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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although occurrence of involuntary movements after thalamic stroke has occasionally been reported, studies using a sufficiently large number of patients and a control population are not available. Between 1995 and 1999, the author prospectively identified 35 patients with post-thalamic stroke delayed-onset involuntary movements, which included all or some degree of dystonia-athetosis-chorea-action tremor, occasionally associated with jerky, myoclonic components. A control group included 58 patients examined by the author during the same period who had lateral thalamic stroke but no involuntary movements. Demography, clinical features and imaging study results were compared. There were no differences in gender, age, risk factors, side of the lesion and follow-up periods. During the acute stage of stroke, the patients who had involuntary movements significantly more often had severe (< or = III/V) hemiparesis (50 versus 20%, P < 0.05) and severe sensory loss (in all modalities, P < 0.01) than the control group. At the time of assessment of involuntary movements, the patients with involuntary movements significantly more often had severe sensory deficit (in all modalities, P < 0.01) and severe limb ataxia (60 versus 5%, P < 0.01) than the control patients, but neither more severe motor dysfunction (7 versus 0%) nor more painful sensory symptoms (57 versus 57%). The patients with involuntary movements had a higher frequency of haemorrhagic (versus ischaemic) stroke (63 versus 31%, P < 0.05). Further analysis showed that dystonia-athetosis-chorea was closely associated with position sensory loss, whereas the tremor/myoclonic movements were related to cerebellar ataxia. Recovery of severe limb weakness seemed to augment the instability of the involuntary movements. Persistent failure of the proprioceptive sensory and cerebellar inputs in addition to successful, but unbalanced, recovery of the motor dysfunction seemed to result in a pathological motor integrative system and consequent involuntary movements in patients with relatively severe lateral-posterior thalamic strokes simultaneously damaging the lemniscal sensory pathway, the cerebellar-rubrothalamic tract and, relatively less severely, the pyramidal tract.
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PMID:Delayed onset mixed involuntary movements after thalamic stroke: clinical, radiological and pathophysiological findings. 1115 57

Background: Although clinically evident and MRI confirmed, basal ganglia involvement, is usual in primary antiphospholipid syndrome, extrapyramidal disorders such as parkinsonism and dystonia are very rare. We were unable to find any report in the literature on dystonia-parkinsonism in patients with primary antiphospholipid syndrome. Here we report an adult patient with dystonia-parkinsonism and primary antiphospholipid syndrome.Case report: A 60 year old, right-handed man came to our attention due to writer's cramp, bradykinesia and stiffness of his right hand. Neurological examination revealed constant, marked dystonic posturing, rigidity and bradykinesia of the right hand. Hyper-gammaglobulinemia was demonstrated on electrophoresis-serum IgG was increased. Anticardiolipin antibodies were examined by counterimmunoelectrophoresis (ELISA): IgG was negative, while IgM was positive. There was also slight thrombocytopenia. Magnetic resonance imaging brain scan axial T2W/UTSE revealed several hyperintense lesions in the basal ganglia and in the periventricular white matter and diffuse hyperintensity of the subcortical white matter bilaterally in the parietal regions. There was asymmetric parenchimal atrophy, more prominent in the left hemisphere. No clinical improvement was achieved by levodopa, dopamine agonists or anticholinergics. According to the criteria for primary antiphospholipid syndrome our patient had thrombocytopenia and high levels of IgG and IgM anticardiolipin antibodies so he was presumed to have a primary antiphospholipid syndrome.Conclusion: Various movement disorders may appear secondary to stroke, antiphospholipid syndrome, Behcet's disease or brain tumor. These cases may help in the understanding of pathophysiology of movement disorders. Dystonia and parkinsonism as well as other movement disorders may be associated with primary antiphospholipid syndrome.
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PMID:Antiphospholipid syndrome and dystonia-parkinsonism. A case report. 1124 96

We have described four patients with slowly progressive aphasia with striatal involvement occurring at different stages in the course of the illness. There were two males and two females, and their ages ranged from 68 to 76 (mean: 72) years. The extrapyramidal signs included tremors, bradykinesia, rigidity, and focal dystonia, and one had weakness resembling stroke. There is a heterogeniety among patients with slowly progressive aphasia and the clinical features correspond to the functional anatomy of the areas involved rather than to the pathology.
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PMID:Slowly progressive aphasia with striatal involvement. 1183 16

PxD are sudden, episodic, involuntary movement disorders that may include any combination of dystonia, chorea, athetosis, or ballism. The majority of reported cases are familial or idiopathic; however, there have been several reports of secondary PxD. We report 20 new cases of secondary, non-psychogenic PxD, and review 130 cases reported in the literature. The results suggest that although PxD is a rare disorder, secondary forms may be more common than previously recognized, accounting for 26% of all cases in our series. Secondary cases are notable for their variability in age of onset, the presence of both kinesigenic and non-kinesigenic symptoms in some patients, the prevalence of sensory precipitants, and most importantly, the reversal of symptoms when the underlying etiology is treated in some patients. In addition to MS, other causes to be considered in patients presenting with PxD include cerebral vascular insufficiency and stroke, trauma, metabolic abnormalities, and CNS infections. Awareness of the association of these etiologies with secondary PxD will permit prompt diagnoses and appropriate interventions. Potential pathophysiologic mechanisms including loss of inhibition or primary neuronal hyperactivity are discussed. In addition, recent hypotheses regarding channelopathies in relation to PxD are presented.
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PMID:Secondary causes of paroxysmal dyskinesia. 1196 64

