Dr Radanov is to be commended in taking a stance on purported brain damage occurring as a result of whiplash ( 2002;44(6):303-306 [9]). I would like to take this opportunity to add some further comments.

The main “evidence” put forward by advocates of whiplash brain injury is that afterwards there are abnormal neuropsychological symptoms and test findings which, however, are non-specific and are not peculiar to traumatic brain injury.[1] The same test results are obtained in depression and chronic pain,[1,2] one or both of which are customary in chronic whiplash. Other confounding variables producing mental distractibility include insomnia and medication effects.

CT or MRI correlates of whiplash brain injury comparable to those in mild contact brain trauma have not been published. Positron emission tomography (PET) findings after whiplash are not those of brain injury, but depression.[3,4]

Brain injury without head contact has been demonstrated experimentally in non-human primates rendered comatose and in harnessed pilots crashing in military aircraft in which the head may decelerate from a velocity of hundreds of kilometres per hour to zero in fractions of a second—the cranium may never contact a solid object, yet the brain is irreversibly damaged.[5] Non-contact forces acting on the brain are very different in everyday circumstances of jolting whiplash injury without a head blow. Rear-end vehicle collisions produce acceleration forces to the human head that are far lower than the calculated necessary threshold for cerebral injury to occur—that threshold is about 100 g or more,[5] depending on how long the force is applied.

In a series of neuropathological examinations of more than 400 road users fatally injured without receiving head impact, McLean[6] found no examples of brain injury.

Very rare instances of delayed subdural hematoma sustained in rear-end accidents have been documented in the literature,[7] ostensibly from tearing of bridging veins. However, there are no histological or biochemical data that would support a concept of primary injury to the brain parenchyma happening without a direct head blow in mature human subjects in everyday life.

Any unbiased physician familiar with the medical literature will come to the reasonable conclusion that traumatic brain injury without head contact is so rare that it is almost never seen in the clinical setting. For a more detailed appraisal the reader is referred to a review article[8] not referenced by Dr Radanov.

—P.M. Rees, MD
Burnaby

References

1. Taylor AE, Cox CA, Mailis A. Persistent neuropsychological deficits following whiplash: Evidence for chronic mild traumatic brain injury? Arch Phys Med Rehabil 1996;77:529-535. PubMed Abstract [10] 
2. Dikmen SS, Machamer JE, Winn R, et al. Neuropsychological outcome at one-year post head injury. Neuropsychology 1995;9:80-90.  
3. Bicik I, Radanov BP, Schafer J, et al. PET with 18fluorodeoxyglucose and hexamethylpropylene amine oxime SPECT in late whiplash syndrome. Neurology 1998;51:345-350.PubMed Abstract [11] 
4. Dolan RJ, Bench CJ, Brown RG, et al. Neuropsychological dysfunction in depression: The relationship to regional cerebral blood flow. Psychol Med 1994;24:849-857. PubMed Abstract [12] 
5. Head Injury. Reilly P, Bullock R (eds). London: Chapman and Hall Medical, 1997. Full Text [13] 
6. McLean AJ. Brain injury without head impact. J Neurotrauma 1995;12:621-625. PubMed Citation [14] 
7. Ommaya AK, Yarnell P. Subdural hematoma after whiplash injury. Lancet 1969 Aug 2;2(7614): 237-239. PubMed Citation [15] 
8. Alexander MP. In the pursuit of proof of brain damage after whiplash injury. Neurology 1998;51:336-340. PubMed Citation [16]