Chronic pain/dysfunction in whiplash-associated disorders.
OBJECTIVE
The purposes of this article are (1) to review current knowledge of and recent concepts pertaining to the causes of chronic pain and/or dysfunction following whiplash-type injuries and (2) to acquaint those who treat these types of injuries with possible mechanisms of continued pain and or dysfunction following whiplash.


METHODS
A review of the literature on mechanisms of injury and neurologic considerations was undertaken. A hand search of relevant medical, neuroscience, chiropractic, and online Index Medicus sources and other sources involving mechanisms of nociception, neurotransmitters, and receptors that might evolve from whiplash-type soft tissue injuries was conducted.


RESULTS
Pain is a complex phenomenon that has great variability. Chronic pain appears to involve a deficient descending inhibitory process and/or ongoing excitatory input.


CONCLUSIONS
There is a wide variety of reactions by individuals to any given type of stimulus. Injury may lead to increases in neuronal activity and prolonged changes in the nervous system. Chronic pain may be seen as part of a central disturbance accompanied by disinhibition or sensitization of central pain modulation, mirrored in the immune and endocrine systems. Patients with chronic whiplash syndrome may have a generalized central hyperexcitability from a loss of tonic inhibitory input (disinhibition) and/or ongoing excitatory input contributing to dorsal horn hyperexcitability. Dysfunction of the motor system may also occur, with or without pain. The purpose of treatment should be not only to relieve pain but also to allow for proper proprioception.
Davis
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D006801:Humans; D008349:Manipulation, Orthopedic; D018377:Neurotransmitter Agents / Q000502:physiology; D010146:Pain / Q000209:etiology*; D014911:Whiplash Injuries / Q000209:etiology / Q000503:physiopathology / Q000628:therapy
D018377:Neurotransmitter Agents