gms | German Medical Science

63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

13. - 16. Juni 2012, Leipzig

Combined deep brain stimulation of GPi and VIM in Lance-Adams syndrome – a case report

Meeting Abstract

  • W. Polanski - Klinik und Poliklinik für Neurochirurgie, Medizinische Fakultät "Carl Gustav Carus", Universitätsklinikum Dresden
  • M. Wolz - Klinik und Poliklinik für Neurologie, Medizinische Fakultät "Carl Gustav Carus", Universitätsklinikum Dresden
  • P. Themann - Klinik für Neurologie, Rehabilitationsklinik "Tharandter Wald", Hetzdorf
  • A. Storch - Klinik und Poliklinik für Neurologie, Medizinische Fakultät "Carl Gustav Carus", Universitätsklinikum Dresden
  • H. Reichmann - Klinik und Poliklinik für Neurologie, Medizinische Fakultät "Carl Gustav Carus", Universitätsklinikum Dresden
  • J. Koy - Klinik und Poliklinik für Neurochirurgie, Medizinische Fakultät "Carl Gustav Carus", Universitätsklinikum Dresden

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocFR.10.11

DOI: 10.3205/12dgnc254, URN: urn:nbn:de:0183-12dgnc2548

Veröffentlicht: 4. Juni 2012

© 2012 Polanski 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

Text

Objective: We report about a 49-year-old man with a severe action triggered myoclonus caused by hypoxic encephalopathy after cardiac arrest with cardiopulmonary reanimation. Because of the therapy resistant myoclonus, combined deep brain stimulation of the VIM and GPi was performed. The patient was treated preoperatively with numerous antiepileptic drugs such as Levetiracetame, Valproat, Clonazepam, Piracetam, Tiapride. Nevertheless, a pronounced dysarthria, dysphagia and an inability to stand and walk as well as to perform activities of daily living caused by the action triggered myoclonus, impaired an independent life while cognitive functions were unaffected. During the observation period of 8 months (1 month preoperatively, 7 months postoperatively) the clinical symptoms were evaluated.

Methods: The implantation of electrodes for deep brain stimulation was performed under general anesthesia with standard coordinates for VIM and GPi. One perioperative epileptic seizure was observed which was terminated with Valproat. No other complications were recorded. The position of the electrodes was checked with a postoperative cerebral computer tomography. Clinical improvement was achieved with the following stimulation parameters: amplitude: both GPi: 3.5 V, left VIM: 1.2 V. impulse length: both GPi: 90µs, left VIM: 60 µs. frequency: both GPi: 180 Hz, left VIM 130 Hz. The right VIM was not used since its stimulation led to apathy. Video recordings were performed pre- and postoperatively.

Results: Initially, the amplitude of the deep brain stimulation of the GPi was increased up to 3.5 V while the impulse length was 60 µs and the frequency was 180 Hz. With these stimulation parameters, the myoclonus worsened. After we increased the impulse length to 90 µs, the myoclonus improved except in proximal arm positions. When we started the stimulation of the left VIM, a marked improvement of the myoclonus was observed in the previously described posture also. The patient even had the ability to walk with a wheeled walker. Unfortunately, dysarthria and dysphagia were not influenced by the deep brain stimulation.

Conclusions: We have shown that combined deep brain stimulation of the VIM and the GPi in patients with Lance-Adams syndrome could be an effective treatment option. This supports the assumption that both targets are involved in action-triggered myoclonus caused by hypoxia.