29 results on '"Chorea physiopathology"'
Search Results
2. Network localization of hemichorea-hemiballismus.
- Author
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Laganiere S, Boes AD, and Fox MD
- Subjects
- Adult, Aged, Aged, 80 and over, Case-Control Studies, Chorea diagnostic imaging, Chorea physiopathology, Connectome, Dyskinesias diagnostic imaging, Dyskinesias physiopathology, Female, Functional Laterality, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Neural Pathways diagnostic imaging, Neural Pathways physiopathology, Reproducibility of Results, Rest, Sensitivity and Specificity, Stroke diagnostic imaging, Stroke physiopathology, Young Adult, Brain diagnostic imaging, Brain physiopathology, Chorea etiology, Dyskinesias etiology, Stroke complications
- Abstract
Objective: To determine whether neuroanatomically heterogeneous strokes causing hemichorea-hemiballismus localize to a common functional network., Methods: We identified 29 cases of lesion-induced hemichorea-hemiballismus from the literature and mapped each lesion volume onto a reference brain. Using a recently validated technique termed lesion network mapping, we tested whether these lesions belonged to the same functional network. To accomplish this, the network of brain regions functionally connected to each lesion was identified using a connectome dataset from healthy participants. Network maps were overlapped to identify any region functionally connected to our set of lesions. Specificity was evaluated using a case-control design; control cohorts included a group of similar lesions randomized to different brain locations and a second group of lesions causing a separate movement disorder, asterixis. Reproducibility was evaluated using an independent cohort of 10 additional hemichorea-hemiballismus cases., Results: Lesions showed heterogeneity in anatomical location, consistent with prior reports. However, at least 90% of these lesions showed network overlap in the posterolateral putamen. This result was specific to lesions causing hemichorea-hemiballismus and reproducible in an independent cohort. The putaminal overlap site was itself connected to a broader motor network that predicted the distribution of lesions causing hemichorea-hemiballismus., Conclusions: Strokes causing hemichorea-hemiballismus, while anatomically heterogeneous, localize to a common functional network. Specifically, lesions occur in regions functionally connected to the posterolateral putamen, a region previously implicated in hyperkinetic movement disorders. Lesion network mapping may be useful in identifying the neuroanatomical substrates of heterogeneous lesion-based disorders., (© 2016 American Academy of Neurology.)
- Published
- 2016
- Full Text
- View/download PDF
3. Paroxysmal kinesigenic dyskinesia: Clinical and genetic analyses of 110 patients.
- Author
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Huang XJ, Wang T, Wang JL, Liu XL, Che XQ, Li J, Mao X, Zhang M, Bi GH, Wu L, Zhang Y, Wang JY, Shen JY, Tang BS, Cao L, and Chen SD
- Subjects
- Adolescent, Adult, Age of Onset, Child, Child, Preschool, Chorea etiology, Chorea physiopathology, Dystonia complications, Dystonia etiology, Dystonia physiopathology, Female, Genetic Association Studies, Homozygote, Humans, Infant, Male, Mutation, Severity of Illness Index, Time Factors, Uniparental Disomy, Young Adult, Chorea genetics, Dystonia genetics, Membrane Proteins genetics, Nerve Tissue Proteins genetics
- Abstract
Objective: We aimed to investigate the clinical and genetic features of paroxysmal kinesigenic dyskinesia (PKD) in a large population and to analyze the genotype-phenotype correlation of PKD., Methods: We analyzed clinical manifestations and conducted PRRT2 screening in 110 patients with PKD. Clinical data were compared between 91 probands with and without PRRT2 mutations., Results: Among the enrolled participants (45 from 26 families, 65 sporadic cases), 8 PRRT2 mutations were detected in 20 PKD families (76.9%) and 14 sporadic cases (21.5%), accounting for 37.4% (34/91) of the study population. Five mutations (c.649dupC, c.649delC, c.487C>T, c.573dupT, c.796C>T) were already reported, while 3 mutations (c.787C>T, c.797G>A, c.931C>T) were undocumented. A patient harboring a homozygous c.931C>T mutation was shown to have inherited the mutation via uniparental disomy. Compared with non-PRRT2 mutation carriers, the PRRT2 mutation carriers were younger at onset, experienced longer attacks, and tended to present with complicated PKD, combined phenotypes of dystonia and chorea, and a positive family history. A good response was shown in 98.4% of the patients prescribed with carbamazepine., Conclusions: PRRT2 mutations are common in patients with PKD and are significantly associated with an earlier age at onset, longer duration of attacks, a complicated form of PKD, combined phenotypes of dystonia and chorea, and a tendency for a family history of PKD. A patient with uniparental disomy resulting in a homozygous c.931C>T mutation is identified in the present study. Carbamazepine is the first-choice drug for patients with PKD, but an individualized treatment regimen should be developed., (© 2015 American Academy of Neurology.)
