Central post-stroke pain

The term "central post-stroke pain" refers to pain and some other sensory disturbances that occur after a stroke. Dejerine and Russi (1906) described intense intolerable pain in the context of the so-called thalamic syndrome (superficial and deep hemianesthesia, sensory ataxia, moderate hemiplegia, mild choreoathetosis) after infarctions in the thalamus area. The most common cause of central pain is vascular damage to the thalamus (its ventroposteriomedial and ventroposteriolateral nuclei). However, central pain can also occur with extrathalamic foci, for example, with damage to the pons and lateral parts of the medulla oblongata. The most common causes of these disturbances are infarctions, hemorrhages, and arteriovenous malformations. The pathogenesis of central pain remains largely unclear; discuss the possible role of damage to afferent somatosensory systems in the brain, as well as disinhibition, sensitization, and secondary neurotransmitter disturbances.

Epidemiology

Central post-stroke pain develops within 1 year after stroke in 8% of patients. Since the prevalence of stroke is high (500 cases per 100,000 population), the absolute number of people with post-stroke pain is quite significant.

In 50% of patients, pain occurs within the first month after a stroke, in 37% - within 1 month to 2 years, in 11% - after 2 years.

Symptoms of central post-stroke pain

Central post-stroke pain most often occurs in the right or left half of the body, although some patients may have local pain (in one arm, leg, or face). Patients often describe the pain as "burning," "aching," "pinching," or "tearing." Post-stroke pain can be aggravated by various factors: movement, cold, heat, emotions. On the contrary, in other patients, the same factors can weaken the pain, especially heat. Central post-stroke pain is often accompanied by other neurological symptoms, such as hyperesthesia, dysesthesia, numbness, changes in sensitivity to heat, cold, touch, and/or vibration. Pathological sensitivity to heat and cold is most often observed and is considered a reliable diagnostic sign of central neuropathic pain. According to research, 70% of patients with central post-stroke pain are unable to feel the difference in temperature in the range from 0 to 50 °C. The phenomenon of allodynia, characteristic of neuropathic pain, is noted in 71% of patients.

Treatment of central post-stroke pain

Amitriptyline (75 mg/day and higher) has been shown to be effective, with the best results being obtained when it was prescribed immediately after the onset of pain. Selective serotonin reuptake inhibitors, despite a more favorable safety profile, are ineffective in central post-stroke pain, the same applies to carbamazepine. No positive effect was observed in the treatment of NSAIDs. The results of using opioid analgesics are also unsatisfactory due to the high incidence of side effects (although some positive effects were noted in a number of studies). The use of some new anticonvulsants is promising. In particular, encouraging results were obtained during preliminary studies using pregabalin (300-600 mg/day for 4 weeks). In patients receiving pregabalin, the quality of life significantly improved, pain decreased, while in most patients in the placebo group these indicators worsened. The most frequently noted side effects of pregabalin were drowsiness, which usually disappeared later. In general, the treatment of patients with central post-stroke pain remains a complex task. Taking into account the different pathogenetic mechanisms of central post-stroke pain, the effectiveness of rational combination pharmacotherapy (antidepressants in combination with anticonvulsants and opioid analgesics) is currently being studied.

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