Xianxiang Wang 王先祥

associate chief physican

the first affiliated hospital
Anhui Medical University

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 Neurosurgery
Chapter 1
Brief
introduction of
neurosurgery

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 Composition of the neurosurgery
center

outpatient department inpatient department

endovascular special
management Center operating
center room

X-knife center Microanatomic

laboratory
general operating room

Combined operating
room
旋转

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• Operating microscope

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  Microanatomical laboratory

cadaveric
 PO

Tentorium of cerebellum \oculomotor \posterior

cerebral artery\
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 视频1
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 Scope of Neurosurgry
 Traumatic diseases of central nervous
system.
 tumors of central nervous system.
 congenital malformation of central nervous
system.
 vascular diseases of central nervous system
 functional diseases of central nervous
system.
 other diseases of central nervous system

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Increased intracranial pressure
Craniocerebral trauma
Brain and spinal tumors
Cerebrovascular diseases
Congenital disease of the nervous system

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 Chapter 2
Increased Intracranial Pressure
(intracranial hypertension )
• Almost all diseases of neurosurgery are
accompanied by increased intracranial
pressure.
• Almost all neurosurgical operations are
aimed to decrease intracranial pressure

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 Physiology of intracranial pressure(ICP)

• Cranial cavity of adult, which is airtight and

unchanged, is formed by cranial bone.

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The proportion of the three
contents in cranial cavity

Blood:7%
Csf:10%
Brain tissue:83% 16
• Brain tissue, cerebrospinal fluid and blood
are contained in cranial cavity, which is
adaptable to the contents, so normal
intracranial pressure is maintained.
• The normal intracranial pressure (ICP) are
0.7-2.0 Kpa in adult and 0.5-1.0 Kpa in
child.

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The ICP wave displaying on the ICP monitor

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• It is defined as increased intracranial pressure
when the ICP continuously exceeds 2Kpa.
• increased intracranial pressure is clinicopathologic
syndrome

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 The causes
1. The volume or quantity of the contents in
cranial cavity is increased
① cerebral edema (caused by every reason)

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② Increasing of CSF, such as all kinds of
hydrocephalus

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③ Increasing of blood caused by:
intracranial arteriovenous malformations and the
dysfunction of cranial venous refluence

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2 Intracranial mass lesions, such as intracranial
hematomas, intracranial tumors, abscesses, etc.

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3 Decreasing of cranial cavity,
such as depressed fracture of skull in large
scope, craniostenosis and basilar
invagination

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Harmful effects of increased ICP

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 1.Decreasing of cerebral blood flow
 CBF=(MAP — ICP）/CVR
CBF:cerebral blood flow
MAP:mean arterial pressure
CVR: cerebral vascular resistance
CPP:MAP-ICP: cerebral perfusion pressure

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 When ICP exceed a limit, autonomous regulative ability
of cerebral blood vessel is lost and CBF decrease
greatly, and so the lives of patients are threatened
directly.

volume / pressure curve

Found by Langlitt in 1965

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 2.Causing of brain herniation

 Severe increasing of ICP can cause any kind of

cerebral hernia which will threaten the lives of
patients directly. （next chapter)
.

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Other Harmful effects such as :
3.Brain edema
4.Cushing reflex (not syndrome)
5.Functional disturbance of gastrointestinal tract
Cushing reflex is a physiological nervous system response to
Increased ICP, It is usually seen in the terminal stages of acute head
injury and may indicate imminent brain herniation . classically
presents as an increase in systolic and pulse pressure.
reduction(decreased) of The heart rate and irregular respiration（
decreased,tidal respiration or sighing respiration ).
In acute inreased ICP.

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Clinical manifestations of increased intracranial
pressure

 “there main signs” of increased

intracranial pressure.
 Other clinical manifestations of increased
intracranial pressure.

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“three main signs” of
increased ICP

 headache
 nausea and vomit
 Papilledema
（memroized by
heart)
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headache

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Nausea and vomit

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Papilledema

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 Atroph
y of
optic
papilledema
nerve

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 Other manifestations of increased ICP

1. Depression of conscious level even to coma

2. Tentorial pressure cone
3. Paralysis of sixth cranial nerve
4. Cushing′s reflex(not syndrome)
5. gastrointestinal disturbance tract hemorrhage
6. Vital sign changes

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 Diagnosis of increased ICP

2 goals of diagnosis:
1. If ICP is increased?
This goal is easy to fulfilled according to clinical
manifestations.
2. What is the causation of increased ICP?
This goal ,some examination methods are needed,
such as CT or MRI, may be needed.

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Precise to know
1. lumbar puncture

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2.Monitor intacranial pressure

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 Treatment
1.General treatment
① Remove mass
② Drain cerebrospinal fluid
③ Fluid management and use of dehydrating agents
（mannitol or and nicorol)
① Surgical decompression

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⑤ Other
Arterial Po2 control
Arterial pCO2 contral
Temperature control
Atrerial pressure control
Venous pressure control

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2.Treatment aimed at decreasing of ICP
3.Treatment aimed at causation of increased ICP

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 Chapter 3
Brain herniation

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 What is brain herniation?

 a part of brain tissue protrude from normal or abnormal

foramen into other cavity and compress important
structure, and thus some typical manifestations present.
This pathophysiological course is called brain
herniation.

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 The brain can shift across such structures as the falx
cerebri, the tentorium cerebelli, and even through the
foramen magnum in the base of the skull (through
which the spinal cord connects with the brain).

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 Herniation can be caused by a number of factors
that increased ICP,these include traumatic brain
injury, intracranial hemorrhage, or brain tumor.

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 The types of brain herniation

1. transtentorial herniation
2. subfalcine herniation
3. tonsillar herniation.

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 Transtentorial herniation
 Transtentorial herniation occurs when the medial aspect of the
temporal lobe (uncus) migrates across the free edge of the
tentorium.
 This causes pressure on the third cranial nerve, interrupting
parasympathetic input to the eye and resulting in a dilated pupil.
This unilateral dilated pupil is the classic sign of transtentorial
herniation and usually (80%) occurs ipsilateral to the side of the
transtentorial herniation.

