Pub Date : 2024-01-17DOI: 10.22141/2224-0713.19.8.2023.1031
I. Zozulya, A. Volosovets
The widespread introduction of cardiological diagnostic methods in clinical angioneurology has significantly enriched the data on the role of cardiovascular diseases in the development of cerebrovascular pathology. Various cardiac disorders play a significant role in the development of cardioembolic and haemodynamic ischaemic strokes. It has been scientifically proven that chronic heart failure, along with hypertension, is a risk factor for the occurrence of a chronic form of cerebrovascular disease — chronic cerebrovascular insufficiency. The characteristic feature of all types of cardiovascular insufficiency is the inability of the circulatory system to deliver to the organs, systems, tissues, including the brain, the amount of blood necessary for their normal functioning, both at rest and especially during exertion. In their daily practice, neurologists encounter patients with chronic heart failure and symptoms of cerebrovascular disease (memory loss, reduced performance, depression). Underestimation of these conditions can result in a shortened life due to irreversible damage to target organs (heart, brain, kidneys). In the absence of adequate treatment, death is possible within the first 5 years after the onset of heart failure. The degree of disease progression depends on many factors: clinical and pathogenetic variant of chronic heart failure, the rate of the pathological process, the presence of myocardial damage and remodeling, complications from target organs. In this article, we tried to analyse the literature data of domestic and foreign authors on the pathogenetic mechanisms of chronic heart failure, the impact on its development and the course of its complications, and, above all, brain damage in the form of chronic cerebrovascular insufficiency.
{"title":"About chronic cerebrovascular insufficiency caused by cardiac pathology (literature review)","authors":"I. Zozulya, A. Volosovets","doi":"10.22141/2224-0713.19.8.2023.1031","DOIUrl":"https://doi.org/10.22141/2224-0713.19.8.2023.1031","url":null,"abstract":"The widespread introduction of cardiological diagnostic methods in clinical angioneurology has significantly enriched the data on the role of cardiovascular diseases in the development of cerebrovascular pathology. Various cardiac disorders play a significant role in the development of cardioembolic and haemodynamic ischaemic strokes. It has been scientifically proven that chronic heart failure, along with hypertension, is a risk factor for the occurrence of a chronic form of cerebrovascular disease — chronic cerebrovascular insufficiency. The characteristic feature of all types of cardiovascular insufficiency is the inability of the circulatory system to deliver to the organs, systems, tissues, including the brain, the amount of blood necessary for their normal functioning, both at rest and especially during exertion. In their daily practice, neurologists encounter patients with chronic heart failure and symptoms of cerebrovascular disease (memory loss, reduced performance, depression). Underestimation of these conditions can result in a shortened life due to irreversible damage to target organs (heart, brain, kidneys). In the absence of adequate treatment, death is possible within the first 5 years after the onset of heart failure. The degree of disease progression depends on many factors: clinical and pathogenetic variant of chronic heart failure, the rate of the pathological process, the presence of myocardial damage and remodeling, complications from target organs. In this article, we tried to analyse the literature data of domestic and foreign authors on the pathogenetic mechanisms of chronic heart failure, the impact on its development and the course of its complications, and, above all, brain damage in the form of chronic cerebrovascular insufficiency.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":"10 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139616496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-17DOI: 10.22141/2224-0713.19.8.2023.1032
M. Trishchynska, O. Kononov, H.V. Lutsenko, Yu.V. Nevgad, I.P. Romanenko
Cerebrovascular pathology occupies the leading position among the causes of mortality and long-term disability in high-, middle- and low-income countries, which indicates the extreme relevance of finding new strategies for the prevention of these diseases. Today, acute ischemic stroke and vascular cognitive disorders, including vascular dementia, are among the most common forms of cerebrovascular diseases. Damage to cerebral small vessels plays a significant role in the pathogenesis of both conditions. The article analyzed literature data on the main and probable pathogenetic mechanisms of cerebral small vessel disease. Keywords used to select the literature in PubMed National Library of Medicine included: small vessel disease, white matter hyperintensity, lacunae, enlarged perivascular spaces, brain atrophy, vascular cognitive disorders. The study of the pathogenetic mechanisms of cerebral microangiopathy or cerebral small vessel disease will allow clinical and scientific research to be directed to the search for pathogenetically justified treatment and prevention strategies, which is extremely important for such patients.
