The review highlights the current understanding of the relationship between particulate matter (PM) in air pollution and the risk of neurodegenerative diseases (NDDs). For this purpose, materials from articles indexed in the PubMed and RSCI databases were used. The results of the short-term and long-term effects of PM on the occurrence and progression of NDDs depending on their size, chemical composition and age of the subjects are considered. PMs with an aerodynamic diameter of ≤ 2.5 microns are recognized as the most dangerous. Epidemiological, clinical and experimental studies have confirmed that air pollution with PM, especially those containing metals, is one of the risk factors for NDDs. Hypotheses of the pathogenesis of the most common NDDs, Alzheimer’s and Parkinson’s diseases, are discussed. Unfortunately, none of the hypotheses provides a clear description of the role of PMs in the pathogenesis of NDDs, in particular, at the molecular or cellular level. Systematized scientific data, especially in the form of formalized descriptions, contribute to the understanding of the pathogenesis and can be used in practical medicine to assess the risk of occurrence, early diagnosis, prognosis and increase the effectiveness of treatment of patients with NDDs.

Thoracic outlet syndrome (TOS) is challenging to diagnose of it`s different etiology and pathophysiology. For now, all the physical examinations and investigations lack sensitivity and/or specificity. Recent efforts have been made to more clearly define a set of diagnostic criteria that will bring consistency to the diagnosis of TOS. Surgical management remains the mainstay of operative treatment for all patients, who have failed conservative therapy, because of it`s low efficiency.

This article aims to review the etiology and pathophysiology, clinical presentations, diagnosis, and management of thoracic outlet syndrome.

Pulmonary arteriovenous malformation (PAVM) is considered a rare cause of ischaemic stroke in young patients. In this article, we present a case series of 5 patients with PAVM-associated ischaemic stroke. We discuss pathophysiology, clinical presentation, diagnostic approaches, and secondary prevention. In addition, two of the aforementioned cases are provided in detail: the one of 32-year-old female with ischaemic stroke associated with sporadic PAVM, the latter being treated with embolization, and the one of 24-year-old male with hereditary hemorrhagic telangiectasia (HHT) who developed PAVM-associated ischaemic stroke, who was treated with intravenous thrombolytic therapy and mechanical thrombectomy on admission, followed by video-assisted thoracoscopic PAVM resection.

Parkinson’s disease (PD) is the second most common neurodegenerative disease in the world, however, structural changes in the brain at different stages and the associated pathophysiological mechanisms remain unclear.
Objective: to study MR-morphometric changes in the cerebral cortex in the early and advanced stages of PD in comparison with the control group.
Material and methods. 88 patients with PD were examined (II stage of the disease — 42 people, III stage — 46 people according to the Hoehn–Yahr scale). The control group consisted of 35 people who did not differ in sex and age with initial manifestations of cerebrovascular insufficiency. All groups included in the study underwent a neurological examination, as well as magnetic resonance imaging of the brain on a Philips Achieva 3.0T apparatus, followed by post-processing processing of the T1 gradient echo images obtained using FreeSurfer 6.0 software.
Results. In patients with stage II PD, compared with the control group, a significant decrease in the thickness of the cortex was found in the gyrus of the precuneus (p = 0.014) of the lateral part of the superior temporal gyrus, inferior frontal gyrus, postcentral sulcus, superior temporal sulcus, which progressed during the transition to the third the stage of the disease and can serve as a marker of the progression of the neurodegenerative process.
Conclusion. A morphometric study of the cerebral cortex in PD makes it possible to clarify some links in the pathogenesis of the formation, including dopamine-independent symptoms of the disease.

Anti-MuSK myasthenia is a chronic autoimmune disease caused by violation of the function of the agrin-MuSK-Lrp4 complex, accompanied by the development of pathological muscle fatigue and often muscle atrophy. The disease can be a primary, as well as a complication of immunosuppressive therapy and hematopoietic stem cell transplantation.
We present a case of anti-MUSK myasthenia gravis that developed after allogeneic HSCT due to acute myeloid leukemia in a 44-year-old patient (born in 1975). A distinctive feature of the case was a generalized injury, including not only extraocular, but also paravertebral muscles, dropped head syndrome in the evening. In addition, laboratory, electroneuromyographic and neuroimaging (MRI of muscles, MR-spectroscopy) data indicating the neurogenic reversible nature of changes in the involved musculature are presented.
Results. This study presents MRI and EMG signs of neurogenic damage of axial musculature in a patient with weakness and swelling of the paravertebral muscles (edematous changes according to STIR, corresponding to MR signs of early functional denervation) for a period of 2–4 months, due to anti-MUSK myasthenia gravis. Clinical manifestations, as well as edematous neurogenic changes in the paravertebral muscles, regressed after pathogenetic therapy.
Conclusion. The article presents up-to-date data on the clinical and instrumental characteristics of myasthenia gravis. The considered clinical example confirms the presence of neurogenic changes at an early stage of anti-MUSK myasthenia gravis and indicates the need for immediate initiation of pathogenetic therapy to avoid the development of atrophy and fatty infiltration of muscles.

