Role of Platelets in the Development of Delayed Neurological Deficits after Subarachnoid Hemorrhage in Mice

Saturday, May 4, 2024

1:30 PM – 1:32 PM CT

Location: Booth 745 Neuro Spotlight

Presenting Author(s)

BS

Bibek Samal

Undergraduate Researcher
Rice University, Houston, Texas, USA

Co-Author(s)

AD

Ari C. Dienel, n/a

Post-Doctoral Researcher
The Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, USA, United States
SH

Sung-Ha Hong, n/a

Post-Doctoral Researcher
The Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, USA, United States
DM

Devin W. McBride, n/a

Principal Investigator
The Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, USA, United States

Submitter(s)

BS

Bibek Samal

Undergraduate Researcher
Rice University, Houston, Texas, USA

Disclosure(s):

Bibek Samal, n/a: No financial relationships to disclose

Introduction: Microthrombosis (platelet aggregation) has been suggested as a major factor contributing to delayed neurological deterioration in patients after subarachnoid hemorrhage (SAH). However, experimental studies on the role of microthrombi in delayed deficits after SAH have not been investigated. Thus, this study aims to elucidate the potential role that platelets have in SAH pathophysiology. Our hypothesis is that, following SAH, mice which develop delayed neurological deficits have a greater number of microthrombi than mice which do not develop delayed neurological deficits.

Methods: SAH was induced in adult male and female C57BL/6 mice via endovascular perforation. Mice were randomly assigned into sham (n=6/sex) or SAH groups (n=22-24/sex). A neurobehavior exam was performed daily for 7 days post-SAH using a composite neuroscore. Animals were sacrificed on the day of delayed deficits or 7 days post-SAH. Microthrombi count and vessel diameters (for vasospasm) were measured using H&E stained brain slices. All outcomes were performed and all data were analyzed by a blinded investigator.

Results: Seventeen percent (4/24) of male mice and thirty-six percent (8/22) of female mice developed delayed deficits on days 3-5 post-SAH. Those mice which developed delayed deficits had significantly more microthrombi in their brains than mice which did not develop delayed deficits; vasospasm did not correlate with delayed deficits. Additionally, female SAH mice develop delayed deficits at a higher frequency than males.

Conclusion : This work found that microthrombi correlated with delayed deficits. The data within this study suggests that preventing platelets and microthrombi may improve functional recovery and reduce the risk of delayed neurological deficits.