Nontraumatic Subarachnoid Hemorrhage Research Articles

High risk for seizures following subarachnoid hemorrhage regardless of referral bias.

To investigate the frequency, predictors, and clinical impact of electrographic seizures in patients with high clinical or radiologic grade non-traumatic subarachnoid hemorrhage (SAH), independent of referral bias. We compared rates of electrographic seizures and associated clinical variables and outcomes in patients with high clinical or radiologic grade non-traumatic SAH. Rates of electrographic seizure detection before and after institution of a guideline which made continuous EEG monitoring routine in this population were compared. Electrographic seizures occurred in 17.6% of patients monitored expressly because of clinically suspected subclinical seizures. In unselected patients, seizures still occurred in 9.6% of all cases, and in 8.6% of cases in which there was no a priori suspicion of seizures. The first seizure detected occurred 5.4 (IQR 2.9-7.3) days after onset of subarachnoid hemorrhage with three of eight patients (37.5%) having the first recorded seizure more than 48h following EEG initiation, and 2/8 (25%) at more than 72h following EEG initiation. High clinical grade was associated with poor outcome at time of hospital discharge; electrographic seizures were not associated with poor outcome. Electrographic seizures occur at a relatively high rate in patients with non-traumatic SAH even after accounting for referral bias. The prolonged time to the first detected seizure in this cohort may reflect dynamic clinical features unique to the SAH population.

Focal subarachnoid haemorrhage mimicking transient ischaemic attack - do we really need MRI in the acute stage?

BackgroundAcute non-traumatic focal subarachnoid haemorrhage (fSAH) is a rare transient ischaemic attack (TIA)-mimic. MRI is considered to be indispensable by some authors in order to avoid misdiagnosis, and subsequent improper therapy. We therefore evaluated the role of CT and MRI in the diagnosis of fSAH patients by comparing our cases to those from the literature.MethodsFrom 01/2010 to 12/2012 we retrospectively identified seven patients with transient neurological episodes due to fSAH, who had received unenhanced thin-sliced multiplanar CT and subsequent MRI within 3 days on a 1.5 T scanner. MRI protocol included at least fast-field-echo (FFE), diffusion-weighted imaging (DWI), T2-weighted fluid-attenuated inversion recovery (FLAIR) and time-of-flight (TOF) MRA sequences. By using MRI as gold-standard, we re-evaluated images and data from recent publications regarding the sensitivity to detect fSAH in unenhanced CT.ResultsfSAH was detected by CT and by FFE and FLAIR on MRI in all of our own cases. However, DWI and T2w-spin-echo sequences revealed fSAH in 3 of 7 and 4 of 6 cases respectively. Vascular imaging was negative in all cases. FFE-MRI revealed additional multiple microbleeds and superficial siderosis in 4 of 7 patients and 5 of 7 patients respectively. Including data from recently published literature CT scans delivered positive results for fSAH in 95 of 100 cases (95%), whereas MRI was positive for fSAH in 69 of 69 cases (100%).ConclusionsThin-sliced unenhanced CT is a valuable emergency diagnostic tool to rule out intracranial haemorrhage including fSAH in patients with acute transient neurological episodes if immediate MRI is not available. However, MRI work-up is crucial and mandatorily has to be completed within the next 24–72 hours.

Utilization And Outcomes Of Ventriculostomy In Non-Traumatic Subarachnoid Hemorrhage During Last Decade In United States (P5.128)

Utilization And Outcomes Of Ventriculostomy In Non-Traumatic Subarachnoid Hemorrhage During Last Decade In United States (P5.128)

Nontraumatic Convexal Subarachnoid Hemorrhage Concomitant with Acute Ischemic Stroke

