In the last two decades many has been published on whiplash injury, which is sometimes looked upon as an accident causing extensive symptomatology without the presence of objective findings. Diagnostics of the late whiplash syndrome is an even more challenging endeavour. So far, functional neuroimaging was rarely utilized in contrast to morphological imaging tools, the latter being inconspicuous in most cases, the first showing significant deficits mainly in the posterior parietal occipital region, as first described in 1995 from Otte et al. with perfusion single-photon emission tomography (SPET) to be followed by some other groups and imaging devices (e.g., Freitag et al., 2001; Lass and Lyczak, 2004).
In this scenario, we were intrigued by the work of Linnman et al. (2009), who found elevated regional cerebral blood flow (rCBF) bilaterally in the posterior parahippocampal and the posterior cingulate gyri, in the right thalamus and the right medial prefrontal gyrus as well as lowered rCBF in the temporo-occipital regions compared to healthy volunteers. One point in the authorś discussion is, however, rather misleading: Never have we stated that our hypoperfusion in the posterior parietal occipital region (which is matching the hypoperfusion reported by Linnman et al. (2009)) is caused by contusion as they write in their discussion section: we always followed the Moskowitz hypothesis in this region with nociceptive afferents causing increased levels of vasopeptides triggering vasoconstriction in the posterior watershed region (Moskowitz and Buzzi, 1991).
To test the hypothesis of nociceptive afferences versus contusion mechanism, we also had re-evaluated our large group of whiplash patients scanned with perfusion SPET and from this identified 15 whiplash-injured drivers who all could remember that they looked to the right side when the rear-end car collision happened (Otte et al., 1998). Ten of the 15 patients reported that they had hit their heads on the steering wheel, the other five could not remember. In statistical parametric mapping, the whiplash patients revealed a significant hypoperfusion in the posterior parietal occipital region of both hemispheres and in the left frontal region (Fig. 1). As the patients looked to the right side during the accident, a contusion mechanism could be discussed for the left frontal and the right posterior parietal occipital region, regardless if this was produced directly by hitting the head to the steering wheel or by the acceleration forces producing indirect head impact. If whiplash injury only was a form of mild head injury with a contusion mechanism, the additional left posterior parietal occipital hypoperfusion in the above patients could not be explained. This analysis, even more, supports the aforementioned Moskowitz hypothesis in whiplash pain syndrome.