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

Forty-four patients with hemiplegia following stroke and 10 nondisabled subjects were studied to examine the contributions inadequate motor unit recruitment and co-contraction attributable to impaired antagonist inhibition play in the movement disorder of the hemiplegic arm. Electromyographic data were recorded from agonist and antagonist muscles while subjects attempted six specified tasks. Data from subjects who could complete the tasks were compared with those who could not complete the tasks. Differences between the two groups were found in the electromyographic data obtained from the agonist muscles. Electromyographic values were consistently and significantly lower in patients who were unable to complete the tasks than in patients who were able to complete the tasks. In the antagonist muscles, a significant difference was noted only once; in this case, the EMG values were again lower in the group of patients who were unable to complete the task. Inadequate recruitment of agonists, not increased activity in the antagonists, was a consistent finding in patients who were unable to carry out the movement tasks. This study theoretically supports aiming treatment efforts at improving motoneuron recruitment rather than reducing activity in antagonists while retraining arm function.
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PMID:Agonist and antagonist activity during voluntary upper-limb movement in patients with stroke. 849 14

Palatal myoclonus is a movement disorder consisting of rhythmic myoclonus of the soft palate, pharynx, larynx, and other muscles derived from the embryonal branchial arches. These movements are continuous and involuntary, and the patients are, in general, unaware of them. In the majority of patients, palatal myoclonus persists for life. In oculopalatal myoclonus, the eyes can be involved in the form of a nystagmus. Often a clicking noise in one or both ears is the initial symptom which can be heard by the examiner. A variety of etiologies have been linked to palatal myoclonus. The most common defined cause is a stroke. The variable delay between the proposed cause and the appearance of the disorder causes difficulties in determining the exact etiology. Pathologic findings show a transsynaptic hypertrophic degeneration of the inferior olivary nucleus which is due to a lesion of a specific, inhibitory, anatomic pathway. This somatotopic pathway leaves the contralateral dentate nucleus, passes through the superior cerebellar peduncle, and crosses the posterior commissure before joining the central tegmental tract and descending to the ipsilateral inferior olive. Treatment of palatal myoclonus is only occasionally effective. Some patients have responded to tryptophan, carbamazepine, and trihexyphenidyl. Surgical attempts have not been successful. - In the present paper the authors report on a case of an oculopalatal myoclonus following Leber's optic atrophy which involved the brain stem.
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PMID:[Etiology and clinical aspects of palatal myoclonus]. 224 51

In this series of 21 patients with hemiballism-hemichorea we found an identifiable cause in all. Unlike most other studies in which stroke was the most important cause of the movement disorder, in almost half (10 of 21) of our patients some other cause was found. Hemiballism-hemichorea was often the presenting feature of underlying medical disease. Besides the subthalamic nucleus, other subcortical structures may be involved in the pathogenesis of this hemihyperkinesia. While the movement disorder often improves spontaneously or with pharmacologic therapy, the underlying disease may result in serious consequences.
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PMID:Hemiballism-hemichorea. Clinical and pharmacologic findings in 21 patients. 234 84

The anatomical location of the thalamic target (ventrolateral nucleus) during stereotactic thalamotomy for a movement disorder was determined using magnetic resonance imaging (MRI) to define the anterior and posterior commissures and the intercommissural plane. Precise targeting was confirmed by intraoperative stereotactic computed tomography (CT), electrophysiological stimulation, and a gratifying postoperative response (disappearance of contralateral tremor and rigidity). The use of a MRI- and CT-compatible stereotactic coordinate frame allowed multiplanar imaging with excellent spatial and contrast resolution, visualization of the source of the tremor (prior embolic stroke affecting the dentatorubrothalamic pathway), and correction for the more medial location of the internal capsule in this patient. Location did not vary among target sites seen with MRI and CT imaging techniques. In this patient MRI during stereotactic thalamotomy supplemented CT and the electrophysiological technique that we conventionally use to define the ventrolateral nucleus. Although the importance of possible magnetic susceptibility imaging artifacts remains to be elucidated, stereotactic MRI may prove sufficiently accurate in the future to replace other imaging techniques used during functional neurosurgery.
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PMID:Magnetic resonance imaging stereotactic thalamotomy: report of a case with comparison to computed tomography. 306 14

Hemiballism is an involuntary uncontrollable movement disorder with grave prognosis. Post stroke anatomical lesions of the subthalamic nucleus are the most frequent but not sole site. Increased cerebrospinal fluid homovanillic acid levels and successful management of hemiballistic symptoms with neuroleptics have suggested a dopaminergic overactivity as the neurochemical pathology. Diazepam, a gamma amino butyric acid (GABA) mimetic drug, has recently been reported to possess therapeutic efficacy. Hemiballism is a treatable condition which responds to neuroleptics and possibly GABA mimetic drugs.
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PMID:Pharmacological approaches to treatment of hemiballism and hemichorea. 613 34

A 9 1/2-year-old boy developed a progressive dyskinesia 7 years after an angiographically demonstrated internal cerebral vein thrombosis. CT revealed bilateral thalamic lesions, more severe on the side contralateral to the movement disorder, without striatal involvement. This is a rare example of survival after internal cerebral vein thrombosis in a child and demonstrates that movement disorders may be delayed consequences of childhood stroke.
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PMID:Progressive dyskinesia due to internal cerebral vein thrombosis. 720 Nov 15

