Central post-stroke pain

The term "central post-stroke pain" refers to pains and some other sensory disorders that occur after a stroke. Dezherin and Russi (1906) described intense intolerable pains within the so-called thalamic syndrome (superficial and deep hemianesthesia, sensitized ataxia, moderate hemiplegia, non-cerebral choreo-athetosis) after infarctions in the visual cusp area. The most common cause of central pain is the vascular lesion of the thalamus (ventroposterei medial and ventroposterolateral its nuclei). Nevertheless, central pain may occur in extralateral foci, for example, in the defeat of the bridge and lateral divisions of the medulla oblongata. The most common causes of these disorders are heart attacks, hemorrhages, arteriovenous malformations. The pathogenesis of central pain remains largely unclear; discuss the possible role of lesions of afferent somatosensory systems in the brain, as well as disinhibition, sensitization and secondary neurotransmitter disorders.

Epidemiology

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

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

Symptoms of central post-stroke pain

Central post-stroke pain often occurs in the right or left half of the body, although in some patients the pain may be local (in one arm, leg or face area). Patients often characterize pain as "burning", "aching", "pinching", "tearing". Post-insult pain can enhance various factors: movement, cold, heat, emotions. On the contrary, in other patients, these same factors can reduce 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 observed most often, it is considered a reliable diagnostic sign of central neuropathic pain. According to research, 70% of patients with central post-stroke pain are not able to sense the temperature difference in the range of 0 to 50 ° C. Characteristic for neuropathic pain, the phenomenon of allodynia is noted in 71% of patients.

Treatment of central post-stroke pain

The effectiveness of amitriptyline (from 75 mg / day and above) was established, and the best results were obtained with his appointment immediately after the onset of pain. Selective serotonin reuptake inhibitors, despite a more favorable safety profile, with central post-stroke pain are ineffective, the same applies to carbamazepine. There was no positive effect in the treatment of NSAIDs. The results of using opioid analgesics are also unsatisfactory because of the high incidence of side effects (although a number of studies have noted some positive effect). It is promising to use some new anticonvulsants. In particular, in preliminary studies, encouraging results were obtained with the use of pregabalin (300-600 mg / day for 4 weeks). In patients receiving pregabalin, the quality of life significantly improved, the pain decreased, while in the majority of patients in the placebo group, these indicators worsened. Of the side effects of pregabalin, drowsiness was most often noted, which was subsequently leveled. In general, treatment of patients with central post-stroke pain remains a challenge. Given 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.

[1], [2], [3], [4], [5]