Reactions 1129 - 25 Nov 2006

[oxcarbazepine] should be included in the list of those drugspotentially able to induce clinical deterioration especially inOxcarbazepine [benign epilepsy with centrotemporal spikes] patients withatypical features."Aggravation of seizures in children with benign

epilepsy with centrotemporal spikes: 3 case reports Grosso S, et al. Oxcarbazepine and atypical evolution of benign idiopathic focalThree children with existing benign epilepsy with epilepsy of childhood. European Journal of Neurology 13: 1142-1145, No. 10, Oct

2006 - Italy 801045647centrotemporal spikes experienced seizure aggravation duringtreatment with oxcarbazepine. Oxcarbazepine wasadministered at a daily dose of 10 mg/kg, in two or three equaldoses per day, and the dose increased every week up to amaximum of 42 mg/kg/day.

A 9-year-old boy received oxcarbazepine (40 mg/kg/day).After 1 month of receiving oxcarbazepine, he developeduncountable daily episodes of atypical absences associatedwith up-gaze, motor arrest, attenuation or loss ofconsciousness, and pallor of < 1 minute’s duration. He hadbehavioural disturbances with bursts of aggressivenessalternated with somnolence. He lost some ability tounderstand language, and he developed stuttering andagrammatism. A 30-minute waking EEG demonstratedgeneralised spike-and-wave complexes at 2.5Hz. The episodeswere associated with impaired consciousness that wastransient and consistent with a diagnosis of atypical absences.An EEG 2 days later demonstrated generalised paroxysmswhich became higher in frequency (3–4Hz), more irregular,and seemed continuous during sleep. Oxcarbazepine wasstopped. His atypical absences disappeared over a few weeksand his EEG anomalies reverted to those noted pretreatment.His language and behavioural disorders resolved. However,3 weeks after oxcarbazepine was stopped, his seizuresreturned, and he began receiving valproic acid. He remainedseizure free for 2.5 years, and had normal schoolperformances; valproic acid was stopped. At a subsequentfollow-up, he remained seizure free; wake and sleep EEGsdemonstrated sporadic spikes, and spike-and-wave dischargesin his right centrotemporal area.

An 8.1-year-old boy began receiving oxcarbazepine (up to42 mg/kg/day) and, 1 month later, he began to complain ofimpaired language comprehension, and scholastic andpronunciation difficulties. He had several daily episodes ofcontact attenuation, motor arrest and eye fluttering. A wakingEEG demonstrated centrotemporal spike-and-wave dischargesthat were more pronounced on the right side, and discharges,of diffuse distribution, during sleep. Two episodes ofattenuation of contact and eyelid fluttering associated with3–4Hz of diffuse epileptiform discharges of up to 10 second’sduration were noted. Oxcarbazepine was discontinued and hisatypical absences disappeared in a few weeks. His EEGanomalies reverted to those noted pretreatment. Heexperienced neuropsychological improvement alongside areduction in EEG anomalies. His partial motor seizurespersisted so valproic acid therapy was given which resulted intotal seizure control. After 22 months of treatment, his wakeand sleep EEGs were normal and valproic acid was stopped.His school performance was normal.

A 6.5-year-old boy began receiving oxcarbazepine(16 mg/kg/day), after valproic acid failed to provide adequateseizure control. Shortly after, the frequency of partial motorseizures increased from one per week, pretreatment, to threeto five per week with oxcarbazepine therapy, and wereprolonged and followed by ictal vomiting and post-ictalsomnolence [time to reaction onset not clearly stated]; thelatter symptoms had never occurred before initiation ofoxcarbazepine. An EEG demonstrated more prominent rightcentrotemporal spike-and-wave discharges that became nearlycontinuous during sleep. Oxcarbazepine was stopped and hisseizures became less frequent; his interictal rightcentrotemporal spike-and-waves reverted to the lowerfrequency (3–5/min) recorded before oxcarbazepinetreatment. He began receiving topiramate and his seizureswere controlled. During a later examination, a wake-and-sleepEEG demonstrated sporadic spikes in his right central region.His school performance was normal.

Author comment: "Our observations suggest that

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