Pub Date : 2022-02-01DOI: 10.15744/2454-4981.8.101.1-14
Bhasin A
{"title":"Characterizing the Etiologies of Seizures and Cortical Myoclonic Activity in Covid-19 Patients and their Impact on Outcomes","authors":"Bhasin A","doi":"10.15744/2454-4981.8.101.1-14","DOIUrl":"https://doi.org/10.15744/2454-4981.8.101.1-14","url":null,"abstract":"","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42321019","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}
J K Cao, K Viray, M Shin, K-L Hsu, K Mackie, R Westenbroek, N Stella
Huntington's Disease is associated with motor behavior deficits that are lessened by few therapeutic options. This preliminary study tested if pharmacological inhibition of α/β-hydrolase domain containing 6 (ABHD6), a multifunctional enzyme expressed in the striatum, rescues behavioral deficits in HdhQ200/200 mice. Previous work has shown that this model exhibits a reduction in spontaneous locomotion and motor coordination at 8 and 10 months of age, with a more severe phenotype in female mice. Semi-quantitative immunohistochemistry analysis indicated no change in striatal ABHD6 expression at 8 months of age, but a 40% reduction by 10 months in female HdhQ200/200 mice compared to female wild-type (WT) littermates. At 8 months of age, acute ABHD6 inhibition rescued motor coordination deficits in female HdhQ200/200 mice without affecting WT performance. ABHD6 inhibition did not impact spontaneous locomotion, grip strength, or overall weight in either group, showing that effects were specific to motor coordination. At 10 months of age, semi-chronic ABHD6 inhibition by osmotic pump delivery also rescued motor coordination deficits in female HdhQ200/200 mice without affecting female WT littermates. Our preliminary study suggests that ABHD6 inhibition improves motor performance in female HdhQ200/200 mice.
{"title":"ABHD6 Inhibition Rescues a Sex-Dependent Deficit in Motor Coordination in The HdhQ200/200 Mouse Model of Huntington's Disease.","authors":"J K Cao, K Viray, M Shin, K-L Hsu, K Mackie, R Westenbroek, N Stella","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Huntington's Disease is associated with motor behavior deficits that are lessened by few therapeutic options. This preliminary study tested if pharmacological inhibition of α/β-hydrolase domain containing 6 (<b>ABHD6</b>), a multifunctional enzyme expressed in the striatum, rescues behavioral deficits in HdhQ200/200 mice. Previous work has shown that this model exhibits a reduction in spontaneous locomotion and motor coordination at 8 and 10 months of age, with a more severe phenotype in female mice. Semi-quantitative immunohistochemistry analysis indicated no change in striatal ABHD6 expression at 8 months of age, but a 40% reduction by 10 months in female HdhQ200/200 mice compared to female wild-type (<b>WT</b>) littermates. At 8 months of age, acute ABHD6 inhibition rescued motor coordination deficits in female HdhQ200/200 mice without affecting WT performance. ABHD6 inhibition did not impact spontaneous locomotion, grip strength, or overall weight in either group, showing that effects were specific to motor coordination. At 10 months of age, semi-chronic ABHD6 inhibition by osmotic pump delivery also rescued motor coordination deficits in female HdhQ200/200 mice without affecting female WT littermates. Our preliminary study suggests that ABHD6 inhibition improves motor performance in female HdhQ200/200 mice.</p>","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10503675/pdf/nihms-1880695.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10635654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-24DOI: 10.21203/RS.3.RS-230223/V1
Jessica K. Cao, Katie Viray, Myungsun Shin, Ku-Lung Hsu, Ken Mackie, R. Westenbroek, Nephi Stella
Huntington's Disease is associated with motor behavior deficits that are lessened by few therapeutic options. This preliminary study tested if pharmacological inhibition of α/β-hydrolase domain containing 6 (ABHD6), a multifunctional enzyme expressed in the striatum, rescues behavioral deficits in HdhQ200/200 mice. Previous work has shown that this model exhibits a reduction in spontaneous locomotion and motor coordination at 8 and 10 months of age, with a more severe phenotype in female mice. Semi-quantitative immunohistochemistry analysis indicated no change in striatal ABHD6 expression at 8 months of age, but a 40% reduction by 10 months in female HdhQ200/200 mice compared to female wild-type (WT) littermates. At 8 months of age, acute ABHD6 inhibition rescued motor coordination deficits in female HdhQ200/200 mice without affecting WT performance. ABHD6 inhibition did not impact spontaneous locomotion, grip strength, or overall weight in either group, showing that effects were specific to motor coordination. At 10 months of age, semi-chronic ABHD6 inhibition by osmotic pump delivery also rescued motor coordination deficits in female HdhQ200/200 mice without affecting female WT littermates. Our preliminary study suggests that ABHD6 inhibition improves motor performance in female HdhQ200/200 mice.
