Carbamazepine
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Reactions 1114 - 12 Aug 2006 Carbamazepine Absence seizures and EEG exacerbation in a child: case report A boy, who was 4 years and 8 months old, developed absence seizures and EEG exacerbation during treatment with carbamazepine for partial seizures. The boy, who had a history of seizures during nocturnal sleep, vomiting and hemiconvulsion and had been receiving carbamazepine 10 mg/kg/day for about 5 months, was diagnosed with Panayiotopoulos syndrome [sic]; an interictal EEG revealed repetitive spike and waves in his left posterior head area, associated with generalisation. About 3 months later, he developed a second seizure during nocturnal sleep. He woke up, vomiting and coughing, and developed a right- sided hemiconvulsion. His hemiconvulsion terminated after a few minutes, but he remained unresponsive and had repeated vomiting for 40 minutes. His carbamazepine dose was subsequently increased to about 22 mg/kg/day and, soon after, he developed episodes of unresponsiveness, which lasted for 10–20 seconds while awake. His seizures were marked by abrupt onset and cessation and a brief interruption of his activities. His attacks occurred several times a day and he began to experience a twitching of his limbs during sleep and wakefulness, especially just after falling asleep. His peak blood carbamazepine concentration was 8.6 µg/mL. About 1 month after his carbamazepine dose was increased, an interictal EEG revealed a further worsening, with diffuse slow spike and waves; the spike and waves were particularly numerous during sleep. EEG findings, when he was awake, showed diffuse spike and wave bursts lasting for several seconds. He was diagnosed with absence seizures. A polygraphic study revealed epileptic myoclonus. His absence seizures, epileptic myoclonus and EEG worsening were attributed to carbamazepine. Carbamazepine was gradually replaced by valproic acid and the boy’s brief-spell episodes disappeared. His valproic acid dose was increased and his EEG improved dramatically, with infrequent spike waves involving his left temporal-occipital area. The amplitude and frequency of his spike discharges decreased, and the generalisation of his spike wave discharges disappeared. He became alert and his appetite improved. Kikumoto K, et al. EEG and seizure exacerbation induced by carbamazepine in panayiotopoulos syndrome. Epileptic Disorders 8: 53-56, No. 1, Mar 2006 - Japan 801041765 1 Reactions 12 Aug 2006 No. 1114 0114-9954/10/1114-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
Transcript of Carbamazepine
Reactions 1114 - 12 Aug 2006
Carbamazepine
Absence seizures and EEG exacerbation in a child:case report
A boy, who was 4 years and 8 months old, developedabsence seizures and EEG exacerbation during treatment withcarbamazepine for partial seizures.
The boy, who had a history of seizures during nocturnalsleep, vomiting and hemiconvulsion and had been receivingcarbamazepine 10 mg/kg/day for about 5 months, wasdiagnosed with Panayiotopoulos syndrome [sic]; an interictalEEG revealed repetitive spike and waves in his left posteriorhead area, associated with generalisation. About 3 monthslater, he developed a second seizure during nocturnal sleep.He woke up, vomiting and coughing, and developed a right-sided hemiconvulsion. His hemiconvulsion terminated after afew minutes, but he remained unresponsive and had repeatedvomiting for 40 minutes. His carbamazepine dose wassubsequently increased to about 22 mg/kg/day and, soon after,he developed episodes of unresponsiveness, which lasted for10–20 seconds while awake. His seizures were marked byabrupt onset and cessation and a brief interruption of hisactivities. His attacks occurred several times a day and hebegan to experience a twitching of his limbs during sleep andwakefulness, especially just after falling asleep. His peak bloodcarbamazepine concentration was 8.6 µg/mL. About 1 monthafter his carbamazepine dose was increased, an interictal EEGrevealed a further worsening, with diffuse slow spike andwaves; the spike and waves were particularly numerous duringsleep. EEG findings, when he was awake, showed diffuse spikeand wave bursts lasting for several seconds. He was diagnosedwith absence seizures. A polygraphic study revealed epilepticmyoclonus. His absence seizures, epileptic myoclonus andEEG worsening were attributed to carbamazepine.
Carbamazepine was gradually replaced by valproic acid andthe boy’s brief-spell episodes disappeared. His valproic aciddose was increased and his EEG improved dramatically, withinfrequent spike waves involving his left temporal-occipitalarea. The amplitude and frequency of his spike dischargesdecreased, and the generalisation of his spike wave dischargesdisappeared. He became alert and his appetite improved.Kikumoto K, et al. EEG and seizure exacerbation induced by carbamazepine inpanayiotopoulos syndrome. Epileptic Disorders 8: 53-56, No. 1, Mar 2006 -Japan 801041765
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Reactions 12 Aug 2006 No. 11140114-9954/10/1114-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
