• Nanna B Finnerup, Hanne Gottrup, and Troels S Jensen.
• Department of Neurology and Danish Pain Research Centre, Aarhus University Hospital, Noerrebrogade 44, 8000 Aarhus C, Denmark. finnerup@akhphd.au.dk
• Expert Opin Pharmacother. 2002 Oct 1; 3 (10): 1411-20.

AbstractTreatment of central neuropathic pain (CP) following lesions of the CNS is a great challenge to the clinician. Preclinical and clinical studies indicate that neuronal hyperexcitability in damaged areas of the central nervous system plays a major role in the development of CP. Anticonvulsants are thought to act by increasing gamma-aminobutyric acid-mediated inhibition, decreasing abnormal neuronal hyperexcitability by modulating sodium and calcium channels or by inhibiting excitatory amino acid actions. The resulting inhibition of excess neuronal activity is thought to be the basis for the use of anticonvulsants in epilepsy as well as neuropathic pain. Both first-generation anticonvulsant drugs (e.g., phenytoin, benzodiazepines, valproate and carbamazepine) and second-generation anticonvulsant drugs (e.g., lamotrigine, gabapentin and topiramate) are used in CP conditions. However, few randomised controlled trials on the treatment of this condition have been published. Present suggestions for anticonvulsant treatment of CP are lamotrigine as the first choice, followed by gabapentin or carbamazepine/oxcarbazepine. These compounds are considered as effective as the antidepressant amitriptyline.

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