Vol 40, No 4 (2021)

The article presents the history of the research of neuroinfections at the Nervous Diseases Department of the Imperial Medical Surgical Academy, later the Military Medical Academy, from 1860 until nowadays. One of the outstanding achievements of Russian and world medicine in the twentieth century, constituting an entire era in neurology and virology, was the comprehensive study of tick-borne encephalitis by Aleksandr Gavrilovich Panov. He made a huge contribution to the research of this infection: “Clinic of spring-summer encephalitis” (1938) – the first journal article in the world literature on the clinical aspects of tick-borne encephalitis; the first Ph.D. thesis on the clinical picture of tick-borne encephalitis was successfully defended by A.G. Panov on February 20, 1939 under the leadership of A.V. Triumfov; the first monograph on tick-borne encephalitis and other encephalitis – “Seasonal summer encephalitis” (Vladivostok, 1940) also belongs to A.G. Panov. The results of the research of tick-borne encephalitis in 1934–1949 became the subject of a doctoral dissertation, defended on December 8, 1951. In 1956, the classic monograph by A.G. Panov “Tick-borne encephalitis” was published. At the end of XX and beginning of XXI centuries research work in the field of neuroinfection expanded, studies were carried out in various directions, including neuropathology of herpes–virus, alteration of the nervous system in botulism, acute demyelinating polyneuropathies, neuropathology of chlamydial infection, neuroborreliosis, neuropathology of infective endocarditis, alteration of the blood-brain barrier in meningitis, treatment of neuroinfectious diseases. For more than a century and a half, the staff of the Department of Nervous Diseases of the Imperial Medical Surgical (Military Medical) Academy have created and laid the foundation for the doctrine of neuroinfections for numerous followers, as well as the modern generation of neurologists and doctors of related specialties (bibliography: 10 refs)

The involvement of the nervous system in the pathological process that occurs when COVID-19 is infected is becoming more and more obvious. The question of the possibility of the debut or progression of the already developed Parkinsonism syndrome in patients who have undergone COVID-19 is regularly raised. A large number of hypotheses are put forward to explain this relationship. It is assumed that a violation of iron metabolism in the brain may underlie the development and progression of neurodegenerative diseases, including after the new coronavirus infection SARS-CoV-2. The analysis of stu dies on the possible influence of iron metabolism disorders on the occurrence and mechanism of development of neurodegenerative diseases after infection with SARS-CoV-2 has been carried out. The processes of physiological maintenance of iron homeostasis, as well as the influence of physiological aging on the accumulation of iron in the central nervous system are described. The relationship between hyperferritinemia occurring in COVID-19 and ferroptosis as the basis of the neurodegenerative process in Parkinson’s disease and Alzheimer’s disease is discussed. The main molecular mechanisms involved in ferroptosis are described. Examples of involvement of metal homeostasis disorders in the process of altering the structure of α-synuclein, synthesis of β-amyloid, hyperphosphorylated tau- protein are given. The causes of excessive iron accumulation in certain brain structures are discussed. The question of the possibility of using the assessment of changes in iron metabolism as a new biomarker of the progression of Parkinson’s disease is analyzed. (1 figure, bibliography: 62 refs)

The central nervous system seems to be quite vulnerable to SARS-CoV-2, leading to a variety of alteration pathways, high incidence and variability of the neurological symptoms of COVID-19. The COVID-19 symptoms, possibly associated with alteration to the central nervous system, include hyperthermia, shortness of breath, fatigue, headache, dizziness, dysphonia, dysphagia, hyposmia and anosmia, hypogeusia and ageusia, impairment of consciousness. The impairment of olfaction and gustation are the most common symptoms of the nervous system alteration (98% and 70%, respectively), which is most likely a consequence of the alteration of the receptors. Presumably the pathogenesis of dysphonia and dysphagia may involve neurodegenerative mechanisms or may be associated with a predominantly demyelinating alteration of the caudal cranial nerves. Pathomorphological findings in the brain of the COVID-19 patients include diffuse hypoxic and focal ischemic injuries of various sizes up to ischemic infarctions (in thrombosis of large arteries); microangiopathy; vasculitis; diapedetic and confluent hemorrhages with possible progression to hemorrhagic infarctions and rarely intracerebral hematomas. Acute cerebrovascular accident worsens the course of COVID-19 and can worsen the clinical outcome, taking into account the mechanisms of the central nervous system alteration in highly contagious coronavirus infections (SARS-CoV, MERS, SARS-CoV-2), including embolism, hypoxia, neurodegeneration, systemic inflammatory response and immune-mediated alteartion to the nervous tissue. A fairly rare complication of coronavirus infection, however, acute myelitis requires attention due to the severity of neurological disorders. The literature data show high incidence and polymorphism of the symptoms of the central nervous system alteration, as well as the important role of the cerebrovascular and neurodegenerative pathogenesis of brain alteration in COVID-19, which is taken into account in examining and treating the patients with new coronavirus infection. (1 figure, bibliography: 61 refs)

