Post-stroke pain

Abstract

Pain is one of the most troublesome sequelae of stroke, occurring in 19–74% of patients. A portion 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 among stroke patients is low (1–8%), the persistent, often treatment-refractory, painful sensations can be a major problem, decreasing the affected patient’s quality of life. As the aging population continues to increase, CPSP will become an even more important problem in the future. Although the pathogenesis of CPSP is not yet known, it has been suggested that underlying causes include hyperexcitation in the damaged sensory pathways, damage to the central inhibitory pathways, or a combination of the two. Adrenergic antidepressants are currently the first-line drugs for CPSP, but their effect is frequently incomplete. Antiepileptics, such as lamotrigine, can be used as an adjunctive therapy, while GABAergic drugs, such as gabapentin or pregabalin, have recently emerged as a potentially useful therapy. Nonpharmacological treatments, such as motor cortex stimulation or deep brain stimulation, also appear to be useful in a certain group of patients. Additional studies are urgently needed to improve our understanding of the pathophysiology of CPSP and support the development of better treatment modalities.

Keywords::

• cerebrovascular disease
• pain
• post-stroke pain
• sensation
• spinothalamic sense

Financial & competing interests disclosure

The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.