Neuropathic pain can occur in systemic diseases or toxic states causing purely sensory or sensorimotor peripheral neuropathy and after peripheral nerve injury. Precise estimates of the prevalence of neuropathic pain are not available, but in the USA alone there may be more than 3 million people with painful diabetic neuropathy.1 After nerve injury, estimated incidence of pain is 2-5-5%, and postherpetic neuralgia occurs in 10% of the patients after acute herpes zoster infection. Small-fibre damage and partial axonal injury seem to be prerequisites for the development of neuropathic pain, and the mechanisms involve both peripheral and central sensitisation. Increases in glutamate activity at the NMDA receptor sites and release of other excitatory neurotransmitters (eg, substance P and calcitonin gene-related peptide) are among the best known central changes after nerve injury. Structurally related to gabapentin, pregabalin selectively binds to the alpha_2-8 subunit of the voltage dependent calcium channel thereby blocking the influx of calcium into presynaptic nerve terminals and reducing the release of excitatory neurotransmitters.2 Similarly to gabapentin, which is effective in the treatment of neuropathic pain,13 pregabalin specifically targets an important pronociceptive site of the central sensitisation cascade.
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