Pain. 2003 (Aug); 104 (3): 509–517 ~ FULL TEXT
Michele Sterling, Gwendolen Jull, Bill Vicenzino, Justin Kenardy
The Whiplash Research Unit,
Department of Physiotherapy,
The University of Queensland,
Brisbane 4072, Australia.
Hypersensitivity to a variety of sensory stimuli is a feature of persistent whiplash associated disorders (WAD). However, little is known about sensory disturbances from the time of injury until transition to either recovery or symptom persistence. Quantitative sensory testing (pressure and thermal pain thresholds, the brachial plexus provocation test), the sympathetic vasoconstrictor reflex and psychological distress (GHQ-28) were prospectively measured in 76 whiplash subjects within 1 month of injury and then 2, 3 and 6 months post-injury.
Subjects were classified at 6 months post-injury using scores on the Neck Disability Index: recovered (<8), mild pain and disability (10-28) or moderate/severe pain and disability (>30). Sensory and sympathetic nervous system tests were also measured in 20 control subjects. All whiplash groups demonstrated local mechanical hyperalgesia in the cervical spine at 1 month post-injury. This hyperalgesia persisted in those with moderate/severe symptoms at 6 months but resolved by 2 months in those who had recovered or reported persistent mild symptoms. Only those with persistent moderate/severe symptoms at 6 months demonstrated generalised hypersensitivity to all sensory tests. These changes occurred within 1 month of injury and remained unchanged throughout the study period.
Whilst no significant group differences were evident for the sympathetic vasoconstrictor response, the moderate/severe group showed a tendency for diminished sympathetic reactivity. GHQ-28 scores of the moderate/severe group were higher than those of the other two groups. The differences in GHQ-28 did not impact on any of the sensory measures. These findings suggest that those with persistent moderate/severe symptoms at 6 months display, soon after injury, generalised hypersensitivity suggestive of changes in central pain processing mechanisms. This phenomenon did not occur in those who recover or those with persistent mild symptoms.