Aim of the research was to study the features of the structure of postoperative cerebral dysfunction, establishing the risk factors for the development of postoperative cerebral dysfunction and for the each of the clinical types during operations for malignant neoplasms of the chest and abdomen. The study was conducted in 2 stages: a retrospective study based on medical records and a prospective study. In a retrospective study by the method of directed selection from 93,129 clinical cases of patients, 47 cases of patients with acute stroke after surgery were selected. In prospective study, 102 patients (69 men, 33 women) aged 38 to 85 years were examined, the median age was 67 years. They were divided into two study groups: “thoracic”, “abdominal”. In a retrospective study, the incidence of perioperative stroke was 0.05%. In a prospective study of surgical operations for malignant neoplasms of the chest and abdomen, the incidence of postoperative cerebral dysfunction was 34%, perioperative stroke – 2%, symptomatic delirium of the early postoperative period – 11%, deferred cognitive impairment – 31%. Statistical processing of the prospective study data revealed 10 risk factors for postoperative cerebral dysfunction, 12 risk factors for perioperative stroke, 7 risk factors for symptomatic delirium of the early postoperative period, and 6 risk factors for deferred cognitive impairment. For each of the clinical types of postoperative cerebral dysfunction the Charlson comorbidity index has a significant predictive value, and therefore it seems appropriate to include this parameter in the preoperative examination algorithm (3 tables, bibliography: 8 refs)

Epileptic status is one of the urgent conditions in neurology that requires clear and urgent measures at any stage of medical care. It ranks second among all urgent neurological conditions. The therapeutic principle “time-brain” is applicable not only for urgent measures in acute cerebrovascular accident, but also for the relief of epileptic status, since the worst prognosis is associated with an increase in the duration of seizure activity. According to the standards proposed in the world for the treatment of epileptic status, benzodiazepines, intravenous forms of antiepileptic drugs, and general anesthetics are used. In the Russian Federation, the use of many drugs is limited due to the lack of registration, their lack in standards, and unavailability in hospitals. Due to the lack of studies on the treatment of epileptic status that go beyond the early stage of status, most of the recommendations presented worldwide remain based on case series or expert judgment. The efficacy benefits of anti-status drugs used in the second and third stages of epileptic status therapy remain unclear. Therefore, if there is a choice of anti-status drugs, the decision of which drug, in what dose and in what sequence will be used, should be made by the senior and most trained doctor in this matter, taking into account the characteristics of each patient. Based on modern international and personal experience, the paper presents a step-by-step protocol for the treatment of generalized convulsive epileptic status, discusses the successes and problems of providing care to patients with this pathology in Russia. The quality of medical care in epileptic status can be significantly improved provided that medical personnel at all stages of the treatment protocol are required to evacuate patients with epileptic status to specialized centers of multidisciplinary hospitals with the possibility of examination and therapy, including the availability of EEG monitors, neuroimaging and laboratory capabilities, and also access to modern antiepileptic drugs (1 table, bibliography: 30 refs)

Pancreatic encephalopathy is a formidable complication of acute pancreatitis, significantly aggravating the course and increasing the mortality rate in this disease. For pancreatic encephalopathy, an acute onset and fluctuating course with subsequent cyclic progression are typical, and the severity of neurological symptoms may be directly dependent on the activity of the pancreatic process. The risk of having residual symptoms, primarily in the form of cognitive impairment, increases with repeated episodes of acute pancreatic encephalopathy. In the pathogenesis of pancreatic encephalopathy, an important role is played by a combination of enzymatic and hormonal dysfunction of the pancreas, systemic microcirculation disorders due to hypovolemia, typical for acute pancreatitis, and changes in glucose metabolism associated with the effects of secondary hepatocellular insufficiency and pancreonecrosis. Microscopically, gross changes in the vascular link are revealed in the form of plasmorrhages and diapedesic hemorrhages in the Virchow-Robin spaces and the white matter of the brain, desquamation and dystrophy of endothelial cells, swelling of the adventitia membrane, sludge of blood corpuscles, plasma impregnation and segmental necrosis of the vascular wall with predominant involvement and small caliber. The presence of pancreatic encephalopathy should be suspected if neurological symptoms are detected in patients with symptoms of acute pancreatitis, such as psychomotor agitation, visual and auditory hallucinations, delirium, followed by episodes of deafness, adynamia, drowsiness, up to a state of catatonia and coma. In most cases, psychomotor agitation is combined with manifestations of the syndrome of irritation of the meninges. Focal neurological symptoms, myoclonia, hyperkinesis may be associated with mental and general cerebral symptoms. Mortality in acute pancreatic encephalopathy is due to shock, hemorrhagic complications, ketoacidosis, fatty embolism of cerebral vessels or renal failure (bibliography: 35 refs)

