Review
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
Dominique Caparros-Lefebvrea, Serge Blondb, Marie-Pierre Feltinc, Pierre Pollakc, Alim Louis Benabidc
a Department of
Neurology, Pointe à Pitre University Hospital, French West Indies, b Department of
Neurosurgery, Lille University Hospital, France, c Department of Neurosciences and Unité Inserm U
318, Grenoble University Hospital, France
Correspondence to: Mrs Dominique Caparros-Lefebvre, The Neurological Clinic, French West Indies University Hospital, CHU, Route de Chauvel, 97159 Pointe à Pitre Cedex, Guadeloupe, French West Indies, France. Telephone and fax 0033 590 89 14 35.
Received 2 November
1998 and in revised form 24 February 1999;
Accepted 5
March 1999
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, 22 electrodes; 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 24 patients, dyskinesias 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 stereotaxic atlases. Considering only the
dyskinetic patients, significant differences were found in the
electrode position according to the therapeutic effects on levodopa
dyskinesias, but they were not related to the team membership.
Improvement in levodopa dyskinesias was significantly associated with
deeper and more medial placement of electrodes.
CONCLUSION
The
retrospective analysis of patients treated with DBS using comparable
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 deeper than the VIM, very close to the
CM-Pf. These results are consistent with neuroanatomical and
neurophysiological data showing that the CM-Pf is included in the motor
circuits of the basal ganglia system and receives an important input
from the internal pallidum. This suggests that the CM-Pf could be
involved specifically in the pathophysiology of levodopa peak dose dyskinesias.
Keywords: deep brain stimulation; nucleus centromedianus and parafascicularis; Parkinson's disease; levodopa induced dyskinesias
© 1999 by Journal of Neurology, Neurosurgery, and Psychiatry
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