129 resultados para POSTSTROKE HEMIPARESIS


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Background During gait, the hip flexors generate 40% of the total power. Nevertheless, no device has been tested extensively for clinical purposes to cope with weakness in the hip flexors in patients with stroke. Objective The purpose of this study was to assess the efficacy and safety of a newly developed hip flexion assist orthosis in adult patients with hemiparesis after stroke. Design The study used a prospective, randomized, before-after trial design. The inclusion criteria were hemiparesis resulting from stroke (onset ≥8 weeks); ability to walk, even if with assistance; and hip flexion weakness (Medical Research Council Scale score ≤4).¦METHODS: /b> The main outcome measures were the 10-Meter Walk Test and the Six-Minute Walk Test. Patients also were evaluated with the Trunk Control Test, the Functional Ambulation Categories, the Motricity Index, and hip flexor strength on the Medical Research Council Scale. Sixty-two survivors of stroke were tested in random order with and without the orthosis. Any adverse event associated with its use was recorded.¦RESULTS: /b> Both the Six-Minute Walk Test and the 10-Meter Walk Test scores improved with the use of the orthosis. A significant negative correlation was found for improvement between scores on the 2 main outcome measures with the orthosis and the Functional Ambulation Categories scores. The improvement in Six-Minute Walk Test scores with the orthosis was related inversely to hip flexor strength.¦CONCLUSIONS: /b> The data showed that the use of a hip flexion assist orthosis can improve gait in patients with poststroke hemiparesis, particularly those with more severe walking impairment.

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Objective: To analyze the relation between contralesional and ipsilesional limbs in subjects with stroke during step-to-step transition of walking. Design: Observational, transversal, analytical study with a convenience sample. Setting: Physical medicine and rehabilitation clinic. Participants: Subjects (nZ16) with poststroke hemiparesis with the ability to walk independently and healthy controls (nZ22). Interventions: Not applicable. Main Outcome Measures: Bilateral lower limbs electromyographic activity of the soleus (SOL), gastrocnemius medialis, tibialis anterior, biceps femoris, rectus femoris, and vastus medialis (VM) muscles and the ground reaction force were analyzed during double-support and terminal stance phases of gait. Results: The propulsive impulse of the contralesional trailing limb was negatively correlated with the braking impulse of the leading limb during double support (rZ .639, PZ.01). A moderate functional relation was observed between thigh muscles (rZ .529, PZ.035), and a strong and moderate dysfunctional relation was found between the plantar flexors of the ipsilesional limb and the vastus medialis of the contralesional limb, respectively (SOL-VM, rZ .80, P<.001; gastrocnemius medialis-VM, rZ .655, PZ.002). Also, a functional moderate negative correlation was found between the SOL and rectus femoris muscles of the ipsilesional limb during terminal stance and between the SOL (rZ .506, PZ.046) and VM (rZ .518, PZ.04) muscles of the contralesional limb during loading response, respectively. The trailing limb relative impulse contribution of the contralesional limb was lower than the ipsilesional limb of subjects with stroke (PZ.02) and lower than the relative impulse contribution of the healthy limb (PZ.008) during double support. Conclusions: The findings obtained suggest that the lower performance of the contralesional limb in forward propulsion during gait is related not only to contralateral supraspinal damage but also to a dysfunctional influence of the ipsilesional limb.

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Background. Further clarification is needed with regard to the degree of atrophy in individual muscle groups and its possible relationship to joint torque deficit poststroke. Objective. The purpose of this study was to investigate quadriceps and hamstring muscle volume and strength deficits of the knee extensors and flexors in people with chronic hemiparesis compared with a control group. Design. This was a cross-sectional study. Methods. Thirteen individuals with hemiparesis due to chronic stroke (hemiparetic group) and 13 individuals who were healthy (control group) participated in this study. Motor function, quadriceps and hamstring muscle volume, and maximal concentric and eccentric contractions of the knee extensors and flexors were assessed. Results. Only the quadriceps muscle of the paretic limb showed reduced muscle volume (24%) compared with the contralateral (nonparetic) limb. There were no differences in muscle volume between the hemiparetic and control groups. The peak torque of the paretic-limb knee extensors and flexors was reduced in both contraction modes and velocities compared with the nonparetic limb (36%-67%) and with the control group (49%-75%). The nonparetic limb also showed decreased extensor and flexor peak torque compared with the control group (17%-23%). Power showed similar deficits in strength (12%-78%). There were significant correlations between motor function and strength deficits (.54-.67). Limitations. Magnetic resonance imaging coil length did not allow measurement of the proximal region of the thigh. Conclusions. There were different responses between quadriceps and hamstring muscle volumes in the paretic limb that had quadriceps muscle atrophy only. However, both paretic and nonparetic limbs showed knee extensor and flexor torque and power reduction.

