ABSTRACT
El tratamiento quirúrgico de la enfermedad de Parkinson se ha revitalizado en los últimos años gracias al desarrollo de un modelo fisiopatológico de los ganglios basales. El modelo reconoce que el d,ficit dopamin,rgico que caracteriza al estado parkinsoniano conlleva un aumento en la actividad neuronal del núcleo subtal mico y del globo p lido interno y sustancia negra pars reticulata, los principales núcleos eferentes de los ganglios basales. La cirugía de ganglios basales ha permitido comprobar la idoneidad del modelo para predecir la respuesta terap,tutica a la inhibición funcional o por la lesión de estos núcleos. Tambi,n ha permitido comprobar que la organización somatotópica de los ganglios basales en el hombre es similar a la descrita en el mono. Es necesario ampliar los conceptos del modelo para explicar manifestaciones motoras tópicas de la enfermedad de Parkinson, como la rigidez o el temblor(AU)
Subject(s)
Basal Ganglia , Parkinson Disease/surgery , Subthalamic Nucleus , Movement DisordersABSTRACT
The role of the subthalamic nucleus (STN) in the origen of parkinsonian tremor is discussed. Previous studies in monkeys made parkinsonian by MPTP (1-methyl-4-phenil-1,2,3,6-tetrahydropyridine) administration suggested a direct participation of the STN in the pathophysiology of tremor. We recorded tremor-related activity in the STN in 12 patients with Parkinso's disease (PD) and found that microstimulation of the sensorimotor region of the nucleus, where these neurons are present, stopped the tremor sith a very short latency. Long-term treatment by means of bilateral deep-brain stimulation (DBS) in the same 12 patients led to a significant reduction of tremor as well as other cardinal features of PD. This effect was blindly assessed at 3 months after implantation. In another group of seven patients, a unilaeral lesion of the STN was performed. Both postural and resting tremor were significantly improved on the limbs contralateral to the lesion side. In three patients, tremor disappearedcompletely after 12 months of follow up. The electrophysiologic data and therapeutic effect of inactivating the STN strongly indicated that this structure is directly involved in the origin of paarkinsonian tremor, as suggested by the MPTP model(AU)