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 In addition to pressure on the third cranial nerve,
transtentorial herniation compresses the brainstem, and
thus coma and contralateral hemiplegia present

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 Tonsillar herniation
 Tonsillar herniation occurs when increased pressure
develops in the posterior fossa.
 In this form of herniation, the cerebellar tonsils are
displaced in the foramen magnum and compress on the
lower brainstem and upper cervical spinal cord which is
the center controlling of breath and blood circulation

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The tonsillar herniation always present breath
changing early and quickly change to breathnessless.
before breathnessless the patient always with serious
headache and complusive position ,there are no
unilateral dilated but bilateral dilated pupil present late.

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 Difference between transtentorial heniation and
tonsillar herniation

Change of Change of Change Prognosis

consciousness pupil of breath
Transtentorial present early present in present good
herniation typical late
pattern early

Tonsillar present late bilateral present bad

herniation dilated pupil early
present late

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 Subfalcine herniation

Subfalcine herniation occurs when the cingulate gyrus is

displaced across the midline under the free edge of the falx
and the paracentral lobe is compressed which is
responsible for the paralysis of contralateral leg.

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 Treatment of brain herniation

Emergent treatment
 Airway must be opened quickly. trachea cannula tracheotomy
 Supporting of blood pressure.
 Decreasing of increased intracranial pressure by diuretic
drugs or dehydrating agent .
 Arranging operation as soon as possible

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Surgical treatment
 Drain of csf, which is applicable for hydrocephalus
patients.
 External decompressing operation, mainly craniotomy.
 Removing of intracranial mass lesions.

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

 the end of chapter 3

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 Questions
1.The normal intracranial pressure (ICP) is 0.7-2.0 Kpa in
adult and 0.5-1.0 Kpa in child;
2.What adjust the ICP mainly? (CSF)
3.What is the three main signs of increased ICP ?
(headache ,nausea and vomit,Papilledema)
4. What is brain herniation?
5. The Difference between transtentorial heniation and
tonsillar herniation.
6.Talk about Cushing reflex simply
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 Chapter 4
Craniocerebral Trauma

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 accounts for 10~20% of all traumatic injuries
 mortality of craniocerebral trauma is the No 1.

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200,000 died every year in traffic accidents
3 people every minute,
more than half died of crainocerebral trauma.

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 Classify of craniocerebral trauma

1.According to the causation of injury

blunt injury; sharp injury; firearm injury
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2.According to the integrity of cerebral dural

opened injury; closed injury

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3.According to the severity
There are :
mild injury; moderate injury; severe injury

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4.According to the anatomical structure
scalp injury; skull fracture; brain injury

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 1.Scalp injury

1）Scalp hematoma
2）Scalp laceration
3）Scalp avulsion

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Scalp hematomas can be
classified further into
subcutaneous hematomas,
sub-galea aponeurotic
hematomas and sub-
periosteum hematomas.
blunt impact on scalp.
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 Scalp laceration
 Because of abundant blood vessels of scalp, bleeding is
usually severe.
 If neither brain injury no skull injury is accompanied,
scalp laceration can be sutured even so it is beyond 24
hours.

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 Scalp avulsion

 Not throw away the avulsion

scalp , suture them
pressure dressing
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2.Skull fracture

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 Skullfractures can be classified further into
calvaria fractures and skull base fractures
according to the location of fractures.

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 Skull fractures can be classified into linear fractures and
depressed fractures according to the configuration of
fractures.
 If no brain injury is accompanied, there are always no
clinical significances with linear fractures and no
treatment is needed.

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 The arm should be at if is there cerebral trauma,such as
epidural hematoma ,CT scan is necessary at any time .

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1）Skull base fractures

 Skull base fractures can be

classified further into
 anterior cranial fossa fracture,
middle cranial fossa fracture and
posterior cranial fossa fracture
according to the location which is
involved.
 calvaria

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 The patients with depressed fractures of skull base are
commonly dead at once after injury and cann’t be seen
in clinic, so there is no clinical significance with them,
too.
 Skull base fractures mostly is linear fractures

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 Most of linear fractures of skull base are extended from
calvaria. that is to say ,the origin of force is on the
calvaria ,not at the skull base .
 Diagnostic proof of skull base fractures is clinical
manifestations rather than X-ray film.
 Clinical manifestations of skull base fracture include
delayed gore spot, CSF leakage and cranial nerve injury

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 anterior cranial fossa fracture
 Ecchymosis of eyelid

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 middle cranial fossa fracture

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 posterior cranial fossa fracture

 Battle sign
ecchymosis behind auricle

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 Manifestations of skull base fracture
Delayed gore spot CSF leakage Cranial nerve other
injury
Anterior Around orbit Along frontal sinus, Olfactory, none
cranial ethmoid sinus or optic nerve
fossa sphenoid to nasal
cavity
Middle Around mastoid Along sphenoid Facial, Injury of ICA
cranial process sinus to nasal cavity acoustic nerve and
fossa or along tympanic hypophysis
cavity to external
acoustic meatus
Posterio Behind mastoid none glossopharyng Injury of
r cranial process or below eal, vagus, cerebellum
fossa external occipital accessory and and medulla
protuberance hypoglosal oblongata
nerve
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 Treatment of skull base fracture

 No treatment for fracture itself, and emphasis should be

placed on CSF leakage, cranial nerve injury and
monitoring brain injury.
 All the injury to head is opened if skull base fractures
and CSF leakage are accompanied, so injecting of
antibiotic and TAT is indicated.

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1. The leakage of CSF can not be blocked or swashed
artificially.
2. Most of CSF leakage will stop within 1~2 weeks, and
repairing operation is indicated if spontaneous close of
leakage of CSF can not be achieved beyond 1 month.
3. There is no special treatment or drug on cranial nerve
injury up to now.

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2.Depressed fracture of calvaria

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 depressed fracture of calvaria is not like Skull base
fractures,brain injury is always accompanied.the ICP
should monitored and some time surgery is inevitable
,so ,we should memorized the Surgical indications of it .

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 Surgical indications
1. ICP is increased if brain injury is accompanied or area
of depressed fracture is large.

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2. Brain disfunction present which is caused by depressed
cranial bone compressing on brain.
aphasia, hemiplegy, epilepsy
3. Depressed fracture of frontal bone harm countenance.

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4 The depth of depressed fracture
is beyond 1 centimeter
(0.5centimeter in child). and
epilepsy may occur for the future.

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 If the fracture on the superior sagittal sinus or on over
transverse sinus,the operation is need to be carefully
consideration ,if there is no increased ICP
accompanied,operation is not the first selection.