Nontraumatic convexal subarachnoid hemorrhage (cSAH) rarely occurs subsequent to acute ischemic stroke. The incidence, clinical background characteristics, and outcomes in acute ischemic stroke patients with cSAH were investigated. Our stroke center database was reviewed to identify patients with acute ischemic stroke/transient ischemic attack (TIA) who demonstrated acute cSAH within 14days of admission between 2005 and 2011. Background characteristics, clinical course, and outcomes at discharge and 3months after onset were investigated in these patients. Of 4953 acute stroke/TIA patients, cSAH was observed in 8 (.14%) patients (7 men, mean age 71years): 7 were detected incidentally, and the other was found immediately after a convulsion. Two patients died during their hospital stay, 1 died after discharge, and 3 were dependent at 3months. Major artery occlusion or severe stenosis was observed in 5 patients. Two patients subsequently developed subcortical hemorrhage. On gradient echo imaging, lobar cerebral microbleeds were observed in 2 patients, and chronic superficial siderosis was observed in 2 patients. In this retrospective review of cases with ischemic stroke and cSAH, over half of patients had occlusion of major arteries. Cerebral amyloid angiopathy was suggested by magnetic resonance imaging findings and subsequent events in 3 patients. The overall outcome was unfavorable although the causal relationship with cSAH was unclear.

Clinical Associations and Causes of Convexity Subarachnoid Hemorrhage

It has been previously found noted that ≈15% to 20% of subarachnoid hemorrhage (SAH) is nonaneurysmal. Nontraumatic convexity SAH (cSAH) is increasingly recognized. Data concerning incidence and associations are scant. We identified all SAH-coded cases from South Australian public hospitals between January 2005 and July 2011. Electronic discharge summaries were reviewed, and cases of cSAH were ascertained. Clinical and radiological features were recorded, and pathogenesis was assigned. Of 742 cases with SAH, 41 (6%) cases were cSAH, giving a minimum population annual incidence of 5.1 per million (95% confidence interval, 3.7-7.0). Median age was 70 years (interquartile range, 48-79). Commonest causes were cerebral amyloid angiopathy (39%), reversible cerebral vasoconstriction syndrome (17%), cerebral venous sinus thrombosis (10%), large-vessel stenotic atherosclerosis (10%), and posterior reversible encephalopathy syndrome (5%). No cause was identified in 20% (mostly elderly patients with incomplete evaluation). Most (63%) presented with transient neurological symptoms. Many (49%) were misdiagnosed as transient ischemic attacks and treated inappropriately with antithrombotics. cSAH comprises a significant proportion of SAH. Commonest causes are cerebral amyloid angiopathy in the elderly and reversible cerebral vasoconstriction syndrome in the young, but differential diagnosis is broad. Misdiagnosis is common and leads to potentially harmful treatments.

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Abstract W MP27: Time to Peak Troponin T Levels Following Subarachnoid Hemorrhage

Introduction: Elevations of troponin after subarachnoid hemorrhage (SAH) frequently occur and are associated with cardiopulmonary complications. The time to peak elevation remains poorly described in terms of the natural history after SAH. Our two objectives were to define the temporal profile of troponin T elevation after SAH and correlate levels of troponin T with baseline neurological status. We hypothesized that troponin T would peak early after initial presentation. Methods: We reviewed the medical records of all aneurysmal and non-traumatic SAH patients from March 2011-December 2012. Troponin T from patients with ≥ 2 values was recorded with respect to SAH symptom onset. Patients with ≥ 1 Troponin T value were stratified according to admission Glasgow Coma Scale (GCS). GCS was dichotomized to > 8 or ≤ 8. Fisher’s exact test was performed comparing elevated peak troponin T (≥0.01 ng/ml) versus normal against GCS status cutoffs > 8 or 8 or less. Results: We identified 124 patients who had both troponin T and GCS reported, and 30 patients had ≥2 troponin T measurements within the first 40 hours of hospitalization. The median time to peak troponin T in these patients was 11.2 hours with a standard deviation of 6.2 hours (Range: 4.9-35.0 hours). Elevated troponin T was seen in 52 of 124. GCS of ≤ 8 was present in 43 of 124. Patients with elevated levels of troponin T had a greater chance of lower GCS [Odds ratio = 4.8 (95% CI: 2.2 to 10.7)] (P= <0.0001). Conclusions: The median time to peak troponin T after SAH injury was 11 hours. There was a statistically significant association between troponin T elevation and worse neurologic status at presentation (GCS ≤ 8). Although our small sample size found large variation in time to peak troponin, it supports the hypothesis that troponin peaks early after the initial presentation. Future studies using troponin elevation as a biomarker should focus on sample acquisition at the time of admission and in the first 1-2 days.