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BACKGROUND AND OBJECTIVE: Investigations were performed to establish if repetitive arm cycling training enhances the antispastic effect of intramuscular botulinum toxin (BTX) injections in postischemic spastic hemiparesis. Effects on cerebral activation were evaluated by functional magnetic resonance imaging (fMRI). METHODS: Eight chronic spastic hemisyndrome patients (49 ± 10 years) after middle cerebral artery infarction (5.5 ± 2.7 years) were investigated. BTX was injected into the affected arm twice, 6 months apart. Spasticity was assessed using the Ashworth Scale and range of motion before and 3 months after BTX injections. Images were analyzed using Brain Voyager QX 1.8, and fMRI signal changes were corrected for multiple comparisons. RESULTS: During passive movements of affected and nonaffected hands, fMRI activity was increased bilaterally in the sensorimotor cortex (MISI), secondary somatosensory areas (SII), and supplementary motor area predominantly in the contralesional hemisphere, compared with the rest. Following repetitive arm cycling, fMRI activity increased further in MISI of the lesioned hemisphere and SII of the contralesional hemisphere. For patients with residual motor activity, treatment-related fMRI activity increases were associated with reduced spasticity; in completely plegic patients, there was no fMRI activity change in SII but increased spasticity after training. CONCLUSION: Increased activity in SII of the contralesional hemisphere and in MISI of the lesioned hemisphere reflect a treatment-induced effect in the paretic arm. It is hypothesized that the increased BOLD activity results from increased afferent information related to the antispastic BTX effect reinforced by training.

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A boy with a right congenital hemiparesis due to a left pre-natal middle cerebral artery infarct developed focal epilepsy at 33 months and then an insidious and subsequently more rapid, massive cognitive and behavioural regression with a frontal syndrome between the ages of 4 and 5 years with continuous spike-waves during sleep (CSWS) on the EEG. Both the epilepsy and the CSWS were immediately suppressed by hemispherotomy at the age of 5 years and 4 months. A behavioural-cognitive follow-up prior to hemispherotomy, an per-operative EEG and corticography and serial post-operative neuropsychological assessments were performed until the age of 11 years. The spread of the epileptic activity to the "healthy" frontal region was the cause of the reversible frontal syndrome. A later gradual long-term but incomplete cognitive recovery, with moderate mental disability was documented. This outcome is probably explained by another facet of the epilepsy, namely the structural effects of prolonged epileptic discharges in rapidly developing cerebral networks which are, at the same time undergoing the reorganization imposed by a unilateral early hemispheric lesion. Group studies on the outcome of children before and after hemispherectomy using only single IQ measures, pre- and post-operatively, may miss particular epileptic cognitive dysfunctions as they are likely to be different from case to case. Such detailed and rarely available complementary clinical and EEG data obtained in a single case at different time periods in relation to the epilepsy, including per-operative electrophysiological findings, may help to understand the different cognitive deficits and recovery profiles and the limits of full cognitive recovery.

