Purports of brain damage following presumed whiplash injury

Mild traumatic head injury, with or without direct impact to the head, is a possible consequence of an acceleration-deceleration mechanism of injury (whiplash).[1] Patients may present without a history of significant loss of consciousness and may not demonstrate any short-duration superficial loss of consciousness. Although there may be numerous short-lasting (days) somatic, psychological, or cognitive symptoms following mild whiplash trauma,[1-4] a tissue damage cause, and a basis on which these symptoms may be demonstrated over a prolonged period of time (months), is a matter of controversy. Probably the most prominent debate concerns the very notion that whiplash trauma can lead to any physical brain damage.[5,6]

Patients who purport to have suffered mild traumatic brain injury as a result of a whiplash-type mechanism usually show normal findings on physical, neurological, and/or MRI examination.[1,4,7] But these are not conclusive tests. For this reason functional examinations such as neuropsychological testing and/or neuroimaging studies such as positron emission tomography (PET) or single photon emission computerized tomography (SPECT) may be expected to provide conclusive evidence of brain damage. Such tests, if positive in demonstrating disturbed function of brain structures, should also correlate to psychological or cognitive symptoms before a presumption of traumatic brain damage can be made.

Localization of trauma-induced cognitive impairment

In a proportion of individuals who had suffered whiplash trauma, the principal cognitive impairment was identified within the complex of attentional processing (i.e., concentration, attention, or working memory).[8-9] Could this be due to physical brain damage? Several experimental studies have shown that for unimpaired complex attentional processing, an intact prefrontal cortex is necessary.[10-12] Based on this, if brain damage is the basis of impaired cognitive functioning following mild whiplash trauma, there should be positive neuroimaging findings in the rostral brain areas (frontal or temporal pole, prefrontal cortex).

Brain damage and whiplash

Animal experiments have shown that the likelihood of brain damage following whiplash-type trauma, without direct head impact, will mainly depend on the magnitude of acceleration-deceleration forces and the rotation forces acting upon the skull.[13,14] However, there was not a linear relationship between acceleration-deceleration forces and the size of brain damage.[15] In addition, it was proposed that rotation of the skull is an essential element in the forces that might provoke loss of consciousness.[13] Accordingly, in the clinical assessment of unconsciousness, the most important indicator of possible brain damage is the severity of the trauma. Minor trauma is an unlikely candidate.

Both in experimental research with animals and in postmortem studies with patients who had previously suffered whiplash-like trauma, but died because of a different reason, morphological lesions were found primarily in the periphery of rostral brain areas. The distribution of rostral lesions was observed almost proportionately from the periphery to more central parts of the brain, with the greater traumatic effects being inflicted upon the periphery. Consequently lesions of more central parts of the brain may be expected only in quite severe trauma in which lesions to the periphery will also occur.[14] Based on the tangential acceleration effects caused by a rotation of the skull, a peripheral shearing effect upon brain tissue may occur, which may lead to a diffuse axonal injury that is more profuse at the periphery.[16,17] This may be explained as follows: due to shearing, neurons and small vessels may rupture. Following rupture of neurons, intracellular substances such as the excitatory neurotransmitter glutamate will be released into the intercellular space. Glutamate will lead to an excitation of the additional neurons near the site of primary lesion, which may be excited to death (so-called excitotoxicity).[18] This may lead to a kind of chain reaction that induces death of neurons not primarily damaged by the trauma; for this reason diffuse axonal injury is not limited only to the immediate site of initial damage, but may also include other nearby tissue.

It may be assumed that the rupture of neurons may result in a time-limited interruption of the neuronal network, which may explain loss of consciousness in patients following head trauma. It may be considered that the duration and depth of unconsciousness, including the phenomenon called post-traumatic amnesia, may depend on the extent of the damage (the size of disrupted neuronal network). Consequently, after any type of head or whiplash-type trauma, patients who did not lose consciousness for even a short duration, or suffer any short post-traumatic amnesia, probably did not suffer a diffuse axonal injury.[19] Accordingly in these cases, brain damage could not be observed using neuroimaging (PET or SPECT), nor could be assumed on the basis of cognitive deficits.