{"title":"ABHD6 Inhibition Rescues a Sex-Dependent Deficit in Motor Coordination in The HdhQ200/200 Mouse Model of Huntington's Disease.","authors":"Jessica K. Cao, Katie Viray, Myungsun Shin, Ku-Lung Hsu, Ken Mackie, R. Westenbroek, Nephi Stella","doi":"10.21203/RS.3.RS-230223/V1","DOIUrl":"https://doi.org/10.21203/RS.3.RS-230223/V1","url":null,"abstract":"Huntington's Disease is associated with motor behavior deficits that are lessened by few therapeutic options. This preliminary study tested if pharmacological inhibition of α/β-hydrolase domain containing 6 (ABHD6), a multifunctional enzyme expressed in the striatum, rescues behavioral deficits in HdhQ200/200 mice. Previous work has shown that this model exhibits a reduction in spontaneous locomotion and motor coordination at 8 and 10 months of age, with a more severe phenotype in female mice. Semi-quantitative immunohistochemistry analysis indicated no change in striatal ABHD6 expression at 8 months of age, but a 40% reduction by 10 months in female HdhQ200/200 mice compared to female wild-type (WT) littermates. At 8 months of age, acute ABHD6 inhibition rescued motor coordination deficits in female HdhQ200/200 mice without affecting WT performance. ABHD6 inhibition did not impact spontaneous locomotion, grip strength, or overall weight in either group, showing that effects were specific to motor coordination. At 10 months of age, semi-chronic ABHD6 inhibition by osmotic pump delivery also rescued motor coordination deficits in female HdhQ200/200 mice without affecting female WT littermates. Our preliminary study suggests that ABHD6 inhibition improves motor performance in female HdhQ200/200 mice.","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":"7 1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42320683","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 : 2020-12-01DOI: 10.15744/2454-4981.6.103
Unluturk Z
{"title":"http://www.annexpublishers.co/full-text/JNND/6103/Tetanus-Presenting-with-Back-Pain.php","authors":"Unluturk Z","doi":"10.15744/2454-4981.6.103","DOIUrl":"https://doi.org/10.15744/2454-4981.6.103","url":null,"abstract":"","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42671260","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 : 2020-12-01DOI: 10.15744/2454-4981.6.101
Gonçalves Mvm
In multiple sclerosis (MS), a chronic inflammation of the central nervous system is the major component of the disease’s pathology. If this is the major factor of the disease’s pathogenesis, it’s still a matter of debate nowadays [1,2]. The disease relapses were believed to be a T cell drive process, although recent evidence shows a growing importance of other cell types like B-cells and other peripheral myeloid cells [1,2], as well as CNS primary cells [2]. Once chronic inflammation is associated with cancer [3], a possible correlation between a chronic disease like multiple sclerosis and cancer have been studied throughout the time. There are studies showing decrease or no alteration in cancer risk of multiple sclerosis patients, even though some specific cancers show a different trend [4-8].
