Artikel
Transcranial direct current stimulation influences the incidence of vasospasm-induced delayed cerebral infarction after experimental subarachnoid hemorrhage
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Autoren
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Vesna Malinova
- Klinik für Neurochirurgie, Georg-August-Universität, Göttingen, Germany
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Bogdan Iliev
- Klinik für Neurochirurgie, Georg-August-Universität, Göttingen, Germany
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Ioannis Tsogkas
- Institut für Neuroradiologie, Georg-August-Universität, Göttingen, Germany
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Veit Rohde
- Klinik für Neurochirurgie, Georg-August-Universität, Göttingen, Germany
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Dorothee Mielke
- Klinik für Neurochirurgie, Georg-August-Universität, Göttingen, Germany
| Veröffentlicht: | 8. Juni 2016 |
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Gliederung
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Objective: We previously showed, that transcranial direct current stimulation (tDCS) can change the resting membrane potential of the nerve cells in the brain and can lead to changes of the cerebral perfusion. Anodal tDCS increases the cortical activity and the cerebral perfusion, whereas cathodal tDCS does the opposite. Thereby, tDCS increases the tolerance for ischemia and reduces the infarction volume in an ischemic stroke model in rats. The aim of this study was to evaluate if tDCS could reduce the extent of vasospasm-induced delayed cerebral infarction after experimental subarachnoid hemorrhage (SAH) in rats.
Method: SAH was induced in 13 Sprague Dawley male rats using the double hemorrhage SAH model. Magnetic resonance imaging (MRI) was performed on day 1 (baseline), day 2 (after the second blood injection) and on day 5 at the end of the experiment. The MRI data were analyzed by two blinded neuroradiologists for the presence of vasospasm-induced cerebral ischemia. The cortical perfusion was measured on day 1, day 2 and day 5 using a Laser Doppler Imager. Either anodal or cathodal tDCS was performed on day 2 and 3. The duration of every single stimulation was 15 minutes, and was performed once or twice a day.
Results: A total of 15 rats have completed the experiments so far. Two rats were in the sham group. No vasospasm or infarction was seen in the sham group. Vasospasm was seen in all SAH groups on day 5: control group without tDCS (3/3 (100%)); anodal tDCS once a day (3/4 (75%)); cathodal tDCS once or twice a day (4/6 (68%)). In the cathodal tDCS group vasospasm affected more vessel territories (mean 3 [range 1-6] vs. mean 2 [range 1-3]). A reduction of cerebral perfusion was seen in all SAH groups on day 5 compared to day 2: control group (-238 perfusion units (PU); anodal tDCS (-122 PU) and cathodal tDCS (-155 PU). Infarction occurred more frequent in the group with cathodal tDCS (5/6 (84%)) compared to the group with anodal tDCS (1/4 (25%)) and to the control group (1/3 (34%)).
Conclusions: tDCS can influence the extent of vasospasm-induced delayed cerebral infarction after experimental SAH in a rat model even with stimulation only once or twice a day. Future experiments will show, if this effect can be extended by more frequent or longer duration of tDCS.
