Commentary
The fascination of complex regional pain syndrome

https://doi.org/10.1016/j.expneurol.2009.09.023Get rights and content

Abstract

Complex regional pain syndrome (CRPS) is a pain disorder involving the somatosensory, the somatomotor and the sympathetic nervous systems. Based on experiments conducted by Bove (2009), it is suggested that changes in impulse activity in small-diameter afferents and postganglionic axons generated by neuritis can contribute to signs of early CRPS. The potential mechanisms involved are discussed. These mechanisms include the possibility that CRPS, a disorder of the central nervous system, may be caused by a nerve inflammation.

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:

  • (1)

    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)

  • MoseleyG.L.

    Graded motor imagery is effective for long-standing complex regional pain syndrome: a randomised controlled trial

    Pain

    (2004)
  • MoseleyG.L.

    Is successful rehabilitation of complex regional pain syndrome due to sustained attention to the affected limb? A randomised clinical trial

    Pain

    (2005)
  • RommelO. et al.

    Hemisensory impairment in patients with complex regional pain syndrome

    Pain

    (1999)
  • RommelO. et al.

    Quantitative sensory testing, neurophysiological and psychological examination in patients with complex regional pain syndrome and hemisensory deficits

    Pain

    (2001)
  • SittirachaT. et al.

    Evaluation of the effects of various additives on retrograde labelling by horseradish peroxidase applied to intact and transected hindlimb nerves of rat and rabbit

    Neurosci.

    (1986)
  • WeberM. et al.

    Facilitated neurogenic inflammation in complex regional pain syndrome

    Pain

    (2001)
  • BaronR. et al.

    Sympathetic and afferent somata projecting in hindlimb nerves and the anatomical organization of the lumbar sympathetic nervous system of the rat

    J. Comp. Neurol.

    (1988)
  • BlumbergH. et al.

    Direct evidence of neurally mediated vasodilatation in hairy skin of the human foot

    J. Physiol.

    (1987)
  • BlumbergH. et al.

    Clinical phenomenology and mechanisms of reflex sympathetic dystrophy: emphasis on edema

  • BoveG.M. et al.

    Inflammation induces ectopic mechanical sensitivity in axons of nociceptors innervating deep tissues

    J. Neurophysiol.

    (2003)
  • de MosM. et al.

    Current understandings on complex regional pain syndrome

    Pain Pract.

    (2009)
  • DeuschlG. et al.

    Tremor in reflex sympathetic dystrophy

    Arch. Neurol.

    (1991)
  • GorodetskayaN. et al.

    Functional properties of cutaneous A- and C-fibers 1 - 15 months after a nerve lesion

    J. Neurophysiol.

    (2009)
  • HäblerH.J. et al.

    Reflex patterns in postganglionic neurons supplying skin and skeletal muscle of the rat hindlimb

    J. Neurophysiol.

    (1994)
  • HäblerH.J. et al.

    Interaction of sympathetic vasoconstriction and antidromic vasodilatation in the control of skin blood flow

    Exp. Brain Res.

    (1997)
  • HäblerH.J. et al.

    Functional evidence for the differential control of superficial and deep blood vessels by sympathetic vasoconstrictor and primary afferent vasodilator fibres in rat hairless skin

    Exp. Brain Res.

    (1998)
  • Cited by (0)

    View full text