head injury clinical presentation
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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 sitt ing 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 somepoint 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 durationof posttraumatic amnesia; patients with longer durations of postt raumatic amnesia have poorer
outcomes.[37]
More recent work has suggested that posttraumatic amnesia is somewhat of a misnomer. Because
severe inattention in the postinjury s tate 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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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 ofAPOE4 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 theAPOE4 allele have an almost 14-times
greater likelihood of a poor outcome after head injury than those with otherAPOEgenotypes.[50]
Similarly, football players and boxers with anAPOE4 allele are at greater risk for posttraumatic
cognitive problems thanAPOE4 -negative athletes.[51]
Other studies have called theseAPOE4 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 HealthPlans
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 VeteransAffairs Medical Center; Director, National MS Society Multiple Sc lerosis 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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