Deep brain stimulation for the treatment of Parkinson's disease.
Deep brain stimulation (DBS) is increasingly accepted as an adjunct therapy for Parkinson's disease (PD). It is considered a surgical treatment alternative for patients with intractable tremor or for those patients who are affected by long-term complications of levodopa therapy such as motor fluctuations and severe dyskinesias. Thalamic stimulation in the ventral intermediate nucleus (Vim) leads to a marked reduction of contralateral tremor but has no beneficial effect on other symptoms of Parkinson's disease. The subthalamic nucleus (STN) and the internal segment of the globus pallidus (GPi) are targeted for the treatment of advanced Parkinson's disease. Several studies have proven the efficacy of STN-DBS and GPi-DBS in alleviating off motor symptoms and dyskinesias. Sub-thalamic nucleus deep brain stimulation is currently considered superior to GPi-DBS because the antiakinetic effect seems to be more pronounced, allows a more marked reduction of antiparkinsonian medication, and requires less stimulation energy. More recently, however, a number of reports on possible psychiatric and behavioral side effects of STN-DBS have been a matter of concern. Given the chronic nature of PD and the noncurative approach of DBS, both targets will need to be reevaluated on the basis of their long-term efficacy and their impact on quality of life. Despite the rapidly increasing numbers of DBS procedures, surprisingly few controlled clinical trials are available that address important clinical issues such as: When should DBS be applied during the course of disease? Which patients should be selected? Which target should be considered? Which guidelines should be followed during postoperative care? Here is summarized the available evidence on DBS as a therapeutic tool for the treatment of Parkinson's disease and the current state of debate on open issues.
Volkmann
Jens
J
Department of Neurology, Christian-Albrechts-University, Kiel, Germany. j.volkmann@neurologie.uni.kiel.de
D000978:Antiparkinson Agents / Q000009:adverse effects / Q000627:therapeutic use; D001931:Brain Mapping; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology / Q000628:therapy; D004599:Electric Stimulation Therapy; D005917:Globus Pallidus / Q000503:physiopathology*; D006801:Humans; D007980:Levodopa / Q000009:adverse effects / Q000627:therapeutic use; D009460:Neurologic Examination; D010300:Parkinson Disease / Q000503:physiopathology / Q000628:therapy*; D020531:Subthalamic Nucleus / Q000503:physiopathology*; D016896:Treatment Outcome; D014202:Tremor / Q000503:physiopathology / Q000628:therapy; D020651:Ventral Thalamic Nuclei / Q000503:physiopathology*
D000978:Antiparkinson Agents; D007980:Levodopa