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 Surgical principle of depressed fracture
1. Restoring configuration of cranial bone is primary goal if no
brain injury is accompanied and the fracture is closed.
2. All the broken piece of bone should be removed if fracture is
opened otherwise infection may occur.

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 3.Operation must be deliberative if venous sinus is
involved by depressed fracture because deadly bleeding
may occur.

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 Chapter 5
Traumatic brain injury(TBI)

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 According to pathologic signs:
concussion
Primary TBI diffuse axonal injury
brain contusion and laceration
TBI primary brain stem injury
hypothalamus injury
intracranial hematoma
Secondary TBI
brain edema

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According to the barrier between brain and outside is
intact or not:
Opened TBI; Closed TBI
(details)

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 Mechanism of closed TBI

Dirrect injury (impact injury)

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 In an acceleration injury, as
in a direct blow to the head,
the force applied to the skull
causes the skull to move
away from the applied force.
The brain does not move
with the skull, and the skull
impacts the brain, causing
translation and deformation
of the brain.
acceleration injury

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In a deceleration injury, in which the head
impacts a stationary object, the skull stops
moving almost instantly. However, the brain
continues to move within the skull toward the
direction of the impact for a very brief period
after the head has stopped moving. This
results in significant forces acting on the brain
as it undergoes both translation and
deformation.
In this injury type, impact injury
may be severe, while contra impact
injury is more severe and usually is
the contusion and laceration of
frontal or/and temporal lobe.

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 details

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 Pathologic types of primary TBI

1. cerebral concussion
2. diffuse axonal injury
3. primary brain stem injury
4. cerebral contusion and laceration

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 1.Cerebral concussion

 A concussion is defined as physiologic injury to the

brain without any evidence of structural alteration.
 Diagnosis : head injury medical history ,brief time of
unconsciousness,most no more than half an hour ;
retrograde amnesia,(details)
 some of patients develop postconcussive syndrome
(PCS).

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 PCS consists of a persistence of any combination of the
following after a head injury: headache, nausea,
insomnia , memory loss, dizziness, diplopia, or sleep
disturbances.
 There is no evident abnormal signs on CT or MRI scan
images.
 No special treatment is needed except means aiming at
alleviating symptoms for them.

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 2.Diffuse axonal injury(DAI)

 shear-type forces on axons

 Pathologic signs of DAI include extend
cranny and mini bleeding spots within brain
white matter
 By microscope axon shrinking ball(ASB)
can be seen.

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 Diagnosis : :
1. head injury medical history ,
2. permanent coma and (or)abnormal pupil present after
injury immediately(dilated or decreased ,unilateral or
bilateral )
3. mini bleeding spots can be showed on CT or MRI at
cerebral cortex,callosum,brain stem ,cortex around
ventricle.but some cases no abnormal signs can be
showed on CT or MRI images,
4.Always accompanied the cerebral contusion and
laceration .
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 Supporting and rehabilitation treatment is the main
therapeutical measures for the patients.

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 3.Primary brain stem injury

 Primary brain stem injury(PBSI) is caused by the same

mechanism as that of DAI, it is thought that cerebral
concussion, DAI and PBSI are the different degrees of
same disease mold.
 Permanent coma, change of pupil, no increase of ICP
and no abnormal sign of CT scan.
 The therapeutical as same as that for DAI.

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 4.Cerebral contusion and laceration
 Most of cerebral contusion and laceration are caused by
contra impact injury by decelerating mechanism and
usually locate at bottom of frontal and/or temporal lobe.

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 Pathologic signs of cerebral contusion and laceration
include contusion and laceration of brain tissue and pia
matter which is accompanied by bleeding spots or
hematomas.

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On CT scan images cerebral contusion and laceration
appear as irregular regions, in which high-density
changes (ie, blood) and low-density changes (ie, edema)
are present
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 cerebral edema occurs after 24 hours, peak within 5~7
days and subsides after 2 weeks gradually.
 Increased ICP and abnormal signs on CT images
commonly present.
 Changes of vital sign and appearances of positive signs
of nerve system.
 The main treatments aim at goals of alleviating of brain
edema, decreasing of ICP and preventing from brain
herniation.

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Indications of surgical treatment
1) acute herniation has occurred (transtentorial, Tonsillar
herniation);
2) CT or MRI show midline of brain shift more than 1 cm
or there are signs showing ventricle or cistern be
pressed obviously;
3) Disturbance of consciousness become more and more
serious;
4) Clinical manifestations deteriorate during non-surgical
treatment.

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 Secondary TBI
1. Brain edema
2. Intracranial hematomas

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 1.Brain edema

 Brain edema is defined as abnormal deposit of water

within brain tissue.
 Brain edema may be caused by the breakage of blood-
brain-barrier(BBB) by which water leak from blood
vessels and deposit in interspace of cells, or it may be
caused by injury of neural cells by which excessive
water penetrate cellar membrane and deposit in neural
cells.

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On CT scan images brain edema is shown as a hypo-
density area after 24 hours.

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 The main disadvantage of brain edema is increasing of
ICP and inducing brain herniation, so the main
therapeutic measure aiming at brain edema is injecting
diuretic and dehydrating agent such as nicorol and
mannitol to decrease ICP and preventing from brain
herniation.

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 2.Intracranial hematomas

 According to location intracranial hematomas can be

classified into epidural, subdural, intracerebral, and
intraventricular hematomas.
 According to time at which occur intracranial
hematomas
can be classified into acute(in 3days), subacute(in 3
weeks) and chronic hematoma(more than 3weeks).

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 ⅠAcute epidural hematoma(EDH)

Typical CT image of acute EDH appears as hyper-density

between inner table of skull and dura which shapes as convex lens.

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Middle meningeal artery, which is a main artery
nourishing dural matter, course along bony canal and
easy to be laniated when fracture occur, and so EDH
form most commonly in temporal region
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 temporal region involved with EDH most commonly
(70-80%). In the temporal region, the bone is relatively
thin, and the middle meningeal artery is close to the
inner table of the skull.

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 Clinical manifestation
 Manifestation of increased ICP, mainly headache,
vomit and change of vital signs.
 Manifestation of acute transtentorial herniation, which
are:
1 change of pupil, such as enlargement of ipsilateral pupil
and loss of light response
2 paralyse of contralateral limbs and present of sign of
pyramid tract
3 changes of consciousness.

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pyramid tract sign: Babinski signs,Oppenheim signs
Gordon signs Chaddock signs,et al.

