Элла Александровна Ковалева

RELEVANCE. Establishing the source of thrombosis and embolism is the main step in choosing effective means of preventing recurrent ischemic stroke. It is known that in 30% of patients with cryptogenic stroke, the cause of cerebral embolism is paroxysmal atrial fibrillation. There is a hypothesis that atrial fibrillation is one of the markers of atrial cardiomyopathy. Thus, identifying various markers of atrial cardiomyopathy in patients with cryptogenic stroke can increase the chance of detecting atrial fibrillation. THE AIM OF THE STUDY. To identify factors associated with newly diagnosed atrial fibrillation in patients with initially undetermined etiology stroke according to the TOAST classification, and to create a prognostic model that allows identifying patients with a high and low probability of detecting atrial fibrillation. MATERIAL AND METHODS. A total of 1294 patients hospitalized at the N.V. Sklifosovsky Research Institute for Emergency Medicine with a diagnosis of cerebral infarction were examined. Patients with newly diagnosed paroxysmal atrial fibrillation and initially undetermined etiology stroke and patients whose stroke was classified as cryptogenic at the end of hospitalization underwent a comparative analysis of clinical, laboratory, and instrumental parameters, including markers of atrial cardiomyopathy. RESULTS. Independent predictors of atrial fibrillation detection were (in descending order of importance): larger left atrial diameter (OR 1.18, 95% CI 1.06–1.32, p=0.002), higher pulmonary artery systolic pressure (OR 1.07, 95% CI 1.01–1.12, p=0.013), older age (OR 1.05, 95% CI 1.01–1.10, p=0.023), and higher NIHSS score on admission (OR 1.05, 95% CI 1.01–1.10, p=0.035). A model was developed that was characterized by the following indicators: AUROC 0.856, negative predictive value of 90.3%. CONCLUSION. Atrial fibrillation is detected in 37% of patients with initially undetermined etiology stroke. Factors that are associated with the presence of latent atrial fibrillation: older age, severe neurological deficit according to NIHSS and GCS, elevated NT ProBNP level, large left atrial volume and diameter, left atrial appendage vestibule diameter, low blood flow velocity in the left atrial appendage, widening of the P wave, decreased left ventricular ejection fraction, increased pulmonary artery systolic pressure, large aortic wall thickness. The prognostic model was developed that included the following parameters: age, NIHSS, left atrial diameter and pulmonary artery systolic pressure. The developed model was characterized by good prognostic ability regarding the development of atrial fibrillation (AUROC 0.856) and high negative predictive value, which allows using the model primarily to identify low-risk patients.

OBJECTIVE. Assessment of patients with impaired consciousness is a priority task in the department intensive care. The Glasgow Coma Scale (GCS), which includes assessment of motor , speech and ocular reactions, was the first scale developed for this purpose. The absence of versions of the GCS that passed validation research, reduces quality of its application in Russia and other Russian-speaking countries and limits the possibility of obtaining objective clinical results during evaluation patients with reduced level of wakefulness, significantly decreased availability of the scale for scientific and clinical use.AIM OF STUDY. Rating psychometric parameters of the Glasgow Coma Scale as part of the 2nd stage of the multicenter validation research.MATERIAL AND METHODS. In a group of 171 patients over 18 years old with different levels decreased wakefulness, as well as in clear consciousness, hospitalized in the department resuscitation and intensive care therapy performed assessment psychometric properties (reliability, validity, sensitivity).RESULTS. For the Russian version of the GCS received high levels of validity (pCONCLUSION. In the conducted research demonstrated a sufficient level psychometric properties of the Russian version of the Glasgow Coma Scale, which opens up the possibility of its application in Russia and Russian-speaking countries. The scale is available for downloading on the Validation Group website international scales and questionnaires of the Federal State Budgetary Scientific Institution Scientific Center of Neurology.

