Gabapentin/oxcarbazepine

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Reactions 1001 - 15 May 2004 S Gabapentin/oxcarbazepine Asterixis and encephalopathy in elderly patients: 2 case reports Two elderly women developed asterixis, one of whom also developed toxic encephalopathy, during treatment with gabapentin. One of the women also had subclinical asterixis while receiving oxcarbazepine. The first woman, aged 76 years, had a history of essential tremor. She developed partial seizures possibly related to cerebrovascular disease and was started on oxcarbazepine 600mg twice daily. Approximately 1 month later, her seizures persisted so gabapentin 900 mg/day was added. Several days later she was hospitalised and, at this time, had occasional, disabling, involuntary jerking of her hands. This asterixis was more marked on the right side, and also involved the lower extremities and was confirmed by an electromyogram (EMG). Neuroimaging of the brain revealed multiple lacunar infarcts near the motor areas of the frontal lobes and in the basal ganglia. The dosage of gabapentin was gradually reduced to 300 mg/day and, within 8 days of reaching this dosage, asterixis resolved. The gabapentin dosage was subsequently increased to 900 mg/day and asterixis recurred after 3 days. Gabapentin was stopped and, 20 days later, an EMG showed subclinical asterixis associated with oxcarbazepine. The woman did not experience any further neurological symptoms during follow-up. The second woman, aged 77 years, had sensory diabetic polyneuropathy and had been receiving gabapentin 3600 mg/day for 3 months for pain and paraesthesias in her legs. She was then admitted with subtle personality changes, impairment of recent memory and immediate recall, and fluctuating cognitive impairment. She had a reduced ability to focus, difficulty with attention, and disorientation for time, place and person. Her mental status fluctuated with 15–30 minute episodes of drowsiness and hypoactivity. She also had asterixis of her hands, particularly on the right side. Neuroimaging of the brain revealed multiple lacunar infarcts near the motor areas of the frontal lobes. Her gabapentin dosage was reduced to 1200 mg/day and, 2 weeks later, her asterixis had resolved and she was alert, conscious, cooperative and oriented. Author comment: "High doses of GBT [gabapentin] may induce asterixis related to a reversible encephalopathy. Low doses of GBT, instead, may induce a disabling asterixis when given in combination with OXCBZ [oxcarbazepine] because of a synergistic interaction between these drugs." Sechi G, et al. Asterixis and toxic encephalopathy induced by gabapentin. Progress in Neuro-Psychopharmacology and Biological Psychiatry 28: 195-199, No. 1, Jan 2004 - Italy 807216383 1 Reactions 15 May 2004 No. 1001 0114-9954/10/1001-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

Transcript of Gabapentin/oxcarbazepine

Page 1: Gabapentin/oxcarbazepine

Reactions 1001 - 15 May 2004

SGabapentin/oxcarbazepine

Asterixis and encephalopathy in elderly patients:2 case reports

Two elderly women developed asterixis, one of whom alsodeveloped toxic encephalopathy, during treatment withgabapentin. One of the women also had subclinical asterixiswhile receiving oxcarbazepine.

The first woman, aged 76 years, had a history of essentialtremor. She developed partial seizures possibly related tocerebrovascular disease and was started on oxcarbazepine600mg twice daily. Approximately 1 month later, her seizurespersisted so gabapentin 900 mg/day was added. Several dayslater she was hospitalised and, at this time, had occasional,disabling, involuntary jerking of her hands. This asterixis wasmore marked on the right side, and also involved the lowerextremities and was confirmed by an electromyogram (EMG).Neuroimaging of the brain revealed multiple lacunar infarctsnear the motor areas of the frontal lobes and in the basalganglia. The dosage of gabapentin was gradually reduced to300 mg/day and, within 8 days of reaching this dosage,asterixis resolved. The gabapentin dosage was subsequentlyincreased to 900 mg/day and asterixis recurred after 3 days.Gabapentin was stopped and, 20 days later, an EMG showedsubclinical asterixis associated with oxcarbazepine. Thewoman did not experience any further neurological symptomsduring follow-up.

The second woman, aged 77 years, had sensory diabeticpolyneuropathy and had been receiving gabapentin3600 mg/day for 3 months for pain and paraesthesias in herlegs. She was then admitted with subtle personality changes,impairment of recent memory and immediate recall, andfluctuating cognitive impairment. She had a reduced ability tofocus, difficulty with attention, and disorientation for time,place and person. Her mental status fluctuated with15–30 minute episodes of drowsiness and hypoactivity. Shealso had asterixis of her hands, particularly on the right side.Neuroimaging of the brain revealed multiple lacunar infarctsnear the motor areas of the frontal lobes. Her gabapentindosage was reduced to 1200 mg/day and, 2 weeks later, herasterixis had resolved and she was alert, conscious,cooperative and oriented.

Author comment: "High doses of GBT [gabapentin] mayinduce asterixis related to a reversible encephalopathy. Lowdoses of GBT, instead, may induce a disabling asterixis whengiven in combination with OXCBZ [oxcarbazepine] because ofa synergistic interaction between these drugs."Sechi G, et al. Asterixis and toxic encephalopathy induced by gabapentin. Progressin Neuro-Psychopharmacology and Biological Psychiatry 28: 195-199, No. 1, Jan2004 - Italy 807216383

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Reactions 15 May 2004 No. 10010114-9954/10/1001-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved