Magnetic resonance analysis of deep cerebral venous vasospasm after subarachnoid hemorrhage in rabbits

Abstract

ObjectiveArterial spasm is proved to be an inducer of cerebral ischemia and cerebral infarction, while when a venous spasm occurs, cerebral edema is seen to be caused by a disturbance in cerebral blood flow. However, it is unclear and unproven whether venous spasm occurs after subarachnoid hemorrhage (SAH). To provide the theoretical basis for treating cerebral vasospasm after SAH, magnetic resonance imaging (MRI) was employed to observe the changes in the diameter of deep cerebral veins in rabbits after SAH.MethodsFourteen New Zealand rabbits were randomly divided into the SAH group (n = 10) and the normal saline group (NS group, n = 4). Specifically, the SAH models were established by the ultrasound-guided double injections of blood into cisterna magna. Moreover, the MRI was performed to observe the changes in the diameter of deep cerebral veins (internal cerebral vein, basilar vein, and great cerebral vein) and basilar artery before modeling (0 d) and 1, 3, 5, 7, 9, and 11 d after modeling.ResultsIn the SAH group, the diameter of the basilar artery showed no evident change on the 1st d. However, it became narrower obviously on the 3rd d and 5th d, and the stenosis degree was more than 30%. The diameter gradually relieved from 7th to 9th d, and finally returned to normal on the 11th d. Moreover, the diameter of the internal cerebral vein significantly narrowed on the 1st d, the stenosis degree of which was 19%; the stenosis then relieved slightly on the 3rd d (13%), reached the peak (34%) on the 5th d, and gradually relieved from 7th d to 11th d. Moreover, the stenosis degree of the basilar vein was 18% on the 1st d, 24% on the 3rd d, and reached the peak (34%) on the 5th d.ConclusionAfter SAH in rabbits, the cerebral vasospasm was seen to occur in the basilar artery, and likewise, spasmodic changes took place in the deep cerebral vein. Furthermore, the time regularity of spasmodic changes between the cerebral vein and basilar artery was of significant difference, indicating that the venous vasospasm resulted in active contraction.

Cerebrovascular Responses in a Patient with Lundberg B Waves Following Subarachnoid Haemorrhage Assessed with a Novel Non-Invasive Brain Pulse Monitor: A Case Report

“…The cerebrovascular responses associated with DCI remain poorly understood but include large vessel vasospasm of arteries, veins, microvascular vasoconstriction, microvascular thrombosis, and hyperperfusion. [1][2][3][4][5][6][7] Early detection and treatment of DCI remains a challenge due to limitations in the monitoring methods, uncertainty in the pathogenesis and lack of compelling evidence supporting treatments, such as spasmolysis. 8,9 In patients with impaired conscious states, monitoring largely relies on clinical neurological examination, which often results in delayed recognition of deterioration, increasing the risk of adverse outcomes.…”