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Rapport de synthèse : Cette thèse a étudié en détail le cas d'un enfant souffrant d'une hémiplégie congénitale sur un infarctus prénatal étendu qui a développé une forme particulière d'épilepsie, le syndrome des pointes ondes continues du sommeil (POCS), associé à une régression mentale massive. Les caractéristiques de cette détérioration pointaient vers un dysfonctionnement de type frontal. Une chirurgie de l'épilepsie (hémisphérotomie) a, non seulement, permis la guérison de l'épilepsie mais une récupération rapide sur le plan comportemental et cognitif, suivie d'une reprise plus lente du développement, avec finalement à l'âge de 11 ans un niveau de déficience intellectuelle modérée. L'intérêt de cette étude réside dans le fait que l'enfant a pu être suivi prospectivement entre l'âge de 4.5 ans et 11 ans par des enregistrements électro-encéphalographiques (EEG) ainsi que des tests neuropsychologiques et des questionnaires de comportements sériés, permettant de comparer les périodes pré-, péri- et postopératoires, ce qui est rarement réalisable. Un enregistrement EEG de surface a même pu être effectué durant l'opération sur l'hémisphère non lésé, permettant de documenter l'arrêt des décharges épileptiformes généralisées dès la fin de l'intervention. L'hypothèse que nous avons- souhaité démontrer est que la régression comportementale et cognitive présentée par l'enfant après une période de développement précoce presque normale (retard de langage) était de nature épileptique : nous l'expliquons par la propagation de l'activité électrique anormale à partir de la lésion de l'hémisphère gauche vers les régions préservées, en particulier frontales bilatérales. L'hémisphérotomie a permis une récupération rapide en déconnectant l'hémisphère gauche lésé et épileptogène de l'hémisphère sain, qui a ainsi pu reprendre les fonctions cognitives les plus importantes. Les progrès plus lents par la suite et l'absence de rattrapage au delà d'un niveau de déficience mentale modérée sont plus difficiles à expliquer: on postule ici un effet de l'épilepsie sur le développement de réseaux neuronaux de l'hémisphère initialement non lésé, réseaux qui sont à la fois à un stade précoce de leur maturation et en cours de réorganisation suite à la lésion prénatale. La littérature sur les déficits cognitifs avant et après hemisphérotomie s'est surtout préoccupée du langage et de sa récupération possible. À notre connaissance, notre étude est la première à documenter la réversibilité d'une détérioration mentale avec les caractéristiques d'un syndrome frontal après hémisphérotomie. La chirurgie de l'épilepsie a offert ici une occasion unique de documenter le rôle de l'activité épileptique dans la régression cognitive puisqu'en interrompant brusquement la propagation de l'activité électrique anormale, on a pu comparer la dynamique du développement avant et après l'intervention. La mise en relation des multiples examens cliniques et EEG pratiqués chez un seul enfant sur plusieurs années a permis d'obtenir des informations importantes dans la compréhension des troubles cognitifs et du comportement associés aux épilepsies focales réfractaires. ABSTRACT : A boy with a right congenital hemiparesis due to a left pre-natal middle cerebral artery infarct developed focal epilepsy at 33 months and then an insidious and subsequently more rapid, massive cognitive and behavioural regression with a frontal syndrome between the ages of 4 and 5 years with continuous spike-waves during sleep (CSWS) on the EEG. Both the epilepsy and the CSWS were immediately suppressed by hemispherotomy at the age of 5 years and 4months. A behavioural-cognitive follow-up prior to hemispheratomy, an per-operative EEG and corticography and serial post-operative neuropsychological assessments were performed until the age of 11 years. The spread of the epileptic activity to the "healthy" frontal region was the cause of the reversible frontal syndrome. A later gradual long-term but incomplete cognitive recovery, with moderate mental disability was documented. T9ris outcome is probably explained by another facet of the epilepsy, namely the structural effects of prolonged epileptic dischazges in rapidly developing cerebral networks which are, at the same time undergoing the reorganization imposed by a unilateral early hemispheric lesion. Group studies on the outcome of children before and after hemispherectomy using only single IQ measures, pre- and postoperatively, may miss particular epileptic cognitive dysfunctions as they are likely to be different from case to case. Such detailed and rarely available complementary clinical and EEG data obtained in a single case at different time periods in relation to the epilepsy, including peroperative electrophysiological findings, may help to understand the different cognitive deficits and recovery profiles and the limits of full cognitive recovery.

