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

Excitotoxic and metabolic impact to periinfarct tissue after malignant hemispheric stroke

Meeting Abstract

  • J. Woitzik - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin; Center for Stroke Research, Charité - Universitätsmedizin Berlin
  • A. Pinczolits - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin; Center for Stroke Research, Charité - Universitätsmedizin Berlin
  • N. Hecht - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin; Center for Stroke Research, Charité - Universitätsmedizin Berlin
  • N. Sandow - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin; Center for Stroke Research, Charité - Universitätsmedizin Berlin
  • P. Vajkoczy - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin; Center for Stroke Research, Charité - Universitätsmedizin Berlin

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. DocDO.17.04

DOI: 10.3205/12dgnc156, URN: urn:nbn:de:0183-12dgnc1567

Veröffentlicht: 4. Juni 2012

© 2012 Woitzik 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: In-hospital lesion progression is a major complication in patients with ischemic stroke. Experimental and clinical research has resulted in potential relief strategies during the early period by clot lysis. However, at later points in time, there is still no treatment option to protect the brain from infarct progression. Experimental data has shown numerous pathways for delayed infarct progression. Here, we tested to what extent excitotoxicity and metabolic impairment within the periinfarct tissue are associated with infarct progression.

Methods: In 15 patients with malignant hemispheric stroke, 2 microdialysis (MD) catheters were placed near (5 mm distance) and distant (15 mm distance) to the infarct rim during decompressive hemicraniectomy. Precise probe placement within the periinfarct tissue was achieved by neuronavigation, laser speckle imaging and MRI flattening techniques. Glutamate, lactate, pyruvate and glucose were monitored for 5 days postoperatively. Infarct progression was assessed by sequential magnetic resonance imaging.

Results: Seven out of 15 (47%) patients developed delayed infarct progression. During the early postoperative period, glutamate was significantly elevated (66.8 μmol/l) but normalized with time (8.5 μmol/l). No difference was detected between the MD catheters placed 5 or 15 mm next to the infarct rim, nor between patients with and without infarct progression. Lactate displayed elevated concentrations at both catheters (6.5 mmol/l), again without differences. However, at the catheter with 15 mm distance to the infarct, rim glucose was significantly elevated in patients without infarct progression (1.7 mmol/l vs. 1.0 mmol/l; p < 0.05). In addition, pyruvate was significantly higher in these patients (183 μmol/l vs. 108 μmol/l; p < 0.05; catheter with 5 mm distance).

Conclusions: Accumulation of glutamate within the periinfarct tissue was not associated with infarct progression. Interestingly, glucose and pyruvate concentrations were significantly elevated in patients without infarct progression and could serve as biomarkers. Whether pyruvate has a neuroprotective function needs further examination.