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Cognitive Complaints After Whiplash

One of the major areas of debate in the whiplash literature in 1998 has been the issue of brain injury. Cognitive and attentional deficits after whiplash injury are fairly well recognized in the medical literature. The question is, however, not whether these symptoms exist but whether they are based on organic pathology of the brain or are secondary symptoms related to whiplash pain in general.

Some researchers, such as Kessels et al1 and Schmand et al2 (STR Volume 3, #3), have reported that the psychological symptoms of whiplash arise only after the patient experiences chronic pain. Bogduk et al3 reported that when the pain was alleviated in whiplash patients, the psychological symptoms vanished.

On the other hand, researchers such as Otte et al4 have repeatedly found that whiplash patients show brain abnormalities when they are tested with sensitive PET and SPECT scans. The source of these abnormalities has been postulated as a direct trauma related to the whiplash motion, or a secondary reaction related to altered nociception in the cervical spine.

In short, this is a new area of study, and one that has not yet been—and may not ever be—proven one way or the other.

Still, a new study5 from Swiss researchers provides some more information on the role of PET and SPECT scans on the brains of whiplash patients, and what abnormalities found on such tests mean.

This study performed SPECT, PET and MRI scans on 13 patients with "late whiplash syndrome" and 16 non-whiplash control subjects. The objectives were: "First, how does the cerebral metabolism of whiplash patients differ from that of healthy subjects? Second, can potential abnormalities be reliably demonstrated for individual patients? Third, what are the implications of potentially abnormal PET or SPECT findings?"

Clinically, 7 of 13 patients (54%) scored below normal on working memory, and 6 of 13 patients (46%) scored below normal on divided attention, indicating some kind of cognitive dysfunction.

Here is a summary of what the researchers found when they reviewed the imaging scans:

"In our study, significantly decreased FDG uptake in the putamen and the frontopolar and lateral temporal cortex was found among patients with persistent symptoms resulting from whiplash injury. An important issue is whether the abnormalities are of purely functional origin or whether there might be microscopic damage. This question cannot be answered with PET or SPECT imaging. Major structural damage as a possible cause was excluded at MRI. The hypometabolism in the pathologic areas could be explained through the presence of depression as indicated by the significant correlation with BDI. Hypometabolism in the frontopolar and lateral temporal cortex and the basal ganglia has been reported among patients with depression without whiplash injury. A significant correlation between BDI scores and FDG uptake was found in the frontopolar region but not in the putamen or the lateral temporal cortex. The frontopolar and lateral temporal areas with pathologically reduced FDG uptake seen in this study correspond to the ones found to have microscopic damage in experimentally induced mild head injury. Frontopolar and laterotemporal microscopic damage in the study group is therefore not excluded. In the putamen, however, microscopic damage seems unlikely, because experimental research has demonstrated that lesions in deeper brain structures may be expected only when high acceleration forces are used. An explanation for the reduced FDG uptake in the putamen might be decreased corticoputaminal input."

In short, the researchers found evidence of brain abnormalities—but they don't know what they represent. From the correlation between BDI scores (the Beck Depression Inventory used to diagnose depression) and areas of cerebral hypometabolism, the abnormalities may be caused by depression. But they may also be due to microscopic damage of the brain tissue itself—a condition provable only by autopsy. Furthermore, the researchers state that even if the abnormalities are due to brain tissue damage, this information provides little help, as treatments for this type of problem "are not yet defined." An editorial6 in the same issue of Neurology sums up the problem well: "At this moment, medical treatment of some of the psychological consequences (depression or anxiety) of whiplash or MTBI is a better developed science than the treatment of the neurologic consequences."
At this point, the researchers can only make one conclusion: something is happening in the brains of patients with chronic whiplash pain, but what exactly that may be is unknown. Therefore, such sophisticated imaging techniques like PET and SPECT scans are at present "of doubtful value in the routine evaluation of late whiplash syndrome."
[Side note: At the "International Symposium, Whiplash '98," this study was mentioned with the statement that it found that there were no signs of brain abnormalities in whiplash patients using PET or SPECT. This is not what the study reported, as we elucidated above. Professionals should be aware, however, that this misconception is out there and is likely to appear in litigation.]

  1. Kessels RPC, Keyser A, Verhagen WIM, et al. The whiplash syndrome: a psychophysiological and neuropsychological study towards attention. Acta Neurologica Scandinavica 1998;97:188-193.
  2. Schmand B, Lindeboom J, Schagen S, et al. Cognitive complaints in patients after whiplash injury: the impact of malingering. Journal of Neurology, Neurosurgery and Psychiatry 1998;64:339-343.
  3. Wallis BJ, Lord SM, Bogduk N. Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomized, double-blind, placebo-controlled trial. Pain 1997;73:15-22.
  4. Otte A, Goetze M, Mueller-Brand J. Statistical parametric mapping in whiplash brain: is it only a contusion mechanism? European Journal of Nuclear Medicine [Letter] 1998;25:306-312.
  5. Bicik I, Radanov BP, Schafer N, et al. PET with 18fluorodeoxyglucose and hexamethylpropylene amine oxime SPECT in late whiplash syndrome. Neurology 1998;51:345-350.
  6. Alexander MP. In the pursuit of proof of brain damage after whiplash injury. Neurology 1998;51:336-340.