed, and the distal
incision posterior to the ear. The advantage end of the proximal catheter can be con-
of posterior shunts is that a single parie- nected to the valve reservoir. Next, distal
to-occipital incision is made and a small flow is confirmed from the abdominal
burr hole is placed. For either approach, a catheter before feeding it into the perito-
pocket in the subcutaneous space is cre- neal cavity. Closure at both incisions is car-
ated for the reservoir and valve. The large ried out in multiple layers to reduce the
tunneler is passed from the cranial to risk of CSF fistulas forming.6
abdominal incision with care taken not to Depending on the institution, VPS may
plunge into deeper spaces; structures at be completed with the assistance of a gen-
direct risk during tunneling are the carotid eral surgeon for the abdominal exposure
and jugular vasculature as well as lung api- with or without laparoscopy. A small
ces (making pneumothorax a possible abdominal incision is made with sharp dis-
complication). The distal catheter is passed section of fascial layers, muscle is conser-
after the tunneled path is made. A one-way vatively split, and the peritoneum is
116
6.11 Functional
Table 6.2 Cranial landmarks for adult and pediatric shunt placement
Point Landmarks Direction and length
Dandy’s point 2 cm lateral to midline and 3 Perpendicular to cortex, slightly
(occipital) cm above inion; approximately cephalic, and approximately 4–5
location of intersection between cm
lamboid suture and midpupillary
line
Frazier’s point 3–4 cm lateral to midline and 6 Perpendicular to cortex,
(occipital) cm above inion approximately 4–5 cm
Keen’s point 2.5–3.0 cm posterior to ear and Perpendicular to cortex,
(parietal) 2.5–3.0 cm above the ear approximately 4–5 cm
Kocher’s point 3.0 cm lateral to Trajectory towards ipsilateral
(frontal) midline (approximately parallel medial canthus (coronal plane)
to the midpupillary line) and and towards tragus of ear
1 cm anterior to the coronal (sagittal plane) to approximately
suture. Often measured as 11 cm 6.5 cm to 3rd ventricle and 4–5
posterior from nasion and 3 cm cm to lateral ventricle
lateral to midline
carefully incised to reveal the abdominal coordinate placement and calculation of

cavity. Lifting the peritoneum with mos- coordinates. Coordinates are calibrated to
quito clamps helps ensure no direct bowel several midline structures including the
injury. anterior and posterior commissures,
Sylvian aqueduct, septum pellucidum

junction with splenium of corpus callo-
6.11 Functional sum, and interpeduncular point.
Small incisions are made anterior to
6.11.1 Deep Brain the coronal suture to allow placement of
a lateral burr hole. The microelectrode
Stimulation
recording center is prepared and these
Deep brain stimulation (DBS) is gaining are inserted via guide tubes using the
increased utilization and indications for a determined coordinates. Extreme care is
variety of conditions, especially movement taken to avoid ventricular entry since
disorders such as Parkinson disease, dysto- excessive loss of CSF causes brain relax-
nia, and essential tremor. Patients are posi- ation which distorts coordinates. When
tioned in a stereotactic frame with local electrodes are inserted, the recordings
rather than general anesthesia. Depending are verified to those expected for the dis-
on the patient’s specific symptom profile, tinct target and then are locked in place.
one of multiple targets may receive DBS After electrode placement is complete,
electrodes including the subthalamic the second phase is to place the DBS gen-
nucleus (STN), globus pallidus internal erator. Generators are often placed in a
segment (GPi), and ventralis intermedius pocket at the infraclavicular space. A tun-
nucleus of the thalamus (Vim). Possibly neler is used to pass the cable between
most important in DBS is understanding electrode and generator.6
117
Operating Room
3. Failure to complete which of the fol-

Pearls
lowing while placing an external ven-
• When tunneling an EVD using a tricular drain has the potential to lead
trocar, travel medially. In cases where to the MOST SEVERE complication?
there are refractory elevated ICPs, the a) Accidentally throwing away the
drain would not be in the way of your capping red nipple
incision site. b) Tunneling the EVD too short a
• The farther an EVD is tunneled from distance
Kocher’s point, the lower the risk of c) Measuring the ventricular catheter
an infection. to 7.5 cm
• For interbody fusions, additional d) Accidentally stitching through the
methods exist for measuring EVD while securing it
spinopevlic parameters including
preoperative planning applications. 4. Which structure listed below is re-
• Intraoperative MRI is becoming a tracted laterally during an ACDF?
more readily available tool in a) Sternocleidomastoid muscle
functional procedures, including b) Carotid artery
magnetic resonance-guided laser-in- c) Esophagus
duced thermal therapy for obliteration d) Trachea
of recurrent brain metastasis.23
5. Where, in relation to skull landmarks,
• The Neurosurgical Instrument Guide
provides an additional resource for a is a keyhole burr hole placed?
description of the common tools used a) Half the distance of a line connect-
in neurosurgery. ing the bregma and inion
b) Pterion (Intersection of frontal,
parietal, temporal, and sphenoid
bones)
6.12 Top Hits c) Within 1 cm of anterior tragus and
1 cm above zygomatic arch
6.12.1 Questions d) Intersection of zygoma, superior
temporal line, and superior orbital
1. Which of the following is NOT part of
ridge
the appropriate management of intra-
operative air embolism? 6. The intercristal line, a horizontal line
a) Copiously irrigating operative field between the most superior point of
b) Elevating the head of the bed both iliac crests, approximates what
c) Aspiration of air from right atrium lumbar spinal level?
using central venous pressure a) L1–L2
catheter b) L2–L3
d) Lowering the head of the bed c) L3–L4
e) Compressing jugular vein d) L4–L5
e) L5–S1
2. Which of the following structures is
NOT directly at risk of harm during a 7. When using Mayfield three-point fixa-
pterional craniotomy? tion for pinning, where should the
a) Frontalis branch of facial nerve two-pins generally be placed?
b) STA a) Superior temporal line
c) Supraorbital nerve b) Frontal sinus
d) Zygoma
118
6.12 Top Hits
c) The dependent position of the incision. Sensitive structures include

head the STA, frontalis branch of facial nerve,
d) Vertex and supraorbital nerve. The location of
the former two may be estimated given
8. Which of the following is NOT em- knowledge of the zygoma.
ployed in standard positioning for a 3. c. Measuring the catheter to greater
pterional craniotomy? than 7.0 cm runs the risk of placing a
a) Ipsilateral shoulder roll catheter too deep and injuring essen-
b) Neck extension 10–15° tial neural and vascular structures.
c) Maxillary eminence as highest part The additional choices all represent
of operative field poor outcomes but are not nearly as
d) Thorax elevation 10–15° severe. Throwing away the cap neces-
e) Contralateral head rotation 75° sitates reopening an additional pack-
age. Tunneling the catheter a short
9. Which of the following is NOT a rou- distance increases infection risk.
tine mechanism of perioperative pe- Stitching through the EVD mandates
ripheral nerve injury? replacement of the EVD as overdrain-
a) Stretch ing and infection are further risks.
b) Shear 4. a. The sternocleidomastoid is identi-
c) Ischemia fied and typically retracted laterally.
d) Compression The remaining options are classically
retracted medially.
10. Resection of which of the following
5. d. Keyhole burrs are placed at the in-
during a laminectomy will lead to
tersection of the zygoma, superior
instability?
temporal line, and supraorbital ridge.
a) Lateral two-third of facet
6. d. L4–L5. Studies have demonstrated
b) Medial one-third of facet
that the level localized by palpation may
c) Lamina
vary based on gender and body habitus.
d) Spinous process
7. c. The arm with two-pins should be
e) Ligamentum flavum
placed in the most dependent portion
of the head in its final position. This is
done to reduce risk of slipping of the
6.12.2 Answers
head out of the Mayfield due to grav-
1. b. Elevating the head of bed is not a part ity. The pins can be placed at the supe-
of the appropriate management of air rior temporal line but this is not
embolism, it will rather make the issue always the case. Care should be taken
worse. The appropriate management to avoid placement of the pins in the
includes irrigating the field copiously, frontal sinus.
packing off veins from further bleeding 8. e. Rotating the head 75° risks kinking
and air entry, lowering the head of the of jugular veins, elevation of ICPs, and
bed, compressing the jugular vein if prevents appropriate brain relaxation
possible, and aspirating air using a cen- during the approach. For any proce-
tral venous pressure catheter. dure which necessitates rotation of the
2. d. The zygoma is not at direct risk head greater than 30°, an ipsilateral
during a pterional craniotomy. The shoulder roll is helpful to reduce mus-
zygoma may be used as a landmark in cular tension and allow additional ro-
determining the lowest extent of the tation without compromising venous
119
Operating Room
outflow. Typically, the most rotation ropathies. Practice advisory for the prevention of
perioperative peripheral neuropathies: an updated
needed in a pterional craniotomy is report by the American Society of Anesthesiol-
approximately 60° for reach anterior ogists Task Force on prevention of perioperative
fossa lesions. peripheral neuropathies. Anesthesiology. 2011;
114(4):741–754
9. b. Shear is not a routine method of [12] Kamel IR, Drum ET, Koch SA, et al. The use of so-
perioperative peripheral nerve injury. matosensory evoked potentials to determine the
The remaining mechanisms of stretch, relationship between patient positioning and im-
pending upper extremity nerve injury during spine
compression, and ischemia are classi- surgery: a retrospective analysis. Anesth Analg.
cally involved in perioperative periph- 2006; 102(5):1538–1542
eral nerve deficits. [13] Saladino A, Lamperti M, Mangraviti A, et al. The
semisitting position: analysis of the risks and surgi-
10. a. Resection of the lateral portion of
cal outcomes in a contemporary series of 425 adult
the facet joint may cause instability of patients undergoing cranial surgery. J Neurosurg.
the posterior column of the spinal col- 2016:1–10
[14] Zhang L, Li M, Lee CC. Venous air embolism during
umn. Up to one-third of the medial
neurosurgery. In: Brambrink AM, Kirsch JR, eds.
facet can be removed without compro- Essentials of Neurosurgical Anesthesia & Critical
mising vertebral stability. Lamina, spi- Care: Strategies for Prevention, Early Detection, and
Successful Management of Perioperative Complica-
nous process, and ligamentum flavum
tions. New York, NY: Springer New York; 2012:355–
are frequently removed during a 362
laminectomy. [15] Laroche MHM, Manley GT. Invasive Neuromoni-
toring Techniques. New York, NY: Thieme Medical
Publishers; 2015
[16] Connoly ES, McKhann II GM, Huang J, Choudri TF,
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Techniques in Neurosurgery. New York, NY: Thieme
[1] Greenberg MS. Handbook of Neurosurgery. 7th ed. Medical Publishers; 2010
New York, NY: Thieme Medical Publishers; 2010 [17] Chaddad-Neto F, Campos Filho JM, Dória-Netto HL,
[2] Thamburaj V. Textbook of Contemporary Neuro- Faria MH, Ribas GC, Oliveira E. The pterional crani-
surgery. Vol 1. New Delhi: Jaypee Brothers Medical otomy: tips and tricks. Arq Neuropsiquiatr. 2012;
Publishers; 2012 70(9):727–732
[3] Fossut DTCA. Operative Neurosurgical Anatomy. [18] Tubbs RS, Loukas M, Shoja MM, Cohen-Gadol AA.
New York, NY: Thieme Medical Publishers; 2002 Refined and simplified surgical landmarks for the
[4] Nader RGC, Berta SC, Sabbagh AJ, Levy ML. Neuro- MacCarty keyhole and orbitozygomatic craniot-
surgery Tricks of the Trade – Cranial. New York, NY: omy. Neurosurgery. 2010; 66(6, Suppl Opera-
Thieme Medical Publishers; 2014 tive):230–233
[5] Zwagerman NT, Zenonos G, Lieber S, et al. Endo- [19] Ma CY, Shi JX, Wang HD, Hang CH, Cheng HL, Wu W.
scopic transnasal skull base surgery: pushing the Intraoperative indocyanine green angiography in
boundaries. J Neurooncol. 2016; 130(2):319–330 intracranial aneurysm surgery: Microsurgical clip-
[6] Jandial RMP, Black PM. Core Techniques in Opera- ping and revascularization. Clin Neurol Neurosurg.
tive Neurosurgery. Philadelphia, PA: Elsevier; 2011 2009; 111(10):840–846
[7] Lu J, Ebraheim NA, Nadim Y, Huntoon M. Anterior [20] Hsieh CY, Vanderford JD, Moreau SR, Prong T. Lum-
approach to the cervical spine: surgical anatomy. bosacral transitional segments: classification, prev-
Orthopedics. 2000; 23(8):841–845 alence, and effect on disk height. J Manipulative
[8] Sandwell S, Kimmell KT, Silberstein HJ, et al. Physiol Ther. 2000; 23(7):483–489
349 Safety of the Sitting Cervical Position for Elec- [21] Apazidis A, Ricart PA, Diefenbach CM, Spivak JM.
tive Spine Surgery. Neurosurgery. 2016; 63(Suppl The prevalence of transitional vertebrae in the lum-
1):203 bar spine. Spine J. 2011; 11(9):858–862
[9] Theologis AA, Burch S, Pekmezci M. Placement of [22] Albasheer MAM, AlMusrea K, Attia WI. Anterior
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B(5):696–702 figurelegend=on&text=on&references=on. Accessed
[10] Kamel I, Barnette R. Positioning patients for April, 2017
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related complications. World J Orthop. 2014; netic resonance-guided laser-induced thermal
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[11] American Society of Anesthesiologists Task Force strip after stereotactic radiosurgery. Cureus. 2016;
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7 Neurocritical Care
Xiaoran Zhang, Lori Shutter
7.1 Introduction ischemic strokes, infection, and mass