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OBJECTIVE: To explore the potential relationship between fatigue following strokes and poststroke mood, cognitive dysfunction, disability, and infarct site and to determine the predictive factors in the development of poststroke fatigue (PSF) following minor infarcts. METHODS: Ninety-nine functionally active patients aged less than 70 years with a first, nondisabling stroke (NIH Stroke Scale score ≤6 in acute phase and ≤3 after 6 months, modified Rankin Scale score ≤1 at 6 months) were assessed during the acute phase and then at 6 (T1) and 12 months (T2) after their stroke. Scores in the Fatigue Assessment Inventory were described and correlated to age, gender, neurologic and functional impairment, lesion site, mood scores, neuropsychological data, laboratory data, and quality of life at T1 and T2 using a multivariate logistic regression analysis in order to determine which variables recorded at T1 best predicted fatigue at T2. RESULT: As many as 30.5% of the patients at T1 and 34.7% at T2 (11.6% new cases between T1 and T2) reported fatigue. At both 6 and 12 months, there was a significant association between fatigue and a reduction in professional activity. Attentional-executive impairment, depression, and anxiety levels remained associated with PSF throughout this time period, underlining the critical role of these variables in the genesis of PSF. There was no significant association between the lesion site and PSF. CONCLUSION: This study suggests that attentional and executive impairment, as well as depression and anxiety, may play a critical role in the development of PSF.

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OBJECTIVE: To assess whether thalamic strokes presenting with a central Horner's syndrome (HS) show specific clinicoanatomic patterns. METHODS: From the Lausanne Stroke Registry (period 1993 to spring 2002), the authors selected all patients with thalamic stroke presenting with ipsilateral HS. Patients with complete infarction of the posterior cerebral artery territory, with involvement of middle cerebral artery territory or bilateral lesions, were excluded. Lesions on brain MRI were correlated with standard neuroanatomic templates. RESULTS: Nine patients with thalamic infarction presenting with central HS were found; all showed contralateral ataxic hemiparesis (AH). Lesions involved the anterior or paramedian thalamus and extended to the hypothalamic or rostral paramedian mesencephalic area in all but one subject. Associated clinical signs included dysphasia (two patients), somnolence (six), vertical gaze paresis (two), asterixis (two), and hemihypesthesia (three). CONCLUSION: The alternate clinical pattern of central HS with contralateral AH is a stroke syndrome of the diencephalic-mesencephalic junction, resulting from the involvement of the common arterial supply to the paramedian/anterior thalamus, the posterior hypothalamus and the rostral paramedian midbrain.

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OBJECTIVE: To investigate the association between early depressive behavior after stroke onset and occurrence of poststroke depression (PSD) at 3- and 12-month follow-up evaluations. METHODS: The study prospectively included 273 patients with first-ever single uncomplicated ischemic stroke. In the stroke unit, nurses scored crying, overt sadness, and apathy daily using an observational method to include patients with comprehension deficits. The Barthel Index was used to assess disability. Follow-up evaluation at months 3 and 12 included psychiatric assessment based on the Diagnostic and Statistical Manual of Mental Disorders, 4th edition. RESULTS: Crying (19.8%), overt sadness (50.5%), and apathy (47.6%) were observed. Of the patients observed crying, 4 showed pathologic crying, 19 emotionalism, and 12 catastrophic reactions. Crying and overt sadness, but not apathy, were associated with a subjective experience of depression (p < 0.05). Thirty of 52 (58%) patients observed crying, 12 of 19 (63%) patients with emotionalism, and 5 of 12 (41%) patients with catastrophic reactions developed PSD within the first year. Multiple logistic regression analysis showed that only severe functional disability (odds ratio [OR], 4.31; 95% CI, 2.41 to 7.69), crying behaviors (OR, 2.66; 95% CI, 1.35 to 5.27), and an age <68 years (OR, 2.32; 95% CI, 1.30 to 4.13) were (p < 0.05) predictors of late PSD development (13% of the variance). CONCLUSIONS: In the stroke unit, crying and overt sadness are more reliable indicators of depressed mood than apathy. In patients with first-ever stroke, crying behaviors soon after stroke, a younger age, and severe disability are predictors of poststroke depression occurrence within the first year after stroke onset.

