2. 3 Neurophysiology of Manipulation: a Central effects

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2.3 Neurophysiology of Manipulation:
a) Central effects
HVLA has been reported to cause numerous neurophysiological effects at both the spinal cord and cortical levels. One of the proposed central effects is called facilitation or sensitisation. This refers to the increased excitability or responsiveness of dorsal horn neurons to an afferent input. An alteration between vertebral segments may produce a biomechanical overload leading to the alteration of signalling from mechanically or chemically sensitive neurons in paraspinal tissues. These changes in afferent input are believed to alter neural integration either by directly affecting reflex activity and/or by affecting central neural integration within motor and neuronal pools [Pickar].
Denslow et al were one of the first groups to investigate this phenomenon, and their findings suggested that motoneurons could be held in a facilitated state because of sensory bombardment from segmentally related dysfunctional musculature. It has been shown that central facilitation increases the receptive field of central neurons and allows innocuous mechanical stimuli access to central pain pathways [Woolf]. Essentially this means that sub-threshold stimuli may become painful as a result of increased central sensitisation. As discussed in the other sections of this proposal, spinal manipulation is believed to be able to overcome this facilitation by making biomechanical changes to the joint [Pickar], and/or by creating a barrage of afferent inputs into the spinal cord from muscle spindle and small-diameter afferents, ultimately silencing motoneurons. [Korr].
Melzack and Wall’s [#] Gate Control Theory dsecribes the dorsal horn of the spinal cord as having a gate-like mechanism which not only relays sensory messages but also modulates them. Nociceptive afferents from small diameter Aγ and C fibres tend to open this gate, and non-nociceptive large diameter Aβ fibres (from joint capsule mechanoreceptor, secondary muscle spindle afferents, and cutaneous mechanoreceptors) tend to close the gate to the central transmission of pain. This modulation takes place in the lamina of the dorsal horn. Simplistically, Aβ afferents enter lamina II and V, stimulating an inhibitory interneuron in lamina II (which connects to lamina V); Aγ and C fibres enter lamina V. Consequently, the central transmission of pain is a balance between the influences of these opposing stimuli. [Potter, Kandel] HVLAT may modulate the pain gate mechanism in the dorsal horn by producing a barrage of non-nociceptive input from large diameter myelinated Aβ afferents from muscle spindles and facet joint mechanoreceptors to inhibit nociceptive C fibres [Besson & Chaouch].
b) Cortical/motoneuronal effects
Dishman et al recently published an article which questioned some of their own previous research findings. In this subsequent paper, the authors stated that the H-reflex technique is susceptible to the effects of pre-synaptic inhibition of the afferent arm of the reflex pathway. So, by using transcranial magnetic stimulation to directly measure the effect of corticospinal inputs on the alpha motor neuron pool, they were able to perform an experiment which showed a transient (20–60 s) increase in motor alpha neuron excitability post manipulation. This paper lends further support to the theory that spinal manipulation produces a brief activation of the motor alpha neuron leading to brief muscle contraction.
Descending pathways also influence pain perception. Stimulation of the Periaqueductal gray produces analgesia via the descending PAG pathways[Morgan MM]. Stimulation of the dorsal PAG (dPAG) in the brain produces selective analgesia to mechano-nociception, whereas temperature nociception is modulated via the ventral PAG (vPAG). It is also known that sympatho-excitation results from stimulation of the dPAG, in contrast to sympatho-inhibition which occurs as a result of stimulating vPAG[Morgan MM]. Activation of the descending dPAG is a possible mechanism for the antinociceptive effects of spinal manipulation. Sterling et al measured changes in pain and sympathetic outflow by comparing a C5/6 HVLA to a sham intervention (manual contact but with no movement). The authors demonstrated HVLA produced mechanical hypoalgesia, measured by an increase in pain pressure threshold, and increased sympathetic outflow, measured by decreased blood flow, decreased skin temperature, and increased skin conductance. However, there was no alteration to thermal pain thresholds. Given such selective mechanical anti-nociception and sympathoexcitation, this supports the theory that the mechanism of effect is due to activation of the dPAG descending pain mechanism. Vincenzino et al conducted a similar experiment on subjects with epicondylitis and showed again that cervical spine HVLA lead to selective analgesia to mechanical stimulus and sympatho-excitation, adding further weight to the argument that spinal manipulation may influence the perception of pain by activation of the descending dPAG. This does not prove conclusively that there is definitely direct activation of dPAG, only that the effects of HVLA are give similar findings to what you would expect with stimulation of the dPAG, hence there is a plausible link between the two, and it is inferred that HVLA may lead to stimulation of the dPAG.
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