The risk of ischemic stroke in inpatients is higher than in the general population. This is due to both the greater comorbidity of inpatients and the presence of additional risk factors, the most studied of which are iatrogenic interventions. At the same time, the higher the probability of developing an ischemic stroke, the more risk factors the patient has. An important link in the pathogenesis of in-hospital ischemic stroke is the activation of the hemostasis system, which is an obligate consequence of a typical pathological process underlying diseases and injuries that led to hospitalization: blood loss, inflammation, mechanical tissue damage, dehydration, etc. In foreign literature, this condition is attributed to the group of acquired thrombophilia, in domestic literature the term hypercoagulation syndrome has become more widespread. Iatrogenic effects can also play an important role in the pathogenesis of hypercoagulation syndrome. It is characterized by increased readiness for thrombosis, clinical and laboratory signs of hypercoagulation, activation of various factors and components of coagulation, decreased fibrinolysis, but without the development of acute thrombosis. Hypercoagulation syndrome is rarely assessed in routine practice as a risk factor for ischemic stroke, however, it can act as an additional and main risk factor for the development of all subtypes of ischemic stroke (according to the TOAST classification), including the ESUS concept. In this regard, it is advisable to distinguish in its structure: chronic (existing before hospitalization: hereditary and/or acquired) and acute (situational, developed as a result of the underlying disease, its complications or iatrogenic effects) hypercoagulation syndromes. To designate a group of acute pathological conditions predisposing to the development of hypercoagulation syndrome, systemic and/or local thrombotic complications, including in-hospital ischemic stroke, and requiring increased preventive measures, it seems pathogenetically justified, understandable and convenient to use the term situational hypercoagulation conditions (1 table, bibliography: 19 refs)

Disability after a stroke is most often associated with decreased patient activity due to walking disorder. In case of severe paresis, the function of the limb in the early stages of recovery is advisable to support with the help of partial prosthetics, using methods that provide functional stimulation. The complex treatment of central paresis includes botulinum therapy, which is due to the high incidence of spasticity.

Aim: of the study: evaluation of the efficacy of functional electrical stimulation in a complex of multimodal effects in restoring movement in stroke patients with lower limb paresis.

Materials and methods: Stimulation and neuroprosthetic methods (“Bioness L300”) were used as the main therapeutic program of rehabilitation treatment for patients with motor disorders of the lower limb after an ischemic stroke (n = 70). The median period of stroke was 21 [11; 47] days, median age 54 [42; 65] years. Scales and questionnaires were used to assess the loss of strength and volume of movement disorders, spasticity, walking speed and self-care (Medical Research Council Weakness Scale (1981, MRC), Barthel Index (1965), Modified Ashworth Scale (MAS), 10-meter test).

Results: The effectiveness of personalized therapy with the use of a neuroprothesis (“Bioness L300”) in patients in the acute and early recovery period of ischemic stroke was shown. The additional use of botulinum toxin made it possible to eliminate the inhibitory effect of spasticity, which expanded the possibility of using intensive methods of physical rehabilitation. There was an increase in daily activity, walking speed, and the level of self-care of patients in 90 % of cases.

Conclusion: The use of a complex of stimulating personalized techniques in the acute period of a stroke is justified and safe. The functional electrical stimulation helps to overcome power paresis, increases the overall level of physical activity of patients after a stroke, motivation for recovery and improves the quality of life. (1 figure, 2 tables, bibliography: 9 refs)

Understanding age-related and functional changes in cerebral venous circulation is critical for the development of new preventive, diagnostic and therapeutic approaches to maintaining brain health in the elderly. Chronic cerebral ischemia is one of the widespread socially significant vascular diseases caused by a decrease in the level of blood circulation. To assess the role of venous outflow through the internal jugular veins in cognitive decline and neural networks in patients with chronic cerebral ischemia, 30 men and 40 women (average age 66.5 years), cognitive functions and organization of neural networks were studied at high and low levels of cerebral venous blood flow through the internal jugular veins. To assess the venous outflow, the systolic blood flow rate was measured by the internal jugular veins. A higher rate of venous outflow through internal jugular veins is associated with a more successful performance of the Luria test for verbal memory. A higher or lower blood flow rate affects the formation of neural networks of the brain. At a higher blood flow rate, the predominant areas of the resting neural networks (the passive mode network of the brain and the salient network) are localized in the frontal regions, at a low blood flow rate, the predominant neural network (frontal-parietal) is located in the left hemisphere. The state of faster and slower venous outflow forms neural networks using different neural formations that affect verbal memory. Reorganization of neural networks in this case, apparently, is the central mechanism responsible for cognitive decline in chronic cerebral ischemia (2 figs, 1 table, bibliography: 10 refs)