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Introduction It was observed that women with aneurysmal subarachnoid hemorrhage (aSAH) tended to have earlier menses than a typical 21- to 28-day cycle. The goal was to determine whether there is an association between aSAH and early onset of menses. Methods All cases of aSAH in women aged 18 to 55 years who were admitted to our facility's neuroscience intensive care unit from June 1, 2011, to June 30, 2012, were reviewed. The electronic healthcare record for each of these patients was examined for documentation of menses onset, computed tomography of the head, brain aneurysm characteristics, modified Fisher score and Glasgow Coma Scale on admission, presence/absence of vasospasm, medical/surgical history, and use of medications that affect the menstrual cycle. The mean onset of menses in this study population was compared with the mean of 21 to 28 days with the 1-sample t test. Results During the study period, 103 patients with subarachnoid hemorrhage were admitted. Sixty-one were women, and 15 were aged 18 to 55 years. Nine of the 15 (60%) had documentation of menses occurring during their initial week of hospitalization; 1 patient had documentation of menses on hospital day 12. There is a significant difference when the mean onset of menses in our patient population is compared with the approximate normal menstrual cycle of 21 to 28 days (P Conclusion Early onset of menses or abnormal uterine bleeding after SAH may occur in women with aSAH and typically within the first 7 to 10 days after intracranial aneurysm rupture. The physiologic cause of early onset of menses after aSAH, whether primary or secondary, remains unknown.

Background The management of aneurysmal subarachnoid hemorrhage (aSAH) has changed dramatically in the last few decades with the publication of a few major studies, including ISAT (International Subarachnoid Aneurysm Trial, the International Cooperative Study on the Timing of Aneurysm Surgery Study). The aim of this study is to analyze the outcome of patients with aSAH based on a contemporary series, identify the risk factors for poor outcome, and focus on patients with good-grade aSAH (to match the ISAT cohort). Methods Baseline demographic and outcome data (modified Rankin Scale) were available for the 803 patients recruited from the STASH (Simvastatin in Aneurysmal Subarachnoid Haemorrhage) trial for post hoc analysis, using a χ2 test or 2-sample t test. Logistic regression analysis was performed to assess the risk factors for poor outcome at 6 months. Propensity matched analysis comparing coiling and clipping, and subgroup analysis of good-grade patients (World Federation of Neurosurgical Societies grade I–II) were also performed. Results Logistic regression analysis showed that the treatment modality (i.e., coiling or clipping) was not associated with poor outcome at 6 months (P = 0.839). The risk factors associated with poor outcome at 6 months were poor admission World Federation of Neurosurgical Societies grade (P < 0.0001), Fisher grade on initial computed tomography scan (P = 0.013), and the development of delayed cerebral ischemia (P < 0.0001). Subgroup analysis for good-grade patients only showed that 82% of patients after coiling and 78% of patients after clipping were classed as good outcome at 6 months (P = 0.181). Conclusions In the current era of aSAH management, apart from patients' admission status, SAH blood load and the development of delayed cerebral ischemia, treatment modality with either coiling or clipping was not associated with poor outcome difference at 6 months.

Headache after aneurysmal subarachnoid hemorrhage (SAH) is very common and is often described as the “worst headache imaginable.” SAH-associated headache can persist for days to weeks and is traditionally treated with narcotics. However, narcotics can have significant adverse effects. We hypothesize that gabapentin (GBP), a non-narcotic neuropathic pain medication, would be safe and tolerable and would reduce narcotic requirements after SAH. We retrospectively reviewed the clinical, radiographic, and laboratory data of SAH patients at the neuroscience intensive care unit at Mayo Clinic in Jacksonville, Florida, from January 2011 through February 2013. Headache intensity was quantified by a visual analog scale score. Total opioid use per day was tabulated using an intravenous morphine equivalents scale. Cerebrospinal fluid was also reviewed when available. There were 53 SAH patients who were treated with GBP along with other analgesics for headache. Among these SAH patients, 34 (64 %) were women, with a mean age of 54 years (SD 12.3). Severe headache was observed in all SAH patients. GBP dosing was rapidly escalated within days of SAH up to a median of 1,200 mg/day, with a range of 300 mg three times a day to 900 mg three times a day. Approximately 6 % of patients treated with GBP had nausea (95 % CI 1–16 %), and only one patient (1.8 %) had to discontinue GBP. GBP appears to be relatively safe and tolerable in SAH patients with headache and may be a useful narcotic-sparing agent to prevent narcotics-associated complications, such as gastrointestinal immobility, ileus, and constipation.

Background and Purpose— Recently, a novel locus at 17q25 was associated with white matter hyperintensities (WMH) on MRI in stroke-free individuals. We aimed to replicate the association with WMH volume (WMHV) in patients with ischemic stroke. If the association acts by promoting a small vessel arteriopathy, it might be expected to also associate with lacunar stroke. Methods— We quantified WMH on MRI in the stroke-free hemisphere of 2588 ischemic stroke cases. Association between WMHV and 6 single-nucleotide polymorphisms at chromosome 17q25 was assessed by linear regression. These single-nucleotide polymorphisms were also investigated for association with lacunar stroke in 1854 cases and 51 939 stroke-free controls from METASTROKE. Meta-analyses with previous reports and a genetic risk score approach were applied to identify other novel WMHV risk variants and uncover shared genetic contributions to WMHV in community participants without stroke and ischemic stroke. Results— Single-nucleotide polymorphisms at 17q25 were associated with WMHV in ischemic stroke, the most significant being rs9894383 ( P =0.0006). In contrast, there was no association between any single-nucleotide polymorphism and lacunar stroke. A genetic risk score analysis revealed further genetic components to WMHV shared between community participants without stroke and ischemic stroke. Conclusions— This study provides support for an association between the 17q25 locus and WMH. In contrast, it is not associated with lacunar stroke, suggesting that the association does not act by promoting small-vessel arteriopathy or the same arteriopathy responsible for lacunar infarction.

The range of behavioral changes occurring after stroke has not yet been fully characterized. To evaluate behavioral symptoms after stroke and clinical characteristics that may influence the number and frequency of such symptoms, we compared 53 survivors of mild ischemic stroke with 30 stroke-free controls. Stroke survivor and control participants completed self-ratings of behavioral symptoms and were administered measures of cognitive status (ie, Beck Depression Inventory II, Mini-Mental State Examination, and Controlled Oral Word Association Test). Informants of stroke survivors and controls completed ratings of behavioral symptoms and functional status (ie, Neuropsychiatric Inventory Questionnaire, Informant Questionnaire on Cognitive Decline in the Elderly, and Functional Activities Questionnaire). More behavioral symptoms were observed in stroke survivors than in controls (mean [standard deviation] total number of symptoms on the Neuropsychiatric Inventory Questionnaire, 2.1 [2.0] vs 1.1 [1.5]; P = .02). Informants of stroke survivors were more likely to recognize behavioral symptoms than were stroke survivors themselves. Higher initial stroke severity was associated with more behavioral symptoms. With more behavioral symptoms, there was more functional impairment. Our findings suggest that behavioral symptoms can have unique and troublesome effects on stroke patients. Future research is needed to understand how the identification of behavioral symptoms after stroke can improve care in stroke survivors.