lesions in the medulla can also dampen
Care of neurosurgical patients does not stop respiratory drive. It is important to note
at the end of an operation. These patients that mechanical compression from pontine
are often some of the sickest patient in the herniation is also a cause of decreased
hospital and knowledge of neurocritical respiratory drive. Demyelinating diseases
care is crucial to ensuring good outcome. and high cervical spine trauma can lead to
the inability of CNS efferents to transmit
signals from the respiratory center, leading
7.2 Respiratory to respiratory paralysis.
Physiology The airway includes the oropharynx,
trachea, and bronchi. Mechanical or soft
Respiration describes the body’s ability to tissue obstruction in any segment can
oxygenate and ventilate. The definition of quickly lead to respiratory failure. Patients
respiratory failure is therefore the inability with diminished mental status or patholo-
of the respiratory system to meet the oxy- gies involving the lower cranial nerves can
genation and ventilation requirements of be at risk of airway compromise and respi-
the patient.1 Furthermore, respiratory fail- ratory failure due to either inability to pro-
ure is divided into two types with type 1 tect the airway from saliva/vomitus, or
being hypoxemic (pO2 < 60 mmHg) and experience obstruction of the airway by
type 2 being hypercapnic (pCO2 > 50 soft tissue in the oropharynx. Optimal gas
mmHg). The respiratory system can be exchange is dependent on unobstructed
divided into four interconnecting compo- air flow through the pulmonary system
nents: (1) the central nervous sys- and adequate blood flow to the pulmonary
tem (CNS), (2) airway, (3) alveoli, and (4) vasculature (perfusion). Common causes
thorax. Failure in one or more components to impaired gas exchange include pro-
can lead to acute respiratory failure. cesses both intrinsic and extrinsic to the
The CNS components include chemore- lung. Intrinsic pulmonary processes, such
ceptors responsible for sensing oxygen and as pneumonia, pulmonary edema, and
carbon dioxide in blood, the respiratory acute respiratory distress syndrome, can
center in the brainstem responsible for lead to decreased ventilation. Extrinsic
respiratory drive, and CNS efferents processes, such as pulmonary artery
responsible for transmitting signals from embolism from either thrombus or fat, can
the brainstem to the muscles that carry out lead to poor perfusion.2 Components of the
the movements necessary for ventilation. thorax include the muscles necessary for
CNS respiratory failure secondary to breathing, the chest wall, and pleural
changes in respiratory drive or ability of space, which are responsible for the
CNS efferents to transmit signal are com- mechanical movements of respiration.
monly seen in the neurological intensive Demyelinating disorders, cervical spinal
care unit (NICU). Dampened respiratory cord injuries, neuromuscular condi-
drive secondary to medication effects can tions (e.g., myasthenia gravis, Guil-
be seen in cases of excessive use of opioids, lain-Barre syndrome, and amyotrophic
sedatives, and medications associated with lateral sclerosis), or traumatic injuries can
CNS depression. Hemorrhagic and prevent the normal movement of muscles
121
Neurocritical Care
necessary for respiration. Injuries to the positional change can also potentially lead
chest wall including rib fractures can lead to improved outcomes. Studies have shown
to significant pain and poor respiratory that aggressive diuresis or corticosteroid
effort. Pneumo- and hemothoraces can therapy does not have a role in the man-
prevent the normal expansion of lung. agement of ARDS.
Patients with morbid obesity can have
impaired respiratory mechanics and
chronically retain carbon dioxide, which 7.2.2 Ventilator Basics
places them at a higher risk of type 2 respi-
ratory failure perioperatively. Patients who are suffering from acute
respiratory failure that is refractory to non-
invasive methods of ventilation undergo
7.2.1 Acute Respiratory intubation with an endotracheal tube for
Distress Syndrome mechanical ventilation. The position of the
endotracheal tube is generally described by
Acute respiratory distress syn- the distance from the tip of the tube to the
drome (ARDS) is an important cause of teeth. Placement of the tube is confirmed
acute respiratory failure. As many as 35% of by end-tidal carbon dioxide color change
NICU patients have some form of ARDS.3 It and auscultation of the lungs, with final
is characterized by widespread inflamma- confirmation and determination of tube
tion of the lungs facilitated by infiltration position done by chest X-ray. Ideally, the tip
and accumulation of neutrophils which of the tube is positioned between 5 and 7
leads to breakdown of endothelial and epi- cm above the carina for adults. The endo-
thelial barriers resulting in extravascular tracheal tube is connected to the ventilator
accumulation of edema and subsequent through a series of plastic tubing called
impaired gas exchange. ARDS is clinically “the circuit”. The ventilator has several
defined as an acute (< 7 days) onset of variables that can be set to tailor when and
respiratory distress with radiographic evi- how a breath is delivered. Ventilation mode
dence of bilateral pulmonary infiltrates on dictates the threshold for when a breath
chest CT or X-ray.4,5 Mild ARDS is defined is delivered. The most common modes
as PaO2/FiO2 of 200–300 with associated include continuous mandatory ventila-
mortality of 27%. Moderated ARDS is PaO2/ tion (CMV), assist control (AC), and pres-
FiO2 of 100–200 with associated mortality sure support (PSV). Under CMV, a breath is
of 35%. Severe ARDS is PaO2/FiO2 of less delivered at fixed time intervals (i.e., every
than 100 with associated mortality of 5 s). CMV is generally reserved for patients
45%. The exact pathogenesis of ARDS is not who are unable to initiate their own breaths
well understood; however, development of either due to several neurologic injury or
ARDS is known to be associated with deep sedation. Under AC, a breath is deliv-
pathologies commonly seen in the NICU ered at a fixed time interval unless the
setting such as sepsis, severe trauma, patient initiates a breath at which point the
blood transfusions, pneumonia, and aspi- ventilator will help the patient breathe a
ration pneumonitis.6 Treatment of ARDS sufficient volume. AC is the most com-
consists mainly of supportive therapy. Low monly used setting in the NICU as it allows
volume ventilation with a target tidal vol- the patients to breathe on their own as
ume of no higher than 6 mL/kg in ideal much as possible with “safety” pro-
body weight has been shown as the most grammed to ensure proper ventilation
important intervention at improving out- regardless of patient effort. Under PSV, the
comes.7 Intermittent supine to prone patient initiates the breath and controls the
122
7.3 Shock
volume with the ventilator only providing 7.3.2 Cardiogenic Shock

some additional positive pressure. PSV is
typically used in patients who are candi- Cardiogenic shock is failure of tissue perfu-
dates for extubating and serves as a test to sion secondary to decreased cardiac out-
determine whether they are able to inde- put. In neurosurgical patients, common
pendently initiate breaths with sufficient causes include myocardial infarction and
volume and with only minimal positive stress cardiomyopathy, both of which are
pressure support. Important settings to associated with aneurysmal subarachnoid
know on a ventilator include tidal vol- hemorrhage (SAH). Classical presentation
ume (Vt), respiratory rate (RR), FiO2, and includes symptoms of fluid overload such
positive end expiratory pressure (PEEP). Vt as pulmonary edema. It is characterized by
is how much air a patient is taking in per increased preload, decreased cardiac out-
breath, typically the setting is 5–8 mL/kg of put, and increased afterload. Treatment
ideal body weight. RR is typically set at options are limited to supportive therapy,
12–14 breaths per minute. FiO2 is the con- diuresis, and afterload reduction.
centration of oxygen being delivered to the
patient; typically start at 100% and decrease
as tolerated. PEEP is the positive pressure 7.3.3 Distributive Shock
being delivered to the patient, typically
There is failure of vascular autoregulation
start at PEEP of 5–7 cm H2O. It is important
leading to inadequate distribution of
to note that the circuit itself will require a
blood. This is most commonly seen in neu-
PEEP of 5 cm H2O to overcome, so PEEP is
rosurgery in the setting of systemic vasodi-
never less than 5 cm H2O.
lation secondary to sepsis or neurogenic
shock. It is important to note that neuro-
7.3 Shock genic shock from spinal trauma can also
have elements of cardiogenic shock, as it
Shock is acute failure in tissue perfusion may involve decreased sympathetic drive.
across multiple organ systems. It is classi- Common symptoms include hypotension
cally divided into four categories based on and poor systemic oxygenation in the set-
etiology and physiologic characteristics ting of adequate volume status and cardiac
including preload, cardiac output, and function. Preload and cardiac output can
afterload. both be either normal or increased, after-
load is always decreased. In neurogenic
shock, other symptoms include bradycar-
7.3.1 Hypovolemic Shock dia and hypothermia. Treatment primarily
This is defined as the loss of effective intra- consists of adequate resuscitation and
vascular volume secondary to inadequate vasoactive agents.
intake, excessive loss, or a mixture of both.
In neurosurgical patients, common causes 7.3.4 Obstructive Shock
include blood loss secondary to trauma or
surgery, cerebral salt wasting (CSW), or This is characterized by mechanical
diabetes insipidus (DI). Hypovolemic shock obstruction to blood flow through cardiac
classically presents with tachycardia and chambers. Most important causes of
tachypnea. It is characterized by decreased obstructive shock in neurosurgical patients
preload, decreased cardiac output, and include postoperative venous thrombosis,
increased afterload. Treatment requires tension pneumothorax from central line
volume resuscitation. placement, and air embolus from surgeries
123
Neurocritical Care
in sitting position or involving dural venous elevated urine osmolality (> 100 mOsm/kg
sinuses. Presentation includes profound and often > 300 mOsm/kg). Treatment of
hypotension and hypoxia in the setting of CSW differs significantly from SIADH as it
normal to high preload, decreased cardiac is treated with fluid repletion and usage of
output, and increased afterload. Treatment fludrocortisone to promote renal sodium
requires adequate oxygenation, proper reabsorption. Although the efficacy of
positioning, removal of obstruction via enteric sodium repletion strategies is con-
thrombectomy, or chest tube placement. troversial, sodium chloride tablets and
Gatorade are commonly used as an adjunct
treatment for hyponatremia.
7.4 Fluid and The determination must be made
Electrolytes between SIADH and CSW prior to treat-
ment as they entail very different
approaches. Patients with SIADH are fluid
7.4.1 Hyponatremia
neutral or overloaded and thus treatment
Hyponatremia is defined as serum sodium is with fluid restriction, given fluid will
of less than 135 mEq/L. Symptoms of hypo- serve to exacerbate symptoms of fluid
natremia include lethargy, confusion, overload and further worsen hyponatre-
coma, and seizure. The differential for mia. Patients with CSW are fluid depleted
hyponatremia in neurosurgical patients or “dry.” The treatment is then fluid resus-
most commonly includes syndrome of citation with the goal of at least maintain-
inappropriate antidiuretic hormone secre- ing an even intake and output.
tion (SIADH) and CSW. SIADH, as its name Fludrocortisone is a mineralocorticoid that
suggests, involves the inappropriate secre- can be used to increase renal reabsorption
tion of antidiuretic hormone (ADH) in the of sodium. Fluid restriction in SAH patients
absence of its normal physiologic trigger, with CSW can be dangerous due to the risk
serum hyperosmolality. It is classically of worsening vasospasm.
seen in the setting of lung neoplasm. Neu-
rosurgical causes of SIADH includes men-
ingitis, traumatic brain injury (TBI),
intracranial hypertension, SAH, and neo- Correction of hyponatremia should be no
plastic processes. Other causes include faster than 1.3 mEq/h and no more than
medication side effects, most notably car- 8 mEq in 24 h and 18 mEq in 48 h.
bamazepine. Diagnosis of SIADH is made
with the criteria of hyponatremia (< 134
Overly quick correction can lead to central
mEq/L), high urine sodium (> 18 mEq/L),
pontine myelinolysis, which can produce
and low serum osmolality (< 280 mOsm/L).
quadriplegia, pseudobulbar palsy, and cra-
Definite diagnosis is through a water-load
nial nerve abnormalities.
test. Treatment of acute SIADH is fluid
restriction to typically less than 1 L/day.
CSW is the renal loss of sodium secondary
to an intracranial process. The exact mech- 7.4.2 Hypernatremia
anism of CSW is unclear. In neurosurgical
patients, CSW is most commonly seen in Hypernatremia is defined as serum sodium
patients with SAH and TBI. Diagnosis of of greater than 150 mEq/L. DI is the most
CSW is made with the criteria of hypona- common cause of hypernatremia in neuro-
tremia (< 134 mEq/L), high urine output, surgical patients. In patients with DI, there
high urine sodium (> 40 mEq/L, and an is an abnormally low levels of serum ADH
124
7.5 Cerebral Metabolism and Perfusion
which results in excessive loss of free water on the cellular level corresponding with
through urination and increasing serum severely suppressed EEG and loss of con-
sodium. Common causes of DI in neurosur- sciousness. Cellular ionic pumps begin to
gical population includes TBI, neoplastic fail at CBF of 10–12 mL/100 g/min which
(primarily pituitary region lesions), menin- leads to cellular swelling and cytotoxic
gitis, and autoimmune causes. Manipula- edema that can be seen on imaging. Com-
tion of the pituitary gland during plete failure of cellular metabolism and
transphenoidal surgeries can lead to either irreversible brain damage occurs at CBF
permanent or temporary DI depending on less than 10 mL/100 g/min.8
the degree of injury to the posterior pitu- The driving force of CBF is cerebral per-
itary gland and pituitary stalk. A unique fusion pressure (CPP), which is the differ-
phenomenon known as the “triphasic ence in pressure between arterial inflow
response” is sometimes seen in patients and venous outflow. Arterial inflow pres-
after pituitary surgery where patient ini- sure is the mean arterial pressure (MAP).
tially presents with symptoms of DI, fol- Venous outflow pressure correlates closely
lowed by a period of normalization prior to with intracranial pressure (ICP), thus ICP is
going back into DI. The theory behind the often used as a surrogate. In short, CPP can
triphasic response is that the initial injury be mathematically described as9:
causes lack of ADH secretion promoting the
patient to go into DI. Over the next 48 hours,
apoptosis of injured ADH secreting cells can
CPP = MAP – ICP
cause a sudden release of ADH leading to
normalization or even overcorrection of
serum sodium. After all the ADH has been An important concept in cerebral perfu-
utilized, the patient again goes back into DI. sion and metabolism is cerebral autoregu-
Diagnosis of DI is made with urine output lation, which describes the ability of
greater than 250 mL/h, serum sodium of cerebral vasculature to regulate its own
greater than 140 mEq/L, and urine osmolal- blood flow through either relaxation or
ity of less than 200 mOsm/L. Definitive constriction in response to metabolic or
diagnosis is made with water deprivation pressure cues in order to maintain blood
test. DI is treated with desmopressin. flow to provide brain oxygenation. One of
the most important metabolic cues is car-
bon dioxide, to which the cerebral vascula-
7.5 Cerebral ture is very sensitive.10 It is estimated that
a change of 1 mmHg of PaCO2 results in a
Metabolism and 4% change in CBF. This property is taken
Perfusion advantage of in situations where a tempo-
rary reduction in ICP is desired. Cerebral
Cerebral blood flow (CBF) is a measure- autoregulation is only effective within a set
ment of the volume of blood (mL) that regulatory plateau. At CPP below the pla-
passes through a fixed amount of tissue (g) teau, there is passive collapse of blood ves-
in a given amount of time (min). Normal sels. At CPP above the plateau, there is
CBF is estimated to be 40–60 mL/100 g/ segmental dilatation of blood vessels with
min. When CBF drops to 20–30 mL/100 g/ breakdown of the blood brain barrier.
min, slowing can be seen on an electroen- A good understanding of cerebral metab-
cephalogram (EEG), and disturbances of olism and cerebral autoregulation is crucial
consciousness occur. CBF of less than in management of SAH patients. The clinical
20 mL/100 g/min leads to electrical failure course of a SAH patient battling vasospasm
125
Neurocritical Care
frequently pushes the boundary of cerebral space, or brain parenchyma. In addition

autoregulation. The pathophysiology of SAH to direct transduction of ICP, an EVD
will be discussed in further detail in the vas- offers the added advantage of allowing
cular chapter see section 12.2. for therapeutic drainage of cerebrospinal
fluid. When compared to other modali-
ties, EVD placement is more invasive and
7.5.1 Intracranial Pressure associated with risks of catheter tract
Monitoring hemorrhage and infections that can lead
to ventriculitis.11,12 In patients who have
The importance of ICP lies in its relation- difficult-to-correct coagulopathy and
ship with CPP. As previously discussed, CPP pathology that is unlikely to require CSF
is the difference between MAP and ICP, and diversion, indirect methods of measuring
thus persistently elevated ICP can lead to ICP can be considered.
decreased CPP with resultant cerebral
hypoperfusion and neurologic injury.
7.6 Hematology and
Coagulation
The concept of ICP is best explained by
the classic Monro-Kellie Hypothesis Regardless of whether it is a lumbar
which states that the human cranium is a puncture or a deformity correction sur-
fixed space occupied by three major com- gery, it is critically important to confirm
ponents, brain parenchyma, blood, and that the patient can tolerate a procedure
cerebrospinal fluid (CSF), and an increase from the hematological and coagula-
in any of the components or the intro- tion standpoint prior to starting. Typical
duction of a new mass lesion can lead to preprocedure laboratory tests include
an elevation in ICP. hemoglobin, platelet count, interna-
tional normalized ratio (INR), and partial
thromboplastin time (PTT). If the patient
Lesions that cause increased ICP can be is on antiplatelet medications (i.e., aspi-
divided based on which component is rin, clopidogrel), platelet function assays
affected. Common lesions that can cause may also be routinely sent. For patients
an increase in ICP include mass lesions undergoing a procedure with small
such as subdural or epidural hematomas, expected blood loss, a hemoglobin of 7.0
neoplasm, abscess, and intraparenchy- g/dL is typically considered the minimal
mal hemorrhages; cerebral edema from threshold prior to transfusion with
trauma, infarction, or inflammation; and packed red blood cells (pRBC). A unit of
hydrocephalus. pRBC (~350 mL) will on average increase
There are many methods of continu- hemoglobin by 1.0 g/dL. A platelet count
ous ICP monitoring, the gold standard of of 100,000/µL is the preprocedural mini-
which is through an external ventricular mum for neurosurgical patients. Platelet
drain (EVD) as it directly transduces the concentrates are usually administered
fluid pressure inside the ventricular sys- as a pool of 6 units. In the average
tem. Other monitoring modalities involve adult, each of these platelet concentrates
placement of monitoring devices such as will increase the platelet count by
fiberoptic transducers or piezoresistive 5,000–10,000/µL. As such an entire pool
sensors in the epidural space, subdural may increase the platelet count by
126
7.6 Hematology and Coagulation
30,000–50,000/µL. Platelet administra- we perform laboratory testing every 6