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 Changes of consciousness
 Typical change of consciousness present as the
procession of “from coma to conscious and to re-
coma” , which is charactered by a conscious interval
between two phase of coma.

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 First , most because of the cerebral concussion to
coma,there is no sever brain injury ,the coma last no
more than half an hour ,but epidural
hematoma(EDH)become larger and larger ,cause the
ICP is increasing ,than to acute transtentorial
herniation,patient become coma again ,so there is a
period of conscious time between two coma
,memorized it.

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 Atypical changes of consciousness present as the “from
conscious to coma” or “ from mild coma to severe
coma”, which are charactered by no conscious interval.

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 Diagnosis of acute epidural hematoma
1. A history of traumatic impact on head.
2. Symptoms and signs of increased ICP present,
3. Clinical manifestations of acute transtentorial
herniation present, such as typical changes of
consciousness and pupils.
4. CT scan of head show typical sign of acute epidural
hematoma.

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 Treatment of acute epidural hematoma
The prognosis of patients with acute epidural hematoma
is determined only by the therapeutical methods it is the
one of a few head traumatic diseases which can be
cured completely,
so neurosurgeons should do their best to treat them at
any time.

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Indications of surgical treatment of intracranial
hematoma(epidural ,subdural, intracerebral ):
1) acute herniation has occurred (transtentorial, Tonsillar
herniation);
2) brain herniation is very likely to occur if supertentorial
hematomas exceed 30ml(some books refer to 40 ml) or
infratentorial hematoma exceed 10 ml;
3) disturbance of consciousness become more and more
serious

126
4)ICP exceed 270 millimeter of water continuously
5)Hematoma is not large while the midline of brain shift
more than 1 cm.or there are signs showing the ventricle
or cistern be pressed obviously (on CT or MRI)
6) Clinical manifestations deteriorate during non-surgical
treatment.
7) Hematoma is in the temporal region ,it is easy to cause
transtentorial herniation ,operationg should be take even
though the hematoma is not too large.

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 Principal of surgical treatment
1) operation should be performed as soon as possible;
2) only evacuation of hematoma is adequate, if no primary
brain injury is accompanied and brain herniation has
not occured;
3) removing of bony flap and opening dura wide besides
evacuation of hematoma are indicated if primary brain
injury is accompanied and brain herniation has
occurred.

128
 Sketch map of removing of acute EPH

Removing hematoma
129
Incision should large enough
 ⅡChronic subdural hematoma
 the hematoma is between dural and cerebral pia
mater,like a crescentiform.(convex,epibdural)

130
 CT scan image of chronic SDH
The characteristic evolution of an SDH appearance on
CT scan is as follows: In the first week, the SDH is
hyperdense to brain tissue. In the second and third
weeks, the SDH appears isodense to brain tissue. After
the third week, the SDH is hypodense to brain tissue.

131
 MRI of chronic SDH

T1-weight T2-weight
 An MRI is helpful in imaging chronic SDH when CT images
are difficult to show an isodense hematoma.
 MRI may be particularly helpful in diagnosing bilateral chronic
SDH because a midline shift may not be apparent.
132
 Treatment of chronic SDH
 Surgical treatment is need for
almost all of the chronic SDH
once the diagnosis is confirmed.
 trepanation and drainage of
hematoma adapt to most of
patients suffer from chronic
SDH.

133
 Opened traumatic brain injury

 All opened traumatic brain injury indicate surgical

treatment which aim at closing wound, clearing
penetrating objects and necrotic brain tissue to avoid
infections of brain and aim at decreasing ICP.

134
 Ⅲ Acute intracerebral hematoma

Acute intracerebral hematoma appear as increased

density in brain tissue, surround by edema belt

135
 No surgical treatment but diuretic drugs is needed for
very small intracranial hematomas, while large
hematomas which increase ICP greatly and may cause
brain herniation must be treated by operation

136
Management of theTraumatic brain injury

137
 First aid for patients with traumatic
craniocerebral injury
1. Inquiring causation and course of injury simply and
swiftly is needed. At the same time examining vital
signs is imperative.
2. Ensuring airway opened is the first important job. For
this aim suction of secretion in airway even trachea-
intubatton or tracheotomy are needed.
3. Stabilizing circular system is the second important job
because hypotension will cause severe ischemic injury
to brain by decreasing brain perfusion pressure.

138
 Once a patient has been stabilized from the
cardiopulmonary standpoint, CT scanning of head
should be performed as soon as possible with the goal
of confirming the degree of injury to head.

139
 Grade is performed according to the degree of injury to
head which is shown by clinical manifestation(eg.
symptoms and neurological signs) and imagining
examining.

140
 Glasgow Coma Scale (GCS)
GCS is the most widely used neurotrauma scale
From 3 to 15
Eye opening:grade from 1 to 4;
Verbal response :grade from 1 to 5;
Motor response: grade from 1 to 6
Total:15
(details ,please look at the page 128 of your text book)

141
 Glascow coma scale
Eye opening score Verbal response score Motor response score

spontaneously 4 Oriented and 5 Obeys to command 6

converses
To verbal 3 Disoriented and 4 Localizes to pain 5
command converses
To pain 2 Inappropriate 3 Flexion withdrawal 4
words
No response 1 Incomprehensib 2 Flexion abnormal 3
le sounds
No response 1 extension 2

No response 1

142
 Grade of patients with traumtic traniocerebral
injury
 After first aid grading the patients is needed so that
appropriate treatments are performed.
 Grade is performed according to the degree of injury to
head which is shown by clinical manifestation(eg.
symptoms and neurological signs) and imagining
examining.
 In general, patients with craniocerebral traumatic injury
can be classified into there grades which are mild,
moderate and severe craniocerebral injury.
143
 mild, moderate and severe(many scales used )
Accroding to patients conditons
 Mild :only consussion ,with or without skull fracture
,unconsciousness no more than 20 minutes .no brain
injury on CT or MRI.
 Moderate: unconsciousness no more than 6 hours,CT or
MRI show small area of cerebral contusion and
laceration or subarachnoid hemorrhage, intracerebral
hematoma no more than 25-30 ml.
144
 Severe
1. large area of skull fracture ,
2. large area of cerebral
3. contusion and laceration ,
4. brain stem injury,
5. unconsciousness more than 6 hours,
6. CT or MRI show
7. large area of cerebral contusion and laceration
8. intracerebral hematoma no more than 30ml,
9. Midline shift more than 1 cm

145
Accroding to GCS
Mild: unconsciousness no more than 6 hours,GCS from
13 –15.
Moderate:8—12.
Severe :3-7
Most severe:3-5,or present the herniation or accompanied
other( moderate to severe )organ injury .
Together with the patients conditons
146
 An important character of patients with traumatic
craniocerebral injury is swift change of state of illness,
so intensive monitoring for them is imperative.
 The elementary monitoring method is “five examining”
which is examining of breath, pulse, blood pressure,
consciousness and pupil.
 A very useful and simple monitoring method is CT
scanning of head.
 Monitoring of ICP is useful but is very inconvenient.