- Published
- 2015
- Full Text
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4. Child Neurology: PRRT2-associated movement disorders and differential diagnoses.
- Author
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Ebrahimi-Fakhari D, Kang KS, Kotzaeridou U, Kohlhase J, Klein C, and Assmann BE
- Subjects
- Adolescent, Diagnosis, Differential, Dystonia, Female, Humans, Chorea diagnosis, Chorea genetics, Chorea physiopathology, Membrane Proteins genetics, Nerve Tissue Proteins genetics
- Published
- 2014
- Full Text
- View/download PDF
5. Head drop in Huntington disease: insights into the pathophysiology.
- Author
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Morgante F, Girlanda P, and Martino D
- Subjects
- Athetosis etiology, Chorea etiology, Female, Humans, Huntington Disease complications, Male, Middle Aged, Athetosis diagnosis, Athetosis physiopathology, Chorea diagnosis, Chorea physiopathology, Head physiopathology, Huntington Disease diagnosis, Huntington Disease physiopathology
- Published
- 2013
- Full Text
- View/download PDF
6. Reduced postmovement cortical inhibition in patients with paroxysmal kinesigenic dyskinesia.
- Author
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Hsu WY, Liao KK, Tseng YJ, Kwan SY, Chen RS, and Lin YY
- Subjects
- Adolescent, Adult, Brain Mapping, Dystonia, Electromyography, Female, Functional Laterality, Humans, Magnetoencephalography, Male, Middle Aged, Psychomotor Performance physiology, Reaction Time physiology, Young Adult, Chorea physiopathology, Cortical Synchronization physiology, Evoked Potentials, Motor physiology, Motor Cortex physiopathology, Neural Inhibition physiology
- Abstract
Objective: To characterize movement-related neural oscillatory activity and to clarify its neurophysiologic role in paroxysmal kinesigenic dyskinesia (PKD)., Methods: We recorded neuromagnetic event-related desynchronization (ERD) and event-related synchronization (ERS) activities in response to a self-paced finger-lifting task in 16 patients with PKD and 17 healthy controls., Results: The amplitude of α-ERD was comparable between the healthy controls and patients with PKD, whereas either the contralateral or ipsilateral β-ERS was decreased. The peak latency of contralateral β-ERS was delayed in patients with PKD. Patients with less frequent dyskinetic attacks demonstrated a larger ipsilateral β-ERS. Moreover, some patients with PKD revealed a lesser degree of contralateral preponderance of β-ERS generation., Conclusions: The present data imply a decreased postmovement inhibition of motor cortex in patients with PKD, and the inhibitory function in the contralateral hemisphere is more affected than that in the ipsilateral hemisphere.
- Published
- 2013
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7. Teaching Video NeuroImages: paroxysmal kinesigenic dyskinesia.