tion in patients who are on antiplatelet hours for hemoglobin, hematocrit, platelet
medications is controversial and the count, INR, PTT, and fibrinogen. Prompt
practices are widely different. At our transfusion of pRBC, platelets, fresh frozen
institution, prior to a procedure, we do plasma (INR/PTT), and cryoprecipi-
not typically transfuse patients who take tate (fibrinogen) based on suboptimal lab-
aspirin, but we will transfuse patients on oratory results can potentially prevent
clopidogrel with a positive response catastrophic hemorrhages.
assay because in our experience, clopi-
dogrel use is associated with more pro-
found intraoperative blood loss. INR is a 7.6.2 Venous
functional measurement of the extrinsic Thromboembolism
coagulation pathway with a typical cut-
off of between 1.2 and 1.4 and PTT is the Venous thromboembolism is a dreaded
measure of the intrinsic pathway with a and possibly life-threatening complica-
cutoff of 40 seconds. Increased INR can tion that is not uncommon in postopera-
be due to a variety of factors such as tive patients. As the name suggests, deep
medication effect (warfarin, direct oral vein thrombosis (DVT) is defined as the
anticoagulants [DOACs]), poor nutrition, formation of blood clots in one of the deep
poor liver synthetic function, and certain veins. Pulmonary embolism (PE) is the
disease states. Reversal of increased INR most clinically significant complication of
is discussed in detail in Cranial chapter DVT, which occurs when a piece of the clot
(Chapter 8). breaks off and travels to the pulmonary
circulation leading to increased ventilatory
dead space and difficulty with gas
7.6.1 Disseminated exchange. PE manifests clinically in the
form of tachycardia, tachypnea, and oxy-
Intravascular Coagulation
gen desaturation. A helical chest CT angio-
Disseminated intravascular coagula- gram is the most valuable tool for diagnosis
tion (DIC) is a dangerous phenomenon of PEs. PE treatments primarily consist of
where there is abnormal generation of supportive therapy with anticoagulation in
microthrombi that can lead to organ dys- the form of heparin drip, therapeutic low
function, and at the same time, there is molecular weight heparin (LMWH; i.e.,
significantly increased risk of bleeding due lovenox), warfarin, or DOAC. Common
to consumption of coagulation factors and neurosurgical conditions that increase the
platelets by the abnormal thrombi forma- risk for developing DVTs include neoplasm,
tion. DIC often presents as a manifestation immobility, and multisystem trauma. In
of underlying disease processes. In neuro- these patients, DVT prophylaxis is
surgical patients, the most common dis- extremely important. Typical prophylaxis
ease processes that can lead to DIC include consists of sequential compression devices,
sepsis, severe multisystem trauma, and in subcutaneous heparin or prophylactic
patients who required significant amounts lovenox, and improving mobility, espe-
of blood products to replace either intra- cially ambulation. It is important to note
operative or traumatic losses. In these that therapeutic LMWH can be dangerous
high-risk patients, frequent laboratory in postoperative neurosurgical patients as
testing and repletion of coagulation com- it cannot be titrated which can lead to
ponents is important. At our institution, potentially fatal bleeding events.
127
Neurocritical Care
Pearls 7.7.2 Answers
• In managing critically ill neurosurgi-
cal patients, ABC (airway, breathing, 1. Polydipsia and polyuria in patients
and circulation) come before the who had recently undergone transphe-
neurological system. noidal surgery should immediately
• Always remember there are make one concerned for DI. Workup of
noninvasive interventions for elevated DI includes testing serum sodium
ICPs and they should be utilized prior (> 140 mEq/L) and urine osmolality
to invasive interventions. (< 200 mOsm), and measuring urine
• In managing patients with suspected output (> 250 cc/h).
DI, close monitoring is necessary to 2. CPP = MAP − ICP.
prevent rapid shifts in serum sodium 3. Presentation of bradycardia and hypo-
from triphasic response. tension in the setting of suspected
spine trauma is concerning for neuro-
genic shock. This patient should be
7.7 Top Hits managed with vasopressors and intra-
venous fluid.
7.7.1 Questions 4. This patient has multiple risk factors
for developing ARDS such as trauma
1. A 37-year-old female, on postopera- and significant blood transfusion.
tive day one from endoscopic endona- Management of ARDS is supportive
sal resection of pituitary adenoma, is therapy with low volume ventilation,
complaining of polydipsia and poly- and diuresis.
uria. What you do suspect? How do 5. The Monro-Kellie hypothesis states that
you work it up? the human cranium is a fixed space oc-
2. How is CPP mathematically calculated? cupied by three major components,
3. A 52-year-old male is brought to the brain parenchyma, blood, and CSF, and
emergency department after being in- an increase in any of the components or
volved in a high velocity motor vehicle the introduction of a new mass lesion
collision. On arrival, his heart rate is can lead to an elevation in ICP.
42, blood pressure is 82/45 mmHg,
and temperature is 35°C. His chest
X-ray is negative for pneumothorax.
His trauma FAST evaluation was nega-
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olds of focal cerebral ischemia in awake monkeys. ES, Jr. Ventriculostomy-related infections: a crit-
J Neurosurg. 1981; 54(6):773–782 ical review of the literature. Neurosurgery. 2002;
[9] Bratton SL, Chestnut RM, Ghajar J, et al; Brain Trau- 51(1):170–181, discussion 181–182
ma Foundation. American Association of Neurolog- [12] Gardner PA, Engh J, Atteberry D, Moossy JJ. Hemor-
ical Surgeons. Congress of Neurological Surgeons. rhage rates after external ventricular drain place-
Joint Section on Neurotrauma and Critical Care, ment. J Neurosurg. 2009; 110(5):1021–1025
AANS/CNS. Guidelines for the management of
129
8 Traumatic Brain Injury
Christine Mau, Shelly Timmons
8.1 Introduction (5 points), and eye response (4 points) for a

minimum score of 3 and maximum score
The Centers for Disease Control and Preven- of 15. There is a separate way to assess pedi-
tion reported that in 2013, there were at atric patients using the GCS score depen-
least 2.8 million emergency department dent on age (▶Table 8.2; see section 14.4,
visits, hospitalization, or deaths related to chapter 14). Based on the GCS, the severity
traumatic brain injury (TBI).1 To put this in of TBI can be estimated (▶Table 8.3).
perspective, every hour, there are an aver-
age of 204 TBI-related emergency depart-
ment visits, 33 TBI-related hospitalizations; The common phrase “less than 8, then in-
and 6 TBI-related deaths.1 Overall, TBIs con- tubate” speaks more to the inability for
tribute to 30% of all injury-related deaths.1 the patient to protect his/her airway.
The range of TBI spans from mild to
life-threatening and the subsequent treat-
ment ranges from observation and medical In fact, 56—60% of patients with GCS
optimization to emergent surgical interven- score less than or equal to 8 have one or
tion. Understanding TBI is critical to effec- more other organ systems injured.2 Fur-
tively evaluate and treat these patients. thermore, 4–5% have associated spine frac-
tures. GCS can be affected by factors other
than neurological injury including pharma-
8.2 Classification of cologics, respiratory compromise, and met-
abolic abnormalities. Re-evaluation once
Head Injury underlying issues are addressed is essential
for accurate prediction of prognosis.
8.2.1 Examination to
Assess Head Injury
8.2.2 Recommendations
The Glasgow Coma Scale (GCS) serves as an
for Imaging
initial way to assess the severity of head
injury (▶Table 8.1). It is composed of three In patients with minor head injury, the deci-
components: motor (6 points), verbal sion to obtain CT imaging can be difficult
Table 8.1 Adult Glasgow Coma Scale

Response 1 point 2 points 3 points 4 points 5 points 6 points
Eye No Open to pain Open to Open spon-
response voice taneously
Verbal No Incomprensi- Incoherent Disoriented Appro-
response ble sounds words or confused priate
responses
Motor No Extensor Flexor Withdraws Localizes Follows
response (decerebrate) (decorticate) from pain to pain com-
posturing posturing mands
130
8.2 Classification of Head Injury
Table 8.2 Pediatric Glasgow Coma Scale

Response Age 1 point 2 points 3 points 4 points 5 points 6 points
Eye <1 No Open to Open to Open
year response pain shouting spontane-
ously
>1 No Open to Open to Open
year response pain com- spontane-
mand ously
Verbal <2 No Grunts, Persistent Cries and Smiles
years response agitated, inappro- consola- or coos
restless priate ble appropri-
crying or ately
screaming
2–5 No Grunts Persistent Inappro- Appro-
years response crying priate priate
and words word
screaming phrases
>5 No Incompre- Inappro- Disori- Oriented
years response hensible priate ented or
sounds words confused
Motor No Extensor Flexor With- Localizes Sponta-
response (decer- (decor- drawal to pain neous
ebrate) ticate)
posturing posturing
Table 8.3 Traumatic brain injury grading Canadian CT Head Rule

Category Criteria • Applies to patients with GCS 13–15
with witnessed loss of conscious-
Mild GCS 13–15
ness (LOC), amnesia, or disorientation.
Moderate GCS 9–12 • High risk of need for intervention:
Severe GCS 3–8 ◦ GCS scores less than 15 at 2 hours
after initial injury.
Abbreviations: GCS, Glasgow Coma Scale. ◦ Suspected open or depressed skull
fracture.
compared to ordering CT imaging on a ◦ Any sign of basilar skull fracture
patient with clear neurological deficit. There (raccoon sign, otorrhea, rhinorrhea,
are two major published recommendations Battle’s sign, hemotympanum etc).
to aid in decision making: the Canadian ◦ More than one episode of emesis.
Head CT rule and the New Orleans criteria. ◦ Age 65 years or older.
131
Traumatic Brain Injury
• Medium risk for brain injury on CT: mortality increases with the presence of
◦ Amnesia before injury for more than an intracranial lesion, edema causing
30 minutes. compression of the cisterns, midline shift
◦ Dangerous mechanism including (MLS) more than 5 mm, and volume of the
pedestrian struck, ejection from lesion more than 25 mL. Contrasted scans
vehicle, fall from height over 3 feet, are often not indicated in most trauma
or fall down more than five stairs. situations unless there is suspicion for

significant brain edema (visible on non-
contrasted scan) secondary to suspected
New Orleans Criteria neoplasm or suspected altered sensorium
CT is recommended for patients with from infectious epidural collection.
minor head injury (GCS 15) with any one
of the following findings:
X-rays
1. Headache.
Skull X-rays may be helpful in certain
2. Vomiting.
situations such as penetrating injuries. How-
3. Age more than 60 years.
ever, X-ray has low sensitivity for detecting
4. Drug or alcohol intoxication.
intracranial abnormalities (roughly 25%).3 If
5. Persistent anterograde amnesia.
a CT cannot be obtained, then X-rays can be
6. Visible trauma above the clavicle.
used to identify pneumocephalus, skull frac-
7. Seizure.
tures, pineal shift, and air-fluid levels.
8.2.3 Imaging to Modalities

Magnetic Resonance Imaging
Computed Tomography MRI is usually not used for acute head inju-
Non-contrast CT scans of the brain can also ries given its lower availability on an acute
be used to predict mortality using the basis, contraindication in critical patients
Marshall Grade (▶Table 8.4). Predicted who may not be able to tolerate lying
Table 8.4 Marshall Grade to predict mortality2

Category Cisterns Midline shift Intracerebral Mortality
hemorrhage
Diffuse injury I No visible No visible No visible 9.6%
pathology pathology pathology
Diffuse injury II No pathology < 5 mm Lesion densities 13.5%
present
Diffuse injury Compressed or < 5 mm Lesion densities 34%
III (swelling) absent < 25 mL
Diffuse injury > 5 mm Lesion densities 56.2%
IV (midline > 25 mL
shift)
Evacuated mass Evacuated 38.8%
lesion
Nonevacuated 52.8%
132
flat or undergoing a longer scan, and

unchanged sensitivity in detecting surgical
lesions.4 MRI scans do have utility after the Hippocampal neurons in the cornu ammo-
patient is stabilized in order to detect evi- nis (CA1) and CA3 layers, cerebellar granu-
dence of diffuse axonal injury (DAI, lar cells, and larger cortical neurons are
although clinical correlation is key in mak- most susceptible to selective neuronal loss.
ing this diagnosis), hypoxic injury, or punc-
tate hemorrhages not seen on CT. When flow is 10 mL/100 g/min or less
for more than 60–90 minutes, infarction
occurs. This dependence on cerebral blood
8.2.4 Brain Injury flow for tissue integrity makes it less sur-
Brain injury secondary to trauma occurs prising that a single episode of hypoten-
from an initial mechanical impact to the sion with systolic blood pressure (SBP) less
brain, sometimes called primary injury or than 90 leads to a 150% increase in mortal-
impact damage. However, secondary injury ity for TBI patients.14
also occurs due to alterations in a variety of
cerebral physiological process, including 8.2.5 Hemorrhage Types
metabolic crisis and ischemia, release of
inflammatory cytokines and cytotoxins, There are various types of hemorrhages
membrane breakdown, excitotoxicity, and depending on etiology, mechanism, and
neurotransmission derangements.5,6 Isch- sometimes age. They vary in both appear-
emia is thought to be the most important ance and location, which can provide
factor leading to secondary damage. The insight into the type of hemorrhage and
brain is dependent on cerebral blood flow subsequently, the management of the
and reduction in oxygen leads to tissue hemorrhage (▶Table 8.5).
damage in a physiologically predictable pro-
cess. Normal, healthy brain that is able to
maintain autoregulation can tolerate a corti-
Epidural Hemorrhages
cal flow reduction to 20 mL/100 g/min. Epidural hemorrhages (EDHs) are classi-
However, below 20 mL/100g/min, loss of cally caused by rupture of the middle
consciousness and coma ensue.7,8,9,10,11 meningeal artery with an overlying frac-
When this flow reduces below 18 mL/100 g/ ture of the temporoparietal bone. How-
min, energy dependent ion pumps are ever, this is actually only the case in
unable to maintain ionic gradients across approximately one-third of adults and
the neuronal cell wall and stops functioning. one-fifth of children.15 EDHs can also be
This can lead to anaerobic metabolism and due to bleeding from the middle menin-
begins to generate lactic acid. At 10 mL/100 geal vein or dural sinus. EDHs are more
g/min, the cell membrane loses stability and common in young adult males aged 20–30
there is a massive influx of calcium leading years. Additionally, skull fractures have
to irreversible damage. On pathology, there been found in 95% of patients with EDH.
is karyorrhexis, or loss of nuclear definition, The classic presentation is a brief loss of
along with vacuolation of perineuronal consciousness after the traumatic event,
astrocytic processes and swelling of the followed by a lucid interval, then rapid
mitochondria, Golgi and intracellular cyto- deterioration over several hours. Almost
plasmic vesicles. When flow is 15–18 half of patients will present with a classic
mL/100g/min for more than 30 minutes, “lucid interval” and 27% will present neu-
selective neuronal loss may occur.12,13 rologically intact.16,17
133
Table 8.5 Types of hemorrhages

Type of Appearance Location Etiology Associations
hemorrhage
Epidural Lens or biconvex Does not cross Arterial bleed- Skull fracture
hemorrhage suture lines ing, often the often overlies
because of dur- middle menin- EDH because
al attachment geal artery high impact
Subdural Crescent Does not cross Venous Elderly patients
hemorrhage shaped midline or bleeding, often have atrophy of
tentorium due to bridging the brain lead-
veins ing to increased
susceptibility of
bridging veins
Subarachnoid Hyperdensity Convexity, Arterial If basilar
hemorrhage along sulci or in Sylvian (starfish
cisterns fissure; Inter- appearance),
hemi-spheric, a ruptured
cisternal aneurysm must
be ruled out
Intraparenchy- Circular or 1. Basal Mechanical Severe impact,
mal hemorrhage ovoid ganglia tearing of poor nutritional
2. Lobar vessel, injury to status
3. Cerebellar vessel leading
to permeability
and subsequent
hemorrhage
Contusion Hyperdense May be in any “Bruising” from “Contrecoup”
blood; May location; Lobar acceleration/ injuries may
be stippled common, deceleration, occur opposite
or multiple; especially direct force to the site of
May be mixed frontal and trajectories, impact
density (both temporal lobes shear and rota-
hyperdense tional forces
blood and
hypotenuse
areas)
Intraventricular Blood within Lateral, 3rd, In trauma, Can be
hemorrhage ventricle and/or 4th often sec- isolated or an
ventricle ondary from extension of
extension from parenchymal or
parenchymal or subarachnoid
subarachnoid hemorrhage;
Isolated more
common in
elderly patients
134
In adults, over 90% of EDHs occur sec- 4. Cardiorespiratory abnormalities.

