Carbamazepine
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Reactions 1081 - 10 Dec 2005 S Carbamazepine Encephalopathy resembling Creutzfeldt-Jakob disease in an elderly patient: case report A 71-year-old man developed encephalopathy resembling Creutzfeldt-Jakob disease (CJD) during treatment with carbamazepine for trigeminal neuralgia. The man, who had a history of hypertension, myocardial infarction and chronic atrial fibrillation, developed left trigeminal neuralgia and started treatment with low-dose carbamazepine. His neuralgia quickly became refractory despite increases in his carbamazepine dosage up to 1200 mg/day. After 4 months, he developed progressive cognitive decline, with memory deficits, psychomotor slowing, confusion, dysphasia, hypersomnia and postural instability. His symptoms quickly worsened and he became dependent and abulic. Neurological examination revealed disorientation, generalised bradykinesia, hypomimia, rigidity with cogwheeling, bilateral and synchronous myoclonus and a low amplitude postural tremor. He also exhibited attention and memory deficits, severe aphasia with paraphasias, preservations and constructional apraxia. A brain MRI scan showed mild brain atrophy, moderate leukoariosis and small lacunae in the basal ganglia, and an EEG was consistent with CJD. Laboratory investigations revealed an elevated serum carbamazepine level of 51 µmol/L (therapeutic range 20–40); serum carbamazepine remained elevated (46 µmol/L) 5 days later. Carbamazepine was discontinued and the man’s symptoms improved over the next 2 weeks. He became alert, his myoclonus resolved and his parkinsonism and cognitive function improved, without recurrence at follow-up 3 months later; a follow-up EEG was also much improved. Author comment: "This severe, CJD-like condition resulted from chronic carbamazepine toxicity, based on a clear temporal relationship between drug initiation and development of the dementing process, serum levels above normal range, and rapid recovery of both clinical and EEG abnormalities following drug discontinuation." Horvath J, et al. Carbamazepine encephalopathy masquerading as Creutzfeldt- Jakob disease. Neurology 65: 650-651, No. 4, 23 Aug 2005 - Switzerland 801019448 1 Reactions 10 Dec 2005 No. 1081 0114-9954/10/1081-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
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Transcript of Carbamazepine
Reactions 1081 - 10 Dec 2005
SCarbamazepine
Encephalopathy resembling Creutzfeldt-Jakobdisease in an elderly patient: case report
A 71-year-old man developed encephalopathy resemblingCreutzfeldt-Jakob disease (CJD) during treatment withcarbamazepine for trigeminal neuralgia.
The man, who had a history of hypertension, myocardialinfarction and chronic atrial fibrillation, developed lefttrigeminal neuralgia and started treatment with low-dosecarbamazepine. His neuralgia quickly became refractorydespite increases in his carbamazepine dosage up to1200 mg/day. After 4 months, he developed progressivecognitive decline, with memory deficits, psychomotorslowing, confusion, dysphasia, hypersomnia and posturalinstability. His symptoms quickly worsened and he becamedependent and abulic. Neurological examination revealeddisorientation, generalised bradykinesia, hypomimia, rigiditywith cogwheeling, bilateral and synchronous myoclonus and alow amplitude postural tremor. He also exhibited attentionand memory deficits, severe aphasia with paraphasias,preservations and constructional apraxia. A brain MRI scanshowed mild brain atrophy, moderate leukoariosis and smalllacunae in the basal ganglia, and an EEG was consistent withCJD. Laboratory investigations revealed an elevated serumcarbamazepine level of 51 µmol/L (therapeutic range 20–40);serum carbamazepine remained elevated (46 µmol/L) 5 dayslater.
Carbamazepine was discontinued and the man’s symptomsimproved over the next 2 weeks. He became alert, hismyoclonus resolved and his parkinsonism and cognitivefunction improved, without recurrence at follow-up 3 monthslater; a follow-up EEG was also much improved.
Author comment: "This severe, CJD-like conditionresulted from chronic carbamazepine toxicity, based on aclear temporal relationship between drug initiation anddevelopment of the dementing process, serum levels abovenormal range, and rapid recovery of both clinical and EEGabnormalities following drug discontinuation."Horvath J, et al. Carbamazepine encephalopathy masquerading as Creutzfeldt-Jakob disease. Neurology 65: 650-651, No. 4, 23 Aug 2005 -Switzerland 801019448
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Reactions 10 Dec 2005 No. 10810114-9954/10/1081-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