147
 Non-surgical treatments
for patients with traumatic craniocerebral
injury
 The general goals of non-surgical treatments are decreasing of
ICP, avoiding the progressing of secondary brain injury and
promoting the restoring of brain.
 Of all no-surgical therapeutic methods decreasing ICP is most
important which is usually performed by diuretic drugs, anti-
metabolic drugs, et al.
 General treatment is the second important methods which
include stabilizing of circular and respiratory system, providing
sufficient nutritious substances, avoiding imbalance of
electrolytes and preventing complications.
 Rehabilitating treatments play a important role which involve
neuro-nutritious drugs, functional exercise, acupuncture, et al.
148
 questions
1. According to the anatomical structure the craniocerebral trauma
can be calssfied into:
2. Principal of treatment of the Scalp laceration
3. Manifestations of skull base fracture
4. Principal of treatment of skull base fracture
5. Surgical principle of depressed fracture
6. Clinical manifestation of Acute epidural hematoma
7. Indications of surgical treatment of acute epidural hematoma
8. Principal of treatment of Opened traumatic brain injury
9. What is “GCS”? Talk about it simply.

149
Tetanus a acute special surgical infection
caused by Clostridium tetani
anaerobic bacterium
Deep wound, blindgut wound
With oxygen-deficient environment
TAT: tetanus antitoxin inject within 24 hours
Does :1500-3000 units
tetanus immune globulin:3000-6000 units
tetanus vaccine
cephalosporin
150
 Chapter 6
Intracranial tumors
(test time )

151
 Brief introduction

 According to the location from which intracranial

tumors originate, they can be classified into primary
group and secondary group.
 Primary intracranial tumors originate from brain tissue,
meninges, cranial nerves, pituitary, blood vessel and
remnants of intracranial embryonic tissue. The
incidence is about 7.8-12.5 per 100 thousands per year,
accounting for the 11th in the list of body tumor
prevalence.

152
 Secondary intracranial tumors are inferred to as
metastasis of extracranial tumors to intracranial cavity.
They account for a large part of intracranial tumors, and
the most common origin is lung cancer.(maligant)

153
 Clinical manifestations
 All clinical manifestations of intracranial tumors can be
divided into two groups: manifestations of chronic
increasing ICP and manifestations of local nerve
impairs.
 Manifestations of chronic increasing ICP include
headache, nausea, vomit, papilledema, diplopia, et al.
they are not differential

154
Manifestations of local nerve impairs are determined by
the location of tumors. It means the location of tumors
can be inferred by them, and so there are diagnostic
significances with them.

155
 Local manifestations of intracranial
tumors

 There are some intracranial special regions which

are commonly involved by tumors. These special
regions are as follows:
1.cerebral hemisphere
2. cerebellum
3. sellar region
4 .cerebellopontine angle (CPA)
5. pineal region.
156
 Local manifestations of a special region is unique and is
called “syndrome”. The syndromes are varied according
to the location which tumors origin and invade,
therefore they have diagnostics significance.

157
 Cerebral hemisphere

The tumors involving cerebral hemisphere are commonly

gliomas and meningiomas.
Frontal lobe involved by tumors may present with
mental dysfunction, epilepsy, et al.
Temporal lobe invaded by tumors may present with
memory and language dysfunction or epilepsy.
.

158
 Parietal lobe impaired by tumors may present with
sensory and motor dysfunction or epilepsy.
 Occipital lobe involved by tumors may present with
visual dysfunction

159
Sellar region
Anatomic sellar region includes many
structures such as anterior and
posterior clinoid processes,
diaphragma sellae, tuberculum sellae,
pituitary gland,et cetra.
The popular benign tumors originating
from sellar region are meningioma,
pituitary adenoma and
craniopharyngioma.
malignancy tumors originating from
sellar region are gonioma ,optic
giloma and chordoma
Typical local manifestations of sellar
region tumors are visual deficit and/or
endocrine dysfunction.
160
Cerebellum
The common lesions involving
cerebellum are gliomas,
meningioma, et cetra.
The patients with cerebellar
tumors may present with ataxia,
nystagmus, vertigo, et al.
Manifestations of increased ICP
usually be severe because tumors
may block the outflow of CSF
and cause hydrocephalus.

161
Cerebellopontine angle (CPA) is
the triangle which is formed by
cerebellum, pons, and ridge of
petrous bone.
The popular benign tumors
originating CPA are neurilemoma,
meningioma, dermoid and
epidermoids cyst .
The typical manifestations of CPA
tumors are commonly caused by
compressing of tumors on multiple
cranial nerves, brain stem and
cerebellum and increased ICP even
hydrocephalus.calle “CPA
syndrome”
162
The tumors involving pineal
region are usually germ cell
tumors.
Parinaud’s syndrome and
increased ICP caused by
hydrocephalus are the typical
manifestations of the patients
with pineal region tumors.

163
Is a supranuclear paralysis of vertical gaze resulting from
damage ot the dorsal midbrain
cause the disorder of eye movements
The clinical features are:
1. a loss of vertical gaze
2. nystagmus on attempted convergence
3. pseudo-Argyll-Robertson pupils
4. large pupils with sluggish reaction to light

164
 Argyll-Robertson pupils :are bilateral small pupils that constrict
when the patient focuses on a near object,but do not constrict
when exposed to bright light (they do not “react” to light).
They are a highly specific sign of neurosyphilis.

165
 Diagnosis of intracranial tumors
 Diagnosis of intracranial tumors includes 3 goals:
1. If does a intracranial tumors exist or not? According to
the clinical manifestations of increased ICP and of
local nerve impair which are revealed by neurological
examining this goal can be achieved in most cases.
2. Where does the tumors exist? If a intracranial tumor is
suspicious CT scan or MRI should be performed to
determined the location of intracranial tumor which is
very important for the aim of surgical treatment.

