Improvement of levodopa induced dyskinesias by thalamic deepbrain stimulation is related to slight variation in electrodeplacement: possible involvement of the centre median andparafascicularis complex

摘要

OBJECTIVE—To define the reason why two teams using the same procedure and the same target for deep brain stimulation (DBS) obtained different results on levodopa induced dyskinesias, whereas in both, parkinsonian tremor was improved or totally suppressed.
METHODS—Deep brain stimulation can replace lesions in the surgical treatment of abnormal movements. After 10 years of experience with DBS in Parkinson's disease, a comparison of results between the teams of Lille (A) and Grenoble (B) was carried out, for as long as they used intraoperative ventriculography. Both teams aimed at the same target, the ventralis intermedius nucleus of the thalamus (VIM), but team A found a clear improvement of choreic peak dose dyskinesias, whereas team B did not consistently. Therefore all teleradioanatomical data of both teams were re-examined and compared with the therapeutic effects. Location of 99 monopolar electrodes of thalamic stimulation applied to treat parkinsonian tremor has been retrospectively measured (team A included 21 patients, 22electrodes; team B included 52 patients, 74 electrodes). Peak dose levodopa dyskinesias were suppressed by DBS in all nine patients of team A, four of which were severely disabling.Only eight out of 32 patients from team B experienced a moderate (four)or clear (four) improvement of dyskinesias, whereas in the remaining 24patients, dyskinesias were unchanged with stimulation.
RESULTS—The meancentre of team A's electrodes was on average 2.9 mm deeper, moreposterior and medial than team B's (t=8.05;p<0.0001). This does not correspond to the coordinates of the VIM, butseems to be closer to those of the centre median and parafascicularis complex (CM-Pf), according to stereotaxic atlases. Considering only thedyskinetic patients, significant differences were found in theelectrode position according to the therapeutic effects on levodopadyskinesias, but they were not related to the team membership.Improvement in levodopa dyskinesias was significantly associated withdeeper and more medial placement of electrodes.
CONCLUSION—Theretrospective analysis of patients treated with DBS using comparablemethodologies provides important information concerning electrodeposition and therapeutic outcome. The position of the electrode isrelated to the therapeutic effects of DBS. The results support thehypothesis that patients experiencing an improvement of dyskinesiasunder DBS are actually stimulated in a structure which is moreposterior, more internal, and deeper than the VIM, very close to theCM-Pf. These results are consistent with neuroanatomical andneurophysiological data showing that the CM-Pf is included in the motorcircuits of the basal ganglia system and receives an important inputfrom the internal pallidum. This suggests that the CM-Pf could beinvolved specifically in the pathophysiology of levodopa peak dose dyskinesias.