Post-stroke Movement Disorders: Clinical Spectrum, Pathogenesis, and Management.

Involuntary movements develop after 1-4% of strokes and they have been reported in patients with ischemic and hemorrhagic strokes affecting the basal ganglia, thalamus, and/or their connections. Hemichorea-hemiballism is the most common movement disorder following a stroke in adults while dystonia is most common in children. Tremor, myoclonus, asterixis, stereotypies, and vascular parkinsonism are other movement disorders seen following stroke. Some of them occur immediately after acute stroke, some can develop later, and others may have delayed onset progressive course. Proposed pathophysiological mechanisms include neuronal plasticity, functional diaschisis, and age-related differences in brain metabolism. There are no guidelines regarding the management of post-stroke movement disorders, mainly because of their heterogeneity.

Botulinum toxin in movement disorders.

Botulinum toxin has gained immense popularity since its introduction for therapeutic use. It is used in a variety of movement disorders like hemi-facial spasm, focal dystonias like blepharospasm, cervical dystonia, oromandibular dystonia, limb dystonias. It is also being used in patients with tremors, tics and for a variety of indications in Parkinson's disease as well. There are eight subtypes of toxins available, but type A and B are the ones used in movement disorder clinics. The toxin mainly acts by inhibiting the release of acetylcholine at the neuromuscular junction and causing weakness. Type B toxin has more effect over the autonomic nervous system and hence is preferred for hyper-secretory disorders. The use of electromyography and ultrasound further improve the accuracy of the procedure. It is a relatively safe therapeutic option with its effect lasting for around three months. It has very few side effects. The key is to start with the lowest possible dose and then gradually increase the dose depending upon the patient's response. Selecting the right muscles for injection is of utmost importance and is guided by the knowledge of anatomy of the muscles.

Post-Stroke Lingual Dystonia: Clinical Description and Neuroimaging Findings.

Background: Lingual dystonia is extremely rare following stroke. We describe clinical features and neuroimaging findings in a series of 11 patients (seven acute and four chronic) with post-stroke lingual dystonia and review the literature. Methods: This was a case series using a preformed structured proforma and review of literature using a PubMed search. Results: In our case series, all patients had dysarthria as a presenting symptom. Seven patients had acute presentation (six had an ischemic infarct and one had thalamic hemorrhage) and four had chronic presentation (all had infarct). All patients except one had small infarcts, with the majority of them in the basal ganglia and subcortical white matter regions. Additional chronic ischemic lesions were seen in all patients with acute presentation. The majority of the patients with acute (five out of seven; 71.42%) presentation had left-sided involvement on imaging. We could identify only one case of acute post-stroke lingual dystonia following the PubMed search. Three other cases of post-stroke lingual dystonia with chronic presentation have been described; however, these were associated with oromandibular or cranial dystonia. Discussion: Our results, based on brain lesions, suggest that all lingual dystonia patients with acute infarcts had underlying chronic infarcts. Overall, more left-sided than right-sided strokes were observed with post-stroke lingual movement disorders including dystonia; however, the data were not significant (p = 1). All patients had dysarthria, with only one having mild tongue weakness and only four having facial weakness. This suggests that the lingual dystonia was responsible for the dysarthria rather than weakness in these patients.

Serum uric acid level as a determinant of the metabolic syndrome: A case control study.

AIMS: To determine whether elevations of uric acid levels are associated with the cluster of disorders described in metabolic syndrome and to evaluate whether hyperuricemia may be considered a component of this syndrome. METHODS: One year case-control study was conducted in Bikaner, Rajasthan, India from January to December 2013. The study population consisted of 200 subjects, 100 with metabolic syndrome (case) and 100 without metabolic syndrome (control) aged between 18 and 80 years, attending OPD at PBM Hospital were studied. Controls were age and sex matched to the cases. Blood tests and all physical variables were examined using standard methods. Subjects were divided into 6 groups according to their possession of 0, 1, 2, 3, 4 or 5 components of the metabolic syndrome. Statistical analysis was done using ANOVA, linear regression analysis and multivariate linear regression model. RESULTS: Mean serum UA level was significantly associated with all components of metabolic syndrome (p<0.001) and had strong positive correlation (r=+0.66 to +0.77, p<0.0001) with all of them except serum HDL with which it showed strong negative correlation(r=-0.71, p<0.0001). It increased as the number of metabolic factors increased showing a highly significant trend (p<0.0001). On multivariate regression analysis UA contributed to 66.84% variance of metabolic syndrome. CONCLUSION: The current multivariate regression analysis clearly infers that uric acid can be considered as a marker and potential modifier of metabolic syndrome.