166
3 .What pathological type is the tumor? According to CT
scan or MRI this goal can be accomplished in about
50~60% cases, and in the others surgical resection and
biopsy is needed.

167
 Treatments of intracranial tumors

 All therapeutical methods aiming at intracranial tumors

are classified further into 2 types: treatments aiming at
decreasing ICP and treatments aiming at intracranial
tumors themselves.
 Treatment aiming at decreasing ICP include
administration of diuretic drugs, drainage of CSF and
removing of lesions or part of skull.
 Treatments aiming at intracranial tumors themselves
include:

168
 Complete or sub-complete resection of tumors by
surgical techniques is the elementary method which
adapts to most cases.
 Radiotherapy, especially stereotactic radiosurgery such
as Gamma knife, adapts to the patients in which cases
surgical resection of tumors is very difficult or the risk
of operation is very great. Radiotherapy can also be
used as a remedial method in the patients in which cases
total removing of tumors is not achieved.
 Chemotherapy still has no positive effect on intracranial
tumors by now.
169
 Clinical characters
of common intracranial tumors
 Gliomas
 Gliomas, originating from neuroepithelial tissue,
account for about 40~50% of primary intracranial
tumors. They commonly locate at cerebral hemispheres,
brain stem, corpus callosum and cerebellum.
 According to the degree of differentiation of tumor cell
gliomas can be classified further into astrocytoma,
glioblastoma, oligodendroglioma, ependymoma and
medulloblastoma

170
 Most of gliomas(perhaps except ependymoma) grow in
the brain tissue diffusely and there in no a clear border
between tumor and brain tissue, therefore complete
resection of the tumor is impossible. For this reason the
prognosis of patients with giomas is very bad, and most
of them will die within 3 years, even treated by the most
active operation and adjuvant radiotherapy.

171
 Plain scan enhanced

A low-grade astrocytoma of right frontal lobe is shown

by CT scan. No positive border exist between the tumor and
brain tissue and there is no contrast effect with the tumor.
172
 Plain scan enhanced

CT scan disclose a glioblastoma locating at the anterior part of

corpus callosum. The lesion is inhomogeneous density and it
is enhanced heterogeneously.
173
MRI show there are necrotic [ne'krɒtɪk] area in the centre of tumor ,illustrate that the tumor growing very fast and it is a high g

174
 Meningiomas

 Intracranial meningiomas are the second common

tumors of primary intracranial tumors. Most of them are
benign while few of them are malignant.
 Meningiomas originate from epithelium of arachnoid
membrane, therefore the common location of
meningiomas are the regions (such as sides of venous
sinus, cerebral falx, cerebellar tentorium, olfactory
groove, sellar region, et al) in which epithelium of
arachnoid membrane is abundant.

175
 There are intercranial and extracranial blood supply to
meningiomas therefore much blood may be lost during
operation.

176
 Thereis a positive border between meningiomas
and brain tissue therefore complete removing of
them can be achieved and the prognosis is very
good.

177
178
 Unfortunately in some cases important nerves or vessels
may be invaded and complete resection of the tumors
will be very dangerous and difficult then subtotal
resection is considered.
 医生(doctor)
医=to cure
生=to give life,
=to give birth
=savage
=student 179
180
.“Meninges tail sign” is the most typical imaging
manifestation of menigioma on CT or MRI

181
Pituitary Adenoma

182
 Pituitary adenomas arise from epithelial pituitary cells
which situates in sellae turcica and develop to above
diaphragma sellae.
 Microadenomas present with symptoms of disorder of
pituitary hormone, while macroadenomas may present
with visual deficits, headache, elevated intracranial
pressure.

183
Based on the adenoma secretes a hormone and cause a
hyper secretory syndrome ,and test the hormone in the
blood serum,classfied in endocrine-active and endocrie-
inactive.
Based on immunohistochemical method to Cell Secretive
Function of adenoma tissure classfied into :
PRL (prolactin) type,
GH(growth hormone) type
ACTH (adrenocorticotrophic hormone )type
Mixed type.
[ə'driːnəʊ-kɔːtɪkəʊ'-trɒfɪk](question) bromocriptine

184
Depending on size ,divided into
Microadenomas(maximal diameter ≤1.0cm )
Macroadenomas(＞1.0cm)
Giant adenomas(＞3.0cm)

185
 Microadenomomas can be treated by radiosurgery( such
as gamma-knife) or medical therapy(bromocriptine),
but macroasenomas can only be treated by surgical
resection to decompress optic nerve and chiasm.
PRL (prolactin) type,is sensitive to
bromocriptine,especially for young grils no married,no
child
 In general complete removing of macroadenomas can
not be achieved therefore adjuvant radiotherapy after
operation is needed.
186
 T1-weithted Contrast

 A macroadenoma is shown by MRI. Pituitary adenoma is

iso-intensity compared with brain tissue on T-1 weighted
image and is homogeneous enhanced after injected with
contrast drugs.
187
 A microadenoma is
shown by MRI. The
lesion is hypo-intensity
compared with pituitary
tissue on T1-weighted
image and the contrast
effect is delayed.

188
 Axial plain image Coronal contrast image
A macroadenoma is shown by CT scan. It is iso-
density on axial plain image but the best display of it can
only be achieved on coronal and contrast image.
189
190
191
192
193
 视屏

194
 Craniopharyngioma

 craniopharyngiomas arise from cellular

remnants of the Rathke pouch, which is an
embryologic structure destined to form both
the infundibulum and anterior lobe of the
pituitary gland.
 Typically, the tumors arise within the sella
or adjacent suprasellar space.

195
 Symptoms are caused by mass effects on adjacent
normal intracranial structures,such as optic nerve and
hypothalamus.
 Craniopharyngiomas are absolutely malignant and
many of them can be cured if they are completely
removed by microsurgical techanique. Unfortunately
complete removing of them is very difficult and
dangerous because many important structures may be
invaded, and so adjuvant radiotherapy after operation is
needed.

196
 Coronal image Sagittal enhanced image

 A multi-cystic craniopharngioma is shown by MRI on

coronal and sagittal enhanced image. Craniopharngiomas
are heterogeneous intensity on T1-weighted image and are
heterogeneous enhanced.
197
198
199
200
 Acoustic neuroma
 Although neuroma can derive from every cranial nerve
the most common cranial nerve from which neuroma
originate is vestibular nerve which account for about
90% of intracranial neuroma.

