Improvement of levodopa induced dyskinesias by thalamic deep brain stimulation is related to slight variation in electrode placement: possible involvement of the centre median and parafascicularis complex

Objective-To define the reason why two teams using the same procedure and t he same target for deep brain stimulation (DBS) obtained different results on levodopa induced dyskinesias, whereas in both, parkinsonian tremor was i mproved or totally suppressed. Methods-Deep brain stimulation can replace lesions in the surgical treatmen t 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 Gren oble (B) was carried out, for as long as they used intraoperative ventricul ography. Both teams aimed at the same target, the ventralis intermedius nuc leus 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 t he therapeutic effects. Location of 99 monopolar electrodes of thalamic sti mulation applied to treat parkinsonian tremor has been retrospectively meas ured (team A included 21 patients, 22 electrodes; team B included 52 patien ts, 74 electrodes). Peak dose levodopa dyskinesias were suppressed by DBS i n 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 24 patients, d yskinesias were unchanged with stimulation. Results-The mean centre of team A's electrodes was on average 2.9 mm deeper , more posterior and medial than team B's (t=8.05; p<0.0001). This does not correspond to the coordinates of the VIM, but seems to be closer to those of the centre median and parafascicularis complex (CM-Pf), according to ste reotaxic atlases. Considering only the dyskinetic patients, significant dif ferences were found in the electrode position according to the therapeutic effects on levodopa dyskinesias, but they were not related to the team memb ership. Improvement in levodopa dyskinesias was significantly associated wi th deeper and more medial placement of electrodes. Conclusion-The retrospective analysis of patients treated with DBS using co mparable methodologies provides important information concerning electrode position and therapeutic outcome. The position of the electrode is related to the therapeutic effects of DBS. The results support the hypothesis that patients experiencing an improvement of dyskinesias under DBS are actually stimulated in a structure which is more posterior, more internal, and deepe r than the VIM, very close to the CM-Pf. These results are consistent with neuroanatomical and neurophysiological data showing that the CM-Pf is inclu ded in the motor circuits of the basal ganglia system and receives an impor tant input from the internal pallidum. This suggests that the CM-Pf could b e involved specifically in the pathophysiology of levodopa peak dose dyskin esias.