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Subthalamic nucleus stimulation restores corticospinal facilitation in Parkinson's disease
Authors:Monika Pötter‐Nerger MD  Tihomir V. Ilic PhD  Hartwiq R. Siebner PhD  Günther Deuschl PhD  Jens Volkmann PhD
Affiliation:1. Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany;2. Outpatients Neurological Department, Military Medical Academy, Belgrade, Serbia
Abstract:We have previously shown that in patients with Parkinson's disease (PD), high‐frequency stimulation (HFS) of the subthalamic nucleus (STN) modifies spinal excitability via subcortical reticulospinal routes. To investigate whether STN‐HFS also modifies spinal excitability via transcortical routes in PD, 10 patients with PD (9 men, 1 woman; 58.3 ± 8.3 years) were investigated in the medical OFF‐state with or without STN‐HFS. The H‐reflex of the right soleus muscle was recorded during slight plantar flexion at 20% of maximum force. A conditioning transcranial stimulus was applied at 95% of active motor threshold to the contralateral primary motor leg area (M1) 0–5 ms after eliciting the H‐reflex. The same paradigm was applied to 8 healthy individuals (5 men, 3 women; 50.8 ± 3.0 years). Transcranial magnetic stimulation (TMS) facilitated the H‐reflex amplitude in healthy controls. A facilitatory effect of the corticospinal input on the H‐reflex was also found in patients with PD, but only with STN‐HFS switched on. When STN‐HFS was discontinued, the H‐reflex was no longer facilitated by the TMS pulse. Accordingly, analysis of variance showed a main effect of stimulation (F = 11.15; P = 0.005), ISI (F = 6.1; P = 0.003), and an interaction between stimulation and group (PD vs. control) (F = 8.9; P = 0.01). STN‐HFS restores the normal facilitatory drive of a transcranially evoked motor cortical response to the spinal motoneuron pool. In addition to subcortical routes, STN‐DBS also alters spinal excitability via transcortical pathways. © 2008 Movement Disorder Society.
Keywords:Parkinson disease  motor cortex  STN DBS  H‐reflex
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