201
 Typical clinical manifestations of acoustic neuroma are
symptoms of impairing of brainstem, cerebellum and
Ⅴ,Ⅶ,Ⅷ cranial nerve.
 All of acoustic neuromas are benign therefore they can
be cured. Macro-neuromas must be treated by surgical
operations with the goal of alleviating the compression
of neuromas on important structures while micro-
neuromas can be treated by radiotherapy

202
 Internal
Internal
auditory
auditory
cannal
cannal

 A huge acoustic neuroma which is hetero-intensity is shown

on MRI coronal and axial enhanced images. Protruding of
tumors into enlarged internal auditory canal is the most typical
finding on CT or MRI.
203
204
 Intracranial metastatic tumors
 Metastatic tumors account for a small part of intracrainal
tumors and the most common location from which
metastatic tumors arise is lung cancer.
 Most of metastatic tumors locate in the brain tissue
below gray matter of cerebral hemispheres or in
cerebellar hemispheres.
 Clinical manifestations of intracranial metastatic tumors
are symptoms of increased ICP and of injury to local
brain tissue.
 Because of malignant character there is no effective
therapeutical methods with intracranial metastatic tumors.
205
 A multiple metastasis tumor which locate in frontal lobe
and vermis of cerebellum is shown by MRI. The typical
imagining characters of metastasis tumors are multiple
and heterogeneous density or intensity.
206
 Chapter 7

Spinal canal tumors

207
 epidural tumor

subdural
intramedullary
tumor

subdural
extramedullary
tumor

208
209
 Clinical manifestations of spinal
canal tumors
 Phase 1. In this phase the main symptom is occasional
pain which involve the region controlled by a nerve
root. This symptom is caused by the stimulation of
tumor to nerve root and is aggravated by cough.

210
 Phase 2. In this phase the main manifestations include
contralateral paralysis, contralateral loss of superficial
sense and ipsilateral loss of deep sense. The
neurological deficits are below the level of location of
the tumor and they are caused by the compressive
injury of tumor to the ipsilateral half of spinal cord

211
 Phase 3. In this phase the main manifestations include
complete paralysis, loss of all sense below the level of
location of the tumor and loss of bowl and bladder
continence. These neurological deficits are caused by
the crossing injury of the tumor to spinal cord.

212
 Diagnosis of spinal canal tumors

The diagnosis of spinal canal tumors involves 2

questions.
1. Is there a spinal canal tumor? This question can
be answered according to typical manifestations.
2. Where and what kind is the spinal canal tumor?
This question can be answered only by MRI.

213
 Treatment of spinal canal cord
 All extramedullary tumors adapt to surgical operation to save
the function of spinal cord as soon as possible. They can be
removed completely and the prognosis is very good, except
malignant part of them.
 Some intramendullary tumors, such as ependymoma, can be
complete removed by microsurgical technique and the
prognosis is relatively good.
 If the tumor is malignant or was not be removed completely
radiotherapy after operation is needed.

214
 Questions
1.Anatomic sellar region includes many structures such as(list 4)
2. The popular benign tumors originating from sellar region are(list
3)
3. Typical local manifestations of sellar region tumors are(list 2)
4. Cerebellopontine angle (CPA) is the triangle which is formed
by(list 3)

215
5.The popular benign tumors originating CPA are(list
3)
6 .Pituitary adenomas arise from?
7.What is the synptoms of Macroadenomas of Pituitary
8.The popular approach to resect the Pituitary adenomas is
9.What is the Typical clinical manifestations of acoustic neuroma
10.According to the location the spinal canal can be classified
into(list 3)

216
 Chapter 8
Cerebrovascular diseases

217
Category of cerebrovascular disease

 According to the main pathological manifestations

cerebrovascular diseases can be classified into 2 groups:
 Hemorrhagic diseases. This group, such as cerebral
aneurysm, cerebrovascular malformation and so on,
present with a common pathological manifestation,
namely cerebral hemorrhage.
 Ischemic disease. This group include cerebral
embolism, formation of cerebral thrombus and so on
which present with a common pathological
manifestation, namely ischemic brain injury.

218
Cerebral aneurysms

219
 Pathology and etiology

 The word aneurysm comes from the Latin word

aneurysma, which means dilatation. Aneurysm is
an abnormal local dilatation in the wall of an artery,
due to a defect, disease, or injury.
 Aneurysms can be true or false. A false aneurysm
is a cavity lined by blood clot. The 3 major types of
true cerebral aneurysms are saccular, fusiform, and
dissecting.

220
 Saccular aneurysms are rounded, berrylike
outpouchings that arise from arterial bifurcation
points. These are true aneurysms, ie, they are
dilatations of a vascular lumen caused by
weakness of all vessel wall layers.
 Most cerebral aneurysms were thought to be
congenital in origin, arising from focal defects in
the media and gradually developing over a period
of years as arterial pressure first weakens and
subsequently balloons out the vessel wall.

221
Most saccular aneurysms arise
on the circle of Willis or the
middle cerebral artery
bifurcation.
Approximately 85% of all
intracranial aneurysms arise on
the anterior circulation. Common
locations are the anterior
communicating artery (30-35%),
the internal carotid artery at the
posterior communicating artery
origin (30-35%), and the MCA
bifurcation (20%).
222
 About 15% of all intracranial
aneurysms arise on the posterior
circulation.5% arise from the basilar
artery bifurcation, and the remaining
1-5% arise from other posterior fossa
vessels. Common posterior fossa
sites include the superior cerebellar
artery and the vertebral artery at the
origin of the posterior inferior
cerebellar artery. Anterior inferior
cerebellar artery aneurysms are rare.

223
 Clinical manifestations
1 rupture and causing SAH.
 The rupturing of cerebral aneurysms account for about 80%
causes of SAH.
 The patients with SAH present with severe headache, vomit or
coma.
 Rupture of aneurysm and SAH may occur many times.

224
 2 Compression of local nerve.
 Some aneurysms, such as aneurysms locating at bifurcation
of ICA and PCoA, may compress oculomotor nerve and
cause enlargement of ipsilateral pupil, loss of opening eye
and loss of pupillary response to light.

225
 In general CT scan of head will
show SAH or intraventricular
hemorrhage. Sometimes very
large aneurysms may be shown
by CT scan.
226
 High quality MRA may reveal the configuration of Will’s
circle and the aneurysms.

