gms | German Medical Science

68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

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Transcranial direct current stimulation influences the extent of neuronal injury after experimental subarachnoid hemorrhage in rats

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  • Vesna Malinova - Universitätsmedizin Göttingen, Klinik und Poliklinik für Neurochirurgie, Göttingen, Deutschland
  • Kim Bleuel - Georg-August-University Göttingen, Klinik für Neurochirurgie, Abteilung für Neuropathologie, Göttingen, Deutschland
  • Bogdan Iliev - Georg-August-Universität, Klinik für Neurochirurgie, Göttingen, Deutschland
  • Walter Schulz-Schaeffer - Georg-August-University Göttingen, Abteilung für Neuropathologie, Göttingen, Deutschland
  • Veit Rohde - Universitätsmedizin Göttingen, Klinik und Poliklinik für Neurochirurgie, Göttingen, Deutschland
  • Dorothee Mielke - Universitätsmedizin Göttingen, Klinik und Poliklinik für Neurochirurgie, Göttingen, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocMi.12.05

doi: 10.3205/17dgnc441, urn:nbn:de:0183-17dgnc4418

Published: June 9, 2017

© 2017 Malinova et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

Text

Objective: Cerebral hypoperfusion is a frequent condition after subarachnoid hemorrhage (SAH), increasing the risk for neuronal injury. In previous experiments transcranial direct current stimulation (tDCS) induced alterations of cerebral blood flow (CBF) in an experimental SAH-model in rats, which again could influence the extent of neuronal injury. In this study a possible correlation between the tDCS and the neuronal injury was evaluated in a SAH-model in rats.

Methods: SAH was induced in 31 Sprague Dawley male rats using the double-hemorrhage SAH-model. The rats were then assigned to the tDCS-group (anodal/cathodal) or to the control-group (no tDCS). The tDCS was applied on day 3 and 4 after the SAH-induction via an epicranial electrode placed over the right hemisphere. Histological analysis with neurons count within the hippocampus formation was performed in all rats. Five rats without SAH were analyzed to establish a reference of normal neurons count within the hippocampus. A correlation analysis of tDCS with neurons loss (NL), as a measure for neuronal injury, was then performed.

Results: 27 rats were assigned to the tDCS-group (15 anodal and 12 cathodal) and 4 rats to the control-group. The cut-off for significant NL was < 720 neurons/mm2 (ROC, AUC 0.93, 95%CI 0.83-1.02, p=0.0003). A significant NL (mean 651 neurons/mm2) was detected in all SAH rats compared to the rats without SAH (mean 840 neurons/mm2). In the control-group a significant NL was observed in 70% (3/4) equally affecting both hemispheres. The cathodal-tDCS correlated with a significant lower rate of NL ipsilateral to the tDCS-application compared to the anodal-tDCS (OR 3.0 95%CI 1.5-5.9, p=0.001). There was no significant difference in the NL in the cathodal-tDCS-group compared to the control-group (OR 0.7 95%CI 0.4-1.4, p=0.54). The anodal-tDCS was associated with a significant higher rate of NL ipsilateral to the tDCS-application in comparison to the control-group (OR 2.4 95%CI 1.1-4.8, p=0.01).

Conclusion: The tDCS can influence the extent of neuronal injury ipsilateral to the applied stimulation in an experimental SAH-model in rats. Future experiments will show if a possible neuroprotective effect of the cathodal-tDCS can be established with a more frequent stimulation.