{"title":"Paroxysmal choreoathetosis.","authors":"C. D. Marsden","doi":"10.32388/898551","DOIUrl":"https://doi.org/10.32388/898551","url":null,"abstract":"","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"70 1","pages":"467-70"},"PeriodicalIF":0.0,"publicationDate":"2019-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48771801","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 : 2018-07-27DOI: 10.1093/med/9780190607555.001.0001
A. Minagar, A. Rabinstein, L. Shulman, W. Weiner
The term movement disorders encompasses a wide range of conditions that cause abnormal movements. This review discusses hypokinetic movement disorders, including bradykinesia, akinesia, akinetic rigid syndrome, and Parkinsonism, an akinetic rigid syndrome that is one of the most common of all the movement disorders which is most often a manifestation of Parkinson disease (PD). The review looks at the epidemiology, etiology, pathology, diagnosis, treatment, and management of PD. Other parkinsonian syndromes include progressive supranuclear palsy, corticobasal syndrome, multiple system atrophy, vascular parkinsonism, normal pressure hydrocephalus, drug-induced parkinsonism, and dementia associated with Parkinson disease. Hyperkinetic movement disorders include tremor, dystonia, tics, myoclonus, and chorea. They include Huntington disease, Wilson disease, tardive dyskinesia, Tourette syndrome, and essential tremor. Figures in this review include examples of generalized dystonia, moderate parkinson disease, affected handwriting, Kayser-Fleischer ring, cervical dystonia, head deviation, and writer's cramp. Tables provide clinical definitions, clues to drug-induced parkinsonism, and a list of drugs that can cause parkinsonism. This review contains 129 references.
{"title":"Movement disorders.","authors":"A. Minagar, A. Rabinstein, L. Shulman, W. Weiner","doi":"10.1093/med/9780190607555.001.0001","DOIUrl":"https://doi.org/10.1093/med/9780190607555.001.0001","url":null,"abstract":"The term movement disorders encompasses a wide range of conditions that cause abnormal movements. This review discusses hypokinetic movement disorders, including bradykinesia, akinesia, akinetic rigid syndrome, and Parkinsonism, an akinetic rigid syndrome that is one of the most common of all the movement disorders which is most often a manifestation of Parkinson disease (PD). The review looks at the epidemiology, etiology, pathology, diagnosis, treatment, and management of PD. Other parkinsonian syndromes include progressive supranuclear palsy, corticobasal syndrome, multiple system atrophy, vascular parkinsonism, normal pressure hydrocephalus, drug-induced parkinsonism, and dementia associated with Parkinson disease. Hyperkinetic movement disorders include tremor, dystonia, tics, myoclonus, and chorea. They include Huntington disease, Wilson disease, tardive dyskinesia, Tourette syndrome, and essential tremor. Figures in this review include examples of generalized dystonia, moderate parkinson disease, affected handwriting, Kayser-Fleischer ring, cervical dystonia, head deviation, and writer's cramp. Tables provide clinical definitions, clues to drug-induced parkinsonism, and a list of drugs that can cause parkinsonism.\u0000\u0000This review contains 129 references.","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"90 1","pages":"213-26"},"PeriodicalIF":0.0,"publicationDate":"2018-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42001162","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 : 2014-01-01DOI: 10.1007/978-3-319-08046-8
Madhavi Thomas
{"title":"Inflammation in Parkinson's Disease","authors":"Madhavi Thomas","doi":"10.1007/978-3-319-08046-8","DOIUrl":"https://doi.org/10.1007/978-3-319-08046-8","url":null,"abstract":"","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"29 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-319-08046-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51002605","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 : 2008-07-11DOI: 10.3109/9780203091708-145
A. A. Balabanov
{"title":"133a. Psychiatric outcome of epilepsy surgery","authors":"A. A. Balabanov","doi":"10.3109/9780203091708-145","DOIUrl":"https://doi.org/10.3109/9780203091708-145","url":null,"abstract":"","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"1 1","pages":"1294-1302"},"PeriodicalIF":0.0,"publicationDate":"2008-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69461503","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}
In summary, the scheme of basal ganglia function presented here, in conjunction with known features of anatomical organization and dopamine neurotransmission provides a hypothesis for the pathophysiology of tics. According to the hypothesis, clusters of striatal neurons (matrisomes) become abnormally active in inappropriate contexts leading to inhibition of GPi or SNpr neurons that would normally be active to supress unwanted movements. The inhibition of htese GPi or SNpr neurons would then disinhibit thalamocortical circuits. Leading to the production of tics. Activity-dependent dopamine effects would inappropriately reinforce these activity patterns leading to stereotyped repetion. Over time, exactly which striatal neuronal clusters are overactive may change under various influences so that the produced movement change over time. This hypothesis is testable directly but requires a valid animal model of tics or higher resolution functional imaging techniques. Continuing work on basic basal ganglia physiology, pathophysiology, and functional imaging in TS is advancing our knowledge of neural circuit abnormalities in TS, but much more work is still needed.
{"title":"Neurobiology of basal ganglia and Tourette syndrome: basal ganglia circuits and thalamocortical outputs.","authors":"Jonathan W Mink","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In summary, the scheme of basal ganglia function presented here, in conjunction with known features of anatomical organization and dopamine neurotransmission provides a hypothesis for the pathophysiology of tics. According to the hypothesis, clusters of striatal neurons (matrisomes) become abnormally active in inappropriate contexts leading to inhibition of GPi or SNpr neurons that would normally be active to supress unwanted movements. The inhibition of htese GPi or SNpr neurons would then disinhibit thalamocortical circuits. Leading to the production of tics. Activity-dependent dopamine effects would inappropriately reinforce these activity patterns leading to stereotyped repetion. Over time, exactly which striatal neuronal clusters are overactive may change under various influences so that the produced movement change over time. This hypothesis is testable directly but requires a valid animal model of tics or higher resolution functional imaging techniques. Continuing work on basic basal ganglia physiology, pathophysiology, and functional imaging in TS is advancing our knowledge of neural circuit abnormalities in TS, but much more work is still needed.</p>","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"99 ","pages":"89-98"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25903762","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}
{"title":"PANDAS: overview of the hypothesis.","authors":"Gavin Giovannoni","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"99 ","pages":"159-65"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25903770","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}
O Carter Snead, Steven J Clapcote, John C Roder, Gabrielle L Boulianne
{"title":"Novel strategies for the development of animal models of refractory epilepsy.","authors":"O Carter Snead, Steven J Clapcote, John C Roder, Gabrielle L Boulianne","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"97 ","pages":"155-71"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25774399","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}
{"title":"Medical comorbidity in intractable epilepsy.","authors":"Richard S McLachlan","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"97 ","pages":"345-9"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25775500","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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