227
 Digital subtract angiography(DSA) can distinctly show
the cerebral blood vessels and the aneurysms.
Nowadays it is the “golden standard” for the diagnosis
of cerebral aneurysm.
228
 Diagnosis of cerebral aneurysm
The diagnosis of cerebral aneurysms
include 2 goals:
1. Is there a cerebral aneurysm? According to
typical clinical manifestations of SAH which
was shown by CT scan this question can be
answered easily.
2. Where is the cerebral aneurysm? This question
can be answered only by MRA or DSA.

229
 Clinical grading scale

 The objectives of clinical grading are evaluating

the severity of illness, choosing surgical
indications and time as well as assessing outcome.
The most useful grading scale is Hunt and Hess
grading system

230
 Grade 1 - Asymptomatic or mild headache
 Grade 2 - Moderate-to-severe headache, nuchal rigidity,
and no neurological deficit other than possible cranial
nerve palsy
 Grade 3 - Mild alteration in mental status (confusion,
lethargy), mild focal neurological deficit
 Grade 4 - Stupor and/or hemiparesis
 Grade 5 - Comatose and/or decerebrate rigidity

231
 Treatment of cerebral aneurysms

Treatment of cerebral aneurysms involves 2

questions as follows:
1. How can the patients be saved from the impact
of SAH caused by rupture of aneurysm?
2. How can the aneurysms be treated to prevent
subsequent SAH?

232
The second question involves the methods dealing
with aneurysms themselves as follows.
1) Clipping of neck of aneurysms by microsurgical
techniques is an old and effective method of
treating of cerebral aneurysms.
2) Embolizing body of aneurysms with detachable
coils by interventional techniques is a fashionable
and mini-invasive method.

233
 Before operation After operation

 An aneurysm locating at the origin of PCoA from ICA was

clipped by our staff.

234
 Before operation After operation

 An aneurysm locating at ACoA was clipped by our staff.

235
 A wide-necked aneurysm locating at ICA was embolized by
our staff because surgical clipping the wide neck of the
aneurysm is very dangerous and difficult.
236
237
Hypertensive cerebral
hemorrhage
(HCH)

238
 Introduction
 Long-standing hypertension
with degenerative changes in
the vessel walls and
subsequent rupture is believed
to be the cause of HCH.
 HCH is very popular in the
population of exceeding 60
years old and has been listed
as one of “the three killers”.

 The common locations which HCH involves usually are

basilar nucleus(including internal capsule, corpus striatum,
thalamus,et al), brain stem, cerebellum and white matter
below cortex.
239
 Clinical manifestations

 Symptoms of acute increased ICP, such as

headache, vomit and nausea.
 Local neurologic deficits, such as hemiplegia.
 Change of consciousness caused by brain
herniation or direct injury to thalamus or brain
stem.

240
CT scan

HCH can be swiftly demonstrated by

CT scan therefore it is the most useful
diagnostic method.

241
 Diagnosis of HCH

 The diagnosis of HCH can be confirmed if the

follows are clear:

（1）a history of hypertension

（2）typical local neurologic deficits;
（3）common hemorrhagic location shown by CT
scan.

242
 Treatment of HCH

 The treatments of HCH include medical treatment and

operative treatment. In general, medical treatment is
passive while operative treatment is active. Choosing
of treatment method is determined by the objective
conditions of a case.

243
The objective conditions determining choosing are
as follows:

1. The age. In general, the older the age is the more bad
the prognosis is.
2. hemorrhagic location. The more superficial the
hemorrhage location is the better the prognosis is.
3. Volume of hematomas. There is no operative need for
very small hematomas(less than 30ml in supratentorial
cavity and 8ml in infratentorial cavity). Beyond this
scope operative treatment is considered.

244
4 Consciousness of patients. There is no operative need
for the very conscious cases or the moribund cases.
Operative treatment is considered if consciousness
deteriorate gradually.

245
 Medical treatments include the methods of decreasing
ICP, preventing rebleeding, protecting brain functions
and preventing secondary brain injury.

246
 Operative treatments include removing hematoma by
craniotomy or drainage of hematoma by burr hole.
Ventriculopuncture and drainage of CSF adapt to
intraventricular hemorrhage.

247
 Chapter 9
Congenital disease of the nervous system
1.Hydrocephalus
2.Spina bifida

248
 1.Hydrocephalus

Hydrocephalus result from change in the normal

relationships of pressure and volume within the
interconnected cerebrospinal fluid compartment of the
brain

249
communicating or
non-communicating
hydrocephalus

250
 In infants and young children there may also be
progressive distention of the cranial vault;
 In older children and adults these pressure –volume
change can result in the cassic symtoms prominent
brain dysfunction follows signs of increased intracranial
Pressure with changes in cerebral blood flow reflected
by increased cerebrospinal fluid lactate
 In elderly ,dementia is prominent without the usual
evidence of increased ICP
251
Diagnosis
In the infant serial head measurement should be part of the
routine examination
Hydrocephalus can be swiftly demonstrated by CT scan
therefore it is also the most useful diagnostic method.

252
 Diagnosis
 Diagnosis of involves 2 questions as follows:
1. is there Hydrocephalus?
2. What kinds of Hydrocephalus, communicating or non-
communicating.
3. If there is non-communicating or obstructive
Hydrocephalus

253
254
255
 Treatment of Hydrocephalus

1.Non-operative
applies to the early stage or not serious patient`s
condition,slow development cases,its methods include:
 Diuretics or dehydrating agent,
 Puncture through anterior fontanel or lumbar discharges
CSF repeatedly.

256
2.Surgical treatment
applies to progressive hydrocephalus,distinct cranial
amplification,and cerebral cortex thickness over
1cm,operation can be taken;it applies to higher
intraventricular pressure(over 200 mmH2O),or the case
which failed by non-operative managemen.t

257
 CSF shunts
 its aim is founding CSF circulation access,relieving the
CSF storage,which is used to communicating or non-
communicating hydrocephalus.The common shunts
include ventriculo-peritoneal shunt,lateral ventricle-
cerebellomedullary cistern shunt,the third ventricle,and
so on.

258
259
2.Spina bifida

260
 cranial
gaps
 congenital encephalocele and
meningoencephalocele

261
 Questions

1. Talk about Clinical manifestations of the aneurysm

2. Clinical grading scale of aneurysm
3. There are two kind of methods dealing with aneurysms, tell me
about them
4. Talk about The objective conditions determining choosing of
HCH

262