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

The delayed-onset focal or segmental dystonia is a rare sequelae of cerebrovascular disease. The responsible lesion sites for the dystonia are variable and the pathogenesis is uncertain. This study reports three patients with delayed-onset focal dystonia as a complication of stroke. The interval between hypoxic insult and onset of dystonia were varied from 1 month to 1 year. Two adults and one child had focal lesions at the contralateral basal ganglia. The interval between the brain damage and dystonia did not appear to be related to the age at the time of hypoxic injury. The site of lesions may serve as an important factor in the pathogenesis.
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PMID:Delayed-onset focal dystonia after stroke. 812 45

Stroke-related nonepileptic transient dyskinesias are rare, and the site of ischemia remains often undetermined. Five cases out of 47 consecutive thalamic infarcts (10.6 per cent) are reported. Patients presented with monochorea (1 case), hemiballism-hemichorea (2 cases), choreoathetosis (1 case with subsequent arm painful dystonia and hand tremor), and asterixis (1 case). Magnetic resonance imaging demonstrated that the subthalamic nucleus was spared in all cases. Transient dyskinesias occurred at any time in the course of infarction (as a warning sign in 1 case, as an associated symptom in 3 cases, or during recovery in 1 case). Moreover, this study suggests that: 1) transient dyskinesias are mainly related to thalamic ischemic injury, and 2) small vessels disease is the main etiology.
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PMID:[Transient involuntary movement disorders and thalamic infarction]. 830 59

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

Small doses of radioactive irradiation were found to be associated with damage to all levels of the nervous system, as evidenced by cliniconeurological investigations. But regulatory functions and vascular system get it most of all. Commonly seen in the sample was vegetovascular dystonia, also revealed were a varying degree discirculatory encephalopathy, acute disturbances in cerebral circulation, dyscirculatory myelopathy. Vascular abnormalities may develop at any age but in young adulthood they tend to occur more frequently. Clinical manifestations of vegetovascular dystonia were characterized by profound mixed type vegetative crises. Even if treated, vegetovascular dystonia tends to acquire remittent-and-progredient course leading to decompensation very soon. Strokes run atypical course: hemorrhages occur more often than not; circulatory disorders come about against the background of normal arterial blood pressure or insignificant its fluctuations. Hemorrhage may run gradually progressing course, which fact makes their diagnosis very difficult even with modern techniques being involved in relevent studies. It is not infrequently that carotid angiography does not find any structural-and-morphologic changes in the main vessels. A separate nozologic form, viz. that of discirculatory encephalopacy due to radiative irradiation, is suggested, as an entity worth introducing into the medical nomenclature.
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PMID:[The characteristics of cerebrovascular disorders in persons exposed to the effect of ionizing radiation as a result of the accident at the Chernobyl Atomic Electric Power Station]. 881 15

Magnetic motor-evoked potential (MEP) study of patients with the syndrome of delayed posthemiplegic hemidystonia, hemiatrophy, and partial or hemi-seizures ('4-hemi' syndrome) has not been described. Among 35 patients investigated for posthemiplegic movement disorders from February 1988 to January 1995, seven showed '4-hemi' syndrome. Clinical work-up, magnetic resonance images (MRI) and/or computed tomography (CT) were performed in all. Transcranial MEP studies were done in five patients. The remote causes of '4-hemi' syndrome were neonatal stroke, trauma, and encephalitis in infancy. The dystonia may occur as long as a decade after the initial insult. MRI or CT showed destructive lesion in the contralateral putamen (five patients), caudate (four), thalamus (five), and atrophy of the contralateral hemisphere (five). Other associations were porencephalic cyst. Wallerian degeneration, and asymmetric compensatory ventriculomegaly. MEP showed abnormalities in the affected upper limbs in four of five patients. The abnormalities were reduced amplitude of the compound muscle action potential following cortical stimulations with or without temporal dispersion, and with or without prolongation of its latency. The peripheral motor conductions following cervical stimulations were normal. MEP abnormalities may not be related to the hemiatrophy and the size of brain lesion per se. The hemidystonia is static after the second decade of life, and it is often difficult to treat.
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PMID:The syndrome of delayed posthemiplegic hemidystonia, hemiatrophy, and partial seizure: clinical, neuroimaging, and motor-evoked potential studies. 888 90

A retrospective study of 13 patients (4 males/9 females) with acquired hemidystonia in childhood is reported. The mean age of onset of hemidystonia was 6.4 years (range 1-13.4 years); the mean duration of dystonia at the time of last follow-up was 11.4 years (range 3.6-23 years). Hemidystonia was caused by ischemic infarction in 9 patients and was attributed to perinatal trauma in 1; in 4 of the 9 patients with stroke and in the remaining 3 patients laboratory investigations were suggestive of primary antiphospholipid syndrome. Eleven of the 13 patients had delayed onset of dystonia: between 1 month and 8.9 years (mean 3.4 years). Ten patients had neuroradiological evidence of contralateral basal ganglia damage. A history of hemiparesis and evidence of striatal damage on CT or MRI were important risk factors for the development of dystonia. Response to medical treatment (trihexyphenidyl dose as high as 40 mg daily) in 5 patients was disappointing; 4 of the 5 patients who underwent functional stereotaxic operations were improved, but dystonia was still present at the end of the follow-up. Our study provides additional evidence that lesions of the striatum may induce dystonia, supporting the theory of striatopallido-thalamic disconnection. Furthermore, our results indicate that the occurrence of delayed dystonia must be considered in the diagnostic approach to childhood-onset dystonia.
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PMID:Acquired hemidystonia in childhood: a clinical and neuroradiological study of thirteen patients. 888 43

