Pathogenesis of neuropathic pain was overwieved and anticonvulsants used for alleviation were reviewed.
Neuropathic pain, whether of peripheral or central origin, is characterized by a neuronal hyperexcitability in
damaged nerve endings Neuropathic pain of peripheral origin exhibit abnormal spontaneous and increased
evoked activity, partly due to an increased and novel expression of sodium channels. In central pain, the
spontaneous pain and evoked pain are also best explained by a neuronal hyperexcitability in dorsal root ganglia, in
the dorsal horn of spinal cord, and in the brain. These changes include abnormal expression of sodium channels,
increased activity at glutamate receptor sites, changes in γ-amynobutiric acid (GABA ergic) inhibition, and
alteration of calcium influx into cells.
The neuronal hyperexcitability and corresponding molecular changes in neuropathic pain have many features in
common with cellular changes in certain forms of epilepsy. This has led to the use of anticonvulsant drugs for the
treatment of neuropathic pain.
Key Words: Neuropathic pain, Mechanism, Anticonvulsant
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