- Author
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Borchert A, Möddel G, and Schilling M
- Subjects
- Brain physiopathology, Chorea drug therapy, Chorea genetics, Dystonic Disorders drug therapy, Dystonic Disorders genetics, Electroencephalography, Humans, Magnetic Resonance Imaging, Male, Movement physiology, Neurology education, Stress, Psychological complications, Treatment Outcome, Video Recording, Anticonvulsants administration & dosage, Carbamazepine administration & dosage, Chorea physiopathology, Dystonic Disorders physiopathology
- Published
- 2009
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8. Pearls & Oy-sters: resolution of hemichorea following endarterectomy for severe carotid stenosis.
- Author
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Galea I, Norwood F, Phillips MJ, Shearman C, McMonagle P, and Gibb WR
- Subjects
- Aged, Brain blood supply, Brain physiopathology, Brain Infarction etiology, Brain Infarction pathology, Brain Infarction physiopathology, Carotid Stenosis diagnostic imaging, Chorea physiopathology, Disease Progression, Female, Humans, Magnetic Resonance Imaging, Male, Paresis etiology, Paresis pathology, Paresis physiopathology, Parietal Lobe blood supply, Parietal Lobe pathology, Parietal Lobe physiopathology, Somatosensory Disorders etiology, Somatosensory Disorders pathology, Somatosensory Disorders physiopathology, Treatment Outcome, Ultrasonography, Doppler, Duplex, Brain pathology, Carotid Stenosis complications, Carotid Stenosis surgery, Chorea etiology, Endarterectomy, Carotid methods
- Published
- 2008
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- View/download PDF
9. Limited chronic focal encephalitis: another variant of Rasmussen syndrome?
- Author
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Gambardella A, Andermann F, Shorvon S, Le Piane E, and Aguglia U
- Subjects
- Adult, Age Factors, Age of Onset, Anticonvulsants therapeutic use, Athetosis drug therapy, Athetosis etiology, Athetosis physiopathology, Atrophy diagnosis, Atrophy etiology, Atrophy physiopathology, Brain pathology, Brain physiopathology, Chemotaxis, Leukocyte immunology, Chorea drug therapy, Chorea etiology, Chorea physiopathology, Chronic Disease, Disease Progression, Encephalitis diagnosis, Epilepsy diagnosis, Female, Humans, Magnetic Resonance Imaging, Movement Disorders diagnosis, Recurrence, Encephalitis complications, Encephalitis physiopathology, Epilepsy etiology, Epilepsy physiopathology, Movement Disorders etiology, Movement Disorders physiopathology
- Abstract
Objective: To describe a more limited and less malignant form of Rasmussen encephalitis (RE)., Methods: Three subjects (all women; 37, 31, and 32 years of age) developed childhood or late onset chronic focal encephalitis, with a relatively nonprogressive form of the disorder., Results: In our patients, clinical features were dominated by partial seizures without marked focal motor deficit and in two with choreo-dystonic movements. The diagnosis of RE was supported by histologic examination and anatomic and functional MRI., Conclusions: These cases extend the phenotypic presentations of Rasmussen encephalitis and confirm Theodore Rasmussen's suggestion that there may be mild and nonprogressive forms of the disease.
- Published
- 2008
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10. Genotype-phenotype correlation of paroxysmal nonkinesigenic dyskinesia.