{"title":"Modern understanding of the pathogenetic mechanisms of small vessel disease","authors":"M. Trishchynska, O. Kononov, H.V. Lutsenko, Yu.V. Nevgad, I.P. Romanenko","doi":"10.22141/2224-0713.19.8.2023.1032","DOIUrl":"https://doi.org/10.22141/2224-0713.19.8.2023.1032","url":null,"abstract":"Cerebrovascular pathology occupies the leading position among the causes of mortality and long-term disability in high-, middle- and low-income countries, which indicates the extreme relevance of finding new strategies for the prevention of these diseases. Today, acute ischemic stroke and vascular cognitive disorders, including vascular dementia, are among the most common forms of cerebrovascular diseases. Damage to cerebral small vessels plays a significant role in the pathogenesis of both conditions. The article analyzed literature data on the main and probable pathogenetic mechanisms of cerebral small vessel disease. Keywords used to select the literature in PubMed National Library of Medicine included: small vessel disease, white matter hyperintensity, lacunae, enlarged perivascular spaces, brain atrophy, vascular cognitive disorders. The study of the pathogenetic mechanisms of cerebral microangiopathy or cerebral small vessel disease will allow clinical and scientific research to be directed to the search for pathogenetically justified treatment and prevention strategies, which is extremely important for such patients.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":"20 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139527331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-17DOI: 10.22141/2224-0713.19.8.2023.1029
S.K. Byelyavsky, B.M. Borysov, V. I. Lutsenko, K. Trinus, L.M. Shipilo, M. Trishchynska
Previously, we showed that Anti-Terrorist Operation (ATO) participants had significant complaints of vestibular disturbances, objective and subjective vertigo, kinetosis. One hundred and ten patients were examined, including 65 participants of ATO with mild traumatic brain injury (mTBI), 44 non-ATO without mTBI. The questionnaire “Types of dizziness” was used according to the International Clinical Protocol for Vertigo Disorders (Dizziness). Complaints of optokinetic nystagmus (OKN) were found in 27 (43.08 %) ATO and 7 (15.91 %) non-ATO patients, F-test = = 0.04, T-test = 0.0026. Thus, complaints of OKN turned out to be a specific feature of patients with blast injury syndrome. Complaints of nausea were detected in 38 (58.46 %) ATO and 11 (25.00 %) non-ATO patients, F-test = 0.38, T-test = 0.00035, indicating that this complaint is present and quantitatively more pronounced in ATO patients, but it is not specific for patients with mTBI. Complaints of vomiting were found in 19 (29.23 %) ATO and 11 (13.64 %) non-ATO patients, F-test = 0.055, T-test = 0.046, showing that this complaint is not typical for patients with mTBI. Complaints of anxiety without a reason were detected in 35 (53.85 %) ATO and 15 (34.09 %) non-ATO patients, F-test = 0.75, T-test = 0.041. Thus, this complaint is present and quantitatively more significant in ATO patients. Complaints of blackout were found in 41 (63.08 %) ATO and 16 (36.36 %) non-ATO patients, F-test = 0.98, T-test = 0.006, demonstrating that this complaint is present and quantitatively more pronounced in ATO patients, but it is not specific for patients with mTBI. Complaints of depression and numbness did not differ reliably according to the statistical indicators used. There were certain correlations. OKN: with scotomas in migraine headaches, kinetoses, descendophobia, and nyctophobia. Nausea: with severity of dizziness, vomiting episodes, blackouts, migraine headaches, increased heart rate, kinetoses, nyctophobia, claustrophobia. Vomiting: with ascendophobia, migraine headaches, increased heart rate. Anxiety without a reason: with impaired movement coordination, depression, blackouts, hyperacusis, weather sensitivity, ascendophobia. Depression without a reason: with subjective vertigo, agoraphobia, blackouts, numbness, throbbing headaches, weather sensitivity, electromagnetic hypersensitivity, increased heart rate. Blackouts: with weight gain, objective vertigo, orthostatic and throbbing headache. Numbness: with dizziness and its severity, agoraphobia, ascendophobia, migraine headaches and increased heart rate. Correlations are discussed from the point of view of vestibular dysfunction.
{"title":"Vestibular disorders in blast injuries: additional symptoms","authors":"S.K. Byelyavsky, B.M. Borysov, V. I. Lutsenko, K. Trinus, L.M. Shipilo, M. Trishchynska","doi":"10.22141/2224-0713.19.8.2023.1029","DOIUrl":"https://doi.org/10.22141/2224-0713.19.8.2023.1029","url":null,"abstract":"Previously, we showed that Anti-Terrorist Operation (ATO) participants had significant complaints of vestibular disturbances, objective and subjective vertigo, kinetosis. One hundred and ten patients were examined, including 65 participants of ATO with mild traumatic brain injury (mTBI), 44 non-ATO without mTBI. The questionnaire “Types of dizziness” was used according to the International Clinical Protocol for Vertigo Disorders (Dizziness). Complaints of optokinetic nystagmus (OKN) were found in 27 (43.08 %) ATO and 7 (15.91 %) non-ATO patients, F-test = = 0.04, T-test = 0.0026. Thus, complaints of OKN turned out to be a specific feature of patients with blast injury syndrome. Complaints of nausea were detected in 38 (58.46 %) ATO and 11 (25.00 %) non-ATO patients, F-test = 0.38, T-test = 0.00035, indicating that this complaint is present and quantitatively more pronounced in ATO patients, but it is not specific for patients with mTBI. Complaints of vomiting were found in 19 (29.23 %) ATO and 11 (13.64 %) non-ATO patients, F-test = 0.055, T-test = 0.046, showing that this complaint is not typical for patients with mTBI. Complaints of anxiety without a reason were detected in 35 (53.85 %) ATO and 15 (34.09 %) non-ATO patients, F-test = 0.75, T-test = 0.041. Thus, this complaint is present and quantitatively