TY  - JOUR
A1  - Albanna, Walid
A1  - Conzen, Catharina
A1  - Weiss, Miriam
A1  - Seyfried, Katharina
A1  - Kotliar, Konstantin
A1  - Schmidt, Tobias Philip
A1  - Kuerten, David
A1  - Hescheler, Jürgen
A1  - Bruecken, Anne
A1  - Schmidt-Trucksäss, Arno
A1  - Neumaier, Felix
A1  - Wiesmann, Martin
A1  - Clusmann, Hans
A1  - Schubert, Gerrit Alexander
T1  - Non-invasive assessment of neurovascular coupling after aneurysmal subarachnoid hemorrhage: a prospective observational trial using retinal vessel analysis
JF  - Frontiers in Neurology
N2  - Delayed cerebral ischemia (DCI) is a common complication after aneurysmal subarachnoid hemorrhage (aSAH) and can lead to infarction and poor clinical outcome. The underlying mechanisms are still incompletely understood, but animal models indicate that vasoactive metabolites and inflammatory cytokines produced within the subarachnoid space may progressively impair and partially invert neurovascular coupling (NVC) in the brain. Because cerebral and retinal microvasculature are governed by comparable regulatory mechanisms and may be connected by perivascular pathways, retinal vascular changes are increasingly recognized as a potential surrogate for altered NVC in the brain. Here, we used non-invasive retinal vessel analysis (RVA) to assess microvascular function in aSAH patients at different times after the ictus.
Y1  - 2021
U6  - http://dx.doi.org/10.3389/fneur.2021.690183
SN  - 1664-2295
VL  - 12
IS  - 12
SP  - 1
EP  - 15
ER  - 
TY  - JOUR
A1  - Conzen, Catharina
A1  - Albanna, Walid
A1  - Weiss, Miriam
A1  - Kürten, David
A1  - Vilser, Walthard
A1  - Kotliar, Konstantin
A1  - Zäske, Charlotte
A1  - Clusmann, Hans
A1  - Schubert, Gerrit Alexander
T1  - Vasoconstriction and Impairment of Neurovascular Coupling after Subarachnoid Hemorrhage: a Descriptive Analysis of Retinal Changes
JF  - Translational Stroke Research
N2  - Impaired cerebral autoregulation and neurovascular coupling (NVC) contribute to delayed cerebral ischemia after subarachnoid hemorrhage (SAH). Retinal vessel analysis (RVA) allows non-invasive assessment of vessel dimension and NVC hereby demonstrating a predictive value in the context of various neurovascular diseases. Using RVA as a translational approach, we aimed to assess the retinal vessels in patients with SAH. RVA was performed prospectively in 24 patients with acute SAH (group A: day 5–14), in 11 patients 3 months after ictus (group B: day 90 ± 35), and in 35 age-matched healthy controls (group C). Data was acquired using a Retinal Vessel Analyzer (Imedos Systems UG, Jena) for examination of retinal vessel dimension and NVC using flicker-light excitation. Diameter of retinal vessels—central retinal arteriolar and venular equivalent—was significantly reduced in the acute phase (p < 0.001) with gradual improvement in group B (p < 0.05). Arterial NVC of group A was significantly impaired with diminished dilatation (p < 0.001) and reduced area under the curve (p < 0.01) when compared to group C. Group B showed persistent prolonged latency of arterial dilation (p < 0.05). Venous NVC was significantly delayed after SAH compared to group C (A p < 0.001; B p < 0.05). To our knowledge, this is the first clinical study to document retinal vasoconstriction and impairment of NVC in patients with SAH. Using non-invasive RVA as a translational approach, characteristic patterns of compromise were detected for the arterial and venous compartment of the neurovascular unit in a time-dependent fashion. Recruitment will continue to facilitate a correlation analysis with clinical course and outcome.
Y1  - 2018
U6  - http://dx.doi.org/10.1007/s12975-017-0585-8
SN  - 1868-601X
IS  - 9
SP  - 284
EP  - 293
PB  - Springer Nature
CY  - Cham
ER  -