Peripheral receptors of pain - free nerve endings lying in skin or other organs - are the distal axons of sensory neurons. Such unmyelinated or only thinly myelinated axons are of small diameter. The termination and central connections of these axons are described on page 196.
The type of stimulus required to activate free endings varies, e.g. in muscle - ischaemia, in abdominal viscera - distension.
Certain substances - bradykinins, prostaglandins, histamine - may stimulate free nerve endings. These substances are released in damaged tissue.
CONTROL OF SENSORY (PAIN) INPUT The Gate control theory
A relay system in the posterior horn of the spinal cord modifies pain input. This involves interneuronal connections within the substantia gelatinosa (a layer of the posterior horn which extends throughout the whole length of the spinal cord on each side).
An afferent impulse arriving at the posterior horn in thick myelinated fibres has an inhibitory effect in the region of the substantia gelatinosa.
An afferent impulse arriving in thin myelinated or unmyelinated fibres (i.e. transmitting pain) has an excitatory effect in the region of the substantia gelatinosa.
The overall interaction of these inhibitory or excitatory effects determines the activity of second order neurons of the spinothalamic pathway.
A reduction in activity of large sensory fibres 'opens' the gate. Stimulation of large sensory fibres theoretically 'closes' the gate.
In addition to these segmental influences, higher centres also control the gate region and form part of a feed-back loop.
The awareness of pain is brought about by projection from the thalamus to cerebral cortex. Personality, mood and neuroticism all influence the intensity of pain perception. Diffuse projections through Lissauer's tract and the reticular core of the spinal cord white matter to the reticular formation and limbic system probably contribute to the unpleasant, emotionally disturbing aspects of pain.
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