Reports of 62 cases with a movement disorder associated with a focal lesion in the thalamus and/or subthalamic region were analyzed. Thirty-three cases had a lesion confined to the thalamus. Sixteen cases had a thalamic lesion extending into the subthalamic region and/or midbrain. Thirteen cases had a lesion in the subthalamic region or a subthalamic lesion extending into the midbrain. Nineteen cases with dystonia, 18 with asterixis, 17 with ballism-chorea, three with paroxysmal dystonia, and five with clonic or myorhythmic movements have been described. No case with isolated tremor has been described. In 53 cases with unilateral thalamic or subthalamic lesions, all but one with bilateral blepharospasm (associated with right posterior thalamic, pontomesencephalic, and bilateral cerebellar lesions) had dyskinesias in the limbs contralateral to the lesion. The other nine cases had bilateral paramedian thalamic lesions; seven developed bilateral dyskinesias, and the remaining two had unilateral dyskinesias. Regarding the 19 patients with dystonia, the two with bilateral blepharospasm had thalamic and upper brainstem lesions, and one with hemidystonia and torticollis had a subthalamic lesion. The other 16 patients all had a unilateral thalamic lesion with contralateral dystonia (10 hemidystonia, five focal dystonia affecting a hand and/or and one segmental dystonia involving face, arm, and hand). The exact location of the thalamic lesion was mentioned in 10 cases; the posterior or posterolateral thalamus was involved in six and the paramedian thalamus in four. These areas are more posterior or medial to the ventrolateral and ventroanterior thalamic nuclei, which receive pallido-thalamic and nigro-thalamic afferents. Two cases developed dystonia immediately after thalamotomy, and one case developed it 4 days after head trauma. The others initially had a hemiplegia and developed dystonia 1-9 months after the acute insult. Fifteen of the 17 patients with chorea had a unilateral lesion in the subthalamic nucleus or subthalamic region (eight due to infarcts, one to hemorrhage, five to mass lesions, and one to multiple sclerosis). All had contralateral hemichorea or hemiballism. One other case had bilateral chorea of the hands and tongue due to paramedian thalamic infarction. Another case with generalized chorea and thalamic atrophy was complicated by stereotaxic surgery. Thirteen of the 18 cases with asterixis had lesions confined to the thalamus. Eight were associated with thalamotomy, and five others had a stroke (four infarction and one hemorrhage) affecting the contralateral thalamus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Movement disorders following lesions of the thalamus or subthalamic region. 799 Aug 45

We studied 53 patients (64% females) with static brain lesions who developed progressive movement disorders. Of these, 50 (94%) had dystonia, 17 (32%) tremor, eight (15%) parkinsonism, seven (13%) myoclonus, and three (6%) chorea. The precipitating insults included perinatal hypoxia/ischemia in 22 (42%), stroke in 12 (23%), head injury in eight (15%), encephalitis in eight (15%), and carbon monoxide poisoning, kernicterus, and radiation necrosis in one patient (2%) each. Among the 30 patients with initial insult occurring at age 2 years or younger (Infant group), distribution of dystonia at follow-up was focal in three (10%), segmental in eight (27%), unilateral in 10 (33%), and generalized in nine (30%). The mean latency between the original injury and onset of movement disorder was 25.5 +/- 16.7 years. Among the nine patients who developed dystonia after an insult occurring between ages 6 and 17 (Childhood group), the distribution of dystonia at follow-up was segmental in two (33%) and unilateral in seven (78%); the mean latency of dystonia onset was 4.9 +/- 7.8 years. Of the 14 patients in the Adult group (injury at age 25 or older), 11 developed dystonia, two developed parkinsonism, and one had carbon monoxide encephalopathy and parkinsonism. The distribution of dystonia in the 11 patients at follow-up was segmental in three (27%) and unilateral in eight (73%). The mean latency of movement disorder onset in the 14 patients of the Adult group was 2.5 +/- 4.9 years. No individuals in the Childhood or Adult groups became left-hand dominant; by comparison, nine of the 30 individuals in the Infant group became left-handed. In conclusion, brain injury at a young age is associated with a longer latency to onset of subsequent movement disorder, a greater tendency to development of generalized dystonia, and a greater probability of altered handedness. These tendencies may result from differences in age-related neuroplasticity.
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PMID:Delayed-onset progressive movement disorders after static brain lesions. 890 76

We reported 8 patients with non-paralytic pontine exotropia (NPPE): 7 men and 1 woman aged from 56 to 79 years (mean: 67.8 years). From 1991 to 1994, 402 patients with acute infratentrial cerebrovascular diseases other than subarachnoid hemorrhage were admitted to our hospital within 7 days after the ouset of their stroke. NPPE was observed in 2% of these patients. NPPE was noted on admission in 6 of them, while it developed during the hospital stay in 2 others with paralytic pontine exotropia and bilateral median longitudinal fasciculus (MLF) syndrome, respectively. Abnormal convergence and alternating exotropia were noted in 6 and 2 patients respectively. The duration of NPPE was 0.5 to 4 days (mean; 2 days), and the ocular movement disorder was transient in all patients. When MRI was performed to detect the causative lesion, a small infarct was found in the upper, middle, and lower pons in 1, 3, and 4 patients, respectively. NPPE is generally considered to develop when the MLF and the paramedian pontine reticular formation (PPRF) are completely and incompletely destroyed respectively. In the present study, however, the pathophysiological features of the NPPE patients with alternating exotropia could not be explained by this mechanism, and severe MLF damage was considered to be a contributory factor.
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PMID:[A study of eight patients with non-paralytic pontine exotropia]. 882 94

We report the unique combination of a mid anterior choroidal artery (AChA) aneurysm and ischemic stroke presenting as a movement disorder in a young man. The mechanism for stroke in the AChA territory may either reflect a cause or an effect of aneurysm formation. We provide evidence for both arguments and speculate on the anatomic basis for the initial presentation of hemibody spasm.
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PMID:Anterior choroidal artery aneurysm and stroke. 885 53


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