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Head Injury Clinical Presentation

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Head Injury Clinical Presentation

Author: David A Olson, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA more... Updated: Sep 5, 2012

History
History in most patients with head injury should be self-evident. However, consider trauma with intracerebral pathology in any patient with a coma of unknown etiology. In the acute setting, the patient may be comatose or confused, and witnesses to the accident or injury are of obvious and crucial importance. Elicit the type and mechanisms of the injury, as these may have prognostic value. Patients sustaining a head injury from an assault or from being struck with a falling object have a markedly greater likelihood of poorer vocational outcomes than patients sustaining the more common acceleration/deceleration injuries, presumably because the former injury types entail greater axonal damage.[24] Ascertain whether the patient lost consciousness. Even a questionable loss of consciousness can be a marker of severe neurological injury. The presence of prior head injuries, particularly prior concussive episodes in sports, can indicate the potential for more severe long-term outcomes. Remote or active drug or alcohol use may raise the risk of intracranial bleeding and cloud the mental status assessment. Present anticoagulant therapy is also worrisome. Among high school athletes with head injuries, on-field dizziness, but not objective balance impairments, at the time of concussion significantly correlated with prolonged return to play compared to athletes with head injuries who did not experience this symptom.[26] Carefully consider past psychiatric disease and a premorbid history of headaches.

Physical
Elemental neurologic examination
The Glasgow Coma Scale (GCS) is the mainstay for rapid neurologic assessment in acute head injury. Both initial and worst GCS postresuscitation scores have correlated significantly with 1-year outcomes following severe head injury. Following ascertainment of the GCS score, focus the examination on signs of external trauma. Bruising or bleeding on the head and scalp and blood in the ear canal or behind the tympanic membranes may be clues to occult brain injuries. Also consider coexistent cervical spine and other systemic injuries. Anosmia is common and probably is caused by the shearing of the olfactory nerves at the cribriform
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plate.[27] If accompanied by rhinorrhea, a CSF leak with the attendant risk of ascending meningitis must be excluded.[28] Abnormal postresuscitation pupillary reactivity correlates with a poor 1-year outcome. In fact, a 2006 study reported no survivors among 173 head-injured patients who presented with bilaterally fixed and dilated pupils and a GCS score of 3[29] , while other researchers have demonstrated that only 9% of 92 such patients attained good outcomes [30] . A unilaterally dilated pupil with or without evidence of ipsilateral cranial nerve (CN) III paralysis, such as ptosis or impaired ocular motility, may indicate impending herniation. Isolated internuclear ophthalmoplegia secondary to traumatic brainstem injuries has been described and has a relatively benign prognosis.[31] CN VI palsies may indicate raised intracranial pressure. CN VII palsy, particularly in association with decreased hearing, may indicate a fracture of the temporal bone. Hearing loss is also frequent with sensory neural loss occurring in 20-30% of patients with head injuries. Low-frequency loss typically improves after 1 year.[32] Dysphagia raises the risk of both aspiration and inadequate nutrition.[33] Focal motor findings may be manifestations of a localized contusion or, more ominously, an early herniation syndrome. Flexor or extensor posturing obviously implies extensive intracranial pathology or raised intracranial pressure. In the chronic phase, motoric manifestations typically include spasticity or, more unusually, akinesia and rigidity. Tremors and dystonia recede with time, but these still can affect as many as 12% of survivors of severe head injury 2 years after the initial trauma.[34] Although postural stability and balance depend on inputs from multiple components of the nervous system, impairments in sitting balance alone have been demonstrated to be predictive of poor functional abilities upon discharge from rehabilitation.[35] Primitive reflexes, despite their presence in some healthy elderly patients, are useful and when multiple can correlate with cognitive deficits.

Bedside cognitive testing

In the acute setting, measurements of the patient's level of consciousness, attention, and orientation are of primary importance. Aphasia obviously implicates localized pathology. Lucid intervals are not unusual. Of 838 patients with severe head injury in one study, 25% talked at some point between the trauma onset and their deterioration into coma. Although 81% of these patients had a focal lesion, 19% exhibited diffuse brain swelling, and approximately one third of these patients demonstrated coexistent subarachnoid hemorrhage or other nonfocal intracranial bleeding. Such diffuse swelling was much more likely in children and adolescents than adults.[36] Some patients acutely recovering from head trauma demonstrate no ability to retain new information. This inability to lay down new memories after a head injury originally was labeled posttraumatic amnesia. The patient's subjective estimate of his or her first recollection of events following the head injury defined the termination of this period. These subjective estimates have yielded in recent years to prospective serial mental status assessments. These mental status assessments have validated the prognostic value of the duration of posttraumatic amnesia; patients with longer durations of posttraumatic amnesia have poorer outcomes.[37] More recent work has suggested that posttraumatic amnesia is somewhat of a misnomer. Because severe inattention in the postinjury state primarily prevents retention of new information, "posttraumatic confusional state" may be a more accurate descriptor.[38] In the long-term setting, bedside cognitive tests are employed to help distinguish damaged and spared realms of cognitive functioning. Even though most of these tests are not quantitative, they readily provide the examiner with immediate information to help in diagnosis and therapy. One standardized test that can be administered easily is the Mini-Mental State Examination. Although this test disproportionately emphasizes left hemisphere functioning, one study has documented that 23% of patients with mild head injuries score less than 24 out of 30 points when assessed with this instrument 1 year after injury.[39] Although all cognitive domains should be assessed, the investigation of frontal or executive systems assumes even greater importance in the long-term setting. While examining mnemonic, visual spatial, and language functioning, the quality of the patient's responses, whether perseverative or impulsive, socially
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Head Injury Clinical Presentation

