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Subarachnoid Hemorrhage (SAH) Triggers Arrest of Cerebral Spinal Fluid (CSF) Circulation
Author(s) -
Federley Richard,
Golanov Eugene,
Wong Stephen,
Britz Gavin
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.149.4
Subject(s) - medicine , basilar artery , subarachnoid hemorrhage , subarachnoid space , cerebrospinal fluid , vasomotion , cisterna magna , vasoconstriction , evans blue , perivascular space , vasospasm , spinal cord , anesthesia , intracranial pressure , pathology , blood flow , psychiatry
SAH, blood accumulation in subarachnoid space (SS), is caused by rupture of intracranial aneurisms or by TBI. CSF circulating throughout SS and brain parenchyma forms glymphatic pathways for waste removal. We explored alterations to CSF circulation following SAH in C57BL mice at various time after perforation SAH. Fluorescent microspheres (μS, 0.02, 1.0 mm) were injected into the cisterna magna (CM). One hour later, their spread across the brain was monitored using in vivo multiphoton or ex vivo fluorescence microscopy. In naive mice, from CM μS spread to the brain stem, paraarterially along Willis circle, and further along middle cerebral artery and the ventral surface vessels toward the olfactory bulb. Caudally μS spread down the spinal cord. One hour after SAH, μS were confined to the CM and brain stem region limited by the rostral pons border indicating significant CSF flow impairment. The number of μS distributed to the spinal cord was also greatly reduced. Four days post SAH CSF flow remained arrested, indicating long‐lasting CSF flow blockade and its independence from acute elevation of intracranial pressure. In vivo examination of vasculature before and after SAH showed significant vasoconstriction as early as 15 minutes post SAH, and suppression of the slow high amplitude vasomotion. The mitigation of vasomotion, in conjunction with the vasoconstriction may contribute to the CSF flow blockade. Acute and prolonged arrest of CSF flow may play an important role in SAH‐induced brain pathology. Supported by The Ting Tsung and Wei Fong Chao Center for BRAIN, John S Dunn Research Foundation, and the Oden Brain Aneurysm Research Foundation.