Neuropsychological and neuroimaging following whiplash

In the region where diffuse axonal injury occurred, changes in tissue metabolism may be expected, and glucose, the most important energy source of the brain, will no longer be utilized.[20] In contrast, brain areas that are still active—such as the speech area during vocalization—will require more energy. In addition, the energy requirements in the brain tissue are highly correlated to tissue perfusion.[21] Accordingly, in the brain tissue where damage has occurred, both diminished glucose metabolism and perfusion should be observed. In a living organism, brain glucose metabolism may be assessed using 18-fluorodeoxyglucose with PET, whereas tissue perfusion may be evaluated using 99Tc-Hexamethylpropylenaminoxim (HMPAO) with SPECT. As a cautionary note, both methods show considerable interindividual variations based on functional status (such as whether the person is vocalizing, the person’s age,[22] and whether the person is anxious or depressed).[23] Furthermore, it has been demonstrated that cognitive problems during the course of a depression may be observed by functional neuroimaging (PET).[24] The latter should be considered while assessing patients following whiplash trauma who may demonstrate changes in emotional functioning.[4]

In some previous studies in patients who suffered a whiplash trauma, significant reductions in both metabolism and perfusion were found bilaterally in the parieto-occipital regions.[5,6] This was initially presumed to be evidence of brain damage. However, the above localization of test anomalies was found in regions of the brain that previously were not considered important for complex functional attention. Although impaired complex functional attention has been observed following whiplash trauma,[8,9] lesions in the parieto-occipital region were not identified.[13,16,17] In one study of post-whiplash patients, reductions of metabolism and perfusion in parieto-occipital regions were identified to reflect the thickness of cortex in these areas of the brain, and therefore reflected an anatomical variation of the morphologically unimpaired brain.[25] In this research, deficits of metabolism and perfusion were also demonstrated bilaterally in frontal pole and putamen. More important, in these same patients there were no significant correlations between scoring of functional attention and neuroimaging findings.[26] An additional study with patients after bona fide mild and moderate traumatic brain injury (loss of consciousness including post-traumatic amnesia less than 5 minutes) demonstrated perfusion deficits in frontal brain areas,[27] the same area as observed in animals and discussed above. Interestingly, in these patients, the observed frontal hypoperfusion was shown to improve at follow-up investigation,[27] which correlates to follow-up studies regarding attentional functioning in which improvement has also been observed over time.[28] These findings overall support the view that if or when impaired attentional functioning follows mild head or whiplash-type trauma, it may be based on a time-limited but fully reversible functional brain impairment; minor brain damage does not cause lasting dysfunction.

Summary

Experimental and clinical research has shown that the severity of the trauma is clearly correlated to the degree of the brain damage. A morphological brain lesion following whiplash-type trauma may be expected if the acceleration-deceleration forces achieved high magnitude. If this magnitude is achieved, lesions will primarily occur in the rostral brain areas (prefrontal cortex, frontal or temporal pole). Very high acceleration-deceleration forces may also lead to more diffuse lesions even in the deeper brain structures. The size of the lesion is in direct correlation to the duration of the loss of consciousness, the depth of coma, and the duration of post-traumatic amnesia. The basis of the impaired consciousness is likely due to diffuse axonal injury. Without significant loss of consciousness and peritraumatic amnesia, brain damage does not occur. Brain regions that are exposed to damage following acceleration-deceleration trauma are the prefrontal cortex, which is crucial for the more complex attentional functioning. Impairment of complex attentional processing may be observed to parallel the more severe trauma cases, so indicators of trauma severity (duration loss and depth of consciousness, post-traumatic amnesia) should be in a significant relationship to the clinical cognitive impairment and neuroimaging findings (PET). If these relationships cannot be established, factors other than brain damage (pain, adverse effect of medication, psychological or psychosocial problems) should be considered as the basis of complaints following purported whiplash trauma. Patients making claims of brain damage but without the prerequisite unconsciousness and peritraumatic amnesia should not be considered bogus; they are still patients, but their therapeutic approach is probably best focused on the psychological and behavioral aspects of their life.

Competing interests

None declared.

Bogdan P. Radanov, MD

Dr Radanov is an associate professor of psychiatry at the University of Berne, Switzerland.