{"title":"Multiple Sclerosis Disease Modifying Therapy and Cancer risks","authors":"Gonçalves Mvm","doi":"10.15744/2454-4981.6.101","DOIUrl":"https://doi.org/10.15744/2454-4981.6.101","url":null,"abstract":"In multiple sclerosis (MS), a chronic inflammation of the central nervous system is the major component of the disease’s pathology. If this is the major factor of the disease’s pathogenesis, it’s still a matter of debate nowadays [1,2]. The disease relapses were believed to be a T cell drive process, although recent evidence shows a growing importance of other cell types like B-cells and other peripheral myeloid cells [1,2], as well as CNS primary cells [2]. Once chronic inflammation is associated with cancer [3], a possible correlation between a chronic disease like multiple sclerosis and cancer have been studied throughout the time. There are studies showing decrease or no alteration in cancer risk of multiple sclerosis patients, even though some specific cancers show a different trend [4-8].","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44850560","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 : 2020-12-01DOI: 10.15744/2454-4981.6.102
S. R
Traumatic brain injury (TBI) is a significant cause of morbidity. In the USA the average lifetime cost of care for a severe TBI patient ranges from $600,000 to $1,875,000 [1]. In India 1.6 million persons sustain TBI annually. Of those 200,000 will die [2]. The survivors face a spectrum of challenges most commonly related to cognitive or corticospinal tract dysfunction. Brain injury related neuropsychological impairment affects quality of life (QoL) [3]. The common presentations of this are: impaired concentration, decreased attention, easy distractibility, impaired visuo-spatial conceptualization, slow verbal/ visual stimulus processing, impaired memory, communication disorder, poor judgment, poor executive function [4]. Participation is a strong predictor of life satisfaction in the differently-abled. These issues lead to ADL dependence when they result in depersonalization [5]. The standard treatment consists of pharmacological agents and therapeutic exercises. Pharmacological agents used vary from agents like Citocholine to Amantadine [6]. Psychological intervention is: Attention process training and tasks for attention deficits, compensatory strategies and errorless learning training for memory deficits, pragmatic language skills and social behavior guidance for cognitive-communication disorder, meta-cognitive strategy, and problem-solving training for executive disorder are the mainstay of therapy for cognitive deficits in persons with TBI [7]. None of these directly address the cortical infrastructure damage. Often, they work with what is preserved. Abstract
{"title":"Hyperbaric Oxygen Therapy Improves Cognition in Patients Severe TBI; A Prospective Study","authors":"S. R","doi":"10.15744/2454-4981.6.102","DOIUrl":"https://doi.org/10.15744/2454-4981.6.102","url":null,"abstract":"Traumatic brain injury (TBI) is a significant cause of morbidity. In the USA the average lifetime cost of care for a severe TBI patient ranges from $600,000 to $1,875,000 [1]. In India 1.6 million persons sustain TBI annually. Of those 200,000 will die [2]. The survivors face a spectrum of challenges most commonly related to cognitive or corticospinal tract dysfunction. Brain injury related neuropsychological impairment affects quality of life (QoL) [3]. The common presentations of this are: impaired concentration, decreased attention, easy distractibility, impaired visuo-spatial conceptualization, slow verbal/ visual stimulus processing, impaired memory, communication disorder, poor judgment, poor executive function [4]. Participation is a strong predictor of life satisfaction in the differently-abled. These issues lead to ADL dependence when they result in depersonalization [5]. The standard treatment consists of pharmacological agents and therapeutic exercises. Pharmacological agents used vary from agents like Citocholine to Amantadine [6]. Psychological intervention is: Attention process training and tasks for attention deficits, compensatory strategies and errorless learning training for memory deficits, pragmatic language skills and social behavior guidance for cognitive-communication disorder, meta-cognitive strategy, and problem-solving training for executive disorder are the mainstay of therapy for cognitive deficits in persons with TBI [7]. None of these directly address the cortical infrastructure damage. Often, they work with what is preserved. Abstract","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46105825","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 : 2019-12-01DOI: 10.15744/2454-4981.5.101
Ahangar Aa
{"title":"Hyponatremia as Parameter in Admission and Discharge Disability of Stroke Survivors, Babol, North of Iran","authors":"Ahangar Aa","doi":"10.15744/2454-4981.5.101","DOIUrl":"https://doi.org/10.15744/2454-4981.5.101","url":null,"abstract":"","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48776809","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 : 2019-12-01DOI: 10.15744/2454-4981.5.102
Baiakmenlang S
We report a 20 year old girl admitted with cognitive decline and abnormal body movement for more than 16 month now bed ridden for last 3 month. On admission patient was conscious following command moving all four limbs. Myoclonic jerk involving limbs at a regular interval were noted .General physical examination was unremarkable. Detailed ophthalmological examination showed a normal fundus with no changes in the retina and optic nerve head. The kidney routine blood test, anti thyroperoxidase antibody, serum ammonia was normal. Viral markers were negative. Case Report