- Author
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Bruno MK, Lee HY, Auburger GW, Friedman A, Nielsen JE, Lang AE, Bertini E, Van Bogaert P, Averyanov Y, Hallett M, Gwinn-Hardy K, Sorenson B, Pandolfo M, Kwiecinski H, Servidei S, Fu YH, and Ptácek L
- Subjects
- Adolescent, Adult, Age of Onset, Caffeine adverse effects, Child, Child, Preschool, Chorea metabolism, DNA Mutational Analysis, Dystonia genetics, Dystonia metabolism, Dystonia physiopathology, Ethanol adverse effects, Female, Genetic Markers genetics, Genetic Testing, Genotype, Humans, Male, Pedigree, Penetrance, Stress, Psychological complications, Chorea genetics, Chorea physiopathology, Genetic Predisposition to Disease genetics, Muscle Proteins genetics, Mutation genetics
- Abstract
Background: Paroxysmal nonkinesigenic dyskinesia (PNKD) is a rare disorder characterized by episodic hyperkinetic movement attacks. We have recently identified mutations in the MR-1 gene causing familial PNKD., Methods: We reviewed the clinical features of 14 kindreds with familial dyskinesia that was not clearly induced by movement or during sleep. Of these 14 kindreds, 8 had MR-1 mutations and 6 did not., Results: Patients with PNKD with MR-1 mutations had their attack onset in youth (infancy and early childhood). Typical attacks consisted of a mixture of chorea and dystonia in the limbs, face, and trunk, and typical attack duration lasted from 10 minutes to 1 hour. Caffeine, alcohol, and emotional stress were prominent precipitants. Attacks had a favorable response to benzodiazepines, such as clonazepam and diazepam. Attacks in families without MR-1 mutations were more variable in their age at onset, precipitants, clinical features, and response to medications. Several were induced by persistent exercise., Conclusions: Paroxysmal nonkinesigenic dyskinesia (PNKD) should be strictly defined based on age at onset and ability to precipitate attacks with caffeine and alcohol. Patients with this clinical presentation (which is similar to the phenotype initially reported by Mount and Reback) are likely to harbor myofibrillogenesis regulator 1 (MR-1) gene mutations. Other "PNKD-like" families exist, but atypical features suggests that these subjects are clinically distinct from PNKD and do not have MR-1 mutations. Some may represent paroxysmal exertional dyskinesia.
- Published
- 2007
- Full Text
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11. Chorea as a manifestation of spontaneous CSF leak.
- Author
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Mokri B, Ahlskog JE, and Luetmer PH
- Subjects
- Blood Patch, Epidural, Cervical Vertebrae, Chorea physiopathology, Dysarthria etiology, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Myelography, Subdural Effusion diagnosis, Subdural Effusion therapy, Thoracic Vertebrae, Tomography, X-Ray Computed, Treatment Outcome, Chorea etiology, Subdural Effusion complications
- Abstract
A 59-year-old man presented with orthostatic headaches, memory complaints, pronounced choreiform movements, and related hyperkinetic dysarthria and titubations. Head MRI findings were suggestive of CSF leak. CSF pressure was low. CT myelography documented CSF leak at the cervicothoracic junction. Targeted epidural blood patch led to resolution of symptoms, including complete disappearance of choreiform movements.
- Published
- 2006
- Full Text
- View/download PDF
12. A family with McLeod syndrome and calpainopathy with clinically overlapping diseases.
- Author
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Starling A, Schlesinger D, Kok F, Passos-Bueno MR, Vainzof M, and Zatz M
- Subjects
- Adolescent, Adult, Amino Acid Transport Systems, Neutral genetics, Chorea complications, Chorea physiopathology, Chromosome Mapping, Codon, Nonsense genetics, DNA Mutational Analysis, Genetic Diseases, X-Linked complications, Genetic Diseases, X-Linked physiopathology, Genetic Testing, Genotype, Humans, Male, Muscle Fibers, Skeletal metabolism, Muscle Fibers, Skeletal pathology, Muscle, Skeletal metabolism, Muscle, Skeletal pathology, Muscle, Skeletal physiopathology, Muscular Dystrophies, Limb-Girdle complications, Muscular Dystrophies, Limb-Girdle physiopathology, Pedigree, Phenotype, Syndrome, Calpain genetics, Chorea genetics, Genetic Diseases, X-Linked genetics, Genetic Predisposition to Disease genetics, Isoenzymes genetics, Muscle Proteins genetics, Muscular Dystrophies, Limb-Girdle genetics, Mutation genetics
- Abstract
The authors describe a family with six patients with muscular dystrophy with a variable course. One is a compound heterozygote for CAPN3 mutations (calpainopathy) and the others have a single CAPN3 mutation. Linkage analysis and sequencing revealed a XK gene mutation (McLeod syndrome). This illustrates the variable phenotype of XK mutations and suggests the possibility that CAPN3 heterozygotes may have their condition caused by nonallelic mutations in other unrelated genes.
