JMPT January 1999 • Volume 22 • Number 1

Dysafferentation: A novel term to describe the neuropathologic effects of joint complex dysfunction—a look at likely mechanisms of symptom generation

To the editor:

I would like to thank Drs Seaman and Winterstein for their efforts at updating neurologic models in which to explain chiropractic subluxation/joint dysfunction.1 However, I would like to take issue with Dr Seaman's belief that dysafferentation from putative joint dysfunction necessarily involves only reduced mechanoreception but provides joint dysfunction. Dr Seaman provides little evidence for his opinion, a point he acknowledges. Most of the evidence cited for the concept of “reduced” mechanoreception comes from motor disturbances, vertigo, and so forth, associated with cervical injury. 1,2 Although it is known that reduction of input from the cervical muscles can cause these symptoms, it has also been shown that stimulation of mechanoreceptors—muscle spindles—can have similar effects. 3,4 For most of the cases Seaman cites, it is not known whether the symptoms were due to decreased or increased mechanoreception.

It has been suggested that because of their extreme density in the intervertebral muscles, muscle spindles are an information-gathering system as complex as vision or audition. 5 Given this complexity, any dysfunction that involves these muscles would, most likely, lead to changes, both increased and decreased, in muscle spindle output (mechanoreception).

A model that would result in increased mechanoreception could be driven by nociception, as Dr Seaman proposes. Activation of nociceptors by injury to a joint generates a reflexive muscle response to guard the joint6; these are termed nocifensive reflexes.7 Contraction of extrafusal muscle unloads associated muscle spindles. 8,9 Loss of spindle Ia and II signal causes increased gamma signals to the spindle, a phenomenon called “automatic gain compensation.”10 Once the nocifensive reflex muscle contraction has abated—injuries heal and nociception is subject to adaptation 7,11—this increased gamma gain results in significantly increased spindle Ia and II output. This phenomenon allows for continued (extrafusal) muscle tension 1216 and mostly Ia (with some II) spindle output 12,1619 without the need for continuing nociceptive input. Experiments in cats have shown that in sampled Ia fibers, discharge rates after muscle contraction increased by 60%; a number of these receptors had been silent before the contraction.12

As Bailey and Dick propose in their model for somatic dysfunction (the osteopathic equivalent of chiropractic subluxation/joint dysfunction), perhaps nociceptive reflexes predominate in the acute phase of injury and mechanoreceptor mechanisms in chronic phases.20 A review of PCSD and related phenomenon and a fusimotor model of chronic subluxation/joint dysfunction have been recently proposed.21

Although evidence is limited that loss of mechanoreception, particularly in the cervical spine, causes symptoms, similar symptoms can be induced by mechanoreceptor stimulation. Intervertebral muscle spindles make up a complex information-gathering system, dysfunction of which is equally likely to cause increased as decreased mechanoreception. And finally, joint dysfunction does cause increased muscle spindle-mechanoreceptor output by means of the phenomenon of postcontraction sensory discharge. I would suggest that Seaman's term dysafferentation for the effects of subluxation/joint dysfunction be moderated to include the possibility of both reduced and increased mechanoreceptor discharge.

Gary A. Knutson, DC

840 W 17th, Suite 5, Bloomington, IN 47404


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