Impaired Cerebral Autoregulation Is Associated With Vasospasm and Delayed Cerebral Ischemia in Subarachnoid Hemorrhage

Cerebral autoregulation may be impaired in the early days after subarachnoid hemorrhage (SAH). The purpose of this study was to examine the relationship between cerebral autoregulation and angiographic vasospasm (aVSP) and radiographic delayed cerebral ischemia (DCI) in patients with SAH. Sixty-eight patients (54±13 years) with a diagnosis of nontraumatic SAH were studied. Dynamic cerebral autoregulation was assessed using transfer function analysis (phase and gain) of the spontaneous blood pressure and blood flow velocity oscillations on days 2 to 4 post-SAH. aVSP was diagnosed using a 4-vessel conventional angiogram. DCI was diagnosed from CT. Decision tree models were used to identify optimal cut-off points for clinical and physiological predictors of aVSP and DCI. Multivariate logistic regression models were used to develop and validate a risk scoring tool for each outcome. Sixty-two percent of patients developed aVSP, and 19% developed DCI. Patients with aVSP had higher transfer function gain (1.06±0.33 versus 0.89±0.30; P=0.04) and patients with DCI had lower transfer function phase (17.5±39.6 versus 38.3±18.2; P=0.03) compared with those who did not develop either. Multivariable scoring tools using transfer function gain>0.98 and phase<12.5 were strongly predictive of aVSP (92% positive predictive value; 77% negative predictive value; area under the receiver operating characteristic curve, 0.92) and DCI (80% positive predictive value; 91% negative predictive value; area under the curve, 0.94), respectively. Dynamic cerebral autoregulation is impaired in the early days after SAH. Including autoregulation as part of the initial clinical and radiographic assessment may enhance our ability to identify patients at a high risk for developing secondary complications after SAH.

Association between serum lactate levels and early neurogenic pulmonary edema after nontraumatic subarachnoid hemorrhage.

Few studies have described the risk factors associated with the development of neurological pulmonary edema (NPE) after subarachnoid hemorrhage (SAH). We have hypothesized that acute-phase increases in serum lactate levels are associated with the early development of NPE following SAH. The aim of this study was to clarify the association between lactic acidosis and NPE in patients with nontraumatic SAH. We retrospectively evaluated 140 patients with nontraumatic SAH who were directly transported to the Nippon Medical School Hospital emergency room by the emergency medical services. We compared patients in whom NPE developed (NPE group) and those in whom it did not (non-NPE group). The median (quartiles 1-3) arrival time at the hospital was 32 minutes (28-38 minutes) after the emergency call was received. Although the characteristics of the NPE and non-NPE groups, including mean arterial pressure (121.3 [109.0-144.5] and 124.6 [108.7-142.6] mm Hg, respectively; P=0.96), were similar, the median pH and the bicarbonate ion (HCO3(-)) concentrations were significantly lower in the NPE group than in the non-NPE group (pH, 7.33 [7.28-7.37] vs. 7.39 [7.35-7.43]); P=0.002; HCO3(-), 20.8 [18.6-22.6] vs. 22.8 [20.9-24.7] mmol/L; P=0.01). The lactate concentration was significantly higher in the NPE group (54.0 [40.3-61.0] mg/dL) than in the non-NPE group (28.0 [17.0-37.5] mg/dL; P<0.001). Multivariable regression analysis indicated that younger age and higher glucose and lactate levels were significantly associated with the early onset of NPE in patients with SAH. The present findings indicate that an increased serum lactate level, occurring within 1 hour of the ictus, is an independent factor associated with the early onset of NPE. Multicenter prospective studies are required to confirm our results.