A 68 year-old man developed progressive hemidystonia and chorea 8 months after a contralateral thalamic stroke. The neurological examination also showed a right pyramidal syndrome without hemiparesis, a right horizontal sectoranopia, and a right hemihypesthesia for all sensory modalities. The MRI revealed infarctions in the left medial temporo-occipital lobes and left posterolateral thalamus, corresponding to the vascular territories of both the thalamo-geniculate and posterolateral choroidal arterial pedicles. The thalamic lesion involved the pulvinar, the lateral geniculate body, and the ventro-postero-lateral, dorso-lateral, posterolateral, and dorso-medial nuclei, but apparently did not extent to the ventrolateral thalamic nucleus, and the subthalamic and midbrain regions. Thalamic and striatopallidal dystonia have not a common pathophysiological mechanism. The involvement of the pulvinar nucleus and of the strategic crossing of proprioceptive, cerebellar, pyramidal, and subthalamic pathways may play a role in the genesis of the posterolateral thalamic dystonia.
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PMID:Delayed-onset hemidystonia and chorea following contralateral infarction of the posterolateral thalamus. A case report. 900 80

A mode is proposed of treatment of chronic cerebrovascular disorders, such as initial manifestations of cerebral blood supply insufficiency (IMBSI) and dyscirculatory encephalopathy (DE) stage I-II in hypertensive disease, involving the use of laser puncture and microclimate of biotron. All patients (n = 162) were exposed to laser puncture (10-12 procedures). Laser puncture treatments were devised according to classical approaches of reflexotherapy, using determinants of electropuncture diagnostic method by Riodoraku. The treatments were carried out with the aid of infrared portable laser "Biomed-001". IMBSI patients presenting with vegetovascular dystonia and about 70% of IMBSI patients presenting with hypertensive disease derived benefit from a course of laser puncture, as evidenced by REG, EEG, acupuncture diagnosis, iridodiagnosis according. In DE stage I-II patients and about 30% IMBSI patients presenting with hypertensive disease good therapeutic effect occurred after treatment in a ward with a stable microclimate of biotron. The proposed method can be used for treating chronic cerebrovascular disorders and administering stroke prophylaxis.
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PMID:[The treatment of patients with chronic cerebral circulatory failure by using laser puncture and the microclimate of the biotron]. 907 33

The phenomenon of delayed-onset dystonia following presumed "static" brain injuries was described after stroke and head trauma. Burke et al. described a different category of secondary dystonia, where perinatal injury (asphyxia) caused minimal or no immediate neurological deficit, with the delay of years before dystonia emerged. This type of dystonia following perinatal injury has been termed "delayed onset dystonia due to static encephalopathy of childhood". According to the definition of dystonia, we were able to select 5 patients with the aetiologic diagnosis of perinatal asphyxia from the group of 347 out- and inpatients (1.4%) treated for various types of dystonia at the Movement Disorders Department (Institute of Neurology, CCS, Belgrade) from November 1986 to November 1994. At onset of dystonia the mean age of patients was 13.2 years (range from 10 to 17), with combined initial involvement of the arm and neck in 3 patients. The period from the onset of the disease to the maximum severity lasted 8.2 years (range from 4 to 14), resulting in segmental brachial dystonia in 3, hemidystonia and generalized dystonia in one patient each (Table 1). The adverse perinatal events are described in Table 2. Three of our patients had delayed achievements of developmental milestones. All patients were regularly schooled and had preserved intellectual capacities, except the patient 3 whose achievements were below average (IQ = 86). Different drugs were administered (Table 3), but moderate effects were achieved only with trihexyphenidyl in two patients (daily doses of 24 mg and 30 mg, respectively), and baclofen (80 mg p.d.) in one patient. In this study we describe 5 new patients who fulfilled the criteria for the diagnosis of delayed-onset dystonia due to perinatal asphyxia (Tables 1 and 2). We accepted the approach of Saint-Hilaire et al. to suggest a relationship between perinatal asphyxia and later occurrence of dystonia in our 5 patients. However, coincident occurrence of a primary dystonia with a static encephalopathy of childhood due to perinatal asphyxia cannot be excluded. This phenomenon of delayed appearance of dystonia was also described in other forms of static cerebral injury; i.e. stroke, head trauma or anoxic brain damage. Interestingly enough, age at the time of anoxia or brain insults seemed to be crucial for the development of dystonia: those who suffer acute brain insults during childhood or early life are more likely to develop dystonia than the older patients. Therefore, the "static" nature of encephalopathy induced by perinatal asphyxia is questionable. Finally, this study strengthens the suggestion that perinatal asphyxia can lead to delayed-onset dystonia, and, since "some of these patients closely resemble cases of idiopathic torsion dystonia, the prior occurrence of asphyxia should be used as a criterion of exclusion for that diagnosis".
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PMID:[Delayed-onset dystonia due to asphyxia in the perinatal period]. 922 23

To establish whether botulinum A toxin (BTX-A) acts on modifying reciprocal inhibition between forearm muscles in spasticity, 20 patients with post-stroke upper limb spasticity lasting for more than 1 year were studied. Clinical examination, physiotherapeutic evaluation, standardized video-tape assessment and electrophysiological testing (flexor carpi radialis muscle M and H responses with study of reciprocal inhibition) were performed at baseline and 2 weeks, 1, 2, 3, 4 months after BTX-A treatment. BTX-A induced a significant decrease of tone and an improvement of motility and functional status, with a significant decrease of the M wave and the H reflex. The reduction in both inhibitory phases of reciprocal inhibition did not change after BTX-A treatment differently from that reported in upper limb dystonia. These findings indicate that the efficacy of BTX-A in upper limb spasticity is mainly due to peripheral effects.
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PMID:Botulinum toxin in upper limb spasticity: study of reciprocal inhibition between forearm muscles. 933 11


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