gms | German Medical Science

Objective: The basilar artery is frequently used as reference vessel for laboratory investigations of cerebral vasospasm (CVS) in many experimental models. However, it is unclear whether this artery is representative in regards to the clinical manifestations and sequelae of basilar artery CVS in humans following aneurysmal subarachnoid hemorrhage (SAH).

Methods: In a prospective observational study we have been analyzing all patients admitted to our department with SAH for the occurrence and sequelae of CVS, beginning January 1, 2016. Age, admission state, Hunt & Hess (HH) grading, Fisher scale, location of cerebral infarction and duration of cerebral vasospasm were taken into account. Specifically, we sought to identify patients with CVS of the basilar artery. All patients were treated on ICU, received nimodipine prophylaxis and underwent CT-A to confirm CVS when suspected from routine TCD examinations. When TCDs were unsuspicious, patients had routine CT-A on day 6-9 following SAH to rule out CVS. When CVS was present, patients received specific treatment, and repeat CT-A was performed to detect CVS associated ischemia and to ascertain normalization of vessel diameter before patient discharge. As per institutional protocol, all patients with CVS detected in the posterior circulation had MRI examinations instead of CT-A.

Results: Between January 1 and October 31, 2016, 67 patients were treated for aneurysmal SAH. 35 (52.2%) patients were HH grades 1 or 2, and 32 (47.8%) patients were HH grades 3 to 5. Median age was 54 years. CVS occurred in 43 (64.2%) patients, and 19 (28.4%) patients developed associated cerebral infarctions. In 10 (14.9%) patients, CVS significantly affected the basilar artery. Poor grade (HH 3-5) patients were more likely to develop basilar artery CVS than other patients (25.0% vs. 5.7%, p<0.05). Patients with basilar CVS developed cerebral infarction in a frequency comparable to other patients with CVS (50% vs. 42.4%, p=0.73), but none of these infarctions occurred in the vertebro-basilar territory (cerebellum, medulla, pons, mesencephalon) even though vessel diameter was dramatically reduced according to CT- and/or MR-angiography.

Conclusion: In an ongoing study, basilar artery CVS does not appear to be followed by cerebral infarction in the basilar artery territory, presumably due to a vascular privilege of this vessel and its perforating branches. In contrast, brain ischemia can frequently be observed in the territories of other major arteries (internal carotid, anterior/middle cerebral arteries) affected by CVS. While the underlying mechanism for this intriguing observation needs to be elucidated, our data question the value of experimental studies on CVS performed with animal basilar arteries.