Stimulation cérébrale profonde dans la maladie de Parkinson: effets moteurs et comportementaux

Abstract

(from the journal abstract) The last 15 years have seen the progressive introduction of deep-brain stimulation (DBS) for the treatment of Parkinson's disease. This advance has been possible thanks to better understanding of the organisation of the basal ganglia with parallel segregated loops involved in the control of movement, behaviour, mood and cognition that interact through interneurons or collateral projections. Deep-brain stimulation, which allows by stimulation adjustments to optimise the benefit/side effect ratio, has made possible bilateral treatments needed for treating Parkinson's disease, while former available lesions were contraindicated because of the substantial side effects they produced. Thalamic ventral intermediate nucleus was the first target. It affects the cerebello-thalamocortical pathway and is mainly effective on tremor with little benefit on the other signs of Parkinson's disease. For Parkinson's disease it has progressively completely been replaced by the two other targets and is currently mainly used to treat medication-resistant essential tremor. Internal posterior part of globus pallidus acts on the common output nucleus of the basal ganglia loops. It has been proven very effective for treating motor fluctuations, mainly dyskinesia. Its effects on motor signs of Parkinson's disease are moderate and variably observed probably secondary to the organisation of this relatively large nucleus, with deep-brain stimulation effects depending upon precise localisation. Globus pallidus deep-brain stimulation does not allow antiparkinsonian medication reduction, in contrast to subthalamic deep-brain stimulation, but necessitates a progressive increase of drugs, with some decrease in efficacy with time. Globus pallidus being very effective on dyskinesia is currently rather used to treat other movement disorders, e.g. dystonia. Subthalamic deep-brain stimulation has become the main target for treating Parkinson's disease. It is acting on the indirect pathway, correcting the subthalamic hyperactivity secondary to disinhibition following dopamine depletion in Parkinson's disease. Subthalamic deep-brain stimulation improves the four major signs of Parkinson's disease, with effects mimicking levodopa: response to levodopa challenge being one of the best predictive parameters of the response to subthalamic deep-brain stimulation. This treatment allows substantial antiparkinsonian drug reduction. The latter is the main responsible for dyskinesia reduction observed after subthalamic deep-brain stimulation. Subthalamic deepbrain stimulation effects are maintained for at least 5 years although increase in axial signs and dementia is observed with Parkinson's disease progression. Beside the motor effects, deep-brain stimulation may induce acute or chronic neurobehavioural changes. The former is probably secondary to direct effect on structures adjacent to the targeted nuclei or involvement of parallel basal ganglia circuitry. The latter, which develops over months or years, is possibly also related to medication changes, neuronal plasticity following deep-brain stimulation, adaptation difficulties and dramatic socio-familial modification induced by the motor effects of deep-brain stimulation. Depression, apathy, anxiety, mania, pathological gambling, sexual behaviours and hallucinations have all been described following deep-brain stimulation. These changes, which underline the importance of basal ganglia circuitry in mood and behaviour, may have severe consequences including suicides. If the acute effects can usually easily be corrected by deep-brain stimulation tuning, the chronic modifications need to be detected and often necessitate a multidisciplinary approach. This careful multidisciplinary (neurologist, neuropsychologist, neurosurgeon, psychiatrist) collaboration is important not only for the selection but also for the follow-up of Parkinson's disease patients treated by deep-brain stimulation. (PsycINFO Database Record (c) 2005 APA, all rights reserved)