Table 5

Studies suggesting central sensitisation is a cause of WAD

First AuthorYear PublishedStudy DesignSummary of FindingsLevel of Study
Borchgrevink1997X-sectional case-controlNo significant alterations in CNS morphology identifiedB
Radanov1999X-sectional cohortNo alterations in CNS perfusion by PET or SPECT scanC
Freitag2001X-sectional case-controlSignificant decrease in BOLD signal in symptomatic patients vs. asymptomatic patients and controlsB
Lorberboym2002X-sectional cohortRegional CNS perfusion abnormalities by SPECT in 13/20 WAD patientsC
Sundstrom2006X-sectional case-controlNo significant changes in WAD group, while non-traumatic neck pain group showed significant altered rCBF pattern compared to controlsB
Sturzenegger2008X-sectional case-controlNo difference in ventricle-brain ratio between WAD patients and healthy controlsB
Obermann2009X-sectional case-controlSignificant decreases in ACC and dorsolateral DLPFC at 3 mo.; resolved by 1 yB
Linnman2009X-sectional case-controlRegional CNS perfusion increases & decreases by PET scanB
Linnman2010X-sectional case-controlAvailability of a pain processing (NK1) receptor was decreased in WAD patientsB
Bakhtadze2012X-sectional cohortParietal and frontal perfusion decreased with increased levels of painC

Tomography, BOLD: Blood-Oxygen-Level-Dependent imaging, rCBF: regional Cerebral Blood Flow, ACC: Anterior Cingulate Cortex, DLPFC: Dorsolateral Prefrontal Cortex, NK1: Neurokinin receptor 1, WAD: Whiplash-associated disorder

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