Possible role of the C-reactive protein and white blood cell count in the pathogenesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage

The delayed ischemic neurologic deficit (DIND) is a common and potentially devastating complication in patients who have sustained subarachnoid hemorrhage (SAH). Recent evidence suggests that various constituents of the inflammatory response may be critical in the pathogenesis of this ischemic complication. The aim of this study was to evaluate the possible relationship between the C-reactive protein (CRP)/white blood cell (WBC) count and DIND. A total of 88 patients with acute SAH were included. CRP and WBC count were estimated on a daily basis. Outcome was evaluated 1 year after the initial ictus according to the Glasgow Outcome Scale. CRP levels on days 5, 6, 7, and 8 were statistically significantly higher in the group of patients developing a DIND (P < 0.025, P < 0.016, P < 0.011, P < 0.0002). WBC counts were higher in this patient group on days 1, 4, 5, 6, and 7 (P < 0.0253, P < 0.0087, P < 0.00167, P < 0.0026, P < 0.0045). Overall CRP values were higher with increasing severity of the initial ictus according to the Hunt and Hess Scale and to the outcome according to the Glasgow Outcome Scale from day 3 on. A statistically significant relationship between WBCs and outcome could not be observed. The presented data do not prove that WBCs and CRP values have a direct contribution to the pathogenesis of ischemic complications following SAH, but it supports the assertion that inflammation may present a common pathogenic pathway in the development of such complications

Effects of temporary clipping during aneurysm surgery

According to our results, it seems to be the possible that temporary vessel occlusion is an additional factor in aggravating vasospasm after aneurysmatic subarachnoid hemorrhage

High re-bleeding rate in young adults after subarachnoid haemorrhage from giant aneurysms

Low re-bleeding rates within the first 14 days of aneurysmal subarachnoid haemorrhage are reported in young patients. Furthermore, re-bleeding rate for giant aneurysms does not exceed 20% according to the literature. Our own clinical impression is that the re-bleeding rate seems to be much higher in giant aneurysms than reported, particularly in young patients. The aim of this study was to evaluate re-bleeding rate after subarachnoid haemorrhage following rupture of giant aneurysms in a younger population. We reviewed records of 23 patients who were treated in our institution for subarachnoid haemorrhage from giant aneurysms between 1994 and 2003. By definition, the aneurysms were larger than 25 mm in diameter. Five patients were younger than 40 years of age at the time of the aneurysmal subarachnoid haemorrhage. All younger patients (<40 years of age) showed re-bleeding after the first subarachnoid haemorrhage within the first 14 days of the initial event. In four patients (20%) older than 40 years at the time of the haemorrhage re-bleeding could be observed within the first 14 days of subarachnoid haemorrhage. We can confirm the re-bleeding rate of approximately 20% in patients suffering from subarachnoid haemorrhage (SAH) in the group of patients older than 40 years of age. However, younger patients seem to be at much higher risk of re-bleeding from giant aneurysms

ICAM-1 and VCAM-1 expression following aneurysmal subarachnoid hemorrhage and their possible role in the pathophysiology of subsequent ischemic deficits

BACKGROUND: The pathophysiology of ischemic cerebral lesions following aneurysmal subarachnoid hemorrhage (SAH) is poorly understood. There is growing evidence that inflammatory reactions could be involved in the pathogenesis of such delayed occurring ischemic lesions. The aim of this study was to evaluate adhesion molecules with regard to these lesions following SAH. METHODS: Serum and cerebrospinal fluid (CSF) samples were taken daily from 15 patients up to day 9 after SAH and evaluated for intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1). RESULTS: CSF and serum samples correlated well during nearly the whole time course (p 0.0001 and p < 0.007) but not to a delayed lesion in the CT scan. CONCLUSION: We believe that inflammatory processes are involved in the pathogenesis of cerebral vasospasm but they might only be a part of a multifactorial pathogenesis