CommentaryThe fascination of complex regional pain syndrome
Section snippets
Experimental neuritis and impulse activity in afferent and efferent (sympathetic) fibers
In a recent issue of Experimental Neurology, Dr. Bove (Bove 2009) puts forward the interesting idea that focal nerve inflammation leads to changes in activity in small diameter afferent neurons (conduction velocity < 4 m/s) and in postganglionic neurons and that these changes in neural activity are responsible for signs of early complex regional pain syndrome (CRPS). He applied complete Freund's adjuvant to the sciatic nerve in rats generating a perineuritis (see Bove et al., 2003). In
The idea
Notwithstanding my concerns about some of the data, the idea about the potential mechanisms underlying the generation of early CRPS is interesting. Dr. Bove argues that the neuritis-induced changes could explain some of the changes observed in patients with CRPS:
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Ongoing pain as a consequence of ongoing activity in small diameter afferents, projected particularly into the deep somatic tissues. This ongoing activity could also be responsible for maintaining the central sensitization of dorsal
Implications for understanding the mechanisms underlying CRPS
We learn from the experiments of Dr. Bove and colleagues, and hopefully will continue to learn in the future (see above), that peripheral neuritis could be a mechanism to start and maintain the early signs of CRPS. Such a hypothetical mechanism is completely compatible with the idea that CRPS is a disorder of the central nervous system (Jänig and Baron, 2002, Jänig and Baron, 2003). Taking the caveats and concerns I have raised above into consideration, Dr. Bove's data could explain some
Conclusions
By mentioning these observations based on quantitative measurements on CRPS patients, I want to emphasize that we have to be very careful about trying to reduce this enigmatic pain disorder to a peripheral pathophysiological process. I think that this was not the intention of Dr. Bove. Two reviews published recently tend to argue that CRPS is primarily a small-fiber neuropathy (Oaklander and Fields 2009) or an inflammatory disease (de Mos et al., 2009). I believe that the peripheral changes
Acknowledgments
Supported by the Deutsche Forschungsgemeinschaft. I thank Elspeth McLachlan for her comments.
References (53)
- et al.
Intradermal injection of norepinephrine evokes pain in patients with sympathetically maintained pain
Pain
(2000) - et al.
Relation between sympathetic vasoconstrictor activity and pain and hyperalgesia in complex regional pain syndromes: a case-control study
Lancet
(2002) Focal nerve inflammation induces neuronal signs consistent with symptoms of early complex regional pain syndromes
Exp. Neurol.
(2009)- et al.
Impaired self-perception of the hand in complex regional pain syndrome (CRPS)
Pain
(2004) - et al.
Complex regional pain syndrome: mystery explained?
Lancet Neurol.
(2003) - et al.
Experimental approach to CRPS
Pain
(2004) - et al.
Is CRPS I a neuropathic pain syndrome?
Pain
(2006) - et al.
Organization of the sympathetic innervation supplying the hairless skin of the cat's paw
J. Auton. Nerv. Syst.
(1981) - et al.
Altered central sensorimotor processing in patients with complex regional pain syndrome
Pain
(2002) - et al.
Body perception disturbance: a contribution to pain in complex regional pain syndrome (CRPS)
Pain
(2007)