Abstract
Post-stroke pain may occur in post-stroke patients. A significant percentage of people develop headaches early after stroke, mostly of the tension type with tendency to chronicity.
Central post-stroke pain (CPSP) occurs in 7-10% of patients after stroke. CPSP usually appears in 1-3 months after stroke; in most people 6 months later.
The most important role in pathophysiology of CPSP play overactivity of the sympathetic nervous system, sensitization of the pain pathway, increased inflammatory response and local nerve tissue hypoxia, respectively. The lesion relates to the pain pathway, particularly in the thalamus, where a slight stimulus of the peripheral pain receptors produces a pronounced painful sensation.
Other structures of the central nervous system (involvement of the spinothalamic pathway in its central part, trigeminothalamic pathway or lemniscus medialis) are also responsible for CSPS. Amitriptyline (75 mg daily), carbamazepine (800 mg daily), gabapentin, pregabalin, lamotrigine, levetiracetam or duloxetine are effective oral pharmacotherapy for CSPS.
In the acute phase after stroke, it is important to start rehabilitation with early mobilization and aerobic exercise, leading to a significant reduction in pain. The most frequent interventions are: epidural administradion of steroids, intradiscal intervention, radiofrequency procedures.