ondary to traffic accidents, falls, and 5. Anisocoria and GCS less than 9.
assaults. In pediatric patients, a 10% drop in
hematocrit should elevate suspicion for an
Subdural Hemorrhages
EDH. In pediatrics, falls account for approx-
imately half of EDHs, while traffic accidents Subdural hemorrhages (SDHs) are the most
account for another one-third.15 Symptoms common traumatic intracranial lesions and
include obtundation, contralateral hemipa- occur in up to 29% of TBI patients.30 Younger
resis (unless Kernohan’s notch phenome- patients most commonly presents after a
non occurs), and ipsilateral pupil dilatation motor vehicle accident and older patients
(up to 44%).17,18 EDH is present in up to 4% most commonly present after a fall.
of TBI patients, and almost 10% will present Patients commonly present obtunded and
in a coma.19,20,21 The single most important up to half present with pupillary abnor-
prognostic factor is the GCS score at time of malities.22,31,32,33 They can arise from injury
presentation. If GCS is 6–8, mortality is 9% or tearing of bridging veins in the subdural
whereas with GCS 3–5, mortality increases space, or bleeding from parenchymal
to 36%.20 Patients with no pupillary find- injuries. SDHs are often associated with

ings have a poor outcome in 30% of cases, damage to the actual underlying brain
one fixed pupil have a poor outcome in 35% parenchyma; therefore, although evacua-
of cases, and bilaterally fixed pupils have a tion may be lifesaving, removal does not
poor outcome in 50%.22 Other poor prog- ensure a good outcome. Regardless of GCS
nostic factors are associated traumatic sub- score at presentation, mortality is between
arachnoid hemorrhage (tSAH), greater than 40 and 60% whereas mortality for patients
50 mL in volume, effacement of basal cis- who present in a coma is 57–68%.30
terns, and MLS more than 1 cm.22,23 There have been a multitude of stud-
If an EDH is diagnosed and treated within ies looking at morbidity and mortality
a few hours, mortality is estimated to be based on the thickness of the SDH, degree
between 5 and 12%.24 More specifically, for of midline shift, presenting GCS score, and
patients that require operative evacuation, age.34,35,36,37 Not surprisingly, larger-sized
one study found that all patients with evacu- SDHs, greater degrees of associated MLS,
ation completed after 70 minutes from the lower presentation GCS scores, and higher
onset of pupillary dilation died.25 Death is ages at presentation are all associated
often secondary to uncal herniation causing with increased mortality and poorer out-
injury to the midbrain leading to respiratory come.34,35,36,37 As with epidural hemato-
arrest. Management ranges from observing mas, earlier evacuation in operative
closely to emergent surgery. patients is associated width better out-
come. Evacuation within 2–4 hours of
clinical decline is associated with
Surgical Indications improved morbidity and mortality.17,29,38
1. Signs of local mass effect (symptom-
atic EDH).
2. Acute asymptomatic EDH more than Kernohan’s notch phenomenon is when
30 cm3, thickness more than 15 mm, the brainstem shifts away from the mass
or more than 5 mm midline shift on and may cause compression of the op-
initial CT regardless of GCS.18,23,26,27,28 posite cerebral peduncle on the tentorial
3. Signs of herniation23,25,29 notch.39 This can cause a false localizing
a) Increased drowsiness, pupillary sign and lead to ipsilateral hemiparesis.
changes, hemiparesis.
135
Surgical Indications increased permeability of vessel walls

causing increased hemorrhage.45 Up to
1. SDH thickness greater than 1 cm or 38% of patients with traumatic IPH may
MLS greater than 5 mm regardless of have an increase in size of the lesion.46
GCS35,36 The presence of SAH, SDH, and higher
2. GCS less than 9, lack of ability to initial volumes (11% risk per cm3) have
localize on motor response should been associated with progressive IPH
undergo intracranial pressure (ICP) enlargement.46 Surgical intervention for
monitoring.37 IPH can be done for hematoma evacua-
3. GCS less than 9 with thickness less tion, cerebral decompression, or both.
than 1 cm and midline shift less than
5 mm should undergo surgical
evacuation if the GCS decreases by 2 Surgical Indications
points, there is an abnormal pupillary
examination, or there is sustained ICP 1. Progressive deterioration of
elevation above 20 mmHg despite neurological examination localizable
medical therapies. to the lesion, medically refractory
intracranial hypertension, signs of
mass effect on CT such as edema,
Subarachnoid Hemorrhages MLS, or compression of the ventricles/
cisterns.47,48,49,50,51
Traumatic SAH occurs in 12–53% of 2. Any lesion with a volume more than
TBIs.40,41,42 It is caused most often by 30 cm3 or MLS more than 5 mm.52
bleeding from cortical arteries, veins,
and capillaries but can also rarely be sec-
ondary to bleeding from the rupture of Contusions
bridging veins or traumatic aneurysms.40,
43 Its presence increases mortality by Contusions are caused by a variety of
twofold. The two main explanations for mechanisms and forces, including direct
this are that either tSAH is an indicator of linear force, rotational and shear forces,
a greater severity of injury or because of and sudden deceleration of the head. They
subsequent vasospasm and ischemia.42,43, may occur in a coup-contrecoup pattern
44 Prognosis of TBI patients with tSAH is and often occur at the frontal, temporal,
related to admission GCS and other asso- and occipital poles as well as the basilar
ciated hemorrhages.40 aspects of the frontal and temporal lobes
because of impact against the inside of the
skull and its bony prominences on the floor
Intraparenchymal of the anterior and temporal fossae. They
typically evolve over time and may enlarge
Hemorrhages
or be associated with progressive edema,
Intraparenchymal hemorrhages (IPH) which may cause mass effect issues and
occur from various mechanisms: tearing require urgent surgical decompression in
of deeper vessels from impact injury, or cases of herniation. Sometimes contusions
vascular disturbances secondary to develop in a delayed fashion in patients
trauma resulting in vasothrombosis and with severe TBI (GCS ≤ 8). These delayed
vasoparalysis which leads to perivascular contusions occur in approximately 10% of
edema and subsequently to perivascular patients usually within 72 hours of the
hemorrhage.45 Additionally, poor nutri- traumatic event.53,54 Mortality is high for
tional status after trauma can lead to these patients and ranges from 50 to 75%.55
136
Surgical Indications • Imaging: Time of last scan (if transferred).

• Important laboratory values: Arterial
1. Progressive deterioration of blood gas (ABG), complete metabolic
neurological examination localizable panel, especially sodium, glucose, and
to the lesion, medically refractory creatinine; complete blood count (CBC),
intracranial hypertension, signs of especially hemoglobin, hematocrit, and
mass effect on CT such as edema, platelet count; partial thromboplastin
MLS, or compression of the ventricles/ time (PTT), prothrombin time (PT) /
cisterns.47,48,49 international normalized ratio (INR);
2. GCS 6–8 with frontal or temporal possibly platelet assays; urinalysis; serum
contusions more than 20 cm3 with alcohol level; and toxicology screen.
MLS more than 5 mm or cisternal
compression.48
3. Any lesion more than 50 cc in 8.2.7 Initial Assessment
volume.48
The initial assessment of a trauma patient
is essential to avoid missing any critical
Intraventricular Hemorrhages injuries. The “ABCDE” method of assess-
ment precedes any imaging or neurological
Intraventricular hemorrhage (IVH) is
exam. In other words, in a patient who is
found in 1.5–5.7% of patients with blunt
unable to protect their airway, intubation
head trauma and present in almost 10%
takes precedent over a neurological exam-
of patients with severe TBI.56,57 IVH may
ination or obtaining imaging to determine
occur from extension of parenchymal
whether they have a potential head injury.
hemorrhages, redistribution of subarach-
noid hemorrhage, or may occur in isola-
tion, especially in the presence of
coagulopathy.56,58 Traumatic IVH is associ-
Resuscitation (A B C D E)
ated with poor outcome and high mortal- • Airway: Ask the patient a question such
ity.56,57 Presence of hemorrhage in all four as “What is your name?” If they are able
ventricles portends worsened outcome to verbalize a response, this means their
and may be associated with diffuse axonal airway is patent. If they do not verbalize a
injury.56 Acute hydrocephalus is relatively response then apply noxious stimulation.
rare after traumatic IVH.56 If they are able to verbalize a response
(including guttural sounds such as a
groan) then their airway is patent.
8.2.6 History and Physical
• Breathing: Listen with a stethoscope to
The following key points should be gleaned both lungs. Unequal breath sounds may
from the history, which often must be indicate a traumatic injury such as a
obtained from family members, friends, pneumothorax or hemothorax.
and first responders at the scene: • Circulation: Palpate for pulses in
• History of present illness: Time of bilateral radial, femoral, posterior tibial,
onset, time of acute decline. and dorsalis pedis arteries. The ability
• Anticoagulation and antiplatelet to palpate the pulse at certain regions is
medications, dosage, indications, time an indicator of blood pressure, and
last taken, time, and result of last asymmetry may indicate a proximal
therapeutic blood level as applicable. arterial injury secondary to trauma.
• Physical examination: Focal neurologi- • Disability: Cursory examination of the
cal deficit. patient overall to look for any gross
137
traumatic injury such as an open long 2. Patients with GCS score 9 to 12 with
bone fracture. concerning mass lesions on CT should
• Exposure: Remove any clothing the be considered for monitoring.
patient may have on to avoid continued 3. Monitoring should be considered in
exposure to any potential toxins and patients with a normal head CT with
cover the patient to prevent hypothermia. any two of the following—age greater
than 40 years, SBP less than 90
mmHg, unilateral or bilateral
Physical Examination posturing (unable to localize).30
• Vitals (Cushing’s reflex)
• GCS 8.3.2 External Ventricular
• Laceration Drains
◦ Is there an underlying open skull
fracture? External ventricular drains (EVD) may be
◦ Is the wound contaminated? used for both ICP monitoring and to drain
• Basal skull fracture cerebrospinal fluid (CSF) to reduce ICP.59Indi-
◦ Battle’s sign: Postauricular ecchy- cations include those delineated above plus
moses (around the mastoid air intracranial hypertension resistant to medi-
sinuses). cal management or upon initiation of moni-
◦ Raccoon sign: Periorbital ecchymoses. toring with radiographic signs of cerebral
◦ Hemotympanum. edema and mass effect. Studies suggest that
◦ Otorrhea, rhinorrhea. continuous drainage, instead of intermittent
drainage, is more effective at lowering ICP.60,
61 However, continuous open drainage pre-
8.3 Monitoring cludes accurate ICP measurements via a flu-

id-coupled measurement mechanism alone,
8.3.1 Intracranial Pressure so either a combination catheter or multiple
Sustained elevated ICP can be devastating. catheters can be used. The use of antimicro-
Less than 3% of patients with a GCS of 14 or bial-impregnated catheters in comparison to
15 later deteriorate into coma, so monitor- standard catheters, has been shown to
ing is generally not used in this group. Of reduce infection rates associated with EVD
note, however, in TBI patients with GCS use.62,63 While EVD has the added benefit of
greater than 8, intracranial hypertension therapeutic CSF drainage, the complication
has been found to develop in over 50% of rates, particularly for infection, are higher
patients with an abnormal head CT com- than those of parenchymal monitors.
pared to 13% of TBI patients with GCS less
than 8 with a normal head CT. Parenchy-
mal monitors have extremely low compli-
8.4 ICP Treatment
cation rates and can be used for longer Normal ICP is generally considered to be
periods of time without infectious risk. less than 20 to 25 mmHg; and treatment is
often initiated in the setting of TBI to keep
Surgical Indications ICP less than 20 mmHg. As previously men-
tioned, a single incidence of SBP less than
1. Patients with a GCS score 3–8 or 90 mmHg is associated with a doubling
patients unable to localize on the of mortality. Another important predictor
motor component of the GCS with an of poor outcome is the duration of time that
intracranial lesion on head CT. ICP is elevated more than 20 mmHg.
138
8.4 ICP Treatment
Cerebral perfusion factor (CPP) is defined as of severe midline shift (especially if out of

the difference between the mean arterial proportion to the thickness of a subdural
pressure (MAP) and ICP. Therefore, with an hematoma), effacement of cisterns, and the
increase in ICP, the CPP decreases unless a presence of other significant lesions are indi-
concomitant increase in BP occurs, and cations that a bone flap may need to be left
thereby deleterious reductions in cerebral out after craniotomy and should prompt a
blood flow to the brain may occur. large exposure. Both mortality and improved
Management of TBI therefore requires outcomes at 6 months based on the Glasgow
a detailed understanding of these relation- Outcome Scale–Extended (GOS–E) after DC
ships as well as the dynamic states of indi- have been shown, with even greater
vidual patients over time. improvements at 12 months, but at least
some studies have shown that the propor-
tion of debilitated survivors may be
When cerebral autoregulation is lost, in- increased, so patient selection is critical.50,67
creases in BP may produce unsafe eleva-
tions in ICP.
Key studies for further reading are the
As previously noted, monitoring of ICP DECRA and RESCUEicp trials.
can include parenchymal ICP monitoring,
external ventricular drainage, or both.
Parenchymal ICP monitoring shows supe- Decompressive craniectomies should
rior accuracy compared to subdural, sub- measure at least 15 cm in diameter to
arachnoid, and epidural monitors. Numeric improve both neurologic outcome and
drift may occur affecting the accuracy after mortality.68,69
one week but this is often minor. EVDs are
the most accurate instruments to measure
8.4.2 Antiepileptic
ICPs due to the fluid coupled mechanism.
However, accuracy may be affected by the Management
presence of hemorrhage in the ventricle Post-traumatic seizures occur in up to 42%
and concomitant catheter occlusion. As up to 3 years after TBI. Patients most at risk
noted, EVDs also offer the advantage of for developing seizures are those with
being able to treat ICPs via drainage of hematomas, depressed skull fractures,
CSF.64 Overall, complications related to and GCS score less than 10.70,71,72 Early
monitors are low. Significant infections are post-traumatic seizures are defined as a sei-
exceedingly rare especially with the use of zure that occurs within the first 7 days after
antibiotic-impregnated catheters and inci- a TBI. These occur in up to 25% of patients.
dence of hematomas actually requiring Preventing early seizures reduces the change
surgical intervention is less than 1%.64,65,66 of epilepsy.71 Additionally, seizures can
cause elevated ICPs, reduce cerebral oxygen-
ation, result in hemodynamic instability,
8.4.1 Decompressive and further damage an already fragile brain.
Craniotomy/Craniectomy
Decompressive craniectomy (DC) is often
utilized to reduce dangerously elevated ICP Phenytoin has been found to be effective
when medical management has failed, or in in reducing early post-traumatic seizures,
conjunction with evacuation of mass lesions but not late post-traumatic seizures.
when cerebral edema is severe. The presence
139
Thus, it is not recommended to main- aspirin use, despite increased mortality, is

