Premium
Electrical Status Epilepticus of Sleep in Association with Topiramate
Author(s) -
Montenegro Maria Augusta,
Guerreiro Marilisa M.
Publication year - 2002
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1046/j.1528-1157.2002.33601_1.x
Subject(s) - topiramate , status epilepticus , medicine , sleep (system call) , association (psychology) , epilepsy , anesthesia , psychology , psychiatry , psychotherapist , computer science , operating system
To the Editor: Most studies suggest that the majority of children taking antiepileptic drugs (AEDs) do not experience clinically relevant cognitive or behavioral adverse events from these medications (1). However, there are a few instances in which the AED may induce serious cognitive decline. We report the occurrence of electrical status epilepticus of sleep (ESES) induced by topiramate (TPM) in a 5-year-old boy with refractory epilepsy. This 5-year-old boy is the first child of unrelated parents, born after an uneventful pregnancy. Developmental milestones were delayed, and he had refractory epilepsy since age 18 months. At age 5 years, he had several drop attacks and myoclonic and tonic seizures, daily. EEG showed multifocal spikes, and generalized spike-andwave complexes, <85%. He was using lamotrigine (LTG), 100 mg/day, and clobazam (CLB), 10 mg/day, when TPM was introduced gradually until 200 mg/day. Seizures improved markedly, but he still had one or two myoclonic seizures a week. Despite that, the family stopped giving him LTG abruptly, without medical advice. Symptoms started gradually, and 11 months after the introduction of TPM, his family reported that he was more somnolent, and 1 month later, it was clear that there was a compromise of previously acquired abilities. Neurologic examination showed only diffuse hypotonia and wide-based gait. Complete blood count (CBC), platelets, Na, K, glucose, blood urea nitrogen (BUN), liver enzymes, evoked potential (visual and brainstem), amino acids, and organic acid chromatography were normal. There were no signs of metabolic acidosis. Magnetic resonance imaging (MRI) was normal. At this time, the EEG showed very frequent, almost continuous, generalized spike-and-wave complexes during >90% of slow sleep (Fig. 1). TPM was discontinued, and when the drug was being tapered off, he already started to improve. One month after drug discontinuation, he recovered completely and returned to his previous neurologic background. Two months after complete drug discontinuation, EEG showed marked improvement, although there was still some slowing and epileptiform activity (Fig. 2). He is currently taking CLB and has weekly tonic and myoclonic seizures. ESES results from the association of various seizure types. The characteristic EEG pattern consists of continuous (>85%) spikes and slow waves during non–rapid eye movement (REM) sleep, and the abnormality is substantially less frequent during the awake state and REM sleep. This condition is associated with neuropsycholog-