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Glioblastoma is the most common primary brain tumour. The aim of this study was to determine trends in survival over a 12-year period. Survival data were collected retrospectively for 625 patients who had surgery for histologically-confirmed glioblastoma between 1993 and 2004 in a single centre. Data including age, sex, preoperative Karnofsky performance score, tumour site, date of surgery, and type of surgical and adjuvant treatment were collected. Overall median survival was 189 days; there was no significant change in survival over 12 years. Multivariate analysis identified the following independent positive prognostic factors: age <60 years (p < 0.0005), Karnofsky score > or = 70 (p < 0.0001), tumour debulking, rather than biopsy (p < 0.001), right-sided lesion (p < 0.05), unilateral tumour (p < 0.05) and radiotherapy (p < 0.0001). Despite neurosurgical advances, the survival of patients with glioblastoma has not changed for more than a decade. Although, overall, glioblastoma has a short survival, our data show that individual patient survival is heterogeneous.

We investigated the role of the glial water channel protein aquaporin-4 in brain edema in a mouse model of subarachnoid haemorrhage in which thirty microliters of blood was injected into the basal cisterns. Brain water content, intracranial pressure and neurological score were compared in wildtype and aquaporin-4 null mice. We also measured blood-brain barrier permeability, and the osmotic permeability of the glia limitans, one of the routes of edema elimination. Wildtype and aquaporin-4 null mice had comparable baseline brain water content, intracranial pressure and neurological score. At six hours after blood injection, aquaporin-4 null mice developed more brain swelling than wildtype mice. Brain water content increased by 1.5 ± 0.1 vs. 0.5 ± 0.2 % (Mean ± Standard Error, P < 0.0005) and intracranial pressure by 36 ± 5 vs. 21 ± 3 mmHg (P < 0.05) above pre-injection baseline, and neurological score was worse at 18.0 vs. 24.5 (median, P < 0.05), respectively. Although subarachnoid hemorrhage produced comparable increases in blood-brain barrier permeability in wildtype and aquaporin-4 null mice, aquaporin-4 null mice had a twofold reduction in glia limitans osmotic permeability. We conclude that aquaporin-4 null mice manifest increased brain edema following subarachnoid hemorrhage as a consequence of reduced elimination of excess brain water. KeywordsAquaporin-4; astrocyte; brain edema; mouse model; subarachnoid hemorrhage; water channel Aneurysmal rupture releases blood at high pressure into the cerebrospinal fluid (CSF). Within hours, subarachnoid hemorrhage (SAH) produces brain edema (Claassen et al., 2002, Liu et al., 2007. Severe brain edema is associated with a large CSF blood load, with reduced consciousness at presentation being an independent predictor of poor outcome (Claassen et al., 2002).

The possibility of an underlying tumor should always be borne in mind so that adequate preoperative planning can be undertaken. The presence of the myxopapillary subtype should not prevent a clinician from excluding other reasons for hemorrhage, and counseling when reinstituting anticoagulation must include warning against a worse prognosis from any future hemorrhage.