gms | German Medical Science

68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
7. Joint Meeting mit der Britischen Gesellschaft für Neurochirurgie (SBNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

14. - 17. Mai 2017, Magdeburg

Impairment of neurovascular coupling after subarachnoid hemorrhage

Meeting Abstract

  • Catharina Conzen - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland
  • Walid Albanna - Department of Neurosurgery, RWTH Aachen University, Aachen, Deutschland
  • Miriam Weiß - Department of Neurosurgery, RWTH Aachen University, Aachen, Deutschland
  • Konstantin Kotliar - Department of Medical Engineering and Technomathematics, FH Aachen University of Applied Sciences, Aachen, Deutschland
  • Hans Rainer Clusmann - Universitätsklinikum der RWTH Aachen, Neurochirurgische Klinik, Aachen, Deutschland
  • Anke Höllig - Department of Neurosurgery, RWTH Aachen University, Aachen, Deutschland
  • Gerrit Alexander Schubert - Department of Neurosurgery, RWTH Aachen University, Aachen, 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.01.01

doi: 10.3205/17dgnc353, urn:nbn:de:0183-17dgnc3539

Veröffentlicht: 9. Juni 2017

© 2017 Conzen et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Objective: Outcome after subarachnoid hemorrhage (SAH) is significantly determined by early brain injury (EBI) and delayed cerebral ischemia (DCI). Experimental data identfied impairment of neurovascular coupling (NVC) as an important contributor to both EBI and DCI, but clinical proof of its existence could not be provided so far. Retinal vessel analysis (RVA) allows non-invasive assessment of the neurovascular unit. Using RVA, we aimed to assess the integrity of NVC in patients with SAH.

Methods: In a prospective study, we performed RVA in 24 patients with acute SAH (group A: day 5-14) and eleven patients at the time of follow-up (group B: mean 90±35ds after SAH), and included 35 age-matched healthy controls (group C). Data was acquired using a Dynamic Vessel Analyzer (Imedos Systems UG, Jena) for examination of retinal vessel dimension and neurovascular coupling (NVC) using flicker-light excitation (FLE).

Results: Diameter of retinal arteries were comparable for all groups, while veins were significantly dilated after SAH compared to the control group (p<0.001). NVC of retinal arteries was significantly impaired early after SAH (A) as characterised by attenuated dilatation (p<0.001) and reduced area-under-the-curve (p<0.01) after FLE when compared to the control group (C). Partial recovery over time was observed for group B, though arterial dilatation was delayed (p<0.05). Venous response to FLE was significantly delayed after SAH (A: p<0.001; B: p<0.05), but not diminished. Vessel response to FLE was not influenced by treatment with nimodipine.

Conclusion: To our knowledge, this is the first clinical study to document impairment of neurovascular coupling in patients with SAH. Using retinal vessel analysis, distinct differences of compromise were detected for the arterial and venous compartment of the neurovascular unit. Recruitment will continue to facilitate a correlation analysis with clinical course and outcome.