[Levodopa-induced psychosis in patients with idiopathic Parkinson disease]. / Psicosis por levodopa en pacientes con enfermedad de Parkinson idiopática.

BACKGROUND: To identify which clinical factors can modify the probability of the appearance of the psychotic syndromes in patients with idiopathic Parkinson's disease treated with levodopa. PATIENTS AND METHODS: 214 patients were retrospectively studied to evaluate the appearance of hallucinosis, delusions or mental confusion, from the beginning of the treatment with levodopa to a transversal evaluation along the course of the disease. To determine which clinical factors were independent predictors of psychosis, a multivariate logistic regression model was obtained, using the variables for which the univariate studies showed p values under 0.25. RESULTS: The multivariate model showed that the probability of developing psychosis during levodopa treatment was higher for the patients with intermediate or advanced stages of the disease (Hoehn and Yarh scale), at the beginning of the treatment (OR: 4.5; 95% CI: 1.86-11.23), when amantadine was administrated as associated drug (OR: 3.31; 95% CI: 1.19-9.23) and for the patients who presented motor fluctuations (OR: 3.08; 95% CI: 1.32-7.16). Univariate studies showed a significant association between levodopa psychosis and dyskinesias (univariate OR: 2.44; 95% CI: 1.12-5.33). Patients who suffered from psychotic complications had received significantly higher mean levodopa daily dose (p = 0.016) and the punctuation reached in the Folstein's Mini-Mental Scale was significantly lower (p = 0.0001). CONCLUSIONS: Levodopa psychosis appears in a "bad prognostic" group of patients, characterized by a greater motor and cognitive impairment and by the occurrence of other levodopa central adverse effects, higher doses of levodopa and a more frequent administration of other antiparkinsonian drugs.

Severe central nervous system toxicity after chronic treatment with cyclosporine.

Severe neurologic complications following treatment with cyclosporine are uncommon. They tend to occur during the first month of treatment and disappear after withdrawal or reduction of the dose of the drug. We report the case of a man who underwent a liver transplantation and subsequently developed severe central nervous system toxicity. After two years receiving cyclosporine, he presented with a brachial monoparesis and a complex visual disturbance. Symptoms slowly worsened during four months. On admission, he had confusion and seizures. Multiple areas of T2 prolongation, located in cerebral white matter, were seen on magnetic resonance imaging (MRI). Symptoms partially improved after cyclosporine withdrawal, but brain lesions shown on MRI persisted in serial imaging studies after two years of follow-up. We discuss the mechanisms that have been proposed to explain this clinical picture. Severe cyclosporine-associated neurotoxicity can also occur after chronic administration, even with serum levels in therapeutic range.