RESUMEN
Twelve patients with Parkinson disease and psychosis were included in an open-label 12-week trial of ziprasidone. Two patients withdrew from the treatment because of adverse effects. The remaining 10 patients reported a significant improvement in psychiatric symptoms. Altogether, there was no deterioration of motor symptoms (UPDRS III score: basal 40.4 +/- 11.1, first month 41.1 +/- 10.8; final visit, 37.7 +/- 13.3). Two patients (20%) suffered a slight deterioration in motor symptoms and another patient suffered deterioration of gait. No analytic alterations or serious adverse effects that could limit the use of ziprasidone were observed. Although controlled trials are needed, the findings suggest that ziprasidone may be effective in parkinsonian patients with psychosis.
Asunto(s)
Antipsicóticos/uso terapéutico , Enfermedad de Parkinson/complicaciones , Piperazinas/uso terapéutico , Trastornos Psicóticos/tratamiento farmacológico , Tiazoles/uso terapéutico , Anciano , Anciano de 80 o más Años , Antipsicóticos/administración & dosificación , Antipsicóticos/efectos adversos , Femenino , Humanos , Hipotensión Ortostática/fisiopatología , Masculino , Persona de Mediana Edad , Enfermedad de Parkinson/psicología , Piperazinas/administración & dosificación , Piperazinas/efectos adversos , Escalas de Valoración Psiquiátrica , Trastornos Psicóticos/psicología , Tiazoles/administración & dosificación , Tiazoles/efectos adversosRESUMEN
This study reports 3 cases of pure hemisensory syndrome due to lacunar infarction at the pons, demonstrated by magnetic resonance. In all patients somatosensory evoked potentials were abnormal. In two out of the 3 cases these potentials remained abnormal even after clinical exploration normalized. Due to the distribution of the sensitive pathways it may be assumed that the hemisensory syndrome would be caused by lesions located from the cortex to the pons. By means of clinico-pathological correlations the hemisensory syndrome was attributed to lesions exclusively located at the cerebral cortex or at the thalamus. However, in 1984 the first case of hemisensory syndrome due to pontine infarction was demonstrated by computerized tomography. After this report a series of approximately 10 patients have been published in the english and french literature. None of them had data on somatosensory potentials. In our experience the study of somatosensory evoked potentials has a high sensitivity. It appears that the distribution of the sensitive defect is independent of the location of the structural lesion.