tain antiepileptics beyond the first 7 days not proven.84,85 A recent multicenter, ran-
after injury as a prophylactic measure (as domized controlled clinical trial showed that
opposed to using for the treatment of ongo- platelet transfusion actually leads to wors-
ing seizures).73 While valproic acid and phe- ened outcomes and thus is not recom-
nytoin, they were approximately equally mended as a routine matter.85 However,
effective, however valproic acid was associ- platelet transfusion may be required prior to
ated with a higher mortality rate so is not or during the conduct of intracranial
usually employed in this setting.74 procedures or operations to provide some
functioning circulating platelets to aid in
clot formation and coagulopathy manage-
8.5 Anticoagulation ment. Conversely, reversal of warfarin is rou-
tinely employed in the acute management
8.5.1 Prophylactic of traumatic hemorrhages (▶Table 8.6).86
Warfarin (vitamin K antagonist) can be
Anticoagulation
reversed with fresh frozen plasma and/or
Patients with TBI have a high incidence of prothrombin complex concentrate (PCC)
deep vein thrombosis (DVT) without any which contains coagulation factors II, VII, IX,
prophylactic treatment with estimates rang- and X.87 Vitamin K must also be given, and it
ing from 33–54%.75 The risk of developing a is imperative that serial laboratory tests be
DVT decreases to 25% in those treated with performed as initial reversal may not be
sequential compression devices (SCDs).76 durable. The reversal of warfarin with PCC is
Factors that increase the risk of DVT are 4–5 times faster in comparison to adminis-
extracranial injuries, increasing age, sub- tration of fresh frozen plasma, and may be
arachnoid hemorrhage, Injury Severity Score better tolerated in elderly patients or those
greater than 15, and increased severity of with congestive heart failure due to the
TBI.75,77 Chemical prophylaxis such as hepa- smaller volumes required.87 With the advent
rin or enoxaparin, can decrease the risk of of new agents such as rivaroxaban (factor Xa
DVT, but may carry the risk of worsening inhibitor) and dabigatran (thrombin inhibi-
intracranial hemorrhage.78,79,80,81,82,83 There tor) management becomes more difficult.88
is no consensus/convincing evidence in the These agents do not reliably reverse with
literature regarding the appropriate medica- standard methods. Theoretically, PCC should
tion, dosage, and timing for initiating DVT be able to reverse both rivaroxaban and dab-
prophylaxis. igatran.88 However, in a study in healthy sub-
jects, PCC administration only reversed the
effect of rivaroxaban, but not dabigatran.88
8.5.2 Reversal of Prior Idarucizumab, is a humanized monoclonal
Anticoagulation Agents antibody that has been developed to reverse
dabigatran and has recently been approved
Regular use of aspirin and use of warfarin for clinical use but has not been studied in
are independent predictors of death after detail in the TBI population.89
spontaneous intracerebral hemorrhage.84
Patients who regularly use aspirin have a
mortality rate over 40% and patients on war-
farin have mortality rates up to 68%.84 While
8.5.3 Skull Fractures
little data exists on outcome after TBI in Skull fractures are a strong predictive factor
patients on antithrombotic medications, for the presence of underlying intracranial
emerging literature shows similar patterns. hemorrhage.90,91 However, they may occur
Whether hemorrhages actually expand with in isolation with no significant brain injury.
140
8.5 Anticoagulation
Table 8.6 Anticoagulation agents and reversal

Anticoagula- Mechanism of Reversal agent Mechanism Half-life
tion agent action of action
Warfarin Vitamin K Fresh frozen All coagula- Limiting factor is
antagonist plasma and tion factors factor VII (4–6 h)
vitamin K
Prothrombin Factors II, Factor II (60–72 h)
complex con- VII, IX, and X Factor VII (4–6 h)
centrate Factor IX (16–20 h)
Factor X (40–45 h)
Rivaroxaban Factor Xa Prothrombin Factors II, Factor II (60–72 h)
inhibitor complex con- VII, IX, and X Factor VII (4–6 h)
centrate Factor IX (16–20 h)
Factor X (40–45 h)
Dabigatran Thrombin Idarucizumab Humanized 10–13 h
inhibitor monoclonal
antibody
Underlying pneumocephalus may indicate fractures may result in a CN VII and/or CN

a basal skull fracture or open fracture. VIII palsy, anterior basal skull fracture
Closed, linear, nondisplaced skull fractures may result in CN I or CN II palsy, and clival
generally do not require surgical interven- fracture (highly lethal) may result in CN VI
tion but overnight observation may be war- injury. If a basal skull fracture is suspected
ranted. Open depressed skull fractures are or diagnosed, certain precautions must be
managed operatively. Fractures involving taken to prevent further complications.
the frontal sinus often require surgical
treatment, especially if the nasofrontal
ducts are involved, pneumocephalus sug- Nasotracheal intubation or insertion of
gesting dural lacerations are present, or if nasogastric tubes must be avoided in

they are comminuted and involving the case of accidental intracranial violation.
posterior wall and cribriform plate. This has been associated with mortality
in 64% of cases.92,93
8.5.4 Basal Skull Fractures
Basal skull fractures are usually exten- About 3% of patients will have a CSF
sions of fractures from the cranial vault. leak after trauma. To avoid unnecessary
They occur in 12–20% of patients after increased ICP, the patient should avoid nose
trauma. Basal skull fractures are charac- blowing and the use of straws. A bowel reg-
terized by several signs on physical exam- imen (including scheduled stool softeners
ination; raccoon eyes (periorbital and laxatives as needed) to avoid Valsalva
ecchymoses), Battle’s sign (postauricular maneuvers during bowel movements
ecchymosis), CSF rhinorrhea/otorrhea, should be implemented as well. Cough sup-
hemotympanum, or epistaxis. Cranial pressants should be employed as needed
nerve (CN) injury can also be indicative of and physical activity involving straining
a skull base fracture. Temporal bone that could lead to a Valsalva maneuver
141
should be avoided. The patient’s head of nonaccidental trauma is suspected, a skele-

bed (HOB) should be elevated to approxi- tal survey (X-ray imaging) and MRI of the
mately 30° at all times. On subjective ques- neuroaxis (brain, cervical, thoracic, and
tioning, it is important to ask about the lumbar spine) may be warranted. Although
presence of a salty or metallic taste at the the majority of linear skull fractures are
back of the mouth or if any nasal drippage nonoperative, the development of a growing
is occurring. Rhinorrhea and otorrhea gen- skull fracture (post-traumatic leptomenin-
erally consist of clear, thin, water-like fluid, geal cyst) is a possibility. These are exceed-
but may also be pink or blood-tinged if ingly rare and only occur in 0.5–0.6% of skull
associated fractures or soft tissue injuries fractures.95 They almost always occur in
exist. Examination of the pillow case for patients less than a year of age and require
CSF may also be helpful if the patient is both a widely separated fracture and a dural
unable to communicate this information. tear. If they do occur, it is usually within 6
The benefit of prophylactic antibiotics is months of injury and present as a scalp
debated.94 If there is mass effect or under- mass. Treatment of a growing skull fracture
lying hematoma, operative intervention is is repair of the dural defect.
indicated. Otherwise, conservative man-
agement of CSF leak associated with basilar
skull fractures (as distinguished from fron- 8.5.6 Depressed Skull
tal sinus fractures) with bed rest (with HOB Fractures
elevation) and observation for CSF leak is
appropriate. If the CSF leak persists, a lum- Depressed skull fractures are often open,
bar drain can be placed for a period of sus- and are associated with infection rates of
tained CSF diversion. If this is not sufficient up to 11% and epilepsy in up to 15%.30,91
to stop the CSF leak, then craniotomy or Depressed skull fractures account for 6% of
endoscopic approach for a dural repair can adult skull fractures and 90% are open. The
be undertaken. If, despite all, a persistent most common location is parietal, followed
CSF leak occurs, a shunt may be indicated by temporal, frontal, and occipital. Mortal-
late in the course. ity from injuries in which a depressed skull
fracture is present are estimated to be as
high as 19%.30 Surgical indications for eleva-
8.5.5 Pediatric Skull tion of depressed skull fractures include
depression greater than the thickness of the
Fractures
skull or beyond the inner table, pneumo-
A linear, nondisplaced skull fracture in an cephalus indicating a dural laceration in the
infant also does not usually require surgical face of an open fracture, neurologic deficit
intervention but there are other consider- related to compression of underlying brain
ations that must be undertaken. In infants, tissue, CSF leak, gross contamination, or
the connective tissue overlying the skull frontal sinus involvement, with cosmesis
fracture more easily expands and given the occasionally playing a role. A relative but
baseline low circulatory volume, a signifi- not absolute contraindication to surgery is
cant amount of blood may be lost into the location of a skull fracture overlying a
overlying cephalohematoma. In addition to venous sinus. The surgical decision-making
physical examination of the cephalohema- follows the same indications as noted
toma, hematocrit should be measured on above, with special care being required
presentation and the next day. In addition, upon elevating the fracture fragments; the
the possibility of nonaccidental trauma surgeon should be prepared for venous
should be assessed, especially if there is sinus repair and control of venous bleeding
underlying intracranial hemorrhage. If prior to opening. Depressed skull fractures
142
8.6 Penetrating Trauma
in the pediatric population are most com- bullet tract, intracranial hemorrhage pat-
mon in the frontal and parietal region. One- terns, status of cisterns, midline shift, and
third are closed and closed fractures tend to cerebral edema CT imaging also helps
occur more often in younger children identify skull fractures as well as bullet
because of thin calvaria. Indications for sur- and bone fragment locations CT angiogra-
gery in simple depressed skull fracture in phy is helpful in identifying vascular inju-
the pediatric population are evidences of ries and should be done at the time of
dural penetration, persistent cosmetic presentation if feasible. Formal angiogra-
defect, or focal neurologic deficit. In new- phy may also be required upon presenta-
borns, a green-stick type of fracture called tion. ICP may be elevated so HOB should
a “ping-pong ball” fracture can occur where be elevated and mannitol administered if
there is a focal indentation of the skull no hypotension is present. An antiepilep-
producing a concavity. Without any focal tic (phenytoin) should be administered.
deficit, temporoparietal ping-pong ball The decision to operate and indications to
fractures usually do not require surgical do so are controversial. Level of conscious-
intervention as the deformity will usually ness is the most important prognostic fac-
correct as the skull grows. Surgical tor.97 Path, trajectory, type of gun, and
indications include an associated neuro- caliber of the bullet are also important for
logic deficit, radiographic evidence of intra- prognosis and surgical decision-making.
parenchymal bone fragments, signs of
increased ICP from related injuries, growing
skull fracture, or CSF leak. Surgery involves
opening the cranium adjacent to the For penetrating non-missile injuries that
depression and pushing out the deformity. are not bullets, the foreign body should
not be removed until the patient is in the
operating room if possible. If there is an
8.6 Penetrating Trauma identical object available to compare, it
can be helpful in planning for extrication.
8.6.1 Gunshot Wounds
Gunshot wounds to the head are the most Intracranial hemorrhage on CT is also a
lethal type of head injury and over 90% in poor prognostic factor. Suicide attempts are
some series were fatal.96,97 Injury from more likely to be fatal. The goals of surgery
gunshot wounds comes from direct injury are debridement of devitalized tissue, evac-
to scalp and facial soft tissue, depressed uation of hematomas, removal of accessible
skull fragments and bullet fragments bone fragments, removal of accessible bul-
which may injure vasculature, and direct let fragments, obtaining hemostasis, dural
injury to brain tissue from the bullet and closure, repair of depressed skull fractures,
from shock waves (blast) secondary to the and decompression of edematous hemi-
force from the bullet. On physical exam- spherers. While surgery is not done strictly
ination, in addition to a neurological for forensic purposes (identification of
examination, it is important to note the entry/exit wounds, retrieval of bullet frag-
appearance and location of entry and exit ment), if surgery performed, evacuated bul-
wounds, presence of gunpowder stippling, let fragments should be submitted to the
presence of bone fragments and brain proper authorities. Delayed imaging with
matter in soft tissue, nasal or oral cavities, angiography should be done to rule out
or external auditory canals, as well as the traumatic pseudoaneurysm, generally at
status of the tympanic membranes. A 7-14 days post-injury and possibly also
non-contrast CT is needed to identify the later. These are more likely for trajectories
143
involving major vascular anatomy, such as

the anterior and middle cerebral artery
8.7 Top Hits
complexes, but may occur in distal branches.
8.7.1 Questions
Trajectories that cross midline at the level 1. What kind of hemorrhage crosses
of the ventricles, involve the basal ganglia suture lines?
or zona fatalis (suprachiasmatic region), a) Subdural hemorrhage
include the posterior fossa or brainstem, b) Epidural hemorrhage
or involve mul tiple lobes have poorer c) Subarachnoid hemorrhage
prognoses. d) All of the above
e) None of the above
The protruding object should be stabi- 2. What is the most important

lized as best as possible during transporta- prognostic factor in the GCS?
tion. CT angiography is warranted if the a) Eye component
object passes through a region concerning b) Voice component
for vascular injury, near the dural sinuses c) Movement component
or there is evidence of arterial bleeding. d) All are equally important
Perioperative anti biotics and tetanus
administration are appropriate in these 3. Which of the following meets
patients, and more prolonged antibiotics operative criteria for a subdural
may be necessary if organic material hemorrhage?
(e.g., tree branches or sticks) are involved. a) 3 mm thickness, 3 mm midline shift
b) 8 mm thickness, 3 mm midline
shift
Pearls c) 3 mm thickness, 8 mm midline
• In TBI, primary injury occurs from shift
impact and secondary injury occurs d) 8 mm thickness, 8 mm midline shift
due to a variety of pathophysiological e) All of the above
processes resulting from that impact. f) c and d
• EDHs requiring surgery must be done
emergently to reduce mortality. 4. Which of the following are operative
• Apart from mass effect, SDHs are often indications for skull fractures?
associated with damage to the underly- a) Open fracture
ing brain parenchyma, which can explain b) Depression of the skull fracture
morbidity despite timely evacuation. below the level of the inner
• Contusions are caused by a variety table
of mechanical forces to the brain, c) Associated intracranial
including acceleration/deceleration, hemorrhage
rotational torque, and brain contact d) Fracture over the venous sinus
with the skull, especially the bony e) b and c
prominences at the skull base. f) a, b and c
• Decompressive craniectomies should g) All of the above
be large enough to adequately decom-
5. What kind of hemorrhage would you
press the hemisphere and extend to
expect in a person who has a “lucid
the middle (temporal) fossa floor to be
interval”?
effective at improving both neurologic
a) Subdural hemorrhage
morbidity and mortality.
b) Epidural hemorrhage
144
8.7 Top Hits
c) Subarachnoid hemorrhage over the tentorium. Epidurals can