RELEVANCE. Wernicke encephalopathy (WE) is an acute life-threatening neurological disease caused by thiamine deficiency. Vitamin B1 is a coenzyme that is involved in the process of maintaining the integrity of cell membranes, and, consequently, the normal functioning of the nervous system, muscles and heart. The prevalence of WE in the population is 0.4–2.8%. In the absence of timely treatment, WE leads to the development of severe disability, and in 20% of cases — to death.AIM OF STUDY. Systematization of data on the role of thiamine in the development of Wernicke encephalopathy.MATERIAL AND METHODS. To achieve this goal, the results of scientific research on WE were analyzed. The literature search was carried out in Scopus, eLibrary, PubMed electronic search engines using the following keywords: Wernicke encephalopathy, thiamine, alcohol abuse, thiamine deficiency. Scientific articles published between 1881 and 2024 were selected for analysis.RESULTS. The most common cause of WE is chronic alcoholism, which accounts for 50% of all cases. However, there are many other diseases and conditions that can lead to the development of WE. Vitamin B1 deficiency plays an important role in the development of WE.CONCLUSIONS. Vitamin B1 deficiency can develop as a result of a malfunction at various stages of the metabolic chain, during various pathological processes in the human body. Wernicke encephalopathy occurs not only in people who abuse alcohol, but also in pregnant women, cancer patients, patients with diseases of the gastrointestinal tract, liver and thyroid gland, after bariatric and other abdominal surgeries, as well as in patients on long-term parenteral nutrition. Thiamine deficiency, and, as a consequence, Wernicke encephalopathy, can lead to irreversible brain damage, severe disability and death.

Giant cell arteritis is a disease characterized by granulomatous inflammation of large and medium-sized arteries. The aorta and its large branches are most susceptible to pathological changes in this arteritis. The course of giant cell arteritis is often complicated by ischemia in the blood supply basin of the artery involved in the pathological process. Variants of such complications may be ischemic optic neuropathy and retinopathy, limb ischemia, and acute cerebrovascular accident. This review presents current data on the etiology and pathogenesis of giant cell arteritis, prevalence, sensitivity, and specificity of clinical and instrumental signs of this disease, as well as practical recommendations for various treatment methods during exacerbation and remission.

Introduction. Osmotic demyelinating syndrome(ODS) is a life-threatening condition caused by water and electrolyte disturbances, usually associated with rapid correction of hyponatremia, manifested by acute demyelination of the brain. The average age of development of patients with ODS varies from 30 to 50 years. The incidence of unfavorable outcome (mortality/complete dependence on outside help) varies from 33 to 55%.Objective. Systematization of data on the etiology, pathophysiology, clinical manifestations, diagnosis and treatment of osmotic demyelinating syndrome.Material and methods. The literature search was performed in the electronic search engines Scopus, eLibrary, PubMed using the keywords: osmotic demyelinating syndrome, central pontine myelinolysis, extrapontine myelinolysis. Scientific articles published between 1959 and 2024 were selected for analysis.Results. The main reason for the development of ODS is water and electrolyte disturbances that occur secondary to severe somatic pathology. Clinical manifestations of ODS are intermittent. Сlinical improvement is typical after rapid correction of osmolarity, followed by the development after 3–5 days of a clinical picture of acute myelinolysis. Currently, there is no specific therapy for ODS. However, early diagnosis of this disease is extremely important due to the high incidence of disorders of consciousness and breathing that require artificial ventilation. The polymorphism of clinical symptoms, as well as the low awareness of doctors, complicate the diagnosis and timely initiation of therapy for ODS. The optimal method of neuroimaging in patients with ODS is MRI in DWI, T2 and T2 FLAIR modes. The rate of correction of hyponatremia by no more than 10 mmol/l in the first 24 hours and no higher than 8 mmol/l every subsequent day is the main way to prevent the development of ODS.

Dysphagia is a common symptom of many diseases. Thus, the incidence of dysphagia in Parkinson’s disease is 11–81%, in patients with traumatic brain injury accounts of 27–30%, in community-acquired pneumonia it reaches 91.7%, in Alzheimer’s disease — up to 85.9%, in mental illnesses — 9–42%. According to observational studies, dysphagia is diagnosed in 8.1–90.0% of patients with acute cerebrovascular accident. We found no report on the use of botulinum toxin in the Russian Federation for the treatment of dysphagia due to spasm of the upper esophageal sphincter (UES). The aim of the work is to describe the first botulinum toxin type A injection experience for spasm of the UES in Russia. The first experience in treating neurogenic cricopharyngeal dysphagia using intrasphincteric injection of botulinum toxin type A Russia is described. We injected 100 units of botulinum toxin diluted in 4 ml of 0.9% sodium chloride solution symmetrically into 4 points (25 units, 1 ml at each point) in the spasm zone of the UES. In our case, the first effect from the injection of botulinum toxin appeared after 24 hours, and the maximum effect was recorded after 6 days. In our case, we observe no side effect after the injection of botulinum toxin. The effect of the procedure persists for 30 days after the injection of botulinum toxin type A into the UES under the control of endoscopic ultrasonography. Conclusion. Dysphagia is a common complication of many neurological diseases, including acute cerebrovascular accident. Aspiration and pneumonia due to swallowing disorder lead to an increase in the duration of hospital treatment, worsen the prognosis of the disease, and the patient’s quality of life. The injection of botulinum toxin type A for the treatment of neurogenic dysphagia due to spasm of the UES under the control of endoscopic ultrasonography is an effective, safe and minimally invasive treatment method, due to which it can be used in the acute period of acute cerebrovascular accident.

