16 research outputs found

    Anti-Gravity Treadmill Training for Freezing of Gait in Parkinson\u27s Disease

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    Background: Parkinson\u27s disease (PD) is a neurodegenerative disorder characterized by motor impairment. Freezing of gait, impaired mobility and falls are common problems in these patients. We aimed to evaluate the effect of a novel therapy for these patients. Methods: We studied patients with moderate to severe freezing of gait who underwent antigravity treadmill training twice a week for 4 consecutive weeks with 50% reduction of body weight. Results: We enrolled 26 consecutive patients with PD, 19 completed the study. There were 10 males; mean age at evaluation was 72.7 ± 10.1 years. Compared to baseline, patients showed improvement in the Freezing of Gait Questionnaire (p = 0.001); and a mean reduction of 7 s in the Timed Up & Go (TUG) test (p = 0.004). Moderate or significant improvement in gait was reported by 84% of patients. Conclusions: Antigravity treadmill training improved freezing of gait and mobility in patients with PD

    The Role of Muscle Strength in the Sit-to-Stand Task in Parkinson\u27s Disease

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    BACKGROUND: Rising from a chair or the sit-to-stand (STS) task is frequently impaired in individuals with Parkinson\u27s disease (PD). These patients commonly attribute such difficulties to weakness in the lower extremities. However, the role of muscle strength in the STS transfer task has not been fully elucidated. OBJECTIVE: We aim at determining the role of muscle strength in the STS task. METHODS: We studied 90 consecutive patients with PD and 52 sex- and age-matched controls. Lower limb strength was determined in both legs by clinical examination using the Medical Research Council Scale, dynamometric (leg flexion) and weighting machine (leg pressure) measures. Patients were interrogated regarding the presence of subjective lower limb weakness or allied sensations. RESULTS: There were 20 patients (22.2%) with abnormal STS task (item 3.9 of the MDS-UPDRS-III ≥2 points). These patients had higher modified Hoehn and Yahr stage (  \u3c  0.001) and higher total motor scores of the MDS-UPDRS(  \u3c  0.001), compared with 70 PD patients with normal STS task. Patients with abnormal STS task endorsed lower limb weakness more frequently and had lower muscle strength in the proximal lower extremities, compared to PD patients with normal STS task and normal controls. The presence of perceived lower limb weakness increased the risk of an abnormal STS task, OR: 11.93 (95% C.I. 1.51-94.32), whereas a hip extension strength ≤9 kg/pressure also increased the risk of abnormal STS task, OR: 4.45 (95% C.I. 1.49-13.23). In the multivariate regression analysis, bradykinesia and decreased hip strength were related to abnormal STS task. CONCLUSIONS: Patients with PD and abnormal STS task complain more commonly of lower limb weakness and have decreased proximal lower limb strength compared to patients with PD and normal STS task, likely contributing to abnormalities in performing the STS task

    A case of tactile agnosia with a lesion restricted to the post-central gyrus

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    Tactile agnosia has been described after lesions of the primary sensory cortex but the exact location and extension of those lesions is not clear. We report the clinical features and imaging findings in a patient with an acute ischemic stroke restricted to the primary sensory area (S1). A 73-year-old man had a sudden onset of a left alien hand, without left hemiparesis. Neurological examination showed intact primary sensory functions, but impaired recognition of shape, size (macrogeometrical) and texture (microgeometrical) of objects; damage confined to the post-central gyrus, sparing the posterior parietal cortex was demonstrated on MRI. An embolic occlusion of the anterior parietal artery was suspected as mechanism of stroke. Tactile agnosia with impaired microgeometrical and macrogeometrical features′ recognition can result from a single lesion in the primary sensory cortex (S1) in the right parietal hemisphere, sparing other regions of the cerebral cortex which presumably participate in tactile object recognition

    Functional (Psychogenic) Movement Disorders Presenting During Sleep

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    BACKGROUND: Functional (psychogenic) movement disorders are involuntary movements that seems to originate from activation of voluntary motor pathways in the brain. The movements typically present during the waking hours with variable frequency. CASE PRESENTATION: We present the case of a 24-year-old woman with FMDs during the waking state, but also during stages 1 and 2 of non-REM sleep and REM sleep, recorded with polysomnography. Such movements caused arousal leading to excessive daytime sleepiness and fatigue. CONCLUSIONS: FMDs may disrupt sleep causing day time somnolence, adding morbidity to the disorder

    Intestinal Decontamination Therapy for Dyskinesia and Motor Fluctuations in Parkinson\u27s Disease

