gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

Physiological target identification of the subthalamic nucleus in surgery for Parkinson’s disease under sedation and general anaesthesia

Meeting Abstract

  • C. Moll - Institut für Neurophysiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf
  • A. Sharott - Institut für Neurophysiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf
  • J. Koeppen - Institut für Neurophysiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf
  • C. Buhmann - Institut für Neurophysiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf
  • M. Westphal - Institut für Neurophysiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf
  • W. Hamel - Institut für Neurophysiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf
  • A. Engel - Institut für Neurophysiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocMI.04-01

DOI: 10.3205/09dgnc183, URN: urn:nbn:de:0183-09dgnc1830

Veröffentlicht: 20. Mai 2009

© 2009 Moll et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

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Objective: To demonstrate the feasibility of a precise delineation of the subthalamic nucleus (STN) in surgery for Parkinson’s disease (PD) under general anesthesia (GA) with the aid of microelectrode-recordings and to characterize the associated changes in neural activity in the STN and adjacent structures.

Methods: 9 patients with advanced PD underwent micro-electrode guided implantation of DBS electrodes in the STN under GA with propofol and remifentanyl. This data was compared to recordings from awake and sedated PD patients undergoing STN surgery, respectively. Single cell activity was recorded from 591 cells in 3 different structures along the STN trajectory: thalamus, STN and substantia nigra, pars reticulata (SNr).

Results: Neural activity under sedation and GA showed major differences to recordings under local anesthesia. Whereas STN units recorded from awake PD patients fired at 34.8±17.4 Hz (mean±SD), they displayed reduced activity levels under sedation (23.4±10.7Hz) and an even stronger reduction under the influence of propofol (17.3±10.3Hz) at moderate dosages (5mg/kg/hr). Higher propofol concentrations caused a near complete silencing of STN neurons. SNr firing rates were generally higher compared to the STN and did not differ between awake (64.8±29.8Hz) and sedated patients (64.0±33.5 Hz). Propofol anesthesia led to a profound reduction of SNr discharge rates (39.0±22.8Hz). The burst index was significantly higher for STN cells recorded under sedation (7.1±5.4) compared to recordings from awake patients (4.3±4.1). Notably, propofol anesthesia was associated with an excessively high burst index in STN units (179.2±110.2). In contrast, burst index values were generally low for SNr cells (typically values <2) and did not differ across vigilance states.

Conclusions: Anesthesia with propofol and remifentanyl is associated with major changes that differentially affect both the discharge rate and -pattern in all 3 investigated subcortical nuclei. STN activity under propofol-anesthesia is characterized by excessive burst discharges of long duration and differs vastly from the typical tonic-irregular activity that is observed in awake PD patients. The reduced discharge rates of STN cells under sedation and GA supports the notion of increased STN activity in the presence of PD symptoms in the awake patient. Taken together, our results demonstrate the possibility of a precise differentiation of the target region in the STN from surrounding structures even under GA.