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History
- December 2, 2021.
Copyright
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
Author Information
- Nicole A. Terpolilli1,2,7,
- R. Dolp2,
- K. Waehner4,
- S. M. Schwarzmaier1,3,7,
- E. Török2,
- Boyan Todorov5,
- Michel D. Ferrari6,
- Arn M.J.M. van den Maagdenberg5,6 and
- Nikolaus Plesnila1,7,*
- 1Institute for Stroke and Dementia Research, Munich University Hospital, Munich, Germany
- 2Department of Neurosurgery, Munich University Hospital, Munich, Germany
- 3Department of Anesthesiology, Munich University Hospital, Munich, Germany
- 4Department of Neurosurgery, Mannheim University, Mannheim, Germany
- 5Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands
- 6Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands
- 7Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
- ↵*Corresponding author:
Dr. Nikolaus Plesnila, Institute for Stroke and Dementia Research, University of Munich (LMU) and Munich University Hospital (KUM), Feodor-Lynen-Str. 17, 81377 Munich, Germany, Tel: +49 89 4400 46 219; Fax: +49 89 4400 46 113, E-mail: nikolaus.plesnila{at}med.uni-muenchen.de
Posted December 02, 2021.
Mutated neuronal voltage-gated CaV2.1 channels causing familial hemiplegic migraine 1 increase the susceptibility for cortical spreading depolarization and seizures and worsen outcome after experimental traumatic brain injury
