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Previous work has shown that non-invasive optical measurement of low cerebral blood flow (CBF) is an acute biomarker of poor long-term cognitive outcome after repetitive mild traumatic brain injury (rmTBI). Herein, we explore the relationship between acute cerebral blood flow and underlying neuroinflammation. Specifically, because neuroinflammation is a driver of secondary injury after TBI, we hypothesized that both glial activation and inflammatory signaling are associated with acute CBF and, by extension, with long-term cognitive outcome after rmTBI. To test this hypothesis, cortical CBF was non-invasively measured in anesthetized mice 4 h after 3 repetitive closed head injuries spaced once-daily, at which time brains were collected. Right hemispheres were fixed for immunohistochemical staining for glial activation markers Iba1 and GFAP while left hemispheres were used to quantify Iba1 and GFAP expression via Western blot as well as 32 cytokines and 21 phospho-proteins in the MAPK, PI3K/Akt, and NF-κB pathways using a Luminex multiplexed immunoassay. N = 8/7 injured/sham C57/black-6 adult male mice were studied. Within the injured group, CBF inversely correlated with Iba1 expression (R = −0.86, p

Subarachnoid hemorrhage (SAH) is a neurosurgical emergency that results from the rupture of an aneurysm in the subarachnoid space. One common complication of SAH is cerebral vasospasm, which can lead to a secondary stroke. Intrathecal (IT) Nicardipine holds promise in treating cerebral vasospasm through its direct vasodilatory effect on the cerebral vasculature. Here, we used diffuse correlation spectroscopy to continuously monitor microvascular cerebral blood flow changes in medium-high grade subarachnoid hemorrhage patients in response to the first dose of IT Nicardipine. To date, we have recruited 9 patients, 3 of whom developed a secondary stroke.

Using non-invasive diffuse correlation spectroscopy measurements of cerebral blood flow, we identify an early functional biomarker of cognitive outcome after repetitive concussion, and we explore potential pathological mechanisms of cognitive deficits.