Treatment of chorea with levetiracetam

Zesiewicz, Theresa A.; Pathak, Amit; Sullivan, Kelly L.; Shamayev, M. I.; Hauser, Robert A.

doi:10.1007/s00228-005-0028-4

Cited by 8 publications

(4 citation statements)

References 4 publications

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“…To the best of our knowledge, our study is the first in the literature to compare the effectiveness of levetiracetam with Na valproate, carbamazepine, and haloperidol in the symptomatic treatment of chorea in patients with SC. Anecdotal case reports indicate that levetiracetam is effective in movement abnormalities of Huntington disease, 21 paroxysmal nonkinesigenic dyskinesia, 22 paroxysmal kinesigenic choreoathetosis, 23 choreoathetosis in dyskinetic cerebral palsy, 24 levodopa‐induced chorea, 25 vascular chorea, 26 and in a case report, 10 in the treatment of SC. The mechanism of action in SC may be related to the regulation of calcium ion flow to basal ganglia neurons preventing neuronal hypersynchronization 25 .…”

Section: Discussionmentioning

confidence: 95%

Efficacy of levetiracetam in the treatment of Sydenham chorea

Direk

Epçaçan

et al. 2020

Pediatrics International

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Background: To study the effect of levetiracetam in treating Sydenham chorea. Methods: We retrospectively collected the data of 140 patients diagnosed with Sydenham chorea in the pediatric neurology and pediatric cardiology outpatient clinics of Van Training and Research Hospital between January 2010 and December 2018. Results: There were 140 patients, 102 (70%) of whom were girls, with mean age of onset 11.8 AE 2.7 years. Symptomatic treatment was initiated in all patients at the time of diagnosis; this medication was changed during follow up in 15 patients. The most frequently prescribed drugs were haloperidol and sodium (Na) valproate, and the most frequently discontinued one was haloperidol, due to side effects. The second-choice drug was most often levetiracetam. Clinical response often began within the first 2 weeks, with Na valproate (P = 0.002), within 4 weeks with carbamazepine (P = 0.037) but 1-6 months with haloperidol (P = 0.018) and levetiracetam (P = 0.008). Time to full remission was similar with Na valproate, carbamazepine, haloperidol, and levetiracetam (P = 0.276). Our study indicated that levetiracetam was as effective as the other commonly used drugs in the symptomatic treatment of Sydenham chorea. Conclusion: Levetiracetam might be an option in the treatment of Sydenham chorea because of its acceptable effect and safety profile. This observation needs further support with evidence obtained through controlled and blinded trials.

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Section: Discussionmentioning

confidence: 95%

Efficacy of levetiracetam in the treatment of Sydenham chorea

Direk

Epçaçan

et al. 2020

Pediatrics International

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“…Additionally, typical neuroleptics and sometimes benzodiazepines are useful in the management of the choreic movements. Topiramate 7 , levetiracetan 8 and tetrabenazine 9 have also been tried in selected cases with favorable outcomes.…”

Section: Figure Mri Scan Showing a Hyperintense Lesion In The Right mentioning

confidence: 99%

Hemichorea-hemiballism as the first presentation of type 2 diabetes mellitus

Felı́cio

Chang

Godeiro-Júnior

et al. 2008

Arq. Neuro-Psiquiatr.

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Hemichorea-hemiballism (HCHB) can be the solely presentation of a wide range of non-neurological clinical pictures, such as metabolic or hydro-electrolyte derangements. HCHB as the first presentation of type 2 diabetes mellitus has been rarely described [1][2][3] . The case depicted herein reinforces this association highlighting that especially in elder patients with newly diagnosed HCHB, non-ketotic hyperglycemia should promptly be recognized. caseA 70-year-old white man presented with one month history of involuntary movements of the left upper and lower limbs. He also noticed polyuria and polydipsia for the last 2 months and lost 10 kg within this period. His past medical history included controlled hypertension and a heart attack three years before. He used to take on a regular basis and at the time of presentation to our emergency department captopril 50 mg per day, hydrochlorothiazide 25 mg per day, propranolol 120 mg per day, aspirin 200 mg per day, and digoxin 0.25 mg per day. He used to be a heavy drinker (stopped 15 years ago) and smoker (stopped 3 years ago). There was no history of diabetes mellitus, other diseases or exposure to neuroleptic medication. No family history of movement disorders was obtained.On admission, he was fully alerted and oriented. He had HCHB involving his left upper and lower limb with normal muscle strength, but mild hypotonia. The movements were almost continuous during wakefulness, and disappeared during sleep. Fasting blood glucose was obtained (560 mg/dL) and type 2 diabetes mellitus was diagnosed. Glycosylated hemoglobin A1c was 6.6%. No ketones were detected in urinalysis and urine pH was normal. Corrected sodium concentration was 140 mmol/L, and estimated serum osmolality was 332 mOsm/L. Other routine blood tests including calcium, potassium, magnesium, and phosphate concentrations, and thyroid and parathyroid hormone tests were normal as well liver and kidney functional status. A brain computer tomography (CT) showed a slight hyperdense lesion on the right putamen. T1-weighted brain magnetic resonance imaging (MRI) showed a right hyperintense lesion on putamen with iso-signal intensity on T2-weighted and Flair images.With the administration of haloperidol (10 mg per day) and glycemia control (10 IU bed time NPH insulin) and 6 mg per day glimepiride his movement disorder decreased in severity and completely disappeared 15 days after the first medical appointment. A nine-month re-scan with MRI showed a normal putamen without the previously seen hyperintense lesion (Figure).The patient signed an informed consent to allow his data publication. discussionThe underlying mechanisms of brain alterations in patients with non-ketotic hyperglycemia-induced HCHB are not known yet, but they have been attributed to base ganglia cerebral blood flow reduction, petechial hemorrhage, depletion of both GABA and acetylcholine, or metabolic acidosis 4 . Interestingly, among neuronal subtypes, striatal medium spiny neurones are highly vulnerable to energy depletion and this might explain ...

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“…This is because, involuntary movements secondary to hyperglycemia is refractory to phenytoin as phenytoin may inhibit insulin secretion and worsens hyperglycemia (Carter et al 1981). However, there were case reports on the use of haloperidol, benzodiazepines, topiramide, and levetiracetam in the management of choreic movements which showed favorable outcomes (Pena et al 2002;Driver-Dunckley & Evidente 2005;Zesiewicz et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia-Induced Involuntary Movements: What You Should Know

Leong¹

2018

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Hemichorea-hemiballismus (HC-HB) adalah gangguan pergerakan tidak terkawal yang melibatkan anggota sebelah badan. Terdapat banyak faktor etiologi yang dijumpai, termasuk strok, jangkitan, dan barah. Walaubagaimanapun, HC-HB yang disebabkan oleh hiperglisemia akut jarang dijumpai. Kami membentangkan dua kes HC-HB yang disebabkan oleh hiperglisemia. Kes-kes yang dibentangkan di sini menunjukkan bahawa HC-HB boleh menjadi antara gejala gangguan neurologi disebabkan diabetes yang tidak dikawal dan boleh dirawat sepenuhnya melalui rawatan bagi hiperglisemia.

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Treatment of chorea with levetiracetam

Cited by 8 publications

References 4 publications

Efficacy of levetiracetam in the treatment of Sydenham chorea

Efficacy of levetiracetam in the treatment of Sydenham chorea

Hemichorea-hemiballism as the first presentation of type 2 diabetes mellitus

Hyperglycemia-Induced Involuntary Movements: What You Should Know

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