Year: 2012
Type: article
Abstract: We were unclear in our wording in describing the manuscript entitled ‘Statistical parametric mapping in whiplash brain: is it only a contusion mechanism?’ by Otte et al. (1998). Already in the 1995 Lancet publication (Otte et al., 1995b), Otte et al. stated that ‘it is unlikely that parieto-occipital hypoperfusion in late whiplash syndrome is a sequel of direct brain injury’. We apologize for the miscitation and we appreciate the opportunity to set the record straight. Both data from Otte et al. (Otte et al., 1996,b, 1997a, 1998,b, 1997b) and our group (Linnman et al., 2009) indicate lower cerebral blood flow in posterior parietal occipital regions. We agree with Dr. Otte in that this is probably not caused by brain contusion. In addition to cerebral blood flow imaging, our patient cohort was also imaged with [11C] GR205171 positron emission tomography (PET) to investigate brain neurokinin 1 (NK1) receptor availability (Linnman et al., 2010), and [11C] D-deprenyl PET to investigate neck inflammation (Linnman et al., 2011). These studies indicated that whiplash patients had reduced NK1 receptor availability in the ventromedial prefrontal, insular and cingulate cortex, the hippocampus, amygdala and the periaqueductal grey area. Patients also had significantly higher uptake of [11C] D-deprenyl, a candidate marker for inflammation, in the regions around the spinous process of the second cervical vertebra, suggestive of local persistent peripheral tissue inflammation. Here we revisited our data in order to investigate if NK1 receptor availability was altered in the posterior parietal occipital region in whiplash patients. A region of interest analysis of the temporal, parietal and occipital lobes, with identical methods as in our original publication (Linnman et al., 2010), indicated that NK1 receptor availability was significantly reduced in the left middle occipital gyrus (MNIxyz −40, −82, −14, PFWE = 0.006), the right middle temporal gyrus (MNIxyz 52, −74, 10, PFWE = 0.001), the left superior temporal gyrus (MNIxyz −60, −62, 24, PFWE = 0.002) and the right superior temporal gyrus (MNIxyz 50, 20, −8, PFWE = 0.001). The results are illustrated in Figure 1. Significantly reduced neurokinin 1 receptor availability in whiplash-associated disorder (grade II) patients (n = 18) versus healthy controls (n = 18). Analysis was restricted to the temporal, occipital and parietal lobes, with results displayed on a template magnetic resonance imaging at p < 0.001 not corrected for multiple comparisons. These results add further detail to the original findings by Dr. Otte and colleagues, indicating that also NK1 receptor availability is compromised in posterior parietal, temporal and occipital regions. As none of our patients lost consciousness at the time of the accident, brain contusion is an unlikely cause of these alterations. Given the prominent role of the posterior parietal occipital region in the brains resting state network, further neuroimaging studies on whiplash-associated disorder are warranted. Clas Linnman received funding from the International Association for the Study of Pain early career award and Swedish Society for Medical research (SSMF). The work presented here was funded by unrestricted grants from the Länsförsäkringar Research Foundation, the Swedish research Council, the Uppsala University Amersham fund and Uppsala Imanet AB. Clas Linnman P.A.I.N. Group, McLean Hospital, Harvard Medical School, Belmont, MA, USA
Source: European Journal of Pain
Author: Clas Linnman
Institutions: Harvard University, McLean Hospital
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W1964310422