CHAPTER 2

The Neurophysiology
of Manipulation

Central Effects

Manipulation 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, 2002).

Denslow, Korr and Krems (1947) were one of the first groups to investigate this phenomenon, and their findings suggested that motor neurons 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, 1994). Essentially, this means that sub-threshold stimuli may become painful as a result of increased central sensitisation. Spinal manipulation is believed to be able to overcome this facilitation by making biomechanical changes to the joint (Pickar, 2002) and/or by creating a barrage of afferent inputs into the spinal cord from muscle spindle and small-diameter afferents, ultimately silencing motor neurons (Korr, 1975).

Melzack and Wall’s (1965) Gate Control Theory describes 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

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