Reversible cerebral vasoconstriction syndrome (RCVS) is a collective term used to describe pathological conditions with a similar clinical and radiological picture which is characterized by thunderclap headaches with a sudden onset and reversible segmental (multifocal) constriction of the cerebral arteries. The article is devoted to issues of terminology, genetic and clinical features of RSCV, and also discusses risk factors, differential diagnosis, complications and prognosis. Modern pathogenetic mechanisms and possible approaches to the treatment of this condition are presented.

Introduction: Wernicke’s encephalopathy is a life-threatening disease caused by thiamine deficiency with the development of damage to brain. Objective: to analyze the etiological factors, clinical, laboratory and instrumental data, as well as clinical outcomes of Wernicke’s encephalopathy.Material and мethods: the study included 36 patients with Wernicke’s encephalopathy. the average age of patients was 54.5 ± 15.9 years, women were 52.8%, men — 47.2%.Results: the most common causes of Wernicke’s encephalopathy were long-term alcohol abuse and diseases of the gastrointestinal tract or liver. A decrease in the level of wakefulness was detected in 63.9% of patients at the onset of the disease and in 72.2% during the entire period of hospitalization. In all patients, MRI of the brain revealed symmetrical areas of increased signal in the T2 FLAIR and DWI modes in the medial parts of both thalami, and in some cases also in the area of the quadrigeminal plate and/or periaqueductal space of the midbrain.Conclusion. Assessment of blood thiamine levels is not mandatory before starting therapy; thiamine administration should be started without laboratory confirmation of deficiency. Preventive administration of thiamine at a dose of 1000 mg per day is justified for any clinical suspicion of Wernicke’s encephalopathy.

The clinical case is presented to demonstrate the importance of differential diagnosis of cerebral circulation disorders in patients with acute or chronic toxic effects of psychoactive substances. In the presented observation, a 50-year-old patient was taken to the N.V. Sklifosovsky Research Institute of SP with depression of the level of wakefulness to deep deafness, denies the fact of using psychoactive substances when collecting anamnesis, bilateral myosis, diffuse decrease in tone in all extremities. Computed angiotomography of the brain, transcranial dopplerography, magnetic resonance imaging of the brain, electroencephalography were performed – without obvious diagnostic findings. During a detailed examination in a neurological clinic, no data were obtained for a violation of cerebral circulation, a chemical and toxicological examination of urine and blood was performed, fentanyl was detected in biological media. Based on the literature data, however, damage to the nervous system usually occurs due to chronic intoxication and it is not always possible to detect psychoactive substances in biological environments. Due to respiratory depression, the patient was intubated and was on artificial ventilation for 72 hours until spontaneous respiration was restored. After repeated demand, the patient admitted the fact of using fentanyl allegedly to relieve pain, after which he refused further treatment. The conclusion is the need for a chemical and toxicological study of biological media in the case of a violation of consciousness of unclear genesis, however, damage to the nervous system usually occurs due to chronic intoxication and it is not always possible to detect psychoactive substances in biological media.

The diagnosis of diseases from the group of autoimmune encephalitis (AE) requires a detailed analysis of clinical data and correlation of results from a wide range of laboratory and instrumental research methods. This article presents three clinical cases of patients with AE. In one patient, AE was associated with a malignant neoplasm, in the second one – with the novel coronavirus infection, and in the third patient, no comorbid pathology was detected. The specific type of encephalitis was determined for each of the three patients. The diagnosis of “autoimmune limbic encephalitis” was established in two patients based on visualization of changes in the medial temporal structures in the magnetic resonance imaging of the brain, detection of pathological bioelectrical activity in the temporal lobe cortex in electroencephalography, and pleocytosis in cerebrospinal fluid. The diagnosis of “anti-NMDA receptor encephalitis” was made based on the detection of specific antibodies to the subunit of the corresponding receptor. Neurological deficit regression was observed in two patients after the application of combined immune therapy methods and in one patient without the use of immune therapy.