gms | German Medical Science

Objective: Cerebral vasopsasm or the delayed ischemic neurological deficit is a potentially devastating complication following aneurysmal subarachnoid hemorrhage. Despite its clinical importance the pathophysiology of ischemic cerebral lesions following aneurysmal subarachnoid hemorrhage is poorly understood. In the last few years there is growing evidence that inflammatory reactions could be involved in the pathogenesis of such delayed occurring ischemic lesions. Aim of the study was to evaluate adhesion molecules with regard to these lesions following SAH.

Methods: 15 Patients could be included. Serum and CSF samples were taken daily up to day 9 after SAH and evaluated for ICAM-1 and VCAM-1. 10 (66%) were female and the remaining 5 (33%) male. The mean age was 47 years with a range from 18 to 68 years. Transcranial doppler ultrasound recordings were made using standard transtemporal and transorbital approaches. All patients received postoperative CT scans within 24 hours after surgery to rule out or confirm an ischemic lesion due to direct surgical manipulation. Symptomatic vasospasm and DIND were defined as a focal neurologic deficit or deterioration in the level of consciousness, with either confirmation of infarction on a CT scan or exclusion of other possible causes. ICAM-1 and VCAM-1 concentrations were determined by using the Quantikine human sVCAM-1 and the Parameter human sICAM-1 Immunoassay Kit (both R & D Systems, Minneapolis, MN) according to the instructions provided by the manufacturer.

Results: CSF and Serum samples correlated well during nearly the whole time course (p<0.0001). A secondary increase of ICAM-1 and VCAM-1 in the serum and CSF correlated with an increase in flow velocity in the transcranial Doppler (p<0.0001 and p<0.007) but not to a delayed lesion in the CT scan.

Conclusions: We believe that inflammatory processes are involved in the pathogenesis of cerebral vasospasm, but they may be only a part of a multifactorial pathogenesis.