Group C Nerve Fiber - Role in Neuropathic Pain

Role in Neuropathic Pain

Activation of nociceptors is not necessary to cause the sensation of pain. Damage or injury to nerve fibers that normally respond to innocuous stimuli like light touch may lower their activation threshold needed to respond; this change causes the organism to feel intense pain from the lightest of touch. Neuropathic pain syndromes are caused by lesions or diseases of the parts of the nervous system that normally signal pain. There are four main classes:

  • peripheral focal and multifocal nerve lesions
    • traumatic, ischemic or inflammatory
  • peripheral generalized polyneuropathies
    • toxic, metabolic, hereditary or inflammatory
  • CNS lesions
    • stroke, multiple sclerosis, spinal cord injury
  • complex neuropathic disorders
    • complex regional pain syndromes

After a nerve lesion of either C fibers or Aδ fibers, they become abnormally sensitive and cause pathological spontaneous activity. This alteration of normal activity is explained by molecular and cellular changes of the primary afferent nociceptors in response to the nerve damage. The abnormal activity of the damaged nerves is associated with the increased presence of mRNA for voltage-gated sodium channels. Irregular grouping of these channels in sites of the abnormal activity may be responsible for lowering the activation threshold, thus leading to hyperactivity.

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