The mitochondrial cytopathies are genetically and phenotypically heterogeneous group of disorders caused by structural and functional abnormalities in mitochondria. To the best of our knowledge, there are very few studies published from India till date. Selected and confirmed fourteen cases of neurological mitochondrial cytopathies with different clinical syndromes admitted between 1997 and 2000 are being reported. There were 8 male and 6 female patients. The mean age was 24.42+/-11.18 years (range 4-40 years). Twelve patients could be categorized into well-defined syndromes, while two belonged to undefined group. In the defined syndrome categories, three patients had MELAS (mitochondrial encephalopathy, lactic acidosis and stroke like episodes), three had MERRF (myoclonic epilepsy and ragged red fibre myopathy), three cases had KSS (Kearns-Sayre Syndrome) and three were diagnosed to be suffering from mitochondrial myopathy. In the uncategorized group, one case presented with paroxysmal kinesogenic dystonia and the other manifested with generalized chorea alone. Serum lactic acid level was significantly increased in all the patients (fasting 28.96+/-4.59 mg%, post exercise 41.02+/-4.93 mg%). Muscle biopsy was done in all cases. Succinic dehydrogenase staining of muscle tissue showed subsarcolemmal accumulation of mitochondria in 12 cases. Mitochondrial DNA study could be performed in one case only and it did not reveal any mutation at nucleotides 3243 and 8344. MRI brain showed multiple infarcts in MELAS, hyperintensities in putaminal areas in chorea and bilateral cerebellar atrophy in MERRF.
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PMID:Neurological mitochondrial cytopathies. 1213 80

Four patients with a stroke developed micrographia. In two patients, the condition was pure and in the two other patients it was associated with signs of writer's cramp. We conclude that infarct of the left lenticular nucleus could either mimic pure micrographia similar to that of Parkinson's disease or micrographia associated with dystonia.
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PMID:Micrographia secondary to lenticular lesions. 1221 Aug 89

We studied the effect of cervical dystonia on quality of life in a cohort of 289 patients by using a generic health status measurement scale (SF36). Cervical dystonia had a significant negative impact on quality of life compared with age-matched general population data. This negative impact was comparable to that seen in multiple sclerosis, Parkinson's disease, and stroke.
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PMID:Impact of cervical dystonia on quality of life. 1221 Aug 91

During the last decade, it has become clear that deep brain stimulation (DBS) therapy provides a dramatic improvement in the symptoms of movement disorders. We have experienced DBS in 110 patients with various types of involuntary movements, and confirmed the benefits of stimulation of the thalamic nucleus ventralis intermedius (Vim), internal globus pallidus (GPi) and subthalamic nucleus (STN) in these patients. DBS therapy affords the best effect on tremor when the Vim is selected as the stimulation site. DBS therapy is also useful for controlling rigidity when the GPi or STN is stimulated. Improvements of bradykinesia and gait disturbance are often induced by DBS therapy involving the GPi or STN. Dopa-induced dyskinesia can be attenuated effectively by the direct and/or indirect effects of DBS therapy. DBS of the Vim also provides excellent control of post-stroke involuntary movements, including hemiballism and hemichoreoathetosis. Dystonia in young patients is controlled effectively by DBS of GPi. Ablative procedures for control of involuntary movement disorders, such as thalamotomy and pallidotomy, always carry a risk associated with creating additional lesions in an already damaged brain. In contrast, there is not such a risk in DBS therapy. This modality of therapy is an important option in treating involuntary movements.
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PMID:[Deep brain stimulation therapy for involuntary movements]. 1223 1

Symptomatic dystonia can be the result of various metabolic, degenerative diseases, the consumption of certain medications or exposure to toxic agents. However, only symptomatic dystonia with focal structural lesion provides a significant "window" for, at least indirect, perception of aetiopathogenesis and pathomorphological substratum of idiopathic dystonia. Our study included 57 patients with symptomatic dystonia, which as a base had focal or multifocal lesions, of whom 7 patients had generalized dystonia, 18 hemidystonia, 6 segmental dystonia, 7 torticollis, 6 blepharospasm, 7 hand dystonia, 3 spasmodic dysphonia, and 3 had oromandibular dystonia. Stroke was highly statistically the most frequent cause of structural lesions (33/57 or 58%). Relevant pathomorphological changes were present in 50/57 (88%) patients, of whom 25 (50%) had lesion in the lenticular nucleus (including individual damage of the putamen and globus pallidus), 12/50 (24%) had damage of the thalamus and 6/50 (12%) had damage of the brainstem. Generalized dystonia was most frequently associated with bilateral lesion of the putamen, hemidystonia with lesion of contralateral putamen, torticollis with damage of the caudate nucleus, hand dystonia with lesion of the thalamus and blepharospasm with lesion of the upper brainstem.
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PMID:[Clinico-pathomorphologic correlations in patients with symptomatic dystonias]. 1239 40

Recent discoveries about the central nervous system's response to injury and how patients reacquire behavioral capabilities by training have yielded promising new therapies for neurorehabilitation. This family of interventions is termed constraint-induced (CI) therapy and is essentially behavioral in nature. Constraining movement of the arm which is less affected by the stroke and training (by shaping) the more affected arm for many hours a day for two consecutive weeks proved effective in the treatment of hemiplegia in many studies. Successful applications other than for stroke have been for traumatic brain injury, cerebral palsy, spinal cord injury, fractured hip, and focal hand dystonia. Extending the principles to other consequences of stroke such as aphasia is examined. Constraint-induced therapy is shown to produce large changes in the organization and function of the brain,which emphasizes the significance of cortical reorganization and learning for neurorehabilitation.
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PMID:[New developments in stroke rehabilitation based on behavioral and neuroscientific principles: constraint-induced therapy]. 1270 2


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