d) All of the above cross the midline and the tentorium.
e) None of the above 2. c. The motor component is the most
important prognostic factor in GCS.
6. An elderly individual presents with 3. f. c (3 mm thickness, 8 mm midline
confusion after falling 1 week ago, shift) and d (8 mm thickness, 8 mm
what kind of hemorrhage do they midline shift).
probably have?
a) Subdural hemorrhage Type of Criteria for
b) Epidural hemorrhage hemorrhage operation
c) Subarachnoid hemorrhage
Subdural > 1cm thickness or >
d) All of the above
hemorrhage 0.5 cm midline shift
e) None of the above
Epidural > 30 cm3 volum
7. A child is hit in the pterional region hemorrhage (volume is calculat-
with a baseball, what vessel is most ed by
likely to be at risk for rupture causing ½ × length × width
hemorrhage? × height)
a) Carotid artery
Intraparenchymal > 30 cm3 volume
b) Internal jugular vein
hemorrhage
c) Middle meningeal artery
d) Bridging veins
e) None of the above 4. f. a (open fracture), b (depression of
the skull fracture 12 mm in thickness)
8. What structure is being compressed
and c (associated intracranial
in a person who presents with a
hemorrhage).
“blown” pupil?
a) Cranial nerve I 5. b. Epidural hemorrhages often have a
b) Cranial nerve II lucid interval because of the lower
c) Cranial nerve III likelihood of underlying brain injury.
d) Cranial nerve IV
e) Cranial nerve VI Operative Contraindications
Indications
9. A baby presents with bilateral acute
on chronic subdurals, what other • Open fracture • Fractures over
imaging should be obtained? • Depression of the venous sinuses
a) Abdominal ultrasound fracture greater may be relative
b) Chest XR
than the thickness contraindications
of the calvarium depending
c) MRI brain
or below the inner upon location
d) Skeletal survey
table
• Cosmetic
8.7.2 Answers • Gross
contamination
1. a. SDHs will cross the suture lines but • Intracranial
not the midline over the convex-
hemorrhage
ity (secondary to the sagittal sinus). • Dural violation
While they can cross the tentorium, it • Frontal sinus
involvement
is more common to see blood layered
145
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Crit Care. 2013; 17(4):234 [77] Van Gent JM, Bandle J, Calvo RY, et al. Isolated trau-
[63] Ratilal BO, Costa J, Pappamikail L, Sampaio C. An- matic brain injury and venous thromboembolism. J
tibiotic prophylaxis for preventing meningitis in Trauma Acute Care Surg. 2014; 77(2):238–242
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tabase Syst Rev. 2015(4):CD004884 RL, McGwin G, Jr, Rue LW, III. Traumatic brain in-
[64] Raboel PH, Bartek J, Jr, Andresen M, Bellander BM, jury is associated with the development of deep
Romner B. Intracranial Pressure Monitoring: Inva- vein thrombosis independent of pharmacological
sive versus Non-Invasive Methods-A Review. Crit prophylaxis. J Trauma. 2009; 66(5):1436–1440
Care Res Pract. 2012; 2012:950393 [79] Scudday T, Brasel K, Webb T, et al. Safety and effi-
[65] Kakarla UK, Kim LJ, Chang SW, Theodore N, Spetzler cacy of prophylactic anticoagulation in patients
RF. Safety and accuracy of bedside external ven- with traumatic brain injury. J Am Coll Surg. 2011;
tricular drain placement. Neurosurgery. 2008; 213(1):148–153, discussion 153–154
63(1, Suppl 1):ONS162–ONS166, discussion [80] Minshall CT, Eriksson EA, Leon SM, Doben AR,
ONS166–ONS167 McKinzie BP, Fakhry SM. Safety and efficacy of
[66] Zabramski JM, Whiting D, Darouiche RO, et al. heparin or enoxaparin prophylaxis in blunt trauma
Efficacy of antimicrobial-impregnated external patients with a head abbreviated injury severity
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domized, controlled trial. J Neurosurg. 2003; sion 399–400
98(4):725–730 [81] Kim J, Gearhart MM, Zurick A, Zuccarello M,
[67] Cooper DJ, Rosenfeld JV, Murray L, et al; DECRA Trial James L, Luchette FA. Preliminary report on the
Investigators. Australian and New Zealand Intensive safety of heparin for deep venous thrombosis
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craniectomy in diffuse traumatic brain injury. N 2002; 53(1):38–42, discussion 43
Engl J Med. 2011; 364(16):1493–1502 [82] Farooqui A, Hiser B, Barnes SL, Litofsky NS. Safety
[68] Jiang JY, Xu W, Li WP, et al. Efficacy of standard and efficacy of early thromboembolism chem-
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[69] Qiu W, Guo C, Shen H, et al. Effects of unilateral lar-weight heparin safe for venous thromboembo-
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13(6):R185 628
[70] Wohns RN, Wyler AR. Prophylactic phenytoin [84] Saloheimo P, Ahonen M, Juvela S, Pyhtinen J,
in severe head injuries. J Neurosurg. 1979; Savolainen ER, Hillbom M. Regular aspirin-use
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[71] Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, orrhage is an independent predictor for death.
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[86] de Gans K, de Haan RJ, Majoie CB, et al; PATCH In- [91] Miller JD, Jennett WB. Complications of depressed
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haemorrhage: study protocol for a multicentre, ran- [92] Başkaya MK. Inadvertent intracranial placement of
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[87] Fredriksson K, Norrving B, Strömblad LG. Emergen- Surg Neurol. 1999; 52(4):426–427
cy reversal of anticoagulation after intracerebral [93] Seebacher J, Nozik D, Mathieu A. Inadvertent intrac-
hemorrhage. Stroke. 1992; 23(7):972–977 ranial introduction of a nasogastric tube, a compli-
[88] Eerenberg ES, Kamphuisen PW, Sijpkens MK, cation of severe maxillofacial trauma. Anesthesiol-
Meijers JC, Buller HR, Levi M. Reversal of rivarox- ogy. 1975; 42(1):100–102
aban and dabigatran by prothrombin complex con- [94] Ignelzi RJ, VanderArk GD. Analysis of the treatment
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over study in healthy subjects. Circulation. 2011; ics. J Neurosurg. 1975; 43(6):721–726
124(14):1573–1579 [95] Lende RA, Erickson TC. Growing skull fractures of
[89] Glund S, Stangier J, Schmohl M, et al. Safety, tolera- childhood. J Neurosurg. 1961; 18:479–489
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149
9 Spinal Trauma
Katherine E Wagner, Jamie Ullman
9.1 Introduction Table 9.1 American Spinal Injury

Association grading system
Traumatic injuries to the spinal column and
cord can be seen following motor vehicle Grade Description
crashes, violence, sports, and even falls. These A Complete injury: No sensory
patients should be evaluated promptly by the or motor function preserved
trauma team and spine surgeon. The basic below the injury, including the
tenets of resuscitation apply; airway, breath- sacral elements S4-S5
ing, and circulation should be evaluated first,
as part of the standard primary survey. An B Incomplete injury: Sensory, but
evaluation of rectal tone is an essential part of not motor, function preserved
the assessment of neurological function in below the neurological level
patients with potential spinal trauma. Fur- C Incomplete injury: Motor
thermore, patients may have concomitant function is preserved below
head trauma, long bone fractures, and inter- the neurological level.
nal injuries. During the initial postinjury More than half of the key
period, patients are generally kept in a hard muscles below the level have <
cervical collar until it is “cleared,” clinically 3 out of 5 strength
and/or radiographically.
D Incomplete: Motor function is
preserved below the neuro-
9.2 Examination logical level
More than half of the key
The American Spinal Injury Association
muscles below the level have
(ASIA) scale, outlined in ▶Table 9.1, is a
≥ 3 out of 5 strength
useful tool in the acute setting, and is
ideally performed within 72 hours of the E Normal motor and sensory
injury. Sometimes, patients with devastat- function
ing injuries show signs of improvement
after 24–72 hours, so the most meaningful
These guidelines stem from the
score is obtained later.1
National Emergency X-Radiography Utili-
zation Study (NEXUS) results.2 Criteria for
9.3 Imaging imaging a patient with suspected blunt
vascular injury are described later.
The decision to image a patient’s spine
Awake patients with neurological
depends on their level of wakefulness and
symptoms should remain in a collar and
ability to participate in a neurological
get a cervical CT scan. If the CT is negative
examination.
but the patient continues to have symp-
toms, including pain or numbness, an MRI
with short inversion time inversion recov-
Awake patients with no neurological symp-
ery (STIR) sequences should be obtained
toms or neck pain, no distracting injuries
within 48 hours to evaluate the disc
with a full, painless range of motion at the
spaces, cord, and ligaments. If that is
neck do not require immobilization or
unremarkable, flexion/extension X-rays
imaging.
are next. If no injury or instability is
150
9.6 Immobilization
found, the collar can be used for comfort. I, II, and III do not demonstrate convincingly
Patients who cannot safely enter the MRI sustained improvements in patient out-
machine (i.e., they have incompatible comes after administration.4,5 There is strong
hardware) can be evaluated with flexion/ evidence linking steroids to gastrointestinal
extension films.2 hemorrhages4 and wound infections.5
Obtunded patients should have a CT
scan of the neuroaxis as part of their
trauma workup and pan-scan. 9.6 Immobilization
Cervical collars may be hard (e.g., Aspen or
Miami J) or soft.
One school of thought suggests obtain-
ing an MRI of the cervical spine within
• Soft collars do not limit motion but can
be useful after surgery for comfort.
48 hours if there is a need to remove the
collar. However, others have suggested
• The compressed foam Philadelphia
collar may be utilized by emergency
that clearance based on careful review of medical techicians. to limit motion in
CT scan alone is sufficient in an obtunded the cervical spine.
trauma patient.
The sterno-occipital-mandibular immobi-
lization device (SOMI brace) has an ante-
9.4 Shock rior piece, rigid shoulder supports, and
removable mandibular support.
Patients can present in hemorrhagic
• The SOMI can help limit motion at the
shock from other injuries, or in frank spi- craniocervical junction, help maintain
nal shock with spinal cord injury (SCI) alignment, and minimize motion in the
above T1. lower cervical spine and cervicothoracic
junction.6
• The Minerva brace, a cervicothoracic
Avoiding hypoxia and hypotension is cru- orthosis, is a similar device in the
cial in minimizing secondary injury to the market.
spinal cord.
The halo vest offers another form for rigid
fixation of the occipital cervical junction
Elevating the mean arterial pressure to (▶Fig. 9.1).6,7
85–90 mmHg with monitoring in an
intensive care unit can result in better
• The pins need to torque to 8 lb at 24
and 48 hours after placement.
outcomes.3 Of note, return of the bulbocav-
ernosus reflex indicates complete SCI as
• Excessive tightening can penetrate or
fracture the skull.7
opposed to just spinal shock.
9.5 Steroids “Snaking” or excessive motion of the

lower cervical spine is a potential issue
There is no Class I evidence supporting the
with the halo vest.
use of steroids like methylprednisolone in
patients with SCI. Animal models with very
early administration of steroids suggest a Thoracolumbosacral and lumbosacral
potential benefit. However, the National orthoses (TLSO/LSO) minimize movement
Acute Spinal Cord Injury Studies (NASCIS) of the torso.
151
Spinal Trauma
Fig. 9.1 Placement of the

Halo. (Reproduced from
Ullman J, Raksin P, Atlas of
Emergency Neurosurgery,
Fig. 9.2 Anterior cord

Quadraparesis syndrome. (Reproduced
Loss of pain and C3 from Alberstone C, Benzel E,
Dorsal columns spared
Temperature sense
Below level of lesion Najm I et al, Anatomic Basis
Lateral spinothalamic tracts
of Neurologic Diagnosis,
Corticospinal tracts

Right Left
C3
9.7 Spinal Cord temperature below the level of the lesion,

and preserved posterior column function.
Syndromes • Outcomes: Poor prognosis; most
patients have no or minimal improve-
These result from incomplete injuries to
ment in their deficits.8
the cord.
9.7.2 Central Cord

9.7.1 Anterior Cord Syndrome
Syndrome
It is the most common spinal cord
• Mechanism: Cord infarction in areas syndrome (▶Fig. 9.3).9
supplied by the anterior spinal • Mechanism: Neck extension
artery (▶Fig. 9.2). ◦ Usually occurs in patients with
• Deficit: Sudden-onset paraplegia or bony spurs, thickened ligaments,
quadriplegia; loss of pain and or herniated discs who suffer
152
9.8 Spinal Column Model
Distal upper extremity sensory loss Fig. 9.3 Central cord

Lateral spinothalamic tract Distal upper extremity syndrome. (Reproduced
(Cervical representation) weakness from Alberstone C, Benzel E,
(Cervical representation)
Najm I et al, Anatomic Basis
Corticospinal tract
Right Left
S LS
L C
Th CTh
S LThC C ThL S
C4-t4
Spinothalamic Corticospinal
tract tract
hyperextension from a fall or motor 9.7.3 Posterior Cord

vehicle accident (MVA).
• Bimodal distribution: Younger patients
Syndrome
with congenital stenosis and severe
traumas and older patients with
• Mechanism: Can result from injury to
the posterior spinal artery.
degenerative stenosis and even minor
traumas.9,10
• Deficit: Results in pain and paresthesias.
• Relatively rare.
• The long tract fibers in the center of the
cord may swell and, since they are
located in a watershed vascular territory, 9.7.4 Brown-Séquard
may suffer temporary ischemia. Syndrome (▶Fig. 9.4)
• Deficit: Greater motor deficits in the
upper extremities than the lower, distal • Mechanism: Cord hemisection, often
more than proximal. Sensory findings traumatic.11
may vary, and some patients become • Deficit: Ipsilateral motor paralysis; loss
frankly myelopathic. of proprioception, vibration sense with
contralateral loss of pain and
• Outcomes: Prognosis is guarded. Lower temperature.
extremity and bowel/bladder function
can recover, while upper extremity • Outcomes: Variable prognosis.
function is variable.9,10
• There is controversy about the timing of 9.8 Spinal Column Model
treatment.9
◦ Some advocate laminectomy and White and Panjabi put forward the concept
possible fusion on the same admis- of spinal stability as the ability of the spine to
sion, while others will do the case limit movements under normal, physiologi-
electively after the patient has some cal conditions to prevent injury to or irrita-
physical therapy/rehabilitation. tion of the spinal cord and nerve roots and
◦ If the patient deteriorates, urgent prevent deformity and mechanical pain.
surgery is warranted. Francis Denis proposed the widely used
◦ Steroid use is also controversial. three-column model for evaluating spine
153
Spinal Trauma
Ipsilateral loss of Fig. 9.4 Brown-Séquard

position and vibration sense
Ipsilateral hemiparesis syndrome. (Reproduced
Contralateral loss from Alberstone C, Benzel E,
T4
of pain and Najm I et al, Anatomic Basis
temperature sense
Lateral spinothalamic tract

Dorsal columns
Corticospinal tracts 1st edition, ©2009, Thieme

Right Left
T4
Fig. 9.5 The Denis classifi-

cation spinal columns—ante-
rior, middle, and posterior,
and major spinal fractures.
(Reproduced from Jallo J,
Vaccaro A, Neurotrauma
and Critical Care of the
Spine, 1st edition, ©2008,
Thieme Publishers,
New York.)
trauma (▶Fig. 9.5).12,13,14,15 His model was outlined five types of fractures seen in the
designed for the thoracic and lumbar spine, thoracolumbar region (refer to thoracolum-
but can be applied to the lower cervical spine bar injury section).
as well. Fractures involving one column are • The anterior column: Anterior
generally stable; fractures involving two or longitudinal ligament (ALL), anterior
three columns are considered unstable and two-thirds of the vertebral body and
may require surgery.12,13,14,15 Denis also disc, including the annulus fibrosus.
154
9.10 Cervical Injuries
• The middle column: Remaining strokes. There is still controversy about

posterior third of the vertebral body which patients should be screened.
and disc, including the annulus fibrosus,
posterior longitudinal ligament (PLL).
• The posterior column: Structures The Denver criteria (below) can be used to
posterior to the PLL; pedicle, facet determine which patients should undergo
joints, ligamentum flavum, interspinous CT angiogram of the head and neck.
ligaments.
The rest of this chapter outlines various • The criteria are divided into signs and
spinal injuries and their management. symptoms of a BCVI and risk factors.
Patients with any of these should be
considered for CTA.
9.9 Cervical Spine • Treatment is generally anticoagulation
Paramedics generally perform spinal immo- or antiplatelet therapy.16,17
bilization and place a cervical collar on ◦ Signs and symptoms: Focal neurolog-
patients who may have a spinal column ical deficit, especially with an exam-
injury. Up to 25% of SCIs occur after the ination inconsistent with patient’s
trauma, secondary to the way the patient is CT head; stroke on CT head; arterial
handled and transported.3 Spinal immobili- hemorrhage, expanding hematoma;
zation is contraindicated in penetrating cervical bruit.
trauma (i.e., gunshots, stabbings), as it has ◦ Risk factors: Le Forte II or III
increased morbidity and mortality with fractures; basilar skull fractures
higher risk of increased intracranial pressure, involving carotid canal; cervical
pressure sores, and aspiration.3 spine fractures, especially those
involving transverse foramen;
diffuse axonal injury with Glasgow
Injuries at or above C3 can produce Coma Scale less than 6 or anoxic
bulbar-cervical dissociation. brain injury with hanging or near
hanging mechanism.
These patients die unless cardiopulmo-
nary resuscitation is started shortly after
injury. Survivors are quadriplegic and ven- 9.10.2 Atlanto-occipital
tilator dependent. Dislocation
• Generally seen in high-energy traumas,
9.10 Cervical Injuries more common in children.18
• Presentation can vary from minimal
9.10.1 Blunt Cerebrovascular neurological findings to bulbar-cervical
Injuries dislocation causing respiratory arrest
and death.18
• Blunt-force trauma to the head, face, or • Type I injuries: The occiput is displaced
neck or high-speed deceleration to the anteriorly to atlas.
thorax can cause blunt cerebrovascular • Type II injuries: The occiput is distracted
injuries (BCVI). away from the atlas.
• Injuries to the carotid and/or vertebral • Type III injuries: The occiput is displaced
arteries may present as devastating posteriorly to atlas.
155
Spinal Trauma
• Radiographic Measurement: Distraction

