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This Article Full Text Full Text (PDF) CME: Take the course for this article: Volume 73, Number 11, September 15, 2009 All Versions of this Article: WNL.0b013e3181b121f5v1 73/11/828    most recent Correspondence: Submit a response Correspondence: View responses Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Fattal-Valevski, A. Articles by Goldberg-Stern, H. PubMed PubMed Citation Articles by Fattal-Valevski, A. Articles by Goldberg-Stern, H. Related Collections All Pediatric All Epilepsy/Seizures EEG Related Article

Epilepsy in children with infantile thiamine deficiency

From the Pediatric Neurology Unit (A.F.-V., U.K.), Tel Aviv Sourasky Medical Center; The Pediatric Neurology and Developmental Unit (A.B.-M.), Loewenstein Rehabilitation Hospital, Raanana; Epilepsy Service (S.K., H.G.-S.), Schneider Children’s Medical Center, Petach Tikva, Israel; Department of Child Neurology and Rehabilitation (E.H.), Assaf Harofeh Medical Center, Zerifin, Israel; Department of Rehabilitation (A.B.), Sheba Medical Center; Pediatric Neurology (R.S.), Schneider Children’s Medical Center, Petach Tikva, Israel; Child Development Center (D.I.), Schneider Children’s Medical Center, Petach Tikva, Israel, All affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Israel.

Address correspondence and reprint requests to Dr. Aviva Fattal-Valevski, Pediatric Neurology Unit, Dana Children’s Hospital, Sourasky Medical Center, 6 Weitzman St., Tel Aviv, 64239, Israel afatal{at}post.tau.ac.il

Objective: To report the follow-up findings of 7 children with severe epilepsy as a result of thiamine deficiency in infancy caused by a defective soy-based formula.

Methods: The medical records of 7 children aged 5-6 years with thiamine deficiency in infancy who developed epilepsy were reviewed and their clinical data, EEG tracings, and neuroimaging results were recorded. The clinical course and present outcome of these children, now 5 years after exposure to thiamine deficiency, are described.

Results: All infants displayed seizures upon presentation, either tonic, myoclonic, or focal. Six infants had an EEG recording at this stage and all showed slow background. Five of them had no epileptic activity and only 1 displayed focal activity. Following a seizure-free period of 1-9 months, the seizures recurred, and all 7 children displayed either myoclonic or complex partial seizures. Multifocal or generalized spike wave complexes were recorded on the EEGs of all 7 patients, and the tracings of 3 children evolved into hypsarrhythmia. The seizures were refractory to most antiepileptic drugs, and 4 children remain with uncontrolled seizures. All children have mental retardation and motor disabilities as well as symptoms of brainstem dysfunction.

Conclusions: Our findings indicate that severe infantile thiamine deficiency may result in epilepsy.

Abbreviations: ACTH = adrenocorticotropic hormone.

Editorial, page 824

e-Pub ahead of print on July 1, 2009, at www.neurology.org.

Disclosure: The authors report no disclosures.

Received November 25, 2008. Accepted in final form May 18, 2009.

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