Head Injury Workup
- Author: David A Olson, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA more...
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Alterations in serum sodium levels are critical and occur in as many as 50% of comatose patients with head injuries. 
- Hyponatremia may be due to the syndrome of inappropriate antidiuretic hormone (SIADH) or cerebral salt wasting. Both syndromes involve decreased serum sodium level in the face of increased urinary sodium losses.
- Unlike SIADH, in which the patient is euvolemic, cerebral salt wasting typically occurs with volume depletion and is caused by the release of a natriuretic hormone. Some researchers suggest that this natriuretic hormone can be measured readily in the serum because it binds to digoxin antibodies and produces a false-positive test for digoxin in patients who are not receiving this medication.
- Elevated sodium levels in head injury indicate simple dehydration or diabetes insipidus.
Magnesium is depleted in the acute phases of both minor and severe head injuries.
- Because this cation blocks the excitotoxic response and functions as an antioxidant, careful monitoring of magnesium may improve outcomes.
- Early administration of magnesium has attenuated experimental brain injury in rats.
Coagulation studies, including prothrombin times (PT), activated partial thromboplastin times (aPTT), and platelet counts, are important to exclude a coagulopathy. A limited trauma-induced coagulopathy as evidence by prolonged PT levels has been found in patients hospitalized for head injury, but PT levels return to normal after 12 hours and the clinical importance of this prolongation is currently unclear. 
Blood alcohol levels and drug screens are important because positive results may help explain subnormal levels of consciousness and cognition in some patients with head trauma.
Obtain renal function tests and creatine kinase levels to help exclude rhabdomyolysis if a crush injury has occurred or marked rigidity is present.
Elevated serum levels of neuron-specific enolase and protein S-100 B obtained within 24 hours of head injury have been demonstrated to correlate with persistent cognitive impairment at 6 months in patients with severe or mild head injuries.  Neuron-specific enolase and S-100 B elevations have even been correlated with frequent "headings" of balls during soccer playing.  Unfortunately, even vigorous soccer training alone increases serum S-100 B as much as playing and heading does, calling into question the specificity of S-100 B as a biomarker of head injury.  Finally, recent research on patients with mild closed head injuries has found that although increased glial fibrillary acid protein (GFAP) levels correlated with abnormal neuroimaging, both GFAP and S100B failed to significantly correlate with clinical outcomes. 
Computerized tomography (CT) is the main imaging modality used in the acute setting.
Controversy exists as to whether all patients with mild head injuries should have neuroimaging. In general, patients with any loss of consciousness should undergo CT scanning.
Some researchers have established clinical criteria to identify those patients who are most likely to have abnormal scans. For example, in a group of 909 consecutive patients who had experienced a mild head injury with a transient loss of consciousness, yet scored a full 15 on their initial GCS, all 57 (6%) patients with abnormal CT scans were identified by the presence of any one of the following clinical features: age older than 60 years, headaches, vomiting, alcohol or drug intoxication, trauma above the clavicles, memory problems, or seizures. More complicated criteria have been invoked to predict abnormal head CT scans even without loss of consciousness; however, these rules are cumbersome. Further validation of such imaging rules is needed.
Repeat CT is needed, of course, when clinical deterioration occurs. The need for routine repeat head CT is unclear. A 2006 multistudy review found neurosurgical interventions resulting from a repeat CT scan occurred in 0-54% of patients.
In addition, emergent brain imaging may be performed for nonmedical reasons. A 10-year study of elderly women with closed head injuries revealed that in general, emergency department physicians who practice in states with tort reform laws ordered significantly less neuroimaging studies than those physicians who practice in states without such legislation.
See the images below.
Magnetic resonance imaging (MRI) is typically reserved for patients who have mental status abnormalities unexplained by CT scan findings. MRI has been demonstrated to be more sensitive than CT scanning, particularly at identifying nonhemorrhagic diffuse axonal injury lesions.
MRI imaging has shown degeneration of the corpus callosum following severe head injuries with axonal damage in adults and children.
Furthermore, increased total lesion volume on fluid-attenuated inversion-recovery (FLAIR) MRI images has been demonstrated to correlate with poor clinical outcomes as well.
Remember that white matter hyperintensities in patients with head trauma may recede when initial MRI scans are compared with those obtained in the months following the injury.
See the image below.
Diffusion tensor imaging may document axonal pathologies in patients with head injury even when conventional MRI scans are unremarkable. For example, diffusion tensor imaging has identified impaired water diffusion indicating white matter tract disruption in patients with mild head injuries whose MRI scans were normal. Cortical projection fibers were frequently abnormal, and using an innovative fiber tracking methodology, actual disruption of cortical projection fibers could be visualized in 19% of fiber groups studied. Similarly, attention impairments in patients with mild head injuries have recently been correlated with diffusion abnormalities in cortical projection fibers.
Functional imaging and MRI spectroscopy may have eventual clinical utility. At present, they are promising research tools.
Behavioral disorders, memory, and executive dysfunction correlated with abnormalities of cingulate gyrus metabolism in 13 patients with severe head injuries who underwent resting 18F-fluorodeoxyglucose positron emission tomographic (PET) imaging and a battery of neuropsychological tests. A more recent study found that while only 34% of CT results were abnormal in 92 patients with mild head injury, 63% of SPECT results demonstrated regions of hypoperfusion within 72 hours of the trauma. Frontal hypoperfusion predominated in adults.
Proton magnetic resonance spectroscopy of frontal white matter that appears normal on MRI has shown a decrease in neuronal N-acetylaspartate spectra in patients with mild head injuries indicating aberrant metabolism.
EEG is of limited usefulness in patients with head injuries.
Although certain EEG patterns may have prognostic significance, considerable interpretation is needed, and sedative medications and electrical artifacts are confounding.
The most useful role of EEG in head injuries may be to assist in the diagnosis of nonconvulsive status epilepticus. In a landmark study of continuous EEG monitoring in patients hospitalized with traumatic brain injury, convulsive and nonconvulsive seizures were seen in 22%.  A 2012 study reported that severe slowing on continuous EEG monitoring related to delta waves or burst suppression patterns is associated with poor outcomes at 3 and 6 months in patients with traumatic brain injuries. 
A meta-analysis of the prognostic ability of somatosensory evoked potentials in predicting outcomes in patients with severe brain injuries examined 44 studies and found that if patients with focal lesions, recent decompressive craniotomies, or subdural and extradural fluid collections were excluded, bilaterally absent somatosensory evoked potentials correctly predicted unfavorable outcomes in 99.5% of patients. 
Although a comprehensive discussion of the histology of traumatic brain injury is beyond the scope of this article, several important newer immunohistochemical techniques have further elucidated the pathophysiology of brain injury.
Beta-amyloid precursor protein is made in the neuron and transported to the axon. The shear forces incurred in head injury damage the axon and beta-amyloid accumulates proximal to the injury. Special immunohistochemical stains for this substance have detected beta-amyloid accumulation as early as 35 minutes after severe head injuries in humans. 
As mentioned previously, apoptosis (programmed cell death) is initiated in brain trauma and may account for delayed loss of functioning. Using a combination of enzymatic and immunohistochemical marking, the DNA fragmentation accompanying apoptosis has been documented in human trauma patients and occurs from 2 hours to 12 days after the initial injury. 
Chronic repetitive head injuries in athletes results in a tauopathy, which was previously known as dementia pugilistica (it is not confined to boxers alone). Tau reactive neurofibrillary tangles and astrocytic tangles accumulate primarily in the frontal and temporal cortices in irregular patches, preferentially occupying the depths of sulci. 
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