Clinical and neurological, neurophysiological, and neuropsychological examination of 50 patients aged 50–65 y. o. with an experience of COVID‑19 infection within the last 3 to 6 months, revealed pathological changes in the central nervous system in the form of cerebrastenic and autonomic disorders, motor disorders, vestibulopathy symptoms, which occurred in various combinations, with astheno-vegetative syndrome as obligate. Cognitive impairments were detected in 26% of patients; the mental fatigability index was 1.055 ± 0.124; a high level of situational anxiety was noted in 35% of patients, and a high level of personal anxiety in 50 % of patients with the experience of COVID‑19. The study of brain biopotentials revealed moderate diffuse changes (18%) and irritative disorders on the part of hypothalamic (69 %) and diencephalic structures (20%). All of the above may indicate that, regardless of the form of coronavirus infection occurred in humans, i. e., latent, mild, moderate or severe, one of the targets of the pathological impact of COVID‑19 virus is the median structures of the brain responsible for autonomic and cognitive functions. Nevertheless, in our opinion, these disorders are associated not with a direct pathological effect, but are mediated mainly by circulatory disorders in the microcirculatory bed due to endothelial damage and are rather functional disorders on the part of the central nervous system. This provides the grounds for the selection of pathogenetic therapy aimed at stabilizing the functional state of neurons, and one of the drugs of choice may be citicoline (Noocyl), the action of which is associated with reinforcing the cell membrane of the neuron and normalizing bioelectric processes.

Fibromyalgia (FM) is a mystery of modern rheumatology. Despite the high prevalence of FM according to special epidemiological studies, clinicians make this diagnosis rarely. The modern concept of fibromyalgia was created by Smythe and Moldofsky in the mid-70s. They introduced a new term «fibromyalgia», thereby emphasizing that this condition is more due to pain syndrome than inflammation of connective tissue. A disturbance of sensory information processing in the central nervous system (dysfunction of the pain system with the formation of central sensitization, CS) plays a key role in the pathogenesis of FM. Clinical manifestations of FM include chronic widespread pain associated with a wide range of psychosomatic disorders (sleep disorders, cognitive disorders [fibro fog], anxiety, depression, fatigue, morning stiffness, etc.). The diagnostic criteria for fibromyalgia have undergone significant changes. The latest FM diagnostic criteria were developed by the American College of Rheumatology (ACR) in 2016. According to the ACR (2016) FM criteria, a diagnosis of FM does not exclude the presence of other clinically important illnesses. Concomitant FM among patients with rheumatic diseases (RD) occurs 2–3 times more often than in the general population. Diagnostics and treatment of FM are extremely difficult for clinicians, it is especially difficult with comorbidity of FM with RD. Therefore, FM requires a multidisciplinary approach within a biopsychosocial model of pain syndrome: the treatment of a patient with RD and FM should combine anti-inflammatory therapy with a complex of methods (medications and nondrug therapy) used for FM therapy. The diagnostics of comorbid FM in patients with RD will allow for personalized and more effective analgesic therapy.

Non-steroidal anti-inflammatory drugs (NSAIDs) is a group of drugs used for analgesia, antinflammatory, antipyretical properties, and antiplatelet effects. NSAIDs are widely used in the treatment of osteoarthritis, musculoskeletal pain, gout and other pathological conditions, however, their use is associated with the risk of developing adverse drug reactions, including serious and fatal ones, for example, gastrointestinal bleeding, or myocardial infarction and stroke. Many NSAIDs can also cross the blood-brain barrier and cause central adverse drug reactions that can be mistaken by practical health care professionals for the manifestation of a new pathologies or insufficient effectiveness of treatment of an existing disease, but not with the use of NSAIDs, that may lead to errors in treatment tactics, additional prescription of drugs and an increased risk of complications. The purpose of this article is to inform practical health care professionals about the potential risks of central adverse drug reactions (including psychiatric ones) of NSAIDs, and thus, to increase the effectiveness and safety of therapy.

Purpose of the study. To establish the relationship between neurophysiological status and the level of efficiency in young people with bruxism.

Materials and methods. Two groups of 64 and 53 subjects (males and females) aged 20–35 years old with bruxism and non-bruxers were formed according to questionnaire results and physical examination. The level of efficiency was assessed by the results of sensorimotor tracking of a moving object (the ‘Smile’ model). Spectral analysis was performed for evaluation of the baseline electroencephalograms. Microsoft Excel and Statistica 10.0 programs were used for statistical data processing.

Results. The level of efficiency was statistically significantly lower in the hardest test of Smile model among the individuals with bruxism (p < 0.05). The bruxers also demonstrated a significantly lower dominant frequency and maximum amplitude of alpha-rhythm (p < 0.05), and significantly higher dominant frequency of beta2 rhythm (p < 0.05). The dominant frequency and the maximum amplitude of the alpha-rhythm are parameters corresponding to significant coefficients of the regression analysis. A negative relationship was found between the degree of error during sensorimotor tracking and the frequency and amplitude of alpha-rhythm.