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BACKGROUND AND PURPOSE: Previous studies have postulated that poststroke depression (PSD) might be related to cumulative vascular brain pathology rather than to the location and severity of a single macroinfarct. We performed a detailed analysis of all types of microvascular lesions and lacunes in 41 prospectively documented and consecutively autopsied stroke cases. METHODS: Only cases with first-onset depression <2 years after stroke were considered as PSD in the present series. Diagnosis of depression was established prospectively using DSM-IV criteria for major depression. Neuropathological evaluation included bilateral semiquantitative assessment of microvascular ischemic pathology and lacunes; statistical analysis included Fisher exact test, Mann-Whitney U test, and regression models. RESULTS: Macroinfarct site was not related to the occurrence of PSD for any of the locations studied. Thalamic and basal ganglia lacunes occurred significantly more often in PSD cases. Higher lacune scores in basal ganglia, thalamus, and deep white matter were associated with an increased PSD risk. In contrast, microinfarct and diffuse or periventricular demyelination scores were not increased in PSD. The combined lacune score (thalamic plus basal ganglia plus deep white matter) explained 25% of the variability of PSD occurrence. CONCLUSIONS: The cumulative vascular burden resulting from chronic accumulation of lacunar infarcts within the thalamus, basal ganglia, and deep white matter may be more important than single infarcts in the prediction of PSD.

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Congenital hemiparesis is one of the most frequent pediatric motor disorders. Upper limb rehabilitation of the hemiparetic child has considerably evolved during the last decade by the use of focal chemical denervation (intramuscular botulinum toxin) and the introduction of novel rehabilitation techniques such as constraint induced movement therapy or robotic reeducation.

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Nervous system involvement in Lyme disease often mimics other conditions and thus represents a diagnostic challenge, especially in an emergency department setting. We report a case of a female teenager presenting with sudden-onset aphasia and transient right-sided faciobrachial hemiplegia, along with headache and agitation. Ischemia, vasculitis, or another structural lesion was excluded by brain imaging. Toxicologic evaluation results were negative. Cerebral perfusion computed tomography and electroencephalography showed left parietotemporal brain dysfunction. Lumbar puncture result, although atypical, suggested bacterial infection and intravenous ceftriaxone was initiated. Finally, microbiological cerebrospinal fluid analysis revealed Lyme neuroborreliosis, showing specific intrathecal antibody production and high level of C-X-C motif chemokine 13. The patient rapidly recovered. To our knowledge, this report for the first time illustrates that acute-onset language and motor symptoms may be directly related to Lyme neuroborreliosis. Neuroborreliosis may mimic other acute neurologic events such as stroke and should be taken into diagnostic consideration even in the absence of classic symptoms and evolution.

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Background. With diffusion-tensor imaging (DTi) it is possible to estimate the structural characteristics of fiber bundles in vivo. This study used DTi to infer damage to the corticospinal tract (CST) and relates this parameter to (a) the level of residual motor ability at least 1 year poststroke and (b) the outcome of intensive motor rehabilitation with constraint-induced movement therapy (CIMT). Objective. To explore the role of CST damage in recovery and CIMT efficacy. Methods. Ten patients with low-functioning hemiparesis were scanned and tested at baseline, before and after CIMT. Lesion overlap with the CST was indexed as reduced anisotropy compared with a CST variability map derived from 26 controls. Residual motor ability was measured through the Wolf Motor Function Test (WMFT) and the Motor Activity Log (MAL) acquired at baseline. CIMT benefit was assessed through the pre—post treatment comparison of WMFT and MAL performance. Results. Lesion overlap with the CST correlated with residual motor ability at baseline, with greater deficits observed in patients with more extended CST damage. Infarct volume showed no systematic association with residual motor ability. CIMT led to significant improvements in motor function but outcome was not associated with the extent of CST damage or infarct volume. Conclusion. The study gives in vivo support for the proposition that structural CST damage, not infarct volume, is a major predictor for residual functional ability in the chronic state. The results provide initial evidence for positive effects of CIMT in patients with varying, including more severe, CST damage.