The aim of the study was to assess the incidence and clinical features of headache associated with the use of granulocyte colony-stimulating factor (G-CSF) for stem cell mobilization or neutropenia treatment among oncohematological patients and bone marrow donors.
Material and methods. A prospective observational uncontrolled study included 39 participants: 20 bone marrow donors (group 1) and 19 oncohematological patients (group 2). We evaluated the incidence and clinical features of headache after subcutaneous administration of G-CSF (filgrastim) at doses of 5 to 10 μg/kg for 2 to 5 days.
Results. Headache occurred in bone marrow donors more often compared to patients with hematological malignancies (78.9% vs 35.0%; p = 0.006). There were no significant differences in the time of headache onset, its duration, intensity, features, and localization between two groups. Gender, age, dose of G-CSF, and duration of its use were not associated with headache development in both groups.
Conclusion. Headache occurs more often in bone marrow donors than in patients with hematological malignancies. The phenotype of headache associated with G-CSF exposure is not drug-specific and requires further studies on its semiotics.

Introduction. Affective and cognitive disorders are characteristic manifestations of Parkinson’s disease (PD). The clinical assessment of this disorder in PD is assessed as a negative assessment of the quality of life (QoL) of patients. Issues related to motor, affective, cognitive communities with various aspects of QoL at the stage of PD require mandatory.
Aim: to evaluate the associations between motor, affective, cognitive impairments and QoL indicators in patients in the early stages of PD.
Results. Significant relationships were found between the motor aspects of QOL and affective and cognitive impairments: between the total assessment of AFLD, assessments of mobility/everyday activity of QoL and SSOBP (r = 0.45–0.49, p < 0.05), depression (r = 0.77, p < 0.05), apathy (r = 0.42, p < 0.05), trait anxiety (TA, r = 0.58, p < 0.05), visuospatial functions SCOPA (r = –0,34, p < 0.05), Stroop test 3 (r = 0.33, p < 0.05).
There was a relationship between self-assessment of emotional well-being of QoL and affective, cognitive impairments: depression, TA (r = 0.73, 0.77, p < 0.05), state anxiety (SA), apathy (r = 0.52, r = 0.56, p < 0.05); SCOPA (r = –0.27, p < 0.05), interference index, Stroop test (r = 0.29, p < 0.05), 1 part TMT test (r = 0.31, p < 0.05). A relationship was found between self-assessment of social life and motor, affective disorders: SSOS (r = 0.38, p < 0.05), SA (r = 0.43, p < 0.05), depression (r = 0.48, p < 0.05), apathy (r = 0.57, p < 0.05).
Conclusion. The significant role of depression, anxiety, apathy, cognitive impairments in self-assessment of motor disorders, decreased daily activity, deterioration of emotional and social aspects of QoL already in the early stages of PD justifies the need for diagnosis and treatment of these disorders in each patient. Taking into account the mutual influence of motor, affective and cognitive disorders, complex rehabilitation is required to improve the quality of life of patients.

Purpose of the study: to study the neurological status, anamnesis data and electroencephalography in patients with autism spectrum disorders.
Material and methods. The study involved 54 children with autism spectrum disorders aged from 3 to 7 years. Anamnestic data were studied, neurological and electroencephalographic studies were performed.
Results. The following were identified as the main antenatal and intranatal risk factors for the formation of neurological disorders: gestosis, the threat of termination of pregnancy, weakness of labor and an increase in the duration of the anhydrous period in mothers. A significant number of children were born prematurely and had signs of intrauterine hypoxia at birth. When examining the neurological status, the majority of patients revealed motor and coordination disorders, disorders of tactile sensitivity. Electroencephalography made it possible to register in most patients a delay in the formation of the rhythm of the bioelectrical activity of the brain. Periodic regional decelerations were detected in 9 cases, and epileptiform activity — in 5 cases.
Conclusion. Disorders in the neurological status in children with autism spectrum disorders were noted in the form of mild motor symptoms, disorders of motor coordination and tactile sensitivity.

Ketogenic diet (KD) refers to promising methods of treatment of epilepsy resistant to anticonvulsants. A clinical case of the use of KD in a child with drug resistant epilepsy (DRE) is presented. This clinical case demonstrates the effectiveness of KD in a child with DRE in the form of achieving 100% control over seizures and positive shifts in the psycho-motor development of the child and positive changes in the child’s psychomotor development while ensuring adequate physical health.

Isolated oculomotor disorders caused by central nervous system damage are quite rare. As a rule, they are combined with other signs of cerebral trunk damage. A clinical case with the focus of amyelination in the cerebral trunk area, which manifests itself in the form of bilateral horizontal gaze palsy in the absence of other focal neurological symptoms is presented. A complete regression of oculomotor disorders was observed against the background of glucocorticosteroid therapy. A differential research was carried out among amyelinating, ophthalmic, endocrinologic diseases, ANCA-associated vasculitis (AAV).

The epidemiology of cervical artery dissection (CAD), which is often not thought to be the cause of ischemic stroke and transient ischemic attack (TIA), is discussed. The pathomorphology and pathogenesis of CAD, the key feature of which is the development of intramural hematoma, as well as predisposing conditions, triggers and associated conditions, in particular migraine, are reviewed. The clinical picture of diseases — local symptoms (headache and/ or neck pain, Horner’s syndrome, caudal cranial nerve involvement, cervical radicular syndrome, pulsatile tinnitus) and ischemic events (ischemic stroke or TIA) is presented. Modern approaches to urgent neuro- and angioimaging in CAD are reflected, including the possibilities of CT angiography (direct and indirect signs) and fat sat MRI (crescent symptom). Issues of reperfusion therapy (intravenous thrombolysis, thrombectomy and stenting) are discussed. The course of disease and secondary antithrombotic prophylaxis are analyzed.