via a cervical collar or traction is
contraindicated.18
◦ Powers ratio is defined as the distance
from the tip of the basion to the poste-
rior arch of C1 divided by the distance
from the opisthion to the anterior arch
of C1. Normal is a ratio < 1.
◦ Basion-Dens Interval (BDI): normal
< 12 mm on plain radiographs.
• A halo orthosis may be used to
immobilize the neck, especially before
definitive surgery; some authors state
all patients require a posterior
occipital-cervical fusion.18
• Patients with incomplete injuries may
improve with stabilization. Fig. 9.6 CT scan with fracture of the
occipital condyle and basilar skull.
(Reproduced from Jallo J, Vaccaro A,
9.10.3 Occipital Condyle Neurotrauma and Critical Care of the
Fractures Spine, 1st edition, ©2008, Thieme
• Patients have head trauma and skull
fractures (▶Fig. 9.6).
◦ Normal in Adults < 2–3 mm, Children
< 5 mm
Look for condyle fractures in trauma pa- • Can be traumatic or secondary to
tients with lower cranial nerve pal- certain diseases. ▶Fig. 9.7 shows an
sies (usually cranial nerve [CN] XII; CN VI, injury causing atlanto-axial dislocation.
IX, and X can also be affected). The transverse ligament is now just
attached to a bone fragment as the
result of a comminuted C1 fracture. The
• Persistent neck pain, or reduced mobility C1 lateral mass is displaced and the
in the upper cervical spine.
spine is unstable.
• Displaced bone fragments may ◦ Associated conditions include Down
compress the brainstem.
Syndrome, Morquio Syndrome, and
• Evaluate for rotatory subluxation and rheumatoid arthritis.21
concomitant traumatic brain injury.19,20
◦ A purely traumatic atlanto-axial
• There are two major classification dislocation in the absence of another
schemes for these fractures
predisposing risk factor is rare—
(▶Table 9.2).
evaluate patients with the above
conditions carefully, and rule out
9.10.4 Atlanto-axial these conditions in patients with
Dislocation unexplained deficits localizing to the
high cervical cord.21
• Refers to loss of stability between atlas ◦ Treatments include cervical traction
and axis (C1 and C2). and posterior fusion with or without
• Increased atlanto-dens interval. a transoral odontoidectomy.
156
9.11 C1 Fractures
Table 9.2 Classifications for evaluating occipital condylar fractures

Type Description Stability Treatment
Anderson and I Comminuted; no/minimal Stable Collar
Montesano displacement
II Direct trauma and associated Stable
basilar skull fracture
III Avulsion fracture involving Unstable Halo or
the alar ligament surgical fixation
Tuli et al 1 Nondisplaced Stable Collar
2A Displaced, ligaments intact Stable
2B Displaced, with craniocervical Unstable Halo or
instability surgical fixation
Source: Adapted from Oskouian R, Shaffrey C, Neurotrauma and Critical Care of the
Spine, ©2009, Thieme Publishers, New York.
Fig. 9.7 Anterior atlanto-occipital dislocation. (a) Dissociation of the bony

elements. (b) Decreased basion-dens interval resulting from a posterior ligamen-
tous complex injury. (c) Epidural hematoma. (Reproduced from Jallo J, Vaccaro A,
Neurotrauma and Critical Care of the Spine, 1st edition, ©2008, Thieme Publishers,
New York.)
9.11 C1 Fractures ◦ Associated with diving head first into

shallow water (i.e., axial loading onto
• Isolated C1 fractures do not usually result the head).
in deficits unless they are not properly ◦ If the transverse ligament is intact,
managed (▶Fig. 9.8 and ▶Fig. 9.9).19 the cervical spine should be immobi-
• Evaluate the integrity of the transverse lized for 10–12 weeks (▶Fig. 9.9). If it
ligament. is NOT intact, a C1–C2 fusion or halo
• A Jefferson fracture is a C1 burst fixation for 12 weeks is advised.
fracture, classically with fractures in • The Rule of Spence can help determine
both anterior and both posterior arches the stability of the transverse ligament.
(▶Fig. 9.8).19 The left and right C1 lateral masses
157
Spinal Trauma
Fig. 9.8 Common C1

fractures. (a) Lateral mass
fracture. (b) Posterior arch
fracture. (c) Classic Jeffer-
son fracture. (Reproduced
from Jallo J, Vaccaro A,
Neurotrauma and Critical
Care of the Spine, 1st
edition, ©2008, Thieme
Fig. 9.9 Comminuted C1

lateral mass fracture and
associated atlanto-axial
instability. The attachment
of the transverse ligament to
the spinal column has been
injured. (Reproduced from
Bambakidis N, Dickman C,
Spetzler R et al, Surgery of
the Craniovertebral Junction,
generally do not overhang C2. If the ◦ They are generally stable and treated
sum of the overhang of the left and with a collar, unless atlanto-occipital
right C1 lateral masses is greater than 7 dislocation is present. Then options
mm, the transverse ligament may be include surgery or immobilization
injured, and should be evaluated with with a halo or collar.
a treatment algorithm for isolated atlas
fractures is shown in ▶Fig. 9.10.19
9.11.1 Odontoid (Dens) Type II fractures occur where the odon-

Fractures toid meets the vertebral body. These are
the most common odontoid fractures
• Most common C2 (axis) fractures; make and have a high rate of nonunion. These
up 7–14% of traumatic cervical spine are generally unstable and treated with
injuries. surgery or immobilization. If commi-
• Often present with high cervical pain; nuted fragments are present, the frac-
mechanism of injury can vary.19,20 ture is unstable and surgery should be
• Type I fractures involve the tip of the considered.
dens (▶Fig. 9.11).
158
9.11 C1 Fractures
Fig. 9.10 Management of isolated C1 fractures. (Reproduced from Jallo J, Vaccaro A,

Neurotrauma and Critical Care of the Spine, 1st edition, ©2008, Thieme Publishers,
New York.)
Fig. 9.11 Dens fracture

types (a) Type I. (b) Type II.
(c) Type III. (Reproduced
from Chapman J, Dettori J,
Norvell D, Spine Classifica-
tions and Severity Measures,
159
Spinal Trauma
• Type III fractures go through the • C2 fractures seen in combination with

vertebral body and are generally stable. C1 fractures require careful evaluation
Treat with a cervical collar unless there for spinal stability.
are other injuries rendering the spine
unstable.
9.11.4 Subaxial Cervical
Spine Injuries
9.11.2 Hangman’s Fractures
• The most commonly injured level is
• Vertical or oblique fractures through C5-C6.19
the C2 pars interarticularis, disconnect-
ing the posterior arch from the
• The three kinds of injuries are
compression, flexion/extension/
vertebral body as shown in ▶Fig. 9.12.22 distraction, and rotation (▶Table 9.3).
• Usually caused by hyperextension (MVA • The table includes bony (fracture) and
or diving injury); the posterior C1 ring ligamentous (whiplash) injuries.
and C2-C3 disc should also be evaluated ▶Fig. 9.13 shows a severe fracture-
for injury. dislocation injury.
• Most isolated fractures can be managed
with a collar; displaced, isolated
fractures can be managed with a halo 9.11.5 Jumped Facets
brace.
• Surgery may be indicated if the C2-C3 • Jumped facets can result in severe
facets are locked or the patient has injury to the spinal cord and nerve
other injuries rending the spine roots.19
unstable. • The facets may be perched or frankly
locked depending on the severity of
injury.
9.11.3 Other C2 Fractures • Unilateral injuries can occur when the
spine is rotated. Bilateral injuries
• Isolated, nondisplaced fractures of the usually result from flexion or extension
C2 lamina, vertebral body, and facets that disrupts the posterior ligaments.
are generally stable and heal in a ▶Fig. 9.14 shows perched and locked
collar.22 facet injuries in the cervical spine.
Fig. 9.12 Hangman’s fracture

involving the bilateral C2
pars. (Reproduced from
Meyers S, Differential
Diagnosis in Neuroimaging:
Spine, 1st edition, ©2016,
Thieme Publishers,
New York.)
160
9.11 C1 Fractures
Table 9.3 Classification of cervical injuries

Injury Mechanism Stability and Treatment
Anterior com- Axial loading Stable.
pression (wedge +/- flexion/extension Generally heal with external
fracture) immobilization
Compression
Comminuted Axial loading Generally unstable.

fracture (burst +/- flexion Treat with fusion, and
fracture) decompression if needed
Teardrop fracture Hyperflexion- Unstable—evaluate disc space
compression and ligaments on MRI.
Treat with fusion, decompress
if needed
These injuries below are unstable if the PLL/posterior annulus fails AND
there is anterolisthesis, facet malalignment, end plate angulation > 10
degrees, or vertebral segment distraction
Whiplash with Flexion/extension Stable.
neurologic injury Management is controversial
and can include collar and
physical therapy
Severe whiplash Flexion/extension Re-evaluate integrity of poste-
(sprain) rior ligaments; treat with collar,
physical therapy
Flexion/Extension/Distraction
Bilateral facet Distraction + flexion/ Unstable: Closed or open

fracture-dislocation extension with failure reduction and internal fixation/
of posterior ligamen- fusion.
tous complex Evaluate for herniated discs
with MRI
Unilateral facet Lateral flexion Stable if there is no significant
fracture + rotation subluxation, dislocation, or
kyphosis.
Treat with collar
Fracture separation Extension, Evaluate for other injuries to
of articular pillar compression, determine if stable.
+ rotation Treatments include collar, halo,
surgery.
Unilateral Lateral flexion A perched facet is unstable.
dislocation + rotation Evaluate for nerve root and
cord injury.
Treatments include reduction
and halo or fusion.
Abbreviations: PLL, posterior longitudinal ligament.
161
Spinal Trauma
Fig. 9.13 Fracture-dis-

location injury at C5–C6.
(Reproduced from Fehlings
M, Vaccaro A, Boakye M
et al, Essentials of Spinal
Cord Injury, Basic Research to
Clinical Practice, 1st edition,
New York.)
Fig. 9.14 (a) Perched.

(b) Locked facets.
(Reproduced from Benzel
E, Biomechanics of Spine
Stabilization, 3rd edition,
New York.)
• The bony injury needs to be reduced. ligamentous injuries can be managed

◦ Unilateral injuries may be reduced in with a cervical collar alone. Follow-up
traction and then a halo or surgical in 4–6 weeks and evaluate range of
fusion. motion and cervical tenderness.
◦ Closed traction is controversial in • Patients with rheumatoid arthritis,
bilateral injuries. Generally, patients Down syndrome, ankylosing spondylitis,
will need surgery, with either an and other conditions predisposing them
anterior or posterior approach and to cervical instability require imaging and
intraoperative reduction. careful examination following trauma.
◦ Some surgeons prefer to get an MRI • Patients with hardware from previous
before reduction, to evaluate for disc cervical spine surgery need careful
herniations.19 evaluation. X-rays, CT, and CT
myelograms are useful imaging options.
MRI is necessary to evaluate the spinal
9.12 Additional Principles cord, but evaluation of the bones may
for Cervical Trauma be limited by artifact.
• Plain radiographs will not show the
• Unless atlanto-occipital dislocation is C7-T1 disc space and facets well; if there
present (i.e., the transverse ligament is is concern for a junctional injury CT
torn in its midportion) most isolated and/or MRI are necessary.
162
9.14 Thoracolumbar and Lumbar Spine Injuries
9.13 Thoracic Injuries • Compression fractures and burst

fractures may be stable, depending on
• The spinal cord generally ends at L1-L2, the integrity of the ligaments.
with the cauda equina filling the distal • Seat-belt type injuries and fracture
canal. dislocations are generally
• Significant force is needed to fracture unstable.
the thoracic vertebrae. However, the
canal is narrow and thus the cord
vulnerable to injury from retropulsed The Spine Trauma Group put forth the
or dislodged fragments.19 Thoracolumbar Injury Classification and
• Lesions above this level can result in Severity Score (TLICS) to help guide treat-
complete or incomplete paraplegia and ment. See ▶Table 9.4 below.
bowel/bladder problems with typical
upper motor neuron findings.
• Injuries below may involve different Patients with a TLICS score of less than 4
nerve roots and show lower motor
can usually be treated nonoperatively;
neuron findings.
score equal to 4 may be treated opera-
• Conus medullaris syndrome can tively or nonoperatively; a score of greater
occur with T12-L1 injury. Damage
than 4 usually warrants operative man-
to the sacral nerve roots results in
agement.23,24
bowel and bladder problems. Some
of the lumbar nerve roots may be
intact. Table 9.4 The Thorocolumbar Injury
Classification and Severity scoring system
• The three-column approach to
evaluating spinal stability is discussed Thorocolumbar Injury Classification
below in the next section and useful for and Severity (TLICS) Score
evaluating these injuries.
Morphology Compression: 1 point
Burst: 2 points
Translation/rotation: 3
9.14 Thoracolumbar and points
Lumbar Spine Injuries Distraction:
4 points
Along with his three-column model for Posterior Intact: 0 point
determining spinal stability, Denis classi- ligamentous Suspected or
fied spine injuries into minor injuries— complex indeterminate injury:
articulating process, transverse process, 2 points
spinous process, and pars interarticularis Injured: 3 points
fractures, and major injuries—compres-
sion, burst, seat-belt type fractures, and Neurologic Intact: 0 point
frac t ure-dislocat ions. 12,13,14,15  T hese involvement Nerve roots: 2 points
terms can be used for thoracic and lumbar Cord/conus medulla-
spinal injuries, and the major injuries are ris (incomplete): 3 points
shown in ▶Fig. 9.5. Cord/conus (complete):
2 points
• Minor injuries are generally stable, but Cauda equina:
patients should be evaluated for other
injuries. 3 points
163
Spinal Trauma
9.14.1 Compression 9.14.3 Seatbelt Type Injuries

Fractures • In a seatbelt type injury, the middle and
• Occur when the anterior column fails. posterior columns fail when the patient
• The middle column is intact, so it can is severely flexed.
serve as a hinge. • Patients usually present as restrained
• The posterior column may fail, occupants in a MVA. The anterior
depending on the forces involved. column acts like a hinge, and may be
• Injuries involving more than one injured as well.
column may be unstable. • The spine is unstable in flexion.
• One level injuries may present as a
Chance fracture, which is a fracture
9.14.2 Burst Fractures through the vertebral body and
Denis also broke thoracolumbar burst frac- neural arch, or as a disruption of
tures into five categories, shown in the disc and PLL.
▶Table 9.5. Purely bony injuries can be
managed conservatively in select cases;
however, patients who cannot or will not
9.14.4 Fracture Dislocations
tolerate a brace may get better results with • These occur when all three columns fail.
surgery. In two level injuries, the bone or • The mechanism of injury can vary—
disc of the middle column is injured. These compression, tension, rotation, or shear.
patients may require surgery. • Most of these injuries require surgery.23
Table 9.5 Denis classification of burst fractures11,12,13,14

Type Elements involved Typical cause(s) and site(s)
A Fracture of both endplates without Pure axial load; usually lumbar spine
kyphosis. Bone may be retropulsed into
the canal
B Fracture of superior endplate Axial load and flexion; usually thora-
Most common columbar junction
C Fracture of the inferior endplate Axial load and flexion; no particular
sites commonly involved
D Burst rotation fracture with comminution Axial load and rotation; mid-lumbar
of the vertebral body, possible laminar spine
fractures, and bone retropulsed into canal
E Burst lateral flexion with fractured Axial load and lateral flexion
posterior wall of the vertebral body and
extrusion towards the side of the flexion
164
9.16 Top Hits
9.15 Sacral Fractures Pearls