Clinical and therapeutic profile of patients who are victims of non-traumatic subarachnoid hemorrhage in the unified health system in the municipality of Barbacena - MG

Introduction: The non-traumatic subarachnoid hemorrhage (HSANT) remains with unchanged incidence rates, in contrast to the reduction in the occurrence of other cerebrovascular disorders. It shows high morbidity and mortality and causes disability in young people. Objective: to evaluate the clinical characteristics and treatment of non-traumatic HSA victims. Method: cross-sectional and descriptive study of 91 medical records from victims of non-traumatic HSA undergoing cerebral angiography in the Unified Health System (SUS) in Barbacena, between 2006 and 2010. Result: 55.0% of HSANT occurred in women; 48.3% between 31 and 50 years of age, with an average of 47 years old; explosive headache was the initial complaint in 84.6%; 71.2% hypertense and 65.9% due to aneurysm. Hydrocephalus was developed in 100% of patients undergoing surgery after the 16 th day after surgery; 100% of those infected remained hospitalized for more than six days. Conclusion: HSANT predominates in women between 31 and 50 years of age, having the explosive headache as the main complaint and aneurysmal disease as the main etiology. Hypertension was the major risk factor. The risk of infection is higher in patients admitted for more than six days, and the development of hydrocephalus seems to be associated with late surgical treatment.

Hyponatremia With Intracranial Disease: Not Often Cerebral Salt Wasting

The degree to which hyponatremia occurs primarily as a result of natriuresis has remained controversial for many years. Cerebral salt wasting (CSW) was first proposed by Peters et al (1) in 1950 as an explanation for the natriuresis and hyponatremia that sometimes accompany intracranial disease, particularly subarachnoid hemorrhage (SAH), in which up to one-half of patients often develop hyponatremia. After the first clinical description of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in 1957, such patients were generally assumed to have hyponatremia secondary to nonosmotic arginine vasopressin (AVP) secretion with a secondary natriuresis (2).However, bothclinical andexperimentaldata have suggested that some patients with SAH and other intracranial diseases may actually have a primary natriuresis leading to extracellular fluid (ECF) volume contraction rather than SIADH (3, 4), in which case the elevated measured plasma AVP levels may actually be physiologically appropriate for the degree of volume contraction present. The major clinical question as to the frequency of CSW as a primary or contributory cause of hyponatremia is critically dependent on the criteria used to assess the ECF volume status of these patients; opponents argue that there is insufficient evidence of true hypovolemia despite ongoing natriuresis (5), whereas proponents argue that the combined measures that have traditionally been used to estimate ECF volume do, in fact, support the presence of hypovolemia in many such cases (6). Noticeably lacking from this ongoing debate has been carefully done clinical research that critically assesses the cause of hyponatremia in neurological diseases such as SAH. The article by Hannon et al (7) in this issue of the JCEM addresses this deficiency by carefully studying 100 patients with acute nontraumatic aneurysmal SAH with serial assessments of clinical ECF volume status by a single experienced clinician and measurements of plasma cortisol, AVP, and brain natriuretic peptide (BNP). Their results demonstrated the expected high incidence of hyponatremia in 49% of the patients; but when all analyses were considered, the cause of the hyponatremia was attributable to SIADH in 71.4% of patients and acute glucocorticoid deficiency in 8.2%, with the remaining cases caused by incorrect iv fluid administration or hypovolemia. Most significantly, no cases were found that met historically accepted criteria for a diagnosis of CSW. Thus, as opposed to the current trend to diagnose CSW with a relatively high frequency in neurological cases, this careful analysis indicates that CSW is an exceedingly rare cause of the hyponatremia in SAH and, by analogy, likely in other intracranial disorders as well. Since the original cases studied by Schwartz and Bartter, increased renal sodium excretion has been viewed as one of the cardinal manifestations of SIADH, indeed one that later became embedded in the requirements for its diagnosis (8). However, next to the use of the term “inappropriate,” probably no other aspect of SIADH has been so widely misinterpreted. Demonstration that the natriuresis accompanying administration of antidiuretic hormone is not due to AVP itself, but rather is due to the volume expansion produced as a result of water retention, was unequivocally shown by Leaf et al (9) even before the description of the clinical occurrence of SIADH. Subsequent metabolic balance studies demonstrated that excess urinary sodium excretion and a negative sodium balance occurred during the development of hyponatremia in patients with SIADH, but eventually urinary sodium excre-

CALCITONIN GENE-RELATED PEPTIDE IN SERUM AFTER SPONTANEOUS SUBARACHNOID HEMORRHAGE

Endogenous Calcitonin Gene-Related Peptide (CGRP) stored in perivascular nerve fibers around the cerebral arteries mediates vasodilation and regulates cerebral blood flow under physiological conditions. Increased levels of CGRP have been continually reported in patients with migraine, but the role of CGRP in the pathophysiology of Subarachnoid Hemorrhage (SAH) has not yet been sufficiently evaluated. Over 10 days, serum was prospectively collected from 33 consecutive patients (17 women, 16 men; mean age 52.8 years) with spontaneous non-traumatic SAH. All patients were graded III or IV according to the Fisher Score. CGRP levels were determined by means of an Enzyme-Immunosorbent Assay (EIA). CGRP concentrations were correlated to (1) the anatomical localization of the aneurysm (anterior circulation or posterior circulation), (2) the treatment modality (clipped group, coiled group, or untreated group) and (3) the rate of ischemia determined by computed tomography (ischemia group, non-ischemia group, or iatrogenic ischemia group). (1) Anatomical localization: CGRP levels were significantly higher in patients with a ruptured aneurysm of the anterior circulation (p<0.001). (2) Treatment modality: CGRP levels differed significantly between the groups (coil group, clip group, or untreated group; p<0.001). The highest levels of CGRP were detected in the coil group and the lowest levels in the untreated group. About (3) Ischemia: CGRP levels differed significantly between the three groups (ischemia group, non-ischemia group, or iatrogenic ischemia group; p = 0.038). The highest levels of CGRP were found in the ischemia group. The maximum levels of CGRP in serum were found for patients with a ruptured aneurysm of the anterior circulation and subsequent ischemia treated by endovascular coiling. These findings support the theory that CGRP is produced and excessively released to counteract cerebral vasospasm and subsequent ischemia. Presumably, the serum levels of CGRP are affected by the anatomical localization of the aneurysm and can be stimulated by any endoluminal manipulation of the parent artery.

Hyponatremia Following Mild/Moderate Subarachnoid Hemorrhage Is Due To SIAD and Glucocorticoid Deficiency and not Cerebral Salt Wasting

Hyponatremia is common after acute subarachnoid hemorrhage (SAH) but the etiology is unclear and there is a paucity of prospective data in the field. The cause of hyponatremia is variously attributed to the syndrome of inappropriate antidiuresis (SIAD), acute glucocorticoid insufficiency, and the cerebral salt wasting syndrome (CSWS). The objective was to prospectively determine the etiology of hyponatremia after SAH using sequential clinical examination and biochemical measurement of plasma cortisol, arginine vasopressin (AVP), and brain natriuretic peptide (BNP). This was a prospective cohort study. The setting was the National Neurosurgery Centre in a tertiary referral centre in Dublin, Ireland. One hundred patients with acute nontraumatic aneurysmal SAH were recruited on presentation. Clinical examination and basic biochemical evaluation were performed daily. Plasma cortisol at 0900 hours, AVP, and BNP concentrations were measured on days 1, 2, 3, 4, 6, 8, 10, and 12 following SAH. Those with 0900 hours plasma cortisol<300 nmol/L were empirically treated with iv hydrocortisone. Plasma sodium concentration was recorded daily along with a variety of clinical and biochemical criteria. The cause of hyponatremia was determined clinically. Later measurement of plasma AVP and BNP concentrations enabled a firm biochemical diagnosis of the cause of hyponatremia to be made. Forty-nine of 100 developed hyponatremia<135 mmol/L, including 14/100<130 mmol/L. The cause of hyponatremia, and determined by both clinical examination and biochemical hormone measurement, was SIAD in 36/49 (71.4%), acute glucocorticoid insufficiency in 4/49 (8.2%), incorrect iv fluids in 5/49 (10.2%), and hypovolemia in 5/49 (10.2%). There were no cases of CSWS. The most common cause of hyponatremia after acute nontraumatic aneurysmal SAH is SIAD. Acute glucocorticoid insufficiency accounts for a small but significant number of cases. We found no cases of CSWS.

Detection of Gnathostoma spinigerum Antibodies in Sera of Non-Traumatic Subarachnoid Hemorrhage Patients in Thailand

Gnathostoma spinigerum can cause subarachnoid hemorrhage (SAH). The detection of specific antibodies in serum against G. spinigerum antigen is helpful for diagnosis of neurognathostomiasis. There is limited data on the frequency of G. spinigerum infection in non-traumatic SAH. A series of patients diagnosed as non-traumatic SAH at the Srinagarind Hospital, Khon Kaen University, Thailand between January 2011 and January 2013 were studied. CT or MR imaging of the brain was used for diagnosis of SAH. Patients were categorized as aneurysmal subarachnoid hemorrhage (A-SAH) or non-aneurysmal subarachnoid hemorrhage (NA-SAH) according to the results of cerebral angiograms. The presence of specific antibodies in serum against 21- or 24-kDa G. spinigerum antigen was determined using the immunoblot technique. The detection rate of antibodies was compared between the 2 groups. Of the 118 non-traumatic SAH patients for whom cerebral angiogram and immunoblot data were available, 80 (67.8%) patients had A-SAH, whereas 38 (32.2%) had NA-SAH. Overall, 23.7% were positive for specific antibodies against 21- and/or 24-kDa G. spinigerum antigen. No significant differences were found in the positive rate of specific antibodies against G. spinigerum in both groups (P-value=0.350).

Repeated neurovascular imaging in subarachnoid hemorrhage when initial studies are negative

Approximately 15% of patients with non-traumatic subarachnoid hemorrhage have no causative lesion identified on their initial angiogram. We present two patients with non-traumatic subarachnoid hemorrhage with negative initial angiograms who were subsequently found to have small basilar perforator aneurysms on delayed neurovascular imaging. We discuss the possible mechanisms for false negative diagnostic cerebral angiograms. These patients support the current standard of care with repeat angiography in cases of subarachnoid hemorrhage when no causative lesion can be identified on initial neurovascular imaging.

Management of subarachnoid hemorrhage

Spontaneous non-traumatic subarachnoid hemorrhage (SAH), caused by the intracranial aneurysm rupture, is a severe cerebrovascular emergency. Cerebral and extracerebral complications are frequently associated to SAH and increase significantly the morbidity and mortality. SAH is a severe medical condition in which outcome can be considerably influenced by an early aggressive expert care. Guidelines have been recently published and offer a framework for treatment of SAH patients. The intensivists’ role in the management of SAH victims is crucial and encompasses prompt diagnosis, identification, and treatment of intracranial (as hydrocephalus, intracranial hypertension, metabolic and electric disturbances, vasospasm and delayed cerebral ischemia) along with extracranial complications (mainly cardiovascular, respiratory, endocrine…).

Nontraumatic Subarachnoid Hemorrhage in Maintenance Dialysis Hospitalizations

Subarachnoid hemorrhage (SAH) is associated with high mortality, and patients on maintenance dialysis have been shown to be at higher risk for stroke including SAH. However, the outcomes of patients on maintenance dialysis with SAH are not well known. This study was designed to look at incidence and outcomes of SAH in those on maintenance dialysis. Using the Nationwide Inpatient Sample Database, hospitalizations with nontraumatic SAH were identified. Age-adjusted incidence rates were calculated by direct standardization to the 2000 US standard population. Logistic regression was used to assess the risk factors for mortality. Of an estimated 149,091 hospitalizations with SAH, 1631 patients (10.9%) were on maintenance dialysis. Unadjusted incidence of SAH hospitalizations was higher in maintenance dialysis than in the general population (73.5 