A frequent manifestation of multiple sclerosis (MS) is chronic fatigue syndrome, which can be defined as a subjective decrease in the level of physical and/or mental energy. Chronic fatigue syndrome can be divided into asthenia (fatigue at rest), pathological fatigability (fatigue on physical loading), and fatigue on the background of deterioration of other symptoms (exacerbation of MS). There are both central and peripheral mechanisms for the formation of fatigue. The combination of fatigue and affective disturbances, especially depression and sleep disorders (insomnia, restless legs syndrome) is common in MS and may provide evidence that they share common mechanisms--decreases in the activity of the serotoninergic and noradrenergic systems. An important component in the formation of chronic fatigue syndrome consists of endocrine and autoimmune factors, the latter having a greater effect on asthenia than on pathological fatigue. Further studies of the pathogenetic mechanisms of the formation of asthenia and pathological fatigue and clarification of their differential diagnostic signs should allow not only a better understanding of the nature of this syndrome, but also better selection of individual treatment.
Changes in the emotional background make significant contributions to the clinical picture of multiple sclerosis (MS), seriously reducing patients' quality of life and hindering adaptation during the process of rehabilitation. The relationship between mental state and disease activity has been discussed in the world literature in recent years and the opinion that mental disorders in MS are pathogenetically based is increasingly widespread. The present article discusses the potential role of substances mediating immune responses-cytokines-in the effects of changes in the functional activity of the nervous system and psychoemotional status. The question of their likely involvement in the pathogenesis of the side effects of immunomodulatory therapy of MS with beta-interferons and glatiramer acetate is discussed.
Dysimmune polyneuropathies are the etiologically heterogeneous group of diseases with autoimmune damage to the peripheral nervous system. The rarity of these diseases doesn’t exclude the possibility of their development or exacerbation in patients infected with SARS‑CoV‑2, which will require timely differential diagnosis and urgent specific therapy. The article summarizes current information on the mechanisms of development, clinical features, diagnosis and management of acute and chronic dysimmune polyneuropathies in the context of the COVID‑19 pandemic.
MRI scans were obtained of the cervical section of the spinal cords of 30 patients with remitting multiple sclerosis. During the study period, patients received immunomodulatory agents (seven received interferon beta-1a, 13 received interferon beta-1b, and 10 received glatiramer acetate). Total focus volume in brain matter was assessed before and after treatment, along with the linear size of the spinal cord on sagittal sections at the level of the inferior margin of the body of C2. There was a significant (p = 0.002) reduction in focus volume in the group overall, from 10993 mm(3) (8098-13888 mm(3), p< 0.05; Me = 9336) to 5630 mm(3) (7400-3860 mm(3), p < 0.05, Me = 4180). There were also significant decreases in focus volume on the background of treatment with interferon beta-1b and glatiramer acetate (p = 0.026 and 0.027, respectively). Significant differences between groups were found in the magnitudes of increases in spinal cord atrophy: H (2, n = 30) = 8.06; p = 0.0178. Patients given glatiramer acetate showed a significantly smaller increase in atrophy as compared with those treated with interferon beta (p < 0.02).
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