{"title":"Triphasic Waves in EEG, an Atypical Finding in a Subacute Sclerosing Panencephalitis (SSPE) Adult Patient","authors":"Baiakmenlang S","doi":"10.15744/2454-4981.5.102","DOIUrl":"https://doi.org/10.15744/2454-4981.5.102","url":null,"abstract":"We report a 20 year old girl admitted with cognitive decline and abnormal body movement for more than 16 month now bed ridden for last 3 month. On admission patient was conscious following command moving all four limbs. Myoclonic jerk involving limbs at a regular interval were noted .General physical examination was unremarkable. Detailed ophthalmological examination showed a normal fundus with no changes in the retina and optic nerve head. The kidney routine blood test, anti thyroperoxidase antibody, serum ammonia was normal. Viral markers were negative. Case Report","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42293995","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 : 2019-12-01DOI: 10.15744/2454-4981.5.103
Blanco Vmp
Nowadays, it is estimated that 50% of patients with encephalic traumatic injuries have been involved in traffic accidents. 63% of them are young adults, with ages from 15 and 24 years, and 34% are 1 to 4 year-old children. The existence of proper legislations addressing the risk factors could help reduce the number of dead and injured from traffic accidents. Encephalic traumatic injury is the leading cause of death in these patients, 50 to 75% according to the statistics. This is supported by the fact that in the United States, for instance, the mortality for traumatic brain lesions caused by car accidents in the decade from 1982 to 1992, exceeded the number of dead on the battlefields during the wars in that nation ́s history. The human factor has been responsible for 90% of these accidents [1-4].
{"title":"Epidemiological Approach to Mortal Lesions-Traffic Accident in Yara Municipality, 2007, Cuba","authors":"Blanco Vmp","doi":"10.15744/2454-4981.5.103","DOIUrl":"https://doi.org/10.15744/2454-4981.5.103","url":null,"abstract":"Nowadays, it is estimated that 50% of patients with encephalic traumatic injuries have been involved in traffic accidents. 63% of them are young adults, with ages from 15 and 24 years, and 34% are 1 to 4 year-old children. The existence of proper legislations addressing the risk factors could help reduce the number of dead and injured from traffic accidents. Encephalic traumatic injury is the leading cause of death in these patients, 50 to 75% according to the statistics. This is supported by the fact that in the United States, for instance, the mortality for traumatic brain lesions caused by car accidents in the decade from 1982 to 1992, exceeded the number of dead on the battlefields during the wars in that nation ́s history. The human factor has been responsible for 90% of these accidents [1-4].","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41402834","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 : 2018-12-01DOI: 10.15744/2454-4981.4.302
Duncan Ac
Identity formation comes in various definitions within psychology, neurobiology and spiritual worlds, but universally, it may be agreed that identity is a part of having a sense of self-awareness about who we are as individuals. As humans’ feel, think, sense and experience life in their surroundings, memory deposits formulate. Some argue that it is our memories that define who we are, but what happens when memory is disrupted with a dementia, such as, Alzheimer’s disease (AD)? As persons living with AD or a related dementia experience memory loss, too often, care providers tend to wane in recognizing the person as they treat the disease. Oftentimes, physicians, family, friends and society at large are inclined to talk around the person with the diagnosis as if they were not in the room, speaking directly to their counterpart. Even some with an early diagnosis of AD may take on the disease as their identity, as a 58 year old an accountant with Early Onset AD questioned, “Without my memories, who am I?”
{"title":"Identity in Memory: Ascertaining Consciousness beyond Dementia","authors":"Duncan Ac","doi":"10.15744/2454-4981.4.302","DOIUrl":"https://doi.org/10.15744/2454-4981.4.302","url":null,"abstract":"Identity formation comes in various definitions within psychology, neurobiology and spiritual worlds, but universally, it may be agreed that identity is a part of having a sense of self-awareness about who we are as individuals. As humans’ feel, think, sense and experience life in their surroundings, memory deposits formulate. Some argue that it is our memories that define who we are, but what happens when memory is disrupted with a dementia, such as, Alzheimer’s disease (AD)? As persons living with AD or a related dementia experience memory loss, too often, care providers tend to wane in recognizing the person as they treat the disease. Oftentimes, physicians, family, friends and society at large are inclined to talk around the person with the diagnosis as if they were not in the room, speaking directly to their counterpart. Even some with an early diagnosis of AD may take on the disease as their identity, as a 58 year old an accountant with Early Onset AD questioned, “Without my memories, who am I?”","PeriodicalId":73860,"journal":{"name":"Journal of neurology and neurological disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44355176","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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