Chorea as a rare manifestation of hyperglycaemia.
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Abstract:
We present a case of chorea presenting as a clinical manifestation of hyperglycaemia.The purpose of presenting this case is to highlight the fact that movement disorder may be the clinical presentation of hyperglycaemia and it reverts on treatment of hyperglycaemia.A 66-year-old female known case of type 2 diabetes mellitus and on oral hypoglycaemic drugs presented with abnormal and involuntary movements of the whole body and face since 7 days and high plasma glucose (446 mg/dl) and without ketosis. On controlling the blood sugar, there has been significant decrease in choreiform movements within 48 hrs and complete resolution of involuntary movements found at discharge at 1 week.Movement disorder like chorea may be the clinical presentation of the hyperglycaemia which could completely recover on rapid detection and correction of hyperglycaemia.Keywords:
Choreiform movement
Presentation (obstetrics)
Blood sugar
Ketosis
Movement Disorders
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Movement disorders are rarely reported in association with antiphospholipid syndrome (APS). Although it is a rare manifestation in APS, chorea is the most common movement disorder. We report a case of APS in a patient who presented with hyperkinesia, tics, choreiform movements, and other dyskinetic movements involving the mouth and tongue along with behavioral changes. These abnormal movements improved with aripiprazole.
Choreiform movement
Hyperkinesia
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Perseveration
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SARS-CoV-2 induces an immunological response that can trigger encephalitis and several movement disorders like chorea, opsoclonus, myoclonus, tremor and ataxia. SARS-CoV-2 receptor protein ACE-2 is expressed in the brain and its gene is closely related to the dopamine decarboxylase gene, which catalyzes the conversion of L-DOPA into dopamine which can be altered in COVID-19. The aim is to report a case of COVID-19 presenting with choreiform movement disorder as the core neurological complication. A 86-year-old hispanic male with COVID-19 presented with persistent nocturnal dyspnea, buccopharyngeal dystonia, dysarthria, night sweats, dry mouth, generalized pruritus, insomnia, headache and involuntary movements. Followed by sialorrhea with dysphagia and dystusia. Physical examination showed hypoacusia, tangential thinking, frontal release signs, facial and upper limbs choreiform movements with lip smacking, tongue biting, facial, upper limbs weakness and lower limbs paresthesias, diminished deep tendon reflexes and Romberg's. Bloodwork showed elevated glucose, ESR, CRP, CPK, ferritin, fibrinogen and D-dimer. SARS-CoV-2 IgM and IgG were positive. MRI showed fronto-parietal subcortical ischemic lesions, as well as at the centrum semiovale, and faint hyperintensity of the claustrum and the rostral putamen. The patient received treatment for COVID-19 with corticosteroids, and overcame the infection. Involuntary choreiform movements disappeared improving the rest of his symptoms. Choreiform movement disorders should be taken into account as a neurological complication of SARS-CoV-2 infection as we report in this case.
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We describe acute movement disorders in 92 children, aged 5 days to 15 years, from an Indian tertiary hospital. Eighty-nine children had hyperkinetic movement disorders, with myoclonus in 25, dystonia in 21, choreoathetosis in 19, tremors in 15, and tics in 2. Tetany and tetanus were seen in 5 and 2 children, respectively. Hypokinetic movement disorders included acute parkinsonism in 3 children. Noninflammatory and inflammatory etiology were present in 60 and 32 children, respectively. Benign neonatal sleep myoclonus in 16 and opsoclonus myoclonus syndrome in 7 accounted for the majority of myoclonus cases. Vitamin B 12 deficiency in 13 infants was the most common cause of tremors. Rheumatic fever and encephalitis were the most common causes of acute choreoathetosis. Acute dystonia had metabolic etiology in 6 and encephalitis and drugs in 3 each. Psychogenic movement disorders were seen in 4 cases only, although these patients may be underreported.
Choreoathetosis
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Psychogenic disease
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Choreiform movement
Movement Disorders
Conversion disorder
Pulmonary thromboendarterectomy
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We present a case of chorea presenting as a clinical manifestation of hyperglycaemia.The purpose of presenting this case is to highlight the fact that movement disorder may be the clinical presentation of hyperglycaemia and it reverts on treatment of hyperglycaemia.A 66-year-old female known case of type 2 diabetes mellitus and on oral hypoglycaemic drugs presented with abnormal and involuntary movements of the whole body and face since 7 days and high plasma glucose (446 mg/dl) and without ketosis. On controlling the blood sugar, there has been significant decrease in choreiform movements within 48 hrs and complete resolution of involuntary movements found at discharge at 1 week.Movement disorder like chorea may be the clinical presentation of the hyperglycaemia which could completely recover on rapid detection and correction of hyperglycaemia.
Choreiform movement
Presentation (obstetrics)
Blood sugar
Ketosis
Movement Disorders
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Abstract Two patients with chronic bilateral subdural hematomas developed symmetrical generalized choreiform movements. In one patient the chorea disappeared after evacuation of the hematomas, and in the other the movements improved. The latter patient has a family history of Huntington's disease.
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Chronic Subdural Hematoma
Subdural Hematomas
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Objective. To determine whether children with recent onset of movement disorders (Tourette syndrome, motor and/or vocal tics, chorea, choreiform movements) show evidence of serological antibodies directed against the human central nervous system as previously documented in research on Sydenham's chorea. Methods. Serum antibodies against previously frozen human caudate nucleus sections were analyzed using a blinded design and immunofluorescent staining methods. The sera of one group of 50 children referred for evaluation of attention deficit hyperactivity disorder, behavior disorders, and learning disabilities (24 with an associated movement disorder) seen between June 1989 and June 1990 were analyzed. The study was replicated in 33 children (21 with an associated movement disorder) seen between June 1990 and November 1990. Results. In the original sample of 50 children, those with movement disorders were significantly more likely to have evidence of antineuronal antibodies than were those without movement disorders (odds ratio [OR] 4.80, 95% confidence interval [CI] 2.58 to 8.93). Results of the replication were similar (OR 6.00, 95% CI 2.56 to 14.03). For the total group, the OR was 5.50, (95% CI 3.54 to 8.99), which is highly significant. The percentage of children with a movement disorder whose sera were strongly positive for antineuronal antibodies (44%) was very similar to that previously found in children with Sydenham's chorea (46%). Children with movement disorders were also more likely than children without movement disorders to have at least one antistreptococcal titer elevated. Conclusions. The data strongly suggest an association between antecedent group A β-hemolytic streptococcal infection as inferred from elevated antistreptococcal titers and the presence of serum antineuronal antibodies, which may, in turn, be linked to childhood movement disorders.
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Choreiform movement
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