Neuropathic pain is a complex disorder initiated by a primary lesion or dysfunction in the nervous system (Merskey, 1994). Common causes include diabetes, alcohol, herpes zoster infection, HIV-related neuropathies, toxins, malignancyrelated pain, genetic disorders, and immune mediated disorders. It develops as a consequence of changes in the affected neurons and results in a chronically sustained, spontaneously-occuring pain. In contrast to nociceptive pain which has a crucial, protective role by warning the body of impending or active tissue damage, neuropathic pain is not thought to have a useful biological function.

Neuropathic and nociceptive pain often coexist. It is necessary to distinguish the two entities when formulating a rational and effective treatment plan.

Mechanisms for nerve injury and neuropathic pain are multifactorial, complex and evolve over time. Peripheral and central sensitizations are two proposed models to explain the development of neuropathic pain. Reorganizational changes can occur at the level of the dorsal horn following a peripheral nerve injury. For example, low-threshold mechanoreceptors have been shown to sprout from deep laminae and synapse in laminae I and II of the dorsal horn after peripheral nerve injury.

Peripheral sensitization is a phenomenon involving lowering of nociceptor depolarization threshold and ectopic discharges that occur after nerve injury. It may lead to chronic neuropathic pain. The proposed mechanism is a release of inflammatory mediators that occur after nerve injury. Namely, neuropeptides (substance P) from primary afferent nociceptors and prostaglandins (PGE2) from sympathetic postganglionic neurons are thought to be involved. These substances activate nearby receptors and trigger a process of spreading activation. This leads to accumulation and altered expression of sodium channels in the axon membranes and dorsal root ganglia. Consequently, this results in lowering of nociceptor depolarization threshold and in ectopic discharges.

Central sensitization

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