By understanding the neuroplastic changes following nerve damage, researchers may be able to gain a better understanding of the mechanism of hyperexcitability in the nervous system that is believed to cause neuropathic pain. Peripheral nerve injury A neuron's response to trauma can often be determined by the severity of the injury, classified by Seddon's classification. In Seddon's Classification, nerve injury is described as either neurapraxia, axonotmesis, or neurotmesis. Following trauma to the nerve, a short onset of afferent impulses, termed "injury discharge", occurs. While lasting only minutes, this occurrence has been linked to the onset of neuropathic pain. When an axon is severed, the segment of the axon distal to the cut degenerates and is absorbed by Schwann cells. The proximal segment fuses, retracts, and swells, forming a "retraction bulb". The synaptic terminal function is lost, as axoplasmic transport ceases and no neurotransmitters are created. The nucleus of the damaged axon undergoes chromatolysis in preparation for axon regeneration. Schwann cells in the distal stump of the nerve and basal lamina components secreted by Schwann cells guide and help stimulate regeneration. The regenerating axon must connect to the appropriate receptors to make an effective regeneration. If proper connections to the appropriate receptors are not established, aberrant reinnervation may occur. If the regenerating axon is halted by damaged tissue, neurofibrils may create a mass known as a neuroma. If an injured neuron degenerates or does not regenerate properly, then the neuron loses its function or may not function properly. Neuron trauma is not an isolated event and may cause degenerative changes in surrounding neurons. When one or more neurons lose their function or begin to malfunction, abnormal signals sent to the brain may be translated as painful signals.
Neuralgia
Tietze syndrome  Tietze syndrome  1
Synesthesia
Dysesthesia
Paresis
Palsy
Allodynia
Chromesthesia