• Jong S Kim.
• Department of Neurology, Asan Medical Center, University of Ulsan, Songpa-Gu, 388-1 Pungnap-Dong, Seoul, 138-736, Korea, jongskim@amc.seoul.kr.
• Cns Drugs. 2014 Sep 1;28(9):787-97.

AbstractPain is one of the most troublesome sequelae of stroke. Some of this post-stroke pain is caused by the brain lesion itself; this is called central post-stroke pain (CPSP). Although the prevalence of CPSP is low (1-8 %), persistent, often treatment-resistant, painful sensations are a major problem for stroke patients. The pathogenesis of CPSP remains unknown, but suggested underlying causes include hyperexcitation in the damaged sensory pathways, damage to the central inhibitory pathways, or a combination of the two. For pharmacological treatment, amitriptyline, an adrenergic antidepressant, is currently the first-line drug for CPSP. However, its effect is frequently incomplete and a high dose is commonly not tolerated in stroke patients. Lamotrigine, an antiepileptic, was also found to be effective in a controlled trial and can be used as an alternative or additive therapy. GABAergic drugs with potential calcium channel-blocking effects, such as gabapentin or pregabalin, have recently emerged as a potentially useful therapy. These drugs are effective in various neuropathic pain syndromes, but their effect on CPSP remains to be proven. Pregabalin may improve pain-related anxiety and sleep disturbances. Fluvoxamine and mexiletine may be used adjunctively in some patients. Non-pharmacological treatments such as motor cortex stimulation or deep brain stimulation are used in some centers, but are not proven to be effective. Further well designed clinical trials as well as basic research should be performed to improve our understanding of the pathophysiology of CPSP and to develop better treatment strategies.

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