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Anticonvulsant-Induced Dyskinesias: a Comparison with Dyskinesias Induced by Neuroleptics

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Anticonvulsant-Induced Dyskinesias: a Comparison with Dyskinesias Induced by Neuroleptics J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.12.1210 on 1 December 1976. Downloaded from Joulrnal ofNeurology, Neurosurgery, and Psychiatry, 1976, 39, 1210-1218 Anticonvulsant-induced dyskinesias: a comparison with dyskinesias induced by neuroleptics D. CHADWICK, E. H. REYNOLDS, AND C. D. MARSDEN From the University Department ofNeurology, the Institute ofPsychiatry, and King's College Hospital Medical School, London SYNOPSIS Anticonvulsants cause dyskinesias more commonly than has been appreciated. Di- phenylhydantoin (DPH), carbamazepine, primidone, and phenobarbitone may cause asterixis. DPH, but not other anticonvulsants, may cause orofacial dyskinesias, limb chorea, and dystonia in intoxica- ted patients. These dyskinesias are similar to those caused by neuroleptic drugs and may be related to dopamine antagonistic properties possessed by DPH. by guest. Protected copyright. Overdosage with diphenylhydantoin (DPH) and other dyskinesia with distal chorea of the limbs and dys- anticonvulsant drugs causes an acute syndrome of tonic spasms ofaxial and limb muscles. This syndrome drowsiness, ataxia, dysarthria, and nystagmus has occurred only when DPH is administered in doses (Woodbury et al., 1972). In recent years a variety of causing toxic plasma levels and usually remits when chronic neurological effects of the drugs have been the dose is reduced. The dyskinesias produced by recognised (Reynolds, 1975a) and a number of DPH are reminiscent of those provoked by pheno- reports have noted abnormal involuntary movements thiazine or other neuroleptic drugs, suggesting a (dyskinesias) occurring in patients acutely or chroni- similar cause. cally intoxicated with DPH. The descriptions of those dyskinesias have included chorea, athetosis, dystonia, CASE HISTORIES (Table 2) tremor, and asterixis' (Table 1). They are most often seen in patients with severe epilepsy and significant CASE 1: ASTERIXIS AND CEREBELLAR SYNDROME DUE TO organic brain damage, taking multiple anticonvulsant PHENOBARBITONE INTOXICATION drugs. They have been associated almost exclusively This patient was a 51 year old woman, working as a with toxic serum levels of DPH and have usually packer, who had suffered idiopathic grand mal recovered rapidly with adjustment ofdosage. seizures without aura since the age of 17 years. Her This communication describes a variety of dys- seizures has always been difficult to control in spite of kinesias occurring in patients intoxicated with DPH taking regular anticonvulsant therapy for 24 years. and other anticonvulsants, who were seen in a busy For the previous 12 months she had been taking DPH neurological unit over a period of some 18 general 300 mg/day, phenobarbitone 60 mg/day, primidone http://jnnp.bmj.com/ months. DPH and other anticonvulsants in intoxi- 500 mg/day, and diazepam 15mg/day. cating doses may cause asterixis, as well as a cerebel- She was referred with an episode of drowsiness, lar syndrome. DPH, but not other anticonvulsants, unsteadiness, and 'shakiness' of her hands. A similar appears capable of inducing a syndrome of orofacial episode had occurred six months previously and had lasted for three to four weeks. I We have used the term 'chorea' to denote unpredictable, rapid On examination she was of below normal intelli- non-purposive muscular jerks of face, tongue, and limbs (which occur gence, with a childish personality. She showed a mild at rest and interrupt voluntary activity), and 'dystonia' to denote abnormal sustained muscular contractions which, if continued, result dysarthria, phasic nystagmus on lateral gaze, and a on September 27, 2021 in the maintenance of typically dystonic postures, and if spasmodic, gait ataxia. There was marked asterixis of the out- cause slow movements into such dystonic postures. We have avoided the terms 'athetosis' and 'choreoathetosis' as we believe them to be stretched hands, and the presence of these postural confusing. 'Asterixis' is used to describe irregular postural lapses and lapses resulted in some impairment of finger-nose subsequent corrections, developing after a latent period, during coordination. There were no signs ofliver disease. sustained posture against gravity-for example, of the outstretched hands. Biochemical screening and liver function tests were (Accepted 18 August 1976.) normal with the exception of a raised plasma alkaline 210 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.12.1210 on 1 December 1976. 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The possibility Phenobarbitone was stopped and there was a rapid that DPH might be responsible for her asterixis was clinical improvement with disappearance of nystag- considered and this drug was withdrawn. However, mus and gait ataxia within three to four days (Figure). her asterixis persisted. Repeat anticonvulsant levels done at this time showed a serum phenobarbitone of 135 ,mol/l CASE 2: ASTERIXIS AND CEREBELLAR SYNDROME DUE TO (32 ,ug/ml), primidone 67 Mmol/l (15 ,ug/ml), and DPH PHENOBARBITONE INTOXICATION 49 lLmoIl (12 ,,a1mh Hn4wever as minnr aqterixi.- was still present, the dose ofprimidone was reduced to dA67 year old man, who had had grand mal seizures in 375 mg/day. Eight Mdeoks later the asterixis had com- childhood, developed a recurrence offits at the age of pletely disappeared and the serum phenobarbitone 58 years. Six months previously he had started therapy was 65 tsmol/l (15.5 hg/ml), primidone 8 btmol/l with phenobarbitone 90 mg/day and DPH 300 (1.7 ,.g/ml), and DPIH 48 ,tmol/l (12 ,g/ml). However, mg/dayS. at this time, seizure control deteriorated so the dose of Since then his family had noted an altered person- primidone was incrreased to 500 mg/day. This re- ality with increasing apathy. He was admitted to sulted in a reappearance of mild asterixis without hospital complaining of a severe headache for a other signs of aniticonvulsant intoxication. Re- month. Investigations were negative apart from a estimation of serumi anticonvulsant llevelss showed a variably raised ESR (12-80 mm/h). (Serum anticon- phenobarbitone of 126anticol/lsant(30 sprimidonepimone vulsants were not estimated.) He was treated with by guest. Protected copyright. 40 (6.5 amol/Iand DPH otg/ml),of 22 analgesics and diazepam and discharged. He returned pmol/l jtg/nnil), timol/I (5.4 one week later having been confused and unsteady at home. On admission he was drowsy but orientated and showed a moderate gait ataxia, nystagmus, and I I marked asterixis of the outstretched hands. Investi- gations were again normal apart from serum anti- ASTERIXIS L convulsants, phenobarbitone 395 ,umol/l (94 pg/ml), DPH 29 ,tmol/l (7 jpg/ml).
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