Shoulder pain from glomus tumour.

symptoms, becoming completely normal after 4 weeks. Fluoxetine was reintroduced at the same dose and the depressive syndrome disappeared without recurrence of toxic effects. A second case, a 57 year old woman, developed a generalised secondary partial epilepsy 3 months after an embolic cerebral infarct. Phenytoin was introduced at 400 mg/ day. A year later the patient developed a depressive syndrome and fluoxetine was indicated at a dose of 20 mg/day. Previously the phenytoin plasma level had been 11 5 ug/ml. Ten days later she developed vomiting, difficulty with getting up and sitting and vertigo. The neurological examination showed trunk ataxia, limb dysmetria, and multidirectional nystagmus. Phenytoin plasma level was 47 ,ug/ml. The fluoxetine was suspended and there was a progressive recovery of the signs and symptoms with a complete recovery in approximately three weeks. Four weeks after suspension of fluoxetine, the phenytoin plasma level was 20 ,ug/ml for the same described dose. In human studies an alteration of the pharmacokinetics of fluoxetine was not found when administered simultaneously with other drugs (such as, ethanol, diazepam, chlorothiazide, tolbutamide and warfarin) and viceversa.3 In animal studies it was shown that fluoxetine is a potent inhibitor of hepatic microsomal metabolism,2 this could be responsible for the increase of the pheny-toin plasma level in these cases. The interval between the first administration of fluoxetine and the beginning of the phenytoin overdose symptoms, also suggests a mechanism of the metabolic alteration in the degradation of the anticonvulsant drug. Gamma vinyl GABA in the treatment of Levodopa-induced dyskinesias in Par-kinson's disease In non-human primates blockade of the GABAergic inhibitory strio-pallidal pathways to the lateral segment of the globus pallidus causes chorea, whereas stimulation causes a Parkinsonian syndrome.' This has led to renewed interest in the potential value of gabaminergic agents in the treatment of Parkinson's disease and the complications of levodopa therapy. We have investigated the irreversible inhib-itor of GABAtransaminase, gamma vinyl GABA (GVG) in the treatment of disabling levodopa-induced chorea in 5 patients with Parkinson's disease. The patients had a mean age of 54 (41-74) years, a mean duration of disease of 11 (7-21) years, mean duration of levodopa therapy 9 (6-18) years and a mean levodopa dose of 760 (450-1400) mg/day. All the patients were also receiving subcuta-neous apomorphine, 4 selegiline and 1 bro-mocriptine. The patients' dyskinesias were assessed over a one week baseline period on optimum anti-Parkinsonian therapy. They were then given …