- Published
- 2005
- Full Text
- View/download PDF
13. Psychogenic paroxysmal dyskinesia following paroxysmal hemidystonia in multiple sclerosis.
- Author
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Morgan JC, Hughes M, Figueroa RE, and Sethi KD
- Subjects
- Adult, Anxiety Disorders complications, Anxiety Disorders diagnosis, Anxiety Disorders psychology, Chorea physiopathology, Diagnosis, Differential, Dystonic Disorders physiopathology, Extremities innervation, Extremities physiopathology, Female, Functional Laterality physiology, Humans, Hyperventilation complications, Hyperventilation psychology, Magnetic Resonance Imaging, Muscle, Skeletal innervation, Muscle, Skeletal physiopathology, Psychophysiologic Disorders physiopathology, Chorea etiology, Chorea psychology, Dystonic Disorders complications, Multiple Sclerosis complications, Psychophysiologic Disorders etiology, Psychophysiologic Disorders psychology
- Published
- 2005
- Full Text
- View/download PDF
14. A novel TITF-1 mutation causes benign hereditary chorea with response to levodopa.
- Author
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Asmus F, Horber V, Pohlenz J, Schwabe D, Zimprich A, Munz M, Schöning M, and Gasser T
- Subjects
- Child, Child, Preschool, Chorea physiopathology, Congenital Hypothyroidism genetics, DNA Mutational Analysis, Dopamine Agents administration & dosage, Dopamine Agents therapeutic use, Exons genetics, Fatal Outcome, Female, Genetic Testing, Humans, Levodopa therapeutic use, Male, Pedigree, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Thyroid Nuclear Factor 1, Treatment Outcome, Chorea drug therapy, Chorea genetics, Codon, Nonsense genetics, Levodopa administration & dosage, Nuclear Proteins genetics, Transcription Factors genetics
- Abstract
Presented is a pedigree with infancy-onset benign hereditary chorea (BHC) caused by a novel nonsense mutation in exon 3 (523G-->T, E175X) of the TITF-1 (Nkx2.1) gene. Four confirmed mutation carriers showed the typical movement disorder of BHC and congenital hypothyroidism. Surprisingly, treatment with levodopa improved gait dramatically and reduced chorea in two patients. Dopaminergic drugs should be considered a useful therapeutic option in BHC.
- Published
- 2005
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15. Obsessive compulsive behavior, hyperactivity, and attention deficit disorder in Sydenham chorea.
- Author
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Maia DP, Teixeira AL Jr, Quintão Cunningham MC, and Cardoso F
- Subjects
- Adolescent, Attention Deficit Disorder with Hyperactivity diagnosis, Child, Chorea physiopathology, Cohort Studies, Comorbidity, Cross-Sectional Studies, Female, Humans, Male, Neuropsychological Tests, Obsessive Behavior epidemiology, Obsessive Behavior psychology, Obsessive-Compulsive Disorder diagnosis, Prevalence, Rheumatic Fever physiopathology, Attention Deficit Disorder with Hyperactivity epidemiology, Chorea epidemiology, Obsessive-Compulsive Disorder epidemiology, Rheumatic Fever epidemiology
- Abstract
The authors investigated obsessive-compulsive behavior, obsessive-compulsive disorder (OCD), and attention deficit and hyperactivity disorder (ADHD) in 50 healthy subjects, 50 patients with rheumatic fever without chorea, and 56 patients with Sydenham chorea. Obsessive-compulsive behavior, OCD, and ADHD were more frequent in the Sydenham chorea group (19%, 23.2%, 30.4%) than in the healthy subjects (11%, 4%, 8%) and in the rheumatic fever without chorea group (14%, 6%, 8%). ADHD was more common in persistent Sydenham chorea.
- Published
- 2005
- Full Text
- View/download PDF
16. Recombinant interferon-alpha-induced chorea and frontal subcortical dementia.
- Author
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Moulignier A, Allo S, Zittoun R, and Gout O
- Subjects
- Aged, Chorea physiopathology, Dementia, Vascular physiopathology, Female, Humans, Male, Neuropsychological Tests, Recombinant Proteins, Chorea chemically induced, Dementia, Vascular chemically induced, Frontal Lobe physiopathology, Interferon Type I adverse effects
- Published
- 2002
- Full Text
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17. Hereditary benign chorea: clinical and genetic features of a distinct disease.
- Author
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Fernandez M, Raskind W, Matsushita M, Wolff J, Lipe H, and Bird T
- Subjects
- Adolescent, Adult, Aged, Chorea physiopathology, Chromosomes, Human, Pair 14 genetics, Female, GTP Cyclohydrolase genetics, Genes, Dominant, Genetic Linkage, Genetic Markers, Humans, Lod Score, Male, Middle Aged, Movement, Mutation, Pedigree, Recombination, Genetic, Chorea genetics
- Abstract
Objective: To describe a second family with benign hereditary chorea (BCH, OMIM 118700) and suggestive linkage to chromosome 14q. BCH is an autosomal dominant disorder of early onset that differs from Huntington disease in being nondementing and nonprogressive without other neurologic signs. There has been controversy regarding the existence of BCH as a discrete disorder., Background: A single kindred was recently reported with linkage of BCH to a 20.6-KcM region on chromosome 14q., Methods: In a four-generation family with BCH, linkage was evaluated to markers in a 23-KcM region between D14S49 and D14S66 that contains the putative BCH locus., Results: A multipoint nonparametric lod score of 3.01 is consistent with linkage of disease in this family to the 14q BCH locus. A recombination event in one affected individual enabled the critical region to be narrowed to 6.93 KcM flanked by D14S1068 and D14S1064. This region contains two candidate genes: glial maturation factor beta and guanosine triphosphate cyclohydrolase 1 (GCH1). Survival motor neuron (SMN) interacting protein-1 is eliminated as a candidate gene because it lies outside the critical region. No sequence alteration was identified in the coding region of GCH1 in an affected individual., Conclusion: These data provide further evidence that BCH is a distinct entity, narrow the location of BCH to a 6.93-KcM region on chromosome 14q, and exclude SMN interacting protein-1 as a candidate gene.
- Published
- 2001
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18. Chronic thalamic stimulation for treatment of dystonic paroxysmal nonkinesigenic dyskinesia.
- Author
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Loher TJ, Krauss JK, Burgunder JM, Taub E, and Siegfried J
- Subjects
- Adult, Chorea physiopathology, Follow-Up Studies, Humans, Male, Chorea therapy, Electric Stimulation Therapy, Thalamic Nuclei physiopathology
- Abstract
The authors report the effect of chronic stimulation of the ventrointermediate (Vim) thalamus for treatment of dystonic paroxysmal nonkinesigenic dyskinesias (PNKD). A 37-year-old patient had a 4-year history of severe and painful PNKD of the right arm. Chronic stimulation through a stereotactically implanted monopolar electrode in the left Vim resulted in a decrease of the frequency, duration, and intensity of the dystonic paroxysmal movement disorder. The benefit of stimulation has been maintained over 4 years of follow-up.
- Published
- 2001
- Full Text
- View/download PDF
19. Paroxysmal movement disorders and epilepsy: links across the channel.
- Author
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Berkovic SF
- Subjects
- Ataxia genetics, Ataxia physiopathology, Chorea genetics, Chorea physiopathology, DNA Mutational Analysis, Diagnosis, Differential, Epilepsy genetics, Epilepsy physiopathology, Humans, Ion Channels genetics, Ataxia diagnosis, Chorea diagnosis, Electroencephalography, Epilepsy diagnosis, Ion Channels physiology
- Published
- 2000
- Full Text
- View/download PDF
20. Paroxysmal kinesigenic choreoathetosis.
- Author
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Lambroso CT
- Subjects
- Female, Humans, Athetosis diagnosis, Athetosis physiopathology, Chorea diagnosis, Chorea physiopathology, Movement
- Published
- 1997
- Full Text
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21. Paroxysmal dystonic choreoathetosis linked to chromosome 2q: clinical analysis and proposed pathophysiology.
- Author
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Fink JK, Hedera P, Mathay JG, and Albin RL
- Subjects
- Athetosis physiopathology, Chorea physiopathology, Female, Humans, Male, Movement Disorders physiopathology, Pedigree, Poland ethnology, Athetosis genetics, Chorea genetics, Chromosomes, Human, Pair 2 genetics, Genetic Linkage, Movement Disorders genetics
- Abstract
We describe clinical features of a large Polish-American kindred in which autosomal-dominant, paroxysmal dystonic choreoathetosis (PDC) was linked to a locus on chromosome 2q. Episodes of generalized dystonia and choreoathetosis involving the face and all extremities began in early childhood, lasted for 30 minutes to several hours, and occurred up to several times each week. There was no interruption of consciousness and EEGs were normal during the episodes. Paroxysmal dyskinesia occurred at rest both spontaneously and following caffeine or alcohol consumption. Neurologic examinations were normal between attacks. The cause of PDC is unknown. We deduced a model of PDC pathophysiology from analyzing neurophysiologic effects of alcohol and caffeine (which provoke attacks of PDC), the variably beneficial effects of levodopa-carbidopa, and the occurrence of dystonia and paroxysmal dyskinesia in biopterin synthesis disorders. We propose that nigrostriatal neurons in PDC patients have either marginally deficient dopamine synthesis or excessive alcohol- and caffeine-induced dopamine release; and that following alcohol- and caffeine-induced dopamine release, PDC patients experience a period of dopamine deficiency.
- Published
- 1997
- Full Text
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22. Choreoathetotic movements: A possible side effect of gabapentin.
- Author
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Buetefisch CM, Gutierrez A, and Gutmann L
- Subjects
- Acetates therapeutic use, Adult, Anticonvulsants adverse effects, Anticonvulsants therapeutic use, Athetosis physiopathology, Chorea physiopathology, Dyskinesia, Drug-Induced physiopathology, Epilepsies, Partial drug therapy, Facial Muscles physiopathology, Gabapentin, Humans, Male, Movement, Acetates adverse effects, Amines, Athetosis chemically induced, Chorea chemically induced, Cyclohexanecarboxylic Acids, gamma-Aminobutyric Acid
- Published
- 1996
23. Cocaine-induced choreoathetoid movements ('crack dancing').
- Author
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Daras M, Koppel BS, and Atos-Radzion E
- Subjects
- Adult, Female, Humans, Male, Middle Aged, Athetosis physiopathology, Chorea physiopathology, Crack Cocaine adverse effects, Dyskinesia, Drug-Induced physiopathology, Movement drug effects
- Abstract
We describe seven patients with cocaine-induced movements, including choreoathetosis, akathisia, and parkinsonism with tremor. All were seen in 2 years at a municipal hospital, during which 701 visits were attributed to complications of cocaine. Dopaminergic changes are hypothesized to cause euphoria, addiction, and abnormal movements.
- Published
- 1994
- Full Text
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24. Inconsistent response to divalproex sodium in hemichorea/hemiballism.