Conclusion. Regression models present the relationship between the level of efficiency and the alpha-rhythm severity. The regression equations make it possible to determine the functional state of the subject using an electroencephalogram.

Persistent idiopathic facial pain (PIFP) is often regarded as an undiagnosed condition with a poor prognosis. Extensive research on this topic is limited, and there are few effective treatments. Even with an established diagnosis of PIFP, due to poor awareness of the etiology and pathogenesis of the development of the disease, patients struggle with the acceptance of the ‘all-encompassing’ disorder in search of the causes that led to the disease and often undergo unnecessary tests and procedures in search of alternative diagnoses.

Dysfunction of the pelvic organs in tumor lesions of the spinal cord is up to 20%. Registration of the bulbocavernosus reflex is performed to assess the integrity of the segmental apparatus of the spinal cord. Polymodal neurophysiological monitoring includes registration of the bulbocavernosus reflex during surgery of spinal cord tumors. The effect of the components of general anesthesia on the parameters of the bulbocavernosus reflex varies significantly according to various medical sources. The aim of the work was to compare the effect of inhalation anesthesia (sevoflurane) and total intravenous anesthesia (propofol) on the parameters of the bulbocavernosus reflex in the surgical treatment of spinal cord tumors. Thirty patients with intradural extramedullary and intramedullary tumors of the spinal cord at the level of Th11–S2 vertebrae were included in the study. The amplitude-frequency parameters of the bulbocavernosus reflex and the threshold intensity of stimulation were assessed in the study. The results of the study demonstrate that intraoperative registration of the bulbocavernosus reflex during resection of tumors of the distal spinal cord can be performed both with inhalation and total intravenous anesthesia. A sustained motor response of the bulbocavernosus reflex requires a higher intensity of stimulation with inhalation anesthesia with sevoflurane than with total intravenous anesthesia. If during the operation the depth of propofol's anesthesia increases by 1 mg/kg/h, then it is necessary to increase the current strength during stimulation by 10–11 mA.

The objective of the study is review and analyze scientific publications devoted to the problems of stroke, its relationship with the most common mutations in the MTHFR gene and their individual allelic variants and serum homocysteine levels.

Materials and methods. Analyzing foreign and domestic publications, the relationship of the strongest mutations in the MTHFR gene with an increase in the level of serum homocysteine, which is a predictor of the development of vascular accidents, including acute circulatory disorders of the brain, was revealed.

Results. Stroke is a socially significant disease. All risk factors for acute cerebral stroke are subdivided into modifiable and non-modifiable. To a non-modifiable factor that predisposes to the development of ischemic and hemorrhagic stroke, hereditary factors, including genetic mutations in a number of genes. MTHFR is a genome carrying individual allelic variants that can affect the level of homocysteine in blood serum, causing it to increase, and hyperhomocysteinemia, according to a number of studies, is a likely predictor of diseases of the cardiovascular system, including severe cerebrovascular accidents. At the same time, a large number of studies use the services of the protective role of reducing the elevated level of serum homocysteine using various forms of folic acid and B vitamins. The authors of the article attempted to process, analyze and summarize the data of modern research issues on the topic under consideration.

Conclusions. The relationship between the occurrence of ischemic and hemorrhagic stroke and the most common mutations in the MTHFR gene has been revealed. Hyperhomocysteinemia, separate and developing as a result of these mutations, is an independent risk factor for the development of acute cerebral ischemia. Normalization of elevated serum homocysteine levels is required for all patients as stroke prevention, and includes not only the use of foods enriched with folic acid, but also pharmacological correction of folates and B vitamins.

Based on the example of seasonal epidemics of respiratory viral infections, it is partially possible to model the outcomes of neurological complications from Covid‑19, taking into account the pathogenetic features of the virus effect on the vascular wall and nerve cells. The accumulated experience of doctors of various specialties makes it possible to prevent such life-threatening complications as ACVA, PATE, intoxication, and sepsis. From the first days of the disease, it is necessary to conduct dynamic monitoring of blood rheology, the level of systemic oxygenation, use anticoagulants in preventive doses in patients at the early stages of the disease, conduct therapy aimed at reducing the risk of cytokine storm development.

Sarcopenia is a progressive generalized muscle disorder, associated with an increased risk of falls, fractures, physical disability, and mortality. Sarcopenia criteria are based on an assessment of a triad of symptoms – a decrease in muscle mass, muscle strength, and impaired physical performance. The most common diagnostic methods are handgrip dynamometry, densitometry, bioimpedansometry, and gait speed measurement. These methods have high accuracy and prognostic value, but are not always applicable to neurological patients. The article discusses sarcopenia detection in neurological practice, as well as its connection with neurodegenerative disorders – Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis. Having a number of common pathophysiological mechanisms, each of the diseases is characterized by a specific phenotype of muscle atrophy. The high incidence of sarcopenia symptoms in neurodegenerative diseases and the common mechanisms of their development allow us to treat sarcopenia as an overlap syndrome of neurodegenerative disorders.