Abstract Details

Title Subarachnoid Hemorrhage Leads to Deficits in Neuronal and Hemodynamic Connectivity

Topic General Neurology

Presentation(s) S3 - General Neurology 1 (2:36 PM-2:48 PM)

Poster/Presentation
Number 009

Objective To investigate the impact of subarachnoid hemorrhage (SAH) on neuronal and hemodynamic measures of resting state functional connectivity after SAH and assess its correlation with behavioral deficits.

Background Survivors of SAH suffer from persistent neurocognitive deficits even in the absence of structural brain injury. There is evidence to suggest that long range functional neuronal networks may play a role in the mechanism of these deficits but testing this mechanism is difficult due to human study constraints.

Design/Methods We used neuronal Thy1-GCaMP6f mice which express a calcium fluorophore in excitatory cortical neurons to simultaneously examine neuronal and hemodynamic connectivity under tribromoethanol anesthesia. We calculated several connectivity metrics including a bihemispheric connectivity index (BCI) to determine the overall connectivity between homotopic regions on each hemisphere. We assessed neurocognitive performance with the Barnes maze.

Results Mice with SAH showed significant deficits in neuronal and hemodynamic resting state functional connectivity. The z-transformed correlation between GCaMP and oxy-hemoglobin fluctuations was 1.29 ± 0.17 before and 1.09 ± 0.23 after SAH (p=0.0096, n=16). The BCI using the neuronal signal was 1.01 ± 0.21 before and 0.81 ± 0.19 after SAH (p=0.01). The hemodynamic BCI was 1.10 ± 0.17 before and 0.85 ± 0.13 after SAH (p=0.003). Barnes maze testing in saline (n=7) vs. SAH (n=8) mice revealed differences in secondary escape times (44 vs. 165 sec, p=0.001) and errors (2.3 vs. 15.1, p=0.01).

Conclusions SAH leads to deficits in neuronal and hemodynamic connectivity and associated behavioral deficits. These results provide insight into potential neuronal mechanisms underlying neurocognitive deficits in SAH patients.

Authors/Disclosures
James H. Lai PRESENTER	Mr. Lai has nothing to disclose.
Sanem Aykan (MGH, HMS)	No disclosure on file
Tao Qin	No disclosure on file
David Boas (Boston University)	No disclosure on file
Sava Sakadzic (Massachusetts General Hospital)	No disclosure on file
Cenk Ayata, MD (Massachusetts General Hospital)	Dr. Ayata has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Quris. Dr. Ayata has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Neurelis. The institution of Dr. Ayata has received research support from NIH. The institution of Dr. Ayata has received research support from Takeda. The institution of Dr. Ayata has received research support from Neurelis.
David Y. Chung, MD (Massachusetts General Hospital)	The institution of Dr. Chung has received research support from NIH/NINDS. The institution of Dr. Chung has received research support from Brain Aneurysm Foundation. The institution of Dr. Chung has received research support from Angea Biotherapeutics.

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