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Deep brain stimulation in Parkinson’s disease
  1. T Z AZIZ,
  2. P G BAIN
  1. Department of Neurosciences, Charing Cross Hospital, London, UK
  2. Department of Neurosurgery, Radcliffe Infirmary, Oxford, UK
    1. T Z AZIZ
    1. Department of Neurosciences, Charing Cross Hospital, London, UK
    2. Department of Neurosurgery, Radcliffe Infirmary, Oxford, UK

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      This issue of the Journal sees the publication of two papers that increase our knowledge of the functions of the internal architecture of the thalamus and globus pallidus—an important achievement given the existing literature on stereotactic functional surgery for Parkinson’s disease.

      The paper by Caparros-Lefebvre et al 1 (pp 308–14) is fascinating, because one would have expected that after nearly 50 years of thalamic surgery every possible internal thalamic target would have been explored. However, the surgical outcomes have not always been studied carefully, or published for others to share. Caparros-Lefebvre et al compared the functional results and electrode positions obtained by two teams performing thalamic stimulation for parkinsonism. Anatomical comparisons were possible because ventriculography had been performed by both groups. The two teams used similar techniques for the implantation of electrodes into the ventralis intermedius nucleus of the thalamus (VIM), although there were minor differences in the approach trajectory which led to team A’s electrodes being placed an average of 2.9 mm posteromedial to those of team B. The result of this slight positional difference was that both tremor and drug induced choreic dyskinesias were abolished by the more posteromedial target, whereas only tremor was relieved by the more anterolateral electrode position. Evidence for this antichoreic dyskinetic effect being secondary to involvement of the centre median and parafascicularis complex (CM-Pf) nucleus is provided. It is noteworthy that no effect on dystonic dyskinesias was found, suggesting a segregation of the pathways involved in these two forms of dyskinesias. However, the clinical importance of this paper lies in the demonstration that surgery to a single posteromedial VIM target can achieve the same functional outcome as that involving both VIM and ventralis oralis posterior—a finding that may translate into a reduced risk of side effects.1

      The paper by Durif et al 2 (pp315–22) considers the possible causes for the variability in clinical outcome obtained after pallidal surgery. The study focuses on the precise target site which in most series, including this one, lies within the posterior half of the pallidum. Durif et al report that within their pallidal target, ventral stimulation is more effective than dorsal stimulation for alleviating rigidity, bradykinesia, and drug induced dyskinesias, a finding that concurs with a recent study of pallidotomy and clinical outcome, but differs from the findings obtained by Krack et al who noted that ventral stimulation within GPi caused improvement in rigidity and alleviation of levodopa induced dyskinesias but caused severe akinesia and blocked the antiakinetic effect of levodopa.4 5 There are two possible reasons for this discord: firstly, the target chosen by Krack et al is posterolateral to that selected by Durifet al, and secondly the approach angle may matter.

      These studies show that from detailed assessments of the relation between surgical target and clinical outcome important clinical and physiological questions may be answered about the function of specific areas within the thalamus and globus pallidus.


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