- Author
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Sethi KD and Patel BP
- Subjects
- Aged, Chorea physiopathology, Chorea surgery, Dose-Response Relationship, Drug, Humans, Male, Movement Disorders physiopathology, Movement Disorders surgery, Thalamus surgery, Chorea drug therapy, Movement Disorders drug therapy, Valproic Acid therapeutic use
- Abstract
We report 6 patients with hemichorea/hemiballism of vascular origin who were treated with divalproex sodium (Depakote). Four of 6 responded initially. Marked improvement was seen in 2 patients only and in 1 of these hemiballism recurred despite continuing therapy. Divalproex sodium is not uniformly effective in the treatment of hemichorea/hemiballism.
- Published
- 1990
- Full Text
- View/download PDF
25. A follow-up study of Sydenham's chorea.
- Author
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Bird MT, Palkes H, and Prensky AL
- Subjects
- Adolescent, Chorea complications, Electroencephalography, Female, Follow-Up Studies, Humans, Male, Mental Disorders etiology, Mental Processes physiology, Motor Skills physiology, Rheumatic Fever complications, Syndrome, Chorea physiopathology, Rheumatic Fever physiopathology
- Abstract
Twenty-five patients convalescing from Sydenham's chorea were contrasted by clinical examination, electroencephalograms, and psychometric and psychologic tests to 15 siblings and 20 matched rheumatic fever controls. A group of 10 postchoreic patients who had two or more signs could be identified. Patients in this group had all the signs classified as moderate or severe, performed less well than other choreic subjects on the Bender gestalt test, and had a higher percentage of abnormal electroencephalograms but not a higher incidence of behavioral disorders. This subgroup could not be predicted from a review of neurologic history or from analysis of the acute episode of chorea. Our data would suggest that uncomplicated Sydenham's chorea is not necessarily a benign self-limited affliction of the central nervous system and that some patients are left with definite, albeit minimal, neurologic residua.
- Published
- 1976
- Full Text
- View/download PDF
26. Tendency to late recurrence following rheumatic chorea.
- Author
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Gibb WR and Lees AJ
- Subjects
- Aged, Chorea complications, Female, Humans, Male, Middle Aged, Recurrence, Rheumatic Fever complications, Time Factors, Chorea physiopathology
- Published
- 1989
- Full Text
- View/download PDF
27. Paroxysmal kinesigenic choreoathetosis. An entity within the paroxysmal choreoathetosis syndrome. Description of 10 cases, including 1 autopsied.
- Author
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Kertesz A
- Subjects
- Adolescent, Adult, Athetosis drug therapy, Athetosis genetics, Athetosis pathology, Child, Chorea drug therapy, Chorea genetics, Chorea pathology, Female, Humans, Male, Motion Pictures, Movement, Phenytoin therapeutic use, Placebos, Sensation, Athetosis physiopathology, Chorea physiopathology
- Published
- 1967
- Full Text
- View/download PDF
28. H reflex study in upper motoneuron diseases.
- Author
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Takamori M
- Subjects
- Adolescent, Adult, Aged, Child, Chorea physiopathology, Dystonia Musculorum Deformans physiopathology, Electric Stimulation, Female, Humans, Huntington Disease physiopathology, Male, Middle Aged, Muscle Contraction, Myoclonus physiopathology, Oscillometry, Parkinson Disease physiopathology, Procaine pharmacology, Reflex, Stretch, Sciatic Nerve drug effects, Spasm physiopathology, Motor Neurons, Peripheral Nervous System Diseases physiopathology, Reflex, Abnormal
- Published
- 1967
- Full Text
- View/download PDF
29. Chorea as a manifestation of familial paroxysmal choreoathetosis.
- Author
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Horner FA and Jackson L
- Subjects
- Athetosis physiopathology, Chorea diagnosis, Chorea physiopathology, Extremities physiopathology, Female, Head physiopathology, Humans, Lithuania, Male, Movement Disorders, Thorax physiopathology, Athetosis genetics, Chorea genetics, Spondylitis, Ankylosing complications
- Published
- 1968
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