Pearls
These are less common and are often
• Remember the ABCs of resuscitation.
caused by shear forces.24 They can injure Look for life-threatening injuries in
sacral roots, plexus, and affect pelvic and patients with significant spine
spinopelvic stability. Injuries below S2 injuries. Patients in spinal and/or
should not affect ambulation, but may be hemorrhagic shock need aggressive
unstable and cause pain that improves treatment and careful monitoring.
after surgical fixation. More medial frac- Avoid hypotension in patients with
tures have higher instances of neurologic spinal cord injuries.
injury and worse outcomes.
• Make sure to perform a thorough
▶Fig. 9.15 outlines the three zones into neurological examination on any
which Denis divided the sacrum. patient with suspected spine trauma.
• Zone 1: Lateral to the neural foramina. These findings will guide your
• Zone 2: Through the neural foramina. decision to image the patient.
• Zone 3: Central canal. • Take extra caution when evaluating
Roy and Camille also presented another patients with spinal hardware or
schematic to evaluate Zone 3 fractures. It conditions predisposing them to
was later modified by Strange-Vognsen cord compression and serious
and Lebech, as in ▶Fig. 9.16. neurological injury.
• There are a multitude of conditions
that make individuals more
susceptible to major spine injury from
a seemingly trivial injury. When a
patient presents with an injury that
seems out of proportion to the
mechanism, obtain imaging promptly
and consider these and other
predisposing conditions.
9.16 Top Hits

9.16.1 Questions
1. An elderly man with a history of
untreated cervical stenosis falls down
the stairs and immediately complains
Fig. 9.15 The Denis classification of of numbness and tingling in his hands
sacral fractures. (Reproduced from and weak grip. What is the most likely
Vialle L, AOSpine Masters Series, diagnosis?
Volume 6: Thoracolumbar Spine a) Unilateral jumped facet
Trauma, 1st edition, ©2015, Thieme b) Central cord syndrome
Publishers, New York.) c) Atlanto-axial subluxation
d) Compression fracture of the C6
vertebra
165
Spinal Trauma
Fig. 9.16 Further classifica-

tion of Denis type 3 sacral
fractures. (Reproduced from
Vialle L, AOSpine Masters
Series, Volume 6: Thoraco-
lumbar Spine Trauma, 1st
edition, ©2015, Thieme
2. A 25-year-old man is extricated from 9.16.2 Answers

a burning vehicle and arrives to the
hospital unconscious, intubated, and
1. b. This is a classic presentation of
with a cervical collar in place. Initial
central cord syndrome. Patients
CT head and cervical spine are
present with distal greater than
negative. His injuries include lower
proximal deficits, and many have
extremity fractures requiring
pre-existing cervical stenosis.
orthopedic surgery and a pneumotho-
2. c. The patient cannot undergo a
rax requiring a chest tube. He is
confrontational examination alone, as he
stabilized, extubated, and awake and
has other painful injuries. Any pain on
alert 2 days later. What is the best
confrontation may indicate ligamentous
way to assess the need for his cervical
injury, which can be confirmed or ruled
collar?
out on an MRI at this point.
a) Confrontational examination only
3. d. Bilateral facet fractures result in an
b) Flexion-extension films only
unstable spine and the patient will
c) Confrontational examination and
need instrumentation to restore
MRI
stability.
d) Repeat CT
3. Which of the following injuries will References

most likely require operative
[1] Fawcett JW, Curt A, Steeves JD, et al. Guidelines for
intervention? the conduct of clinical trials for spinal cord injury as
a) A unilateral facet fracture at C4-C5 developed by the ICCP panel: spontaneous recovery
with intact ligaments on MRI after spinal cord injury and statistical power need-
ed for therapeutic clinical trials. Spinal Cord. 2007;
b) Unilateral transverse process frac- 45(3):190–205
tures at L2 and L3 [2] Hoffman JR, Wolfson AB, Todd K, Mower WR.
c) An isolated C7 superior endplate Selective cervical spine radiography in blunt trauma:
methodology of the National Emergency X-Radiog-
fracture raphy Utilization Study (NEXUS). Ann Emerg Med.
d) Bilateral facet fractures at C4-C5 1998; 32(4):461–469
166
9.16 Top Hits
[3] Theodore N, Hadley MN, Aarabi B, et al. Prehospital thoracolumbar burst fractures in the absence of
cervical spinal immobilization after trauma. Neu- neurologic deficit. A comparison between oper-
rosurgery. 2013; 72Suppl 2:22–34 ative and nonoperative treatment. Clin Orthop
[4] Khan MF, Burks SS, Al-Khayat H, Levi AD. The ef- Relat Res. 1984(189):142–149
fect of steroids on the incidence of gastrointesti- [16] Shahan CP, Croce MA, Fabian TC, Magnotti LJ.
nal hemorrhage after spinal cord injury: a case- Impact of continuous evaluation of technology
controlled study. Spinal Cord. 2014; 52(1):58–60 and therapy: 30 years of research reduces stroke
[5] Hurlbert RJ. Methylprednisolone for acute spinal and mortality from blunt cerebrovascular injury.
cord injury: an inappropriate standard of care. J J Am Coll Surg. 2017; 224(4):595–599
Neurosurg. 2000; 93(1), Suppl:1–7 [17] Al-Harthy A, Al-Hinai A, Al-Wahaibi K, Al-Qadhi
[6] Lauweryns P. Role of conservative treatment of H. Blunt cerebrovascular injuries: a review of
cervical spine injuries. Eur Spine J. 2010; 19Suppl the literature. Sultan Qaboos Univ Med J. 2011;
1:S23–S26 11(4):448–454
[7] Weiss N. Application of closed spinal traction. In: [18] Leonard JC, Kuppermann N, Olsen C, et al; Pedi-
Atlas of Emergency Neurosurgery. New York, NY: atric Emergency Care Applied Research Network.
Thieme; 2015:170–178 Factors associated with cervical spine injury in
[8] Schneider RC. The syndrome of acute anterior children after blunt trauma. Ann Emerg Med.
spinal cord injury. J Neurosurg. 1955; 12(2):95– 2011; 58(2):145–155
122 [19] Okonkwo DO, Oskouian RJ, Shaffrey CI. Manage-
[9] Management of Acute Traumatic Central Cord ment of cervical injuries. In: Neurotrauma and
Syndrome. Contemporary Spine Surgery. 2016; Critical Care of the Spine. New York, NY: Thieme;
17(10):1–8 2009:126–142
[10] Ishida Y, Tominaga T. Predictors of neurologic [20] Öner FC. Spinal injury classification systems.
recovery in acute central cervical cord injury In: Neurotrauma and Critical Care of the Spine.
with only upper extremity impairment. Spine. New York, NY: Thieme; 2009:45–67
2002; 27(15):1652–1658, discussion 1658 [21] Yang SY, Boniello AJ, Poorman CE, Chang AL, Wang
[11] Beer-Furlan AL, Paiva WS, Tavares WM, de S, Passias PG. A review of the diagnosis and treat-
Andrade AF, Teixeira MJ. Brown-Sequard syn- ment of atlantoaxial dislocations. Global Spine J.
drome associated with unusual spinal cord injury 2014; 4(3):197–210
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2014; 7(1):316–319 injuries of the craniovertebral junction. In: Sur-
[12] Denis F. Updated classification of thoracolumbar gery of the Craniovertebral Junction. 2nd ed. New
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[13] Denis F. The three column spine and its signifi- [23] Rajasekaran S, Kanna RM, Shetty AP. Management
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[14] Denis F. Spinal instability as defined by the [24] Bellabarba C, Bransford RJ. Spinopelvic fixation.
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167

10 Spine
Robert F Heary, Raghav Gupta, Georgios A Maragkos, Justin M Moore
10.1 Introduction 10.3 Degenerative

Nontraumatic spine diseases affect mil- Cervical Myelopathy
lions of people around the world. These
Nontraumatic degenerative cervical
can include common age-related degen-
myelopathy is the most common cause of
erative diseases of the cervical, thoracic,
spinal cord pathology among the elderly
and lumbar spines which may present
and it is estimated to have a prevalence
with pain, functional deficiencies, and/or
of 605 per million individuals in North
neurological symptoms. Other patholo-
America alone.3,4 These degenerative
gies include vascular, neoplastic, and/or
changes can be subdivided into osteoar-
infectious lesions which can lead to pain
thritic (spondylotic) and nonosteoarthritic
from instability or can compress the
changes though both types can ultimately
neural elements leading to symptoms of
lead to symptomatic spinal cord compres-
spinal cord or nerve root compression.
sion or myelopathy. The various subtypes
In the present chapter, we have provided
of degenerative cervical myelopathy are
an overview of these various conditions
considered in the sections below.
and outlined their pathophysiology, clin-
ical and radiographic presentations,
available treatment options, and clinical
outcomes. 10.3.1 Cervical
Osteoarthritis
10.2 Cervical Spine Degenerative Disc Disease
Degenerative Disease The intervertebral disc, which is an avascular
Degenerative conditions of the cervical fibrocartilaginous structure,5 is comprised of
spine are prevalent and affect nearly an outer annulus fibrosus and the inner
two-thirds of the population at some nucleus pulposus both of which contain
time during their lifetime leading to neck poorly vascularized cells. The former con-
pain and neurological symptoms in a tains fibrocyte-like cells and the latter con-
subset of these patients.1 The baseline tains chondrocyte-like cells. Proteoglycans
prevalence of radiographically-deter- and collagen fibers comprise the extracellu-
mined cervical disc degeneration, for lar matrix (ECM) in which these cells are sus-
example, has been previously reported pended. The disc structure allows for the
to be 21.7%.2 While most degenerative radial redistribution of compressive forces
conditions of the cervical spine follow that would otherwise be transmitted longi-
a benign clinical course, they can also tudinally. However, over time, with excessive
result in compression of the neural ele- or repetitive use, trauma, and/or the influ-
ments leading to myelopathy and/or ence of genetic or environmental factors,
radiculopathy in addition to local disc degeneration can occur.4 Guiot et al have
mechanical neck pain. reported that compromised diffusion of
168
10.3 Degenerative Cervical Myelopathy
substances through the intervertebral disc, fractures and/or dislocations. These can
including oxygen and nutrients, is a central also be used to assess spinal stability by
mechanism by which cell death and disc utilizing dynamic flexion and extension
degeneration occur.5 This degenerative pro- images which can provide information
cess can lead to a redistribution of forces about the s

Lingua

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Agarwal, Neurosurgery Fundamentals (ISBN 978-1-62623-822-0), copyright © 2019 Thieme Medical Publishers.

All rights reserved. Usage subject to terms and conditions of license.

Thieme Publishers Rio de Janeiro,

1 Roadmap to a Career in Neurosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2 History of Neurological Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.2 The Pre-Cushing Era. . . . . . . . . . . . . . 14 2.5 Instrumentation . . . . . . . . . . . . . . . . . 17

2.3 The Cushing Era. . . . . . . . . . . . . . . . . . 15

3.2 Mental Status. . . . . . . . . . . . . . . . . . . . 23 3.7 Gait and Coordination . . . . . . . . . . . . 32

3.3 Cranial Nerves . . . . . . . . . . . . . . . . . . 23 3.8 Special Tests . . . . . . . . . . . . . . . . . . . . 34

3.4 Motor Examination . . . . . . . . . . . . . . . 28 3.9 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 37

3.5 Reflex Examination . . . . . . . . . . . . . . . 31

4.2 Bones of the Skull . . . . . . . . . . . . . . . . 40 4.7 Vertebral Column . . . . . . . . . . . . . . . . 60

4.3 Cerebrum. . . . . . . . . . . . . . . . . . . . . . . 42 4.8 Vascular Anatomy. . . . . . . . . . . . . . . . 69

4.4 Brainstem. . . . . . . . . . . . . . . . . . . . . . . 50 4.9 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 78

5 Neuroradiology for the Neurosurgeon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81

5.2 Computed Tomography. . . . . . . . . . . 81 5.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 95

5.3 Magnetic Resonance . . . . . . . . . . . . . 82

6.2 Operating Room . . . . . . . . . . . . . . . . . 97 6.8 Cranial Approaches . . . . . . . . . . . . . . 104

6.3 Cranial Positioning . . . . . . . . . . . . . . . 97 6.9 Spinal Approaches. . . . . . . . . . . . . . . . 112

6.4 Spinal Positioning . . . . . . . . . . . . . . . . 98 6.10 Pediatric. . . . . . . . . . . . . . . . . . . . . . . . 115

6.5 Positioning-Related Complications. . 100 6.11 Functional . . . . . . . . . . . . . . . . . . . . . . 117

6.6 Cerebral Relaxation . . . . . . . . . . . . . . 101 6.12 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 118

7 Neurocritical Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121

8 Traumatic Brain Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130

8.2 Classification of Head Injury. . . . . . . . 130 8.6 Penetrating Trauma . . . . . . . . . . . . . . 143

8.3 Monitoring. . . . . . . . . . . . . . . . . . . . . . 138 8.7 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 144

8.4 ICP Treatment . . . . . . . . . . . . . . . . . . . 138

9 Spinal Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150

9.2 Examination. . . . . . . . . . . . . . . . . . . . . 150 9.11 C1 Fractures . . . . . . . . . . . . . . . . . . . . 157

9.3 Imaging . . . . . . . . . . . . . . . . . . . . . . . . 150 9.12 Additional Principles for Cervical

9.7 Spinal Cord Syndromes . . . . . . . . . . . 152 9.15 Sacral Fractures. . . . . . . . . . . . . . . . . . 165

9.8 Spinal Column Model . . . . . . . . . . . . . 153 9.16 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 165

9.9 Cervical Spine . . . . . . . . . . . . . . . . . . . 155

10.2 Cervical Spine Degenerative 10.8 Spinal Deformity. . . . . . . . . . . . . . . . . 180

10.6 Spinal Neoplasms . . . . . . . . . . . . . . . . 176 10.13 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 187

11.2 Major Types of Pain . . . . . . . . . . . . . . 197 11.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 209

11.3 Craniofacial Pain Syndromes . . . . . . . 197

12.2 Subarachnoid Hemorrhage . . . . . . . . 225 12.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 240

12.3 Aneurysms. . . . . . . . . . . . . . . . . . . . . . 228

13 Neurosurgical Oncology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245

13.3 Neuroepithelial Brain Tumors . . . . . . 251 13.8 Sellar Tumors. . . . . . . . . . . . . . . . . . . . 261

13.4 Ependymoma and 13.9 Cysts and Tumor-Like

13.5 Pineal Region Tumors. . . . . . . . . . . . . 256 13.10 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 264

14 Pediatric Neurosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 268

14.2 Developmental Anomalies. . . . . . . . . 273 14.5 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 286

14.3 Pediatric Tumors. . . . . . . . . . . . . . . . . 284

15 Movement Disorders and Epilepsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291

15.2 Epilepsy . . . . . . . . . . . . . . . . . . . . . . . . 300

16 Stereotactic Radiosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315

16.2 Radiation Background . . . . . . . . . . . . 315 16.10 Clinical Outcomes. . . . . . . . . . . . . . . . 327

16.3 Types of Radiation. . . . . . . . . . . . . . . . 315 16.11 Radiation-Induced Changes. . . . . . . . 327

16.4 Main SRS Modalities . . . . . . . . . . . . . . 316 16.12 Vasculopathy. . . . . . . . . . . . . . . . . . . . 327

16.5 Dosing . . . . . . . . . . . . . . . . . . . . . . . . . 317 16.13 Cranial Nerve Deficits. . . . . . . . . . . . . 327

16.6 Occupational Exposure. . . . . . . . . . . . 318 16.14 Radiation-Induced Tumors. . . . . . . . . 327

16.7 Adverse Reactions. . . . . . . . . . . . . . . . 318 16.15 Future Directions . . . . . . . . . . . . . . . . 327

16.8 Indications. . . . . . . . . . . . . . . . . . . . . . 319 16.16 Top Hits . . . . . . . . . . . . . . . . . . . . . . . . 328

17 Neurological Infectious Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332

17.2 Microbiological Diagnosis. . . . . . . . . . 332 17.8 Additional Neurological

communication and follow-up inquiries. If things. Sometimes, we were breaking