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
12–16
and mostly Ia (with some II) spindle
output
12,16–19 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
References1.
Seaman DR, Winterstein JF.
Dysafferentation: A Novel Term to Describe the Neuropathophysiological Effects of Joint Complex Dysfunction.
A Look at Likely Mechanisms of Symptom Generation
J Manipulative Physiol Ther 1998 (May); 21 (4): 267-280
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for chronic subluxation. Chiropract Res J. Submitted for
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