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Background The prevalence of hypothalamic-pituitary dysfunction after aneurysmal subarachnoid hemorrhage has not been precisely determined, and conflicting results have been reported in the literature. Objective To perform a systematic review and meta-analysis investigating the prevalence of pituitary insufficiency after aneurysmal subarachnoid hemorrhage and to focus on basal serum and dynamic test differences. Methods The prevalence of pituitary dysfunction was quantified at 3 to 6 months and >6 months after aneurysmal subarachnoid hemorrhage. Proportions were transformed with the logit transformation. A subgroup analysis was performed focusing on the differences in outcome between basal serum and dynamic tests for the diagnosis of growth hormone deficiency (GHD) and secondary adrenal insufficiency. Results Overall prevalence of hypopituitarism differed considerably between studies, ranging from 0.05 to 0.45 in studies performed between 3 and 6 months after the event and from 0 to 0.55 in long-term studies (>6 months), with pooled frequencies of 0.31 (95% confidence interval [CI]: 0.22-0.43) and 0.25 (95% CI: 0.16-0.36), respectively. Pooled frequency of GHD at 3 to 6 months was 0.14 (95% CI: 0.08-0.24). At >6 months, GHD prevalence was 0.19 (95% CI: 0.13-0.26) overall, but ranged from 0.15 (95% CI: 0.06-0.33) with the insulin tolerance test to 0.25 (95% CI: 0.15-0.36) using the growth hormone releasing hormone + arginine test. Conclusion Hypopituitarism is a common complication in patients with aneurysmal subarachnoid hemorrhage, with GHD being the most prevalent diagnosis. We showed that variations in prevalence rates in the literature are partly due to methodological differences among pituitary function tests. Abbreviations ACTH, adrenocorticotropic hormoneaSAH, aneurysmal subarachnoid hemorrhageGHD, growth hormone deficiencyGHRH, growth hormone-releasing hormoneGST, glucagon stimulation testIGF, insulin-like growth factor 1ITT, insulin tolerance testSAH, subarachnoid hemorrhage.

BACKGROUND Chronic subdural hematoma (CSDH) is commonly seen in neurosurgical practice, and the incidence is increasing. Treatment results are highly variable with respect to recurrences and complications. OBJECTIVE To report our single-center experience with the surgical treatment of CSDH in patients on preoperative corticosteroids and to assess possible predictors of outcome. METHODS The medical reports of 496 consecutive patients with CSDHs treated with burr hole craniostomy were analyzed retrospectively. Patient demographics, medication, hematoma, treatment characteristics, and laboratory values were scored in relation to outcome. Data were analyzed with the χ(2) test, independent t test, and multivariate backward regression. RESULTS Mean age was 71.5 ± 13.3 years (range, 18.6-95.4 years); the male-to-female ratio was 3:1. A decreased Glasgow Coma Scale (GCS) was observed in 63.1%, and GCS motor score on admission was < 6 in 25.2%. Recurrence and mortality rates were 11.9% and 5.3%, respectively. Multivariate analysis showed a longer period of preoperative dexamethasone administration (odds ratio [OR], 0.93 per day; P = .02), GCS motor score within 1 week after surgery of 6 (OR, 0.54; P = .02), postoperative complications (OR, 5.3; P < .001), and a left-sided hematoma (OR, 0.42; P = 0.010) to be significantly related to recurrence risk. CONCLUSION The present data suggest that in surgical treatment of CSDH with burr hole craniostomy, extended preoperative corticosteroid administration is associated with a lower recurrence rate. The use of corticosteroids does not seem to be related to a higher incidence of complications and treatment-related death compared with the current literature.

OBJECTIVE: Patients with subarachnoid hemorrhage (SAH) who have been successfully treated for all detected aneurysms are at risk for recurrence of SAH. We assessed the characteristics, complications of re-treatment, and outcomes of patients with recurrent SAH as important factors in determining whether to screen patients for new aneurysms. METHODS: We studied patients admitted between 1987 and 2002 to three hospitals in the Netherlands for recurrent SAH. Patients had received treatment previously for all aneurysms identified after initial SAH. We collected data for age, sex, risk factors, site, and number of the aneurysm(s), time between the first and the second SAH, complications of re-treatment, and outcome after recurrent SAH. RESULTS: We identified 30 patients: 27 women and 3 men. Thirty-two aneurysms were documented; 19 were classified as de novo, 8 were classified as regrowth, and 5 had been missed in retrospect. The mean time between the first and the second SAH was 7.8 years (range, 0.25-17 yr for all aneurysms and 2.8-14 yr for de novo aneurysms). Nine patients (30%) had a family history of SAH. No specific complications were reported with reoperation in 21 patients. Ten patients (33%) died, 4 patients (14%) were severely disabled, and 16 patients (53%) had good outcomes. CONCLUSION: Among patients admitted with recurrent SAH, there is a predominance of women and patients with familial SAH. Reoperation is not associated with specific complications. Outcome after recurrent SAH is similar to that after initial SAH.

OBJECTIVE: To evaluate the efficacy of the conditionally replicating adenovirus (Ad) Ad.d24 for oncolysis of benign and malignant meningiomas.METHODS: Primary meningioma cells and organotypic spheroids were cultured from tumor biopsies of 12 consecutive unselected patients. Four different Ads were constructed and tested on meningioma cells and spheroids: a replication-deficient Ad encoding the luciferase marker gene (Ad.Luc), a replication-competent Ad with complete E1 region (Ad.E1+), a replication-competent Ad encoding the luciferase gene in the E3 region (Ad.E1Luc), and a conditionally replicating Ad with an E1ACR2 deletion (Ad.d24). Replication of the latter is restricted to cells with a defective retinoblastoma pathway, whereas Ad.E1+ and Ad.E1Luc can replicate in all human cells like a wild-type Ad. Their oncolytic activity was compared in primary meningioma cells and spheroids by use of viability and outgrowth assays.RESULTS: Adenoviral penetration into organotypic meningioma spheroids was detected with the replication-competent Ad.E1Luc, whereas infection with the replication-deficient Ad.Luc was limited to the outer layer of the spheroid. Replication of the Ads and oncolysis was demonstrated in primary cell cultures of meningioma cells at high dose, i.e., greater than 50 plaque-forming units per cell. At a lower dose of 5 plaque-forming units per cell, Ad.d24 kills meningioma cells more efficiently than Ad.E1+. Infection of organotypic meningioma spheroids with Ad.d24 resulted in decreased viability and suppression of outgrowth as compared with untreated control spheroids.CONCLUSION: Infection of meningioma cells and spheroids with replication-competent Ads results in efficient oncolysis. The Ad modified to replicate selectively in retinoblast-mutant cells, Ad.d24, seemed to be an efficient oncolytic agent in benign, atypical, and malignant meningiomas.