From: Pain. 2010 Jun 29. [Epub ahead of print]
Widespread sensory hypersensitivity is present in acute whiplash and is associated with poor recovery. Decreased nociceptive flexion reflex thresholds (spinal cord hyperexcitability) are a feature of chronic whiplash but have not been investigated in the acute to chronic injury stage. This study compared the temporal development of sensory hypersensitivity and nociceptive flexion reflex responses from soon after injury to either recovery or to transition to chronicity. It also aimed to identify predictors of persistent spinal cord hyperexcitability. Pressure and cold pain thresholds, nociceptive flexion reflex responses (threshold and pain VAS) were prospectively measured in 62 participants at <3 weeks, 3 and 6 months post whiplash injury and in 22 healthy controls on two occasions a month apart. Pain levels and psychological distress (GHQ-28; IES) were measured at baseline. Whiplash participants were classified at 6 months post-injury using the Neck Disability Index: recovered (8%), mild pain and disability (10-28%) or moderate/severe pain and disability (30%).
All whiplash groups demonstrated spinal cord hyperexcitability (lowered nociceptive flexion reflex thresholds) at 3 weeks post-injury. This hyperexcitability persisted in those with moderate/severe symptoms at 6 months but resolved in those who recovered or reported lesser symptoms at 6 months. In contrast generalized sensory hypersensitivity (pressure and cold) was only ever present in those with persistent moderate/severe symptoms and remained unchanged throughout the study period. This suggests different mechanisms underlie sensory hypersensitivity and nociceptive flexion reflex responses. In multivariate analyses only initial Neck Disability Index scores were a unique predictor of persistent spinal cord hyperexcitability indicating possible ongoing peripheral nociception following whiplash injury.
Related citations
In Pain. 2003 Aug;104(3):509-17. Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery. The conclusion states, “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.”
In Clin J Pain. 2008 Feb;24(2):124-30. Psychologic factors are related to some sensory pain thresholds but not nociceptive flexion reflex threshold in chronic whiplash. The discussion states, “We have demonstrated that psychologic factors have some association with sensory hypersensitivity (cold pain threshold measures) in chronic whiplash but do not seem to influence spinal cord excitability. This suggests that psychologic disorders are important, but not the only, determinants of central hypersensitivity in whiplash patients.”
In Phys Med Rehabil Clin N Am. 2006 May;17(2):287-302. Central hypersensitivity in chronic pain: mechanisms and clinical implications. It is stated, “Treatment strategies for central hypersensitivity in patients have been investigated mostly in neuropathic pain states. Possible therapy modalities for central hypersensitivity in chronic pain of musculoskeletal origin are largely unexplored. The limited evidence available and everyday practice show, at best, modest efficacy of the available treatment modalities for central hypersensitivity. The gap between basic knowledge and clinical benefits remains large and should stimulate further intensive research.”
In BMC Musculoskelet Disord. 2010 Feb 9;11:29. Minimizing the source of nociception and its concurrent effect on sensory hypersensitivity: an exploratory study in chronic whiplash patients. It was concluded, the patients with chronic whiplash associated disorders showed evidence of widespread sensory hypersensitivity to mechanical and thermal stimuli. The whiplash associated disorders group revealed decreased sensory hypersensitivity following a decrease in their primary source of pain stemming from the cervical zygapophyseal joints.