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    Parkinson\u27s disease is neurodegenerative disorder with an initial robust response to levodopa. As the disease progresses, patients frequently develop dyskinesia and motor fluctuations, which are sometimes resistant to pharmacological therapy. In recent years, abnormalities in gut microbiota have been identified in these patients with a possible role in motor manifestations. Dysbiosis may reduce levodopa absorption leading to delayed On or no-On states. Among 84 consecutive patients with PD, we selected 14 with levodopa-induced dyskinesia and motor fluctuations with a Movement Disorders Society Unified Parkinson\u27s Disease Rating Scale (MDS-UPDRS) part IV ≥ 8 points following a trial of pharmacological adjustment 2-3 months prior to study enrollment or adjustments in deep brain stimulation therapy. Patients received treatment with sodium phosphate enema followed by oral rifaximin and polyethylene glycol for 7 and 10 days, respectively. Evaluations between 14 to 21 days after starting treatment showed improvement in MDS-UPDRS-IV (P = 0.001), including duration (P = 0.001) and severity of dyskinesia (P = 0.003); duration of medication Off -state (P = 0.004); functional impact of motor fluctuations (P = 0.047) and complexity of motor fluctuations (P = 0.031); no statistical improvement was observed in Off dystonia (P = 0.109) and total motor scores (P = 0.430). Marked to moderate improvement in dyskinesia was observed in 57% of cases with blinded evaluation of videos. About 80% of patients perceived moderate to robust improvement at follow-up. A therapeutic strategy aimed at decontamination of intestines showed benefit in motor fluctuations and dyskinesia. Further studies should confirm and clarify the mechanism of improvement observed in these patients

    Tics Emergencies and Malignant Tourette Syndrome:Assessment and Management

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    Tourette syndrome (TS) is a complex neurodevelopmental disorder characterized by the presence of tics, frequently accompanied by a variety of neuropsychiatric comorbidities. A subset of patients with TS present with severe and disabling symptoms, requiring prompt therapeutic intervention. Some of these manifestations may result in medical emergencies when severe motor or phonic tics lead to damage of anatomical structures closely related to the tic. Examples include myelopathy or radiculopathy following severe neck (“whiplash”) jerks or a variety of self-inflicted injuries. In addition to self-aggression or, less commonly, allo-aggression, some patients exhibit highly inappropriate behavior, suicidal tendencies, and rage attacks which increase the burden of the disease and are important components of “malignant TS”. This subset of TS is frequently associated with comorbid obsessive-compulsive disorder. Therapeutic measures include intensive behavioral therapy, optimization of oral pharmacotherapy, botulinum toxin injections, and deep brain stimulation

    Tics Emergencies and Malignant Tourette Syndrome:Assessment and Management

    No full text
    Tourette syndrome (TS) is a complex neurodevelopmental disorder characterized by the presence of tics, frequently accompanied by a variety of neuropsychiatric comorbidities. A subset of patients with TS present with severe and disabling symptoms, requiring prompt therapeutic intervention. Some of these manifestations may result in medical emergencies when severe motor or phonic tics lead to damage of anatomical structures closely related to the tic. Examples include myelopathy or radiculopathy following severe neck (“whiplash”) jerks or a variety of self-inflicted injuries. In addition to self-aggression or, less commonly, allo-aggression, some patients exhibit highly inappropriate behavior, suicidal tendencies, and rage attacks which increase the burden of the disease and are important components of “malignant TS”. This subset of TS is frequently associated with comorbid obsessive-compulsive disorder. Therapeutic measures include intensive behavioral therapy, optimization of oral pharmacotherapy, botulinum toxin injections, and deep brain stimulation

    Objective and Self-Perceived Lower Limb Weakness in Parkinson\u27s Disease

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    BACKGROUND: Lower limb weakness is a long-recognized symptom in patients with Parkinson\u27s disease (PD), described by James Parkinson in his seminal report on \u27paralysis agitans\u27. However, little is known on the frequency, clinical correlations, and association with objective decrease in muscle strength in such patients. OBJECTIVE: The objective of this study was to assess the frequency of objective and perceived lower limb weakness in patients with PD. METHODS: We studied 90 consecutive patients with PD and 52 age-matched controls. We recorded clinical and demographic variables, as well as perceived weakness and allied abnormal lower limb sensations, including \u27heavy legs\u27, \u27fatigued legs\u27, and \u27pain\u27. Symptoms consistent with restless legs syndrome were not considered. Lower limb strength was determined in both legs by means of the Medical Research Council scale, dynamometric (leg flexion) and weighting machine (leg pressure) measures. RESULTS: Weakness and allied abnormal lower limb sensations were reported in 69% of patients with PD and 21% of healthy controls. Patients with PD had decreased leg pressure compared with healthy controls ( = 0.002). Among patients with PD, an association between perceived leg weakness (and allied sensations) and gait freezing ( = 0.001) was observed in the multivariate regression analysis; however, these variables only explained 30.4% of the variance. Moreover, PD patients with and without abnormal lower limb sensations had similar muscle strength by objective measurements. CONCLUSION: Perceived lower limb weakness and allied abnormal sensations are common in patients with PD. However, there is a dissociation between perceived weakness and objective muscle strength in the lower limbs. These abnormal sensations were mostly related to gait freezing but a causal association is questionable
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