more significant in ATO patients. Complaints of blackout were found in 41 (63.08 %) ATO and 16 (36.36 %) non-ATO patients, F-test = 0.98, T-test = 0.006, demonstrating that this complaint is present and quantitatively more pronounced in ATO patients, but it is not specific for patients with mTBI. Complaints of depression and numbness did not differ reliably according to the statistical indicators used. There were certain correlations. OKN: with scotomas in migraine headaches, kinetoses, descendophobia, and nyctophobia. Nausea: with severity of dizziness, vomiting episodes, blackouts, migraine headaches, increased heart rate, kinetoses, nyctophobia, claustrophobia. Vomiting: with ascendophobia, migraine headaches, increased heart rate. Anxiety without a reason: with impaired movement coordination, depression, blackouts, hyperacusis, weather sensitivity, ascendophobia. Depression without a reason: with subjective vertigo, agoraphobia, blackouts, numbness, throbbing headaches, weather sensitivity, electromagnetic hypersensitivity, increased heart rate. Blackouts: with weight gain, objective vertigo, orthostatic and throbbing headache. Numbness: with dizziness and its severity, agoraphobia, ascendophobia, migraine headaches and increased heart rate. Correlations are discussed from the point of view of vestibular dysfunction.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":" 23","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139616765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-17DOI: 10.22141/2224-0713.19.8.2023.1033
O.M. Yasnii, D.V. Lebedynets, M. Trishchynska
Acute stroke is a major public health problem in both developing and developed countries and has detrimental effects on the individual, family, and societal levels. Ischemic stroke is a disease with significant prevalence, high disability, high mortality, and high recurrence rate. Diabetes mellitus is one of the most serious and most common chronic diseases today, causing life-threatening complications that lead to disability. Among these complications, one of the most common is acute stroke. People with diabetes are at a 1.5–2 times higher risk of acute ischemic stroke compared to people without this disease. Hyperglycemia doubles the risk of recurrent stroke and increases the risk of death or disability after ischemic stroke. There are several possible mechanisms by which diabetes leads to acute stroke, including cardiac embolism (atrial fibrillation), endothelial dysfunction, increased arterial stiffness at an early age, systemic inflammation and thickening of the capillary basement membrane. Controlling glucose levels through lifestyle changes or medications and modifying other associated risk factors (such as hypertension and dyslipidemia) are critical steps to the effective stroke prevention.
{"title":"Features of the course of acute cerebral stroke in patients with type 2 diabetes","authors":"O.M. Yasnii, D.V. Lebedynets, M. Trishchynska","doi":"10.22141/2224-0713.19.8.2023.1033","DOIUrl":"https://doi.org/10.22141/2224-0713.19.8.2023.1033","url":null,"abstract":"Acute stroke is a major public health problem in both developing and developed countries and has detrimental effects on the individual, family, and societal levels. Ischemic stroke is a disease with significant prevalence, high disability, high mortality, and high recurrence rate. Diabetes mellitus is one of the most serious and most common chronic diseases today, causing life-threatening complications that lead to disability. Among these complications, one of the most common is acute stroke. People with diabetes are at a 1.5–2 times higher risk of acute ischemic stroke compared to people without this disease. Hyperglycemia doubles the risk of recurrent stroke and increases the risk of death or disability after ischemic stroke. There are several possible mechanisms by which diabetes leads to acute stroke, including cardiac embolism (atrial fibrillation), endothelial dysfunction, increased arterial stiffness at an early age, systemic inflammation and thickening of the capillary basement membrane. Controlling glucose levels through lifestyle changes or medications and modifying other associated risk factors (such as hypertension and dyslipidemia) are critical steps to the effective stroke prevention.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":" 694","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139617464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-17DOI: 10.22141/2224-0713.19.8.2023.1028
K. Duve, O.P. Venger
Cognitive impairment can be a consequence of direct and indirect brain injury, hypoxia, edema, metabolic disorders, neurodegenerative processes, metabolic encephalopathies, electrolyte abnormalities, organ failure, the effects of pesticides, toxins, drugs, and infectious processes. The results are presented from the study on correlations between cognitive functioning and syndromic characteristics and neuroimaging changes in patients with chronic post-traumatic (CTE), chronic vascular (CVE), chronic alcohol-induced (CAIE) and post-infectious (PIE) encephalopathies. The data of 520 medical records of patients with CTE (n = 145), CVE (n = 145), CAIE (n = 102) and PIE (n = 128) were analyzed. Neuroimaging was performed using multislice computed tomography. Cognitive functions were examined using the Montreal Cognitive Assessment. Statistical analysis of data was carried out with the help of computer software Microsoft Excel and Statistica 13.0. There was a probable relationship between cognitive functioning and extrapyramidal syndrome in patients with CVE; cognitive impairment and emotional lability disorder in patients with CAIE; cephalalgia syndrome, motor disorder syndrome and cerebellar ataxia syndrome in patients with PIE. In participants with CTE and CAIE, there was a significant correlation between cognitive functioning and ventricular enlargement; in patients with PIE — between cognitive functioning and the enlargement of the subarachnoid spaces.
{"title":"The relationship between cognitive functioning and syndromic characteristics and neuroimaging changes in patients with different types of encephalopathies","authors":"K. Duve, O.P. Venger","doi":"10.22141/2224-0713.19.8.2023.1028","DOIUrl":"https://doi.org/10.22141/2224-0713.19.8.2023.1028","url":null,"abstract":"Cognitive impairment can be a consequence of direct and indirect brain injury, hypoxia, edema, metabolic disorders, neurodegenerative processes, metabolic encephalopathies, electrolyte abnormalities, organ failure, the effects of pesticides, toxins, drugs, and infectious processes. The results are presented from the study on correlations between cognitive functioning and syndromic characteristics and neuroimaging changes in patients with chronic post-traumatic (CTE), chronic vascular (CVE), chronic alcohol-induced (CAIE) and post-infectious (PIE) encephalopathies. The data of 520 medical records of patients with CTE (n = 145), CVE (n = 145), CAIE (n = 102) and PIE (n = 128) were analyzed. Neuroimaging was performed using multislice computed tomography. Cognitive functions were examined using the Montreal Cognitive Assessment. Statistical analysis of data was carried out with the help of computer software Microsoft Excel and Statistica 13.0. There was a probable relationship between cognitive functioning and extrapyramidal syndrome in patients with CVE; cognitive impairment and emotional lability disorder in patients with CAIE; cephalalgia syndrome, motor disorder syndrome and cerebellar ataxia syndrome in patients with PIE. In participants with CTE and CAIE, there was a significant correlation between cognitive functioning and ventricular enlargement; in patients with PIE — between cognitive functioning and the enlargement of the subarachnoid spaces.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":"11 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139527106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-17DOI: 10.22141/2224-0713.19.8.2023.1030
O. Kravets, V.V. Yekhalov, V. Sedinkin, Y. Ploshchenko
The central nervous system is very sensitive to hyperthermia, which causes neurological complications through alteration of the cerebellum, basal ganglia, anterior horn cells, and peripheral nerves. Cerebellar damage is associated with generalized atrophy and signs of Purkinje cell involvement. Heat shock (stroke) is a critical condition caused by hyperthermia, typified by symmetrical damage to the cerebellum. The critical core temperature for the brain is 40–41 °C, but damage to the cerebellum can occur at lower temperatures. In the central nervous system, cerebellar Purkinje cells are most susceptible to hyperpyrexia-induced dysfunction. The degree of their loss correlates with the severity and duration of hyperthermia. Heat hyperpyrexia-induced cerebellar atrophy usually involves both the vermis and the cerebellar hemispheres. Heat stroke can also cause neurological dysfunction, most commonly due to cerebellar damage. During the acute stage, typical neurological disorders are cerebellar ataxia, cognitive impairment, dysphagia, and aphasia. The convalescent period is characterized by transient cerebellar dysfunction; diffuse cerebellar atrophy has been described, and cerebellar degeneration is a well-known consequence of heat stroke. In permanent cerebellar dysfunction after heat stroke, permanent neurological deficit is relatively rare, and the most common manifestation is cerebellar syndrome. The most common X-ray finding in heat stroke is diffuse cerebellar atrophy with preserved brain volume, which is caused by diffuse loss of Purkinje cells and, according to computed tomography and magnetic resonance imaging, mostly affects the vermis or the cerebellar hemispheres, with the hemispheres of the brain mostly remain intact. Cerebellar disorders caused by heat stroke is a complex neurological problem. To rule out an alternative diagnosis, a thorough special examination with neuroimaging is necessary.
中枢神经系统对高热非常敏感，它会通过改变小脑、基底节、前角细胞和周围神经而引起神经系统并发症。小脑损伤伴有全身萎缩和浦肯野细胞受累的迹象。热休克（中风）是一种由高热引起的危重病症，以小脑的对称性损伤为典型特征。大脑的临界核心温度为 40-41 °C，但在较低温度下也会对小脑造成损害。在中枢神经系统中，小脑浦肯野细胞最容易受到高热引起的功能障碍的影响。其损失程度与高热的严重程度和持续时间有关。高热引起的小脑萎缩通常涉及蚓部和小脑半球。中暑也会导致神经功能障碍，最常见的是小脑损伤。在急性期，典型的神经系统疾病是小脑共济失调、认知障碍、吞咽困难和失语。恢复期的特点是一过性小脑功能障碍；弥漫性小脑萎缩已被描述，小脑变性是中暑的一个众所周知的后果。在中暑后出现的永久性小脑功能障碍中，永久性神经功能缺损相对少见，最常见的表现是小脑综合征。中暑时最常见的 X 射线检查结果是弥漫性小脑萎缩，脑容量保留，这是由于普肯耶细胞弥漫性缺失造成的，根据计算机断层扫描和磁共振成像，主要影响蚓部或小脑半球，大脑半球大多保持完好。中暑引起的小脑功能紊乱是一个复杂的神经系统问题。为了排除其他诊断，有必要通过神经影像学进行全面的特殊检查。
{"title":"Cerebellar syndrome in heat stroke (literary review)","authors":"O. Kravets, V.V. Yekhalov, V. Sedinkin, Y. Ploshchenko","doi":"10.22141/2224-0713.19.8.2023.1030","DOIUrl":"https://doi.org/10.22141/2224-0713.19.8.2023.1030","url":null,"abstract":"The central nervous system is very sensitive to hyperthermia, which causes neurological complications through alteration of the cerebellum, basal ganglia, anterior horn cells, and peripheral nerves. Cerebellar damage is associated with generalized atrophy and signs of Purkinje cell involvement. Heat shock (stroke) is a critical condition caused by hyperthermia, typified by symmetrical damage to the cerebellum. The critical core temperature for the brain is 40–41 °C, but damage to the cerebellum can occur at lower temperatures. In the central nervous system, cerebellar Purkinje cells are most susceptible to hyperpyrexia-induced dysfunction. The degree of their loss correlates with the severity and duration of hyperthermia. Heat hyperpyrexia-induced cerebellar atrophy usually involves both the vermis and the cerebellar hemispheres. Heat stroke can also cause neurological dysfunction, most commonly due to cerebellar damage. During the acute stage, typical neurological disorders are cerebellar ataxia, cognitive impairment, dysphagia, and aphasia. The convalescent period is characterized by transient cerebellar dysfunction; diffuse cerebellar atrophy has been described, and cerebellar degeneration is a well-known consequence of heat stroke. In permanent cerebellar dysfunction after heat stroke, permanent neurological deficit is relatively rare, and the most common manifestation is cerebellar syndrome. The most common X-ray finding in heat stroke is diffuse cerebellar atrophy with preserved brain volume, which is caused by diffuse loss of Purkinje cells and, according to computed tomography and magnetic resonance imaging, mostly affects the vermis or the cerebellar hemispheres, with the hemispheres of the brain mostly remain intact. Cerebellar disorders caused by heat stroke is a complex neurological problem. To rule out an alternative diagnosis, a thorough special examination with neuroimaging is necessary.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":" 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139616783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-06DOI: 10.22141/2224-0713.19.7.2023.1023
O. Kravets, V. Yekhalov, V. Sedinkin, O. V. Pylypenko
Based on the understanding of the pathophysiology of heat stroke, it has been suggested that heat stroke can be considered as a form of hyperthermia that is associated with a systemic inflammatory response leading to a syndrome of multiple organ dysfunction in which encephalopathy predominates. Mechanisms of neuronal injury in heat stroke include: cellular effects (damage to membranes, mitochondria, and DNA, stimulation of excitotoxic mechanisms, protein denaturation), local effects (ischemia, inflammatory changes, edema, cytokine release, vascular damage), systemic effects (changes in cerebral blood flow, endotoxemia, translocation of bacteria through a dysfunctional gastrointestinal tract). Neurological manifestations of heat stroke develop in 3 stages according to the time of occurrence: acute, convalescent and late. In the acute stage, cerebral dysfunction prevails. Overheating of the body directly caused polyetiological cerebral dysfunction with deep suppression of consciousness in the acute stage; circulatory shock, hypoxia and cerebral ischemia, excessive accumulation of cytotoxic free radicals and oxidant brain damage developed. During the convalescence stage, cerebral dysfunction gradually decreases. This stage is characterized by transient cerebellar dysfunction. For the late stage, long-term neurological and cardiovascular complications with a constant risk of death are typical. When late stage with permanent neurologic deficits develop, cerebellar dysfunction is the most common symptom. The delayed onset of degeneration and deafferentation suggests that the syndrome is not caused by the primary lesion itself but may be a consequence of postsynaptic hypersensitivity or secondary reorganization of the involved pathways.
根据对中暑病理生理学的理解，有人认为中暑可被视为一种高热，与全身炎症反应相关，导致以脑病为主的多器官功能障碍综合征。中暑导致神经元损伤的机制包括：细胞效应（膜、线粒体和 DNA 损伤、兴奋毒性机制刺激、蛋白质变性）、局部效应（缺血、炎症变化、水肿、细胞因子释放、血管损伤）、全身效应（脑血流变化、内毒素血症、细菌通过功能紊乱的胃肠道转运）。中暑的神经系统表现根据发生时间可分为三个阶段：急性期、恢复期和晚期。急性期主要表现为大脑功能障碍。机体过热直接导致多病因脑功能障碍，急性期意识深度抑制；出现循环休克、缺氧和脑缺血，细胞毒性自由基过度积累和氧化性脑损伤。在康复阶段，脑功能障碍逐渐减轻。这一阶段的特点是短暂的小脑功能障碍。晚期则是典型的长期神经和心血管并发症，并伴有持续的死亡风险。当晚期出现永久性神经功能缺损时，小脑功能障碍是最常见的症状。变性和去感觉延迟发病表明，该综合征并非由原发性病变本身引起，而可能是突触后超敏反应或受累通路继发性重组的结果。
{"title":"Neurological disorders with general overheating of the body (scientific and literary review)","authors":"O. Kravets, V. Yekhalov, V. Sedinkin, O. V. Pylypenko","doi":"10.22141/2224-0713.19.7.2023.1023","DOIUrl":"https://doi.org/10.22141/2224-0713.19.7.2023.1023","url":null,"abstract":"Based on the understanding of the pathophysiology of heat stroke, it has been suggested that heat stroke can be considered as a form of hyperthermia that is associated with a systemic inflammatory response leading to a syndrome of multiple organ dysfunction in which encephalopathy predominates. Mechanisms of neuronal injury in heat stroke include: cellular effects (damage to membranes, mitochondria, and DNA, stimulation of excitotoxic mechanisms, protein denaturation), local effects (ischemia, inflammatory changes, edema, cytokine release, vascular damage), systemic effects (changes in cerebral blood flow, endotoxemia, translocation of bacteria through a dysfunctional gastrointestinal tract). Neurological manifestations of heat stroke develop in 3 stages according to the time of occurrence: acute, convalescent and late. In the acute stage, cerebral dysfunction prevails. Overheating of the body directly caused polyetiological cerebral dysfunction with deep suppression of consciousness in the acute stage; circulatory shock, hypoxia and cerebral ischemia, excessive accumulation of cytotoxic free radicals and oxidant brain damage developed. During the convalescence stage, cerebral dysfunction gradually decreases. This stage is characterized by transient cerebellar dysfunction. For the late stage, long-term neurological and cardiovascular complications with a constant risk of death are typical. When late stage with permanent neurologic deficits develop, cerebellar dysfunction is the most common symptom. The delayed onset of degeneration and deafferentation suggests that the syndrome is not caused by the primary lesion itself but may be a consequence of postsynaptic hypersensitivity or secondary reorganization of the involved pathways.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":"1 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139380340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-06DOI: 10.22141/2224-0713.19.7.2023.1027
K. Duve, S. Shkrobot, Z. Salii
Background. Predicting the individual risk of developing cognitive impairment and functional disability in everyday life among patients with chronic traumatic encephalopathy (CTE) will allow timely and adequate treatment to prevent dementia. Therefore, the study aimed to develop a mathematical model for predicting the risk of cognitive disorders and functional disability in patients with CTE based on the analysis of polymorphic variants of the ACE, AT2R1, eNOS, ePON1, IL-1β, IL-10, TNF-α genes, as well as cofactors (gender, age group, follow-up, presence/absence of somatic comorbidity). Materials and methods. We examined 145 individuals with CTE who were undergoing inpatient treatment in the Communal Non-Profit Enterprise “Ternopil Regional Clinical Psychoneurological Hospital” in 2021–2022 and were included in the retrospective analysis. The molecular and genetic testing was performed for 26 patients. The molecular and genetic differentiation of the studied polymorphic variants of genes was carried out in the molecular and genetic laboratory of the State Institution “Reference Centre for Molecular Diagnostics of the Ministry of Health of Ukraine” in Kyiv. Cognitive functions were studied using the Montreal Cognitive Assessment (MoCA), activities of daily living — with the Barthel index. Statistical analysis was done using Microsoft Excel and Statistica 13.0 computer software. A logistic regression analysis was performed to determine the likelihood of cognitive impairment and functional disability in patients with CTE. Results. When analyzing polymorphic variants of the ACE, AT2R1, eNOS, ePON1, IL-1β, IL-10, TNF-α genes, as well as such cofactors as gender, age group, follow-up, presence/absence of somatic comorbidity in the context of the development of cognitive disorders in patients with CTE, it has been found that the I/D polymorphism of the ACE gene has the most significant prognostic value (in the presence of the D/D genotype, the probability of cognitive impairment is 83.33 %). At the same time, patients with CTE who were carriers of the D allele of the ACE gene had a significant decrease in the MoCA score compared to the group of those who didn’t carry this allele. Regarding the development of functional disability in patients with CTE, the C108T polymorphism of the PON1 gene has the most significant prognostic value (in the presence of the T/T genotype, the risk of functional disability is 41.49 %, with significantly lower Barthel index compared to the C/C homozygotes). Conclusions. It was found that the I/D polymorphism of the ACE gene and the C108T polymorphism of the PON1 gene are likely associated with the development of cognitive impairment and functional disability in patients with CTE that indicates the feasibility of further studies involving a larger sample of patients.
{"title":"Chronic traumatic encephalopathy: predictors of the development of cognitive disorders and functional disability","authors":"K. Duve, S. Shkrobot, Z. Salii","doi":"10.22141/2224-0713.19.7.2023.1027","DOIUrl":"https://doi.org/10.22141/2224-0713.19.7.2023.1027","url":null,"abstract":"Background. Predicting the individual risk of developing cognitive impairment and functional disability in everyday life among patients with chronic traumatic encephalopathy (CTE) will allow timely and adequate treatment to prevent dementia. Therefore, the study aimed to develop a mathematical model for predicting the risk of cognitive disorders and functional disability in patients with CTE based on the analysis of polymorphic variants of the ACE, AT2R1, eNOS, ePON1, IL-1β, IL-10, TNF-α genes, as well as cofactors (gender, age group, follow-up, presence/absence of somatic comorbidity). Materials and methods. We examined 145 individuals with CTE who were undergoing inpatient treatment in the Communal Non-Profit Enterprise “Ternopil Regional Clinical Psychoneurological Hospital” in 2021–2022 and were included in the retrospective analysis. The molecular and genetic testing was performed for 26 patients. The molecular and genetic differentiation of the studied polymorphic variants of genes was carried out in the molecular and genetic laboratory of the State Institution “Reference Centre for Molecular Diagnostics of the Ministry of Health of Ukraine” in Kyiv. Cognitive functions were studied using the Montreal Cognitive Assessment (MoCA), activities of daily living — with the Barthel index. Statistical analysis was done using Microsoft Excel and Statistica 13.0 computer software. A logistic regression analysis was performed to determine the likelihood of cognitive impairment and functional disability in patients with CTE. Results. When analyzing polymorphic variants of the ACE, AT2R1, eNOS, ePON1, IL-1β, IL-10, TNF-α genes, as well as such cofactors as gender, age group, follow-up, presence/absence of somatic comorbidity in the context of the development of cognitive disorders in patients with CTE, it has been found that the I/D polymorphism of the ACE gene has the most significant prognostic value (in the presence of the D/D genotype, the probability of cognitive impairment is 83.33 %). At the same time, patients with CTE who were carriers of the D allele of the ACE gene had a significant decrease in the MoCA score compared to the group of those who didn’t carry this allele. Regarding the development of functional disability in patients with CTE, the C108T polymorphism of the PON1 gene has the most significant prognostic value (in the presence of the T/T genotype, the risk of functional disability is 41.49 %, with significantly lower Barthel index compared to the C/C homozygotes). Conclusions. It was found that the I/D polymorphism of the ACE gene and the C108T polymorphism of the PON1 gene are likely associated with the development of cognitive impairment and functional disability in patients with CTE that indicates the feasibility of further studies involving a larger sample of patients.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":"8 11","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139380382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-06DOI: 10.22141/2224-0713.19.7.2023.1022
S. A. Lysenko, N. M. Lysenko, Y. V. Stoika, Y. O. Botanevych
Background. Vestibular schwannoma is a formation of Schwann cells in the vestibulocochlear zone. Despite the benign nature of the tumor, it carries risks for life, as its massiveness poses a threat to intracranial structures and their functional capacity. The purpose of the study is to conduct an analysis of modern information on the diagnosis and methods of treatment of schwannoma. Materials and methods. A literature search using keywords was conducted in Web of Science, Scopus, PubMed, Elsevier, and Springer databases. Results. In most cases, vestibular schwannoma is diagnosed after a number of symptoms are detected such as dizziness, hearing loss, etc. According to modern research, magnetic resonance imaging and audiogram are the most informative and at the same time gold standard for diagnosis, and verification is carried out based on pathohistology. Most schwannomas are clinically stable; however, when analyzing the information, the main approaches in the presence of such a diagnosis were determined. The safest and most non-invasive one is observation, with control of the dynamics of the clinical picture and the size of the formation. However, there are several surgical techniques for complete tumor removal. The most common of them is access through the middle cranial fossa, which, unfortunately, has several limitations. Translabyrinthine and retrosigmoid approaches are also used. The choice of treatment depends on the size, growth and symptoms of the patients. Radiotherapy is one of the relatively new methods of treatment, it is sometimes combined with a surgery. Conclusions. Thus, vestibular schwannoma requires active monitoring and the use of other treatment methods. In the presence of clinical indications, a combination of different types of treatment allows achieving positive therapeutic outcomes. A perspective for future research is the study of targeted gene therapy.
背景。前庭裂隙瘤是由前庭蜗区内的许旺细胞形成的。尽管这种肿瘤是良性的，但由于其肿块对颅内结构及其功能能力构成威胁，因此具有生命危险。本研究旨在对有关裂隙瘤诊断和治疗方法的现代信息进行分析。材料和方法。使用关键词在 Web of Science、Scopus、PubMed、Elsevier 和 Springer 数据库中进行文献检索。结果。在大多数情况下，前庭分裂瘤是在发现头晕、听力下降等一系列症状后被诊断出来的。根据现代研究，磁共振成像和听力图是信息量最大的诊断方法，同时也是诊断的金标准，并根据病理组织学进行验证。大多数裂隙瘤临床症状稳定，但在分析相关信息时，确定了诊断裂隙瘤的主要方法。最安全、最无创的方法是观察，控制临床表现的动态和形成的大小。不过，也有几种手术技术可以彻底切除肿瘤。其中最常见的是通过中颅窝进入，但不幸的是，这种方法存在一些局限性。经迷路和蛛网膜后入路也可使用。治疗方法的选择取决于肿瘤的大小、生长情况和患者的症状。放射治疗是相对较新的治疗方法之一，有时会与手术相结合。结论因此，前庭分裂瘤需要积极监测并采用其他治疗方法。在有临床指征的情况下，联合使用不同类型的治疗方法可以取得积极的治疗效果。未来研究的一个方向是研究靶向基因疗法。
{"title":"Principles of diagnosis and treatment of vestibular schwannoma: a literature review","authors":"S. A. Lysenko, N. M. Lysenko, Y. V. Stoika, Y. O. Botanevych","doi":"10.22141/2224-0713.19.7.2023.1022","DOIUrl":"https://doi.org/10.22141/2224-0713.19.7.2023.1022","url":null,"abstract":"Background. Vestibular schwannoma is a formation of Schwann cells in the vestibulocochlear zone. Despite the benign nature of the tumor, it carries risks for life, as its massiveness poses a threat to intracranial structures and their functional capacity. The purpose of the study is to conduct an analysis of modern information on the diagnosis and methods of treatment of schwannoma. Materials and methods. A literature search using keywords was conducted in Web of Science, Scopus, PubMed, Elsevier, and Springer databases. Results. In most cases, vestibular schwannoma is diagnosed after a number of symptoms are detected such as dizziness, hearing loss, etc. According to modern research, magnetic resonance imaging and audiogram are the most informative and at the same time gold standard for diagnosis, and verification is carried out based on pathohistology. Most schwannomas are clinically stable; however, when analyzing the information, the main approaches in the presence of such a diagnosis were determined. The safest and most non-invasive one is observation, with control of the dynamics of the clinical picture and the size of the formation. However, there are several surgical techniques for complete tumor removal. The most common of them is access through the middle cranial fossa, which, unfortunately, has several limitations. Translabyrinthine and retrosigmoid approaches are also used. The choice of treatment depends on the size, growth and symptoms of the patients. Radiotherapy is one of the relatively new methods of treatment, it is sometimes combined with a surgery. Conclusions. Thus, vestibular schwannoma requires active monitoring and the use of other treatment methods. In the presence of clinical indications, a combination of different types of treatment allows achieving positive therapeutic outcomes. A perspective for future research is the study of targeted gene therapy.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":"15 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139380562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-06DOI: 10.22141/2224-0713.19.7.2023.1024
V.S. Tkachyshyn
Occupational dyskinesia is a functional damage to the central nervous system, characterized by an impaired coordination of precise movements that are necessary to perform certain operations. The disease develops gradually and manifests in employees with a long work experience. At the same time, other motor functions are preserved. There are convulsive, paretic, ataxic, trembling, neuralgic and mixed clinical forms of this pathology at the present stage. In the initial period, the diagnosis of occupational dyskinesia causes certain difficulties associated with the spread of symptoms exclusively to one action. It is also difficult to verify the presence of dyskinesia itself, which is described by a patient. Treatment should be started as early as possible, as it is effective only at the initial stage of the disease. A complete and sufficiently long cessation of professional activity is necessary. Treatment is long and comprehensive. Preventive measures involve the correct organization of work with an even distribution of professional workload. Since occupational dyskinesia is diagnosed late, at the stage of already developed clinical manifestations, the prognosis for recovery is doubtful. The professional prognosis is unfavorable. Patients need reorientation and retraining for related professions.
{"title":"Dissociative motor disorders — occupational dyskinesia","authors":"V.S. Tkachyshyn","doi":"10.22141/2224-0713.19.7.2023.1024","DOIUrl":"https://doi.org/10.22141/2224-0713.19.7.2023.1024","url":null,"abstract":"Occupational dyskinesia is a functional damage to the central nervous system, characterized by an impaired coordination of precise movements that are necessary to perform certain operations. The disease develops gradually and manifests in employees with a long work experience. At the same time, other motor functions are preserved. There are convulsive, paretic, ataxic, trembling, neuralgic and mixed clinical forms of this pathology at the present stage. In the initial period, the diagnosis of occupational dyskinesia causes certain difficulties associated with the spread of symptoms exclusively to one action. It is also difficult to verify the presence of dyskinesia itself, which is described by a patient. Treatment should be started as early as possible, as it is effective only at the initial stage of the disease. A complete and sufficiently long cessation of professional activity is necessary. Treatment is long and comprehensive. Preventive measures involve the correct organization of work with an even distribution of professional workload. Since occupational dyskinesia is diagnosed late, at the stage of already developed clinical manifestations, the prognosis for recovery is doubtful. The professional prognosis is unfavorable. Patients need reorientation and retraining for related professions.","PeriodicalId":14476,"journal":{"name":"INTERNATIONAL NEUROLOGICAL JOURNAL","volume":"6 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139380657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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