sanctioned or grossly inappropriate, is also important to observe and document. Motor regulation can be assessed rapidly using the Luria "fist, chop, slap" sequencing task. An antisaccade task, in which the patient looks away from the offered visual stimulus, recently has been shown to be impaired in patients with symptomatic brain injury compared to controls, although the sensitivity of this test in detecting brain injury has been questioned.[40] Letter fluency, in which the patient names as many words as possible beginning with a specific letter in 1 minute, and category fluency, in which the patient names as many items as possible in a certain category in 1 minute, provide further information about self-generative frontal processes. An untimed Trails B test, in which the patient alternates between number and letter sequences, allows further qualitative testing of frontal functioning. Be cautious in overinterpreting this or any single test. Malingerers have been shown to fake performance errors on the Trails B.[41]

Causes
Road accidents involving motor vehicle drivers and occupants, cyclists, and pedestrians are the main risk factor for head injuries. Assaults in economically depressed regions and during wartime are other major risk factors. Athletic participation, especially football and soccer, is another important cause of these injuries. Falls cause head injuries in elderly patients and children, occasionally with catastrophic results. The incidence of fall-related traumatic brain injury has been increasing in the United States and in 2005 resulted in 7,946 deaths and 56,423 hospitalizations in the elderly.[42] Blast injuries from incendiary devices can cause head trauma and primarily occur in soldiers, although even civilian tire explosions have been implicated.[43] While the energy from the blast can directly impact the cranium and be transferred to the brain, some researchers have hypothesized that systemic blood vessels may actually transmit the shock waves.[44] Current clinical studies, however, have failed to identify a unique pattern of neuropsychologic deficits in patients who have incurred such blast injuries.[45] Anticoagulants and antiplatelet medications, such as aspirin, raise the risk of intracranial bleeding with even trivial head injuries.[46] For example, among elderly patients with head injuries, clopidogrel use has been associated with a 15 times greater mortality compared with patients not taking antithrombotics.[47] Alcohol use raises the risks of incurring a head injury. Perhaps because it may impede excitotoxicity, alcohol use at the time of injury may decrease the likelihood of a poor outcome. A newer study of intentional head injuries reported that patients consuming alcohol had higher initial GCS scores.[24] Another study of patients with apparently trivial injuries (patients either were found down or fell from heights < 10 ft) found that outcomes were better in patients who were severely intoxicated (blood alcohol levels >200 mg/dL). Methamphetamine use has also been shown to reduce mortality in severe head injury.[48] More recently, patients with severe brain injuries and high blood alcohol levels ( 0.08 mg/L) exhibited a significantly lesser mortality compared with patients with lower levels or the absence of alcohol in their blood.[49] Although the presence of APOE4 alleles is not an established risk factor for head injury, the presence of even one of these alleles increases the risk of a poor outcome. Patients who are homozygous or heterozygous for the APOE4 allele have an almost 14-times greater likelihood of a poor outcome after head injury than those with other APOE genotypes.[50] Similarly, football players and boxers with an APOE4 allele are at greater risk for posttraumatic cognitive problems than APOE4 -negative athletes.[51] Other studies have called these APOE4 associations into question, but a 2008 meta-analysis has supported these observations.[52] Genes regulating the interleukin, dopamine, and apoptotic systems as well as genes associated with angiotensin converting enzyme and calcium channel polymorphisms have all been implicated in head injury outcomes.[53] Other genetic determinants of head injury will undoubtedly surface with further research.

Contributor Information and Disclosures

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Author David A Olson, MD Clinical Neurologist, Dekalb Neurology Associates, Decatur, Georgia David A Olson, MD is a member of the following medical societies: American Academy of Neurology Disclosure: Nothing to disclose. Specialty Editor Board Joseph Carcione Jr, DO, MBA Consultant in Neurology and Medical Acupuncture, Medical Management and Organizational Consulting, Central Westchester Neuromuscular Care, PC; Medical Director, Oxford Health Plans Joseph Carcione Jr, DO, MBA is a member of the following medical societies: American Academy of Neurology Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Florian P Thomas, MD, MA, PhD, Drmed Director, Regional MS Center of Excellence, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, and Sigma Xi Disclosure: Nothing to disclose. Chief Editor Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and Phi Beta Kappa Disclosure: Nothing to disclose.

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