Introduction. COVID-19 can damage the nervous system by direct viral damage to the neural cells or by immunopathology. More serious medical conditions such as cerebral edema, neuronal degeneration, encephalitis, acute disseminated encephalomyelitis, Guillain-Barre syndrome, Bickerstaff’s brainstem encephalitis, Miller-Fisher syndrome, polyneuritis, toxic encephalopathy, and stroke can occur.Case report. We report a case of a 40-year-old patient with previous history of hypertension and no other chronic disease who was admitted to the hospital with respiratory distress due to SARS-CoV-2-induced bilateral pneumonia. A few days later, he developed worsening respiratory function with an acute seizure episode. Head CT scan revealed subarachnoid hemorrhage with diffuse cerebral edema as a lethal neurological complication, possibly secondary to COVID-19.Discussion. COVID-19 induces CNS damage through various mechanisms including ACE-2 receptor damage, cytokine storm syndrome, secondary hypoxia, blood-brain barrier disruption, and neuroinflammation. Neurological symptoms correlate with the severity of COVID-19 disease and may range from asymptomatic infection to severe and lethal forms. Acute cerebral edema, as illustrated by our case, may result from a combination of diffuse en dothelial dysfunction, cytokine release syndrome, and hypoxic damage from pulmonary dysfunction.
{"title":"Acute cerebral edema: a lethal neurological complication in a patient with COVID-19 infection. Case report and literature review","authors":"M. Puodžiūnaitė, R. Sadeckaitė, A. Čikotienė","doi":"10.29014/ns.2022.26.12","DOIUrl":"https://doi.org/10.29014/ns.2022.26.12","url":null,"abstract":"Introduction. COVID-19 can damage the nervous system by direct viral damage to the neural cells or by immunopathology. More serious medical conditions such as cerebral edema, neuronal degeneration, encephalitis, acute disseminated encephalomyelitis, Guillain-Barre syndrome, Bickerstaff’s brainstem encephalitis, Miller-Fisher syndrome, polyneuritis, toxic encephalopathy, and stroke can occur.Case report. We report a case of a 40-year-old patient with previous history of hypertension and no other chronic disease who was admitted to the hospital with respiratory distress due to SARS-CoV-2-induced bilateral pneumonia. A few days later, he developed worsening respiratory function with an acute seizure episode. Head CT scan revealed subarachnoid hemorrhage with diffuse cerebral edema as a lethal neurological complication, possibly secondary to COVID-19.Discussion. COVID-19 induces CNS damage through various mechanisms including ACE-2 receptor damage, cytokine storm syndrome, secondary hypoxia, blood-brain barrier disruption, and neuroinflammation. Neurological symptoms correlate with the severity of COVID-19 disease and may range from asymptomatic infection to severe and lethal forms. Acute cerebral edema, as illustrated by our case, may result from a combination of diffuse en dothelial dysfunction, cytokine release syndrome, and hypoxic damage from pulmonary dysfunction.","PeriodicalId":479531,"journal":{"name":"Neurologijos seminarai","volume":"98 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135697163","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}
A. Judickaitė, A. Zizas, A. Varoniukaitė, L. Šemeklis, B. Glebauskienė
Anisocoria (unequal pupil size) is a condition described as various lacerations in iris sphincter or dilator muscles, innervation abnormalities, or conditions caused by external pharmacological agents. Adie pupil is one of the causes of anisocoria. Adie pupil is a rare neurological disorder which represents itself with unilateral or bilateral mydriasis, unresponsiveness to bright or dim light, and constriction on accommodation. This condition is idiopathic, affecting 25-45-year-old adults, more frequently women. The symptoms are a unilateral or bilateral dilated pupil, photophobia, and blurred vision. The diagnosis is based on patients’ symptoms, clinical examination findings, and a dilute pilocarpine test can also be performed. Most patients do not need treatment. In this article, we review the epidemiology, pathogenesis, etiology, clinical evaluation, diagnostic features, treatment of Adie pupil, its relationship with COVID-19, and other conditions that cause anisocoria.
{"title":"Adie pupil. Literature review","authors":"A. Judickaitė, A. Zizas, A. Varoniukaitė, L. Šemeklis, B. Glebauskienė","doi":"10.29014/ns.2022.26.19","DOIUrl":"https://doi.org/10.29014/ns.2022.26.19","url":null,"abstract":"Anisocoria (unequal pupil size) is a condition described as various lacerations in iris sphincter or dilator muscles, innervation abnormalities, or conditions caused by external pharmacological agents. Adie pupil is one of the causes of anisocoria. Adie pupil is a rare neurological disorder which represents itself with unilateral or bilateral mydriasis, unresponsiveness to bright or dim light, and constriction on accommodation. This condition is idiopathic, affecting 25-45-year-old adults, more frequently women. The symptoms are a unilateral or bilateral dilated pupil, photophobia, and blurred vision. The diagnosis is based on patients’ symptoms, clinical examination findings, and a dilute pilocarpine test can also be performed. Most patients do not need treatment. In this article, we review the epidemiology, pathogenesis, etiology, clinical evaluation, diagnostic features, treatment of Adie pupil, its relationship with COVID-19, and other conditions that cause anisocoria.","PeriodicalId":479531,"journal":{"name":"Neurologijos seminarai","volume":"98 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135696393","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}
COVID-19 infection is affecting more and more people around the world, and as the number of recovered patients increases, so does the knowledge on the potential clinical signs of the disease. Although SARS-CoV-2 virus is commonly associated with damage to the respiratory system, it has been observed that about half of patients with COVID-19 infection may also develop various neurological symptoms such as anosmia, dysgeusia, headache, myalgia, or dizziness. Encephalopathy is singled out as one of the most severe complications of the central nervous system caused by SARS-CoV-2 virus and associated with longer duration of the disease, increased disability, and mortality. Acute encephalopathy is a disorder of the brain that clinically occurs with a sudden change in the level of consciousness in otherwise healthy patients before the onset of symptoms. Risk factors include older age, male gender, quicker hospitalization after the onset of symptoms, and chronic illnesses. In exceptional cases, encephalopathy may be an early or even a major symptom of COVID-19 in young patients. The pathogenesis of COVID-19 encephalopathy is not fully understood. However, the most likely etiology of encephalopathy is multifactorial: systemic disease response, inflammation, coagulopathy, direct viral neuroinvasion, endoartheritis, and possibly post-infectious autoimmune mechanisms. For patients with suspected changes in the level of consciousness due to coronavirus infection, it is recommended to perform a thorough examination of the cerebrospinal fluid (CSF), head imaging with a preference for magnetic resonance imaging (MRI), and electroencephalography (EEG) It is worth noting that blood or imaging tests often do not show specific changes in patients with encephalopathy. As revealed by some studies of CSF examinations, cytosis is usually absent or very low while the protein concentration remains normal. It is important to note that SARS-CoV-2 is detected in the cerebral fluid only in isolated cases. Although the EEG of patients with COVID-19 are often normal, they sometimes show specific encephalopathic changes including excessive generalized frontal delta waves, triphasic waves and lower amplitude alpha and beta waves. The MRI describes a spectrum of neurovisual abnormalities, the most common of which are foci of leukoencephalopathy, changes in diffusion restriction imaging in the white, rarely in the gray matter, signs of microhaemorrhage and leptomeningitis. Treatment for COVID-19 encephalopathy includes supportive care and symptomatic treatment. Some studies have shown that immune modulation therapy, including high-dose corticosteroids and intravenous immunoglobulins, is effective in some severely ill patients.
{"title":"COVID-19 encephalopathy with severe neurological symptoms: a clinical case presentation with literature review","authors":"G. Baranauskienė, N. Tutlienė, G. Kaubrys","doi":"10.29014/ns.2022.26.20","DOIUrl":"https://doi.org/10.29014/ns.2022.26.20","url":null,"abstract":"COVID-19 infection is affecting more and more people around the world, and as the number of recovered patients increases, so does the knowledge on the potential clinical signs of the disease. Although SARS-CoV-2 virus is commonly associated with damage to the respiratory system, it has been observed that about half of patients with COVID-19 infection may also develop various neurological symptoms such as anosmia, dysgeusia, headache, myalgia, or dizziness. Encephalopathy is singled out as one of the most severe complications of the central nervous system caused by SARS-CoV-2 virus and associated with longer duration of the disease, increased disability, and mortality. Acute encephalopathy is a disorder of the brain that clinically occurs with a sudden change in the level of consciousness in otherwise healthy patients before the onset of symptoms. Risk factors include older age, male gender, quicker hospitalization after the onset of symptoms, and chronic illnesses. In exceptional cases, encephalopathy may be an early or even a major symptom of COVID-19 in young patients. The pathogenesis of COVID-19 encephalopathy is not fully understood. However, the most likely etiology of encephalopathy is multifactorial: systemic disease response, inflammation, coagulopathy, direct viral neuroinvasion, endoartheritis, and possibly post-infectious autoimmune mechanisms. For patients with suspected changes in the level of consciousness due to coronavirus infection, it is recommended to perform a thorough examination of the cerebrospinal fluid (CSF), head imaging with a preference for magnetic resonance imaging (MRI), and electroencephalography (EEG) It is worth noting that blood or imaging tests often do not show specific changes in patients with encephalopathy. As revealed by some studies of CSF examinations, cytosis is usually absent or very low while the protein concentration remains normal. It is important to note that SARS-CoV-2 is detected in the cerebral fluid only in isolated cases. Although the EEG of patients with COVID-19 are often normal, they sometimes show specific encephalopathic changes including excessive generalized frontal delta waves, triphasic waves and lower amplitude alpha and beta waves. The MRI describes a spectrum of neurovisual abnormalities, the most common of which are foci of leukoencephalopathy, changes in diffusion restriction imaging in the white, rarely in the gray matter, signs of microhaemorrhage and leptomeningitis. Treatment for COVID-19 encephalopathy includes supportive care and symptomatic treatment. Some studies have shown that immune modulation therapy, including high-dose corticosteroids and intravenous immunoglobulins, is effective in some severely ill patients.","PeriodicalId":479531,"journal":{"name":"Neurologijos seminarai","volume":"95 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135739340","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}
Stiff-person syndrome (SPS) is a rare neurologic disease, most often caused by autoimmune process during which antibodies against glutamic acid decarboxylase (anti-GAD65) are synthesised. The main clinical symptoms, among which are axial and proximal leg muscle stiffness and painful spasms, are often provoked by external triggers. In addition to those, the disease presents with anxiety, phobias, and other psychiatric symptoms. The most notable SPS comorbidities include temporal lobe epilepsy and type 1 diabetes mellitus. In this article, we present a clinical case of a patient illustrating the course of the disease, diagnostic difficulties, and treatment options, all of which are discussed in the literature review.
{"title":"Successful treatment of stiff-person syndrome with plasmapheresis: case report and literature review","authors":"M. Nasvytis, R. Kaladytė Lokominienė","doi":"10.29014/ns.2022.26.22","DOIUrl":"https://doi.org/10.29014/ns.2022.26.22","url":null,"abstract":"Stiff-person syndrome (SPS) is a rare neurologic disease, most often caused by autoimmune process during which antibodies against glutamic acid decarboxylase (anti-GAD65) are synthesised. The main clinical symptoms, among which are axial and proximal leg muscle stiffness and painful spasms, are often provoked by external triggers. In addition to those, the disease presents with anxiety, phobias, and other psychiatric symptoms. The most notable SPS comorbidities include temporal lobe epilepsy and type 1 diabetes mellitus. In this article, we present a clinical case of a patient illustrating the course of the disease, diagnostic difficulties, and treatment options, all of which are discussed in the literature review.","PeriodicalId":479531,"journal":{"name":"Neurologijos seminarai","volume":"25 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135739478","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}
Multiple sclerosis is a chronic autoimmune disease of the central nervous system. Multiple sclerosis causes demyelination, impaired nervous system function, and eventually neurodegeneration. Microglia are cells of the central nervous system that develop from yolk sac macrophages during embryogenesis. These cells perform important functions in the development of the central nervous system and the retina, in the formation of synapses, protect against pathogens, and are involved in the removal of damaged structures. In response to environmental factors, microglia can acquire an inflammatory or anti-inflammatory phenotype. Microglia also play an important role in the pathogenesis of multiple sclerosis, and these cells are thought to be involved in both demyelination and remyelination processes. Microglial cells phagocytose harmful myelin remnants, promote remyelination, and control the proper response of peripheral immune cells, but disruption of these functions can lead to demyelination and neurodegeneration. Many of the disease-modifying drugs used to treat multiple sclerosis also affect microglial cells and inhibit their inflammatory response. Currently, new drugs are being researched that could be used to treat multiple sclerosis promoting the transition of microglia to an anti-inflammatory phenotype. The latest advanced cell therapy drugs have a broader spectrum of action – they inhibit inflammation, promote angiogenesis, perform trophic function, and inhibit oxidative damage.
{"title":"Mikroglijos reikšmė išsėtinės sklerozės patogenezėje ir sąsajos su imunomoduliuojančiu gydymu","authors":"P. Valiukevičius, R. Liutkevičienė, R. Balnytė","doi":"10.29014/ns.2022.26.14","DOIUrl":"https://doi.org/10.29014/ns.2022.26.14","url":null,"abstract":"Multiple sclerosis is a chronic autoimmune disease of the central nervous system. Multiple sclerosis causes demyelination, impaired nervous system function, and eventually neurodegeneration. Microglia are cells of the central nervous system that develop from yolk sac macrophages during embryogenesis. These cells perform important functions in the development of the central nervous system and the retina, in the formation of synapses, protect against pathogens, and are involved in the removal of damaged structures. In response to environmental factors, microglia can acquire an inflammatory or anti-inflammatory phenotype. Microglia also play an important role in the pathogenesis of multiple sclerosis, and these cells are thought to be involved in both demyelination and remyelination processes. Microglial cells phagocytose harmful myelin remnants, promote remyelination, and control the proper response of peripheral immune cells, but disruption of these functions can lead to demyelination and neurodegeneration. Many of the disease-modifying drugs used to treat multiple sclerosis also affect microglial cells and inhibit their inflammatory response. Currently, new drugs are being researched that could be used to treat multiple sclerosis promoting the transition of microglia to an anti-inflammatory phenotype. The latest advanced cell therapy drugs have a broader spectrum of action – they inhibit inflammation, promote angiogenesis, perform trophic function, and inhibit oxidative damage.","PeriodicalId":479531,"journal":{"name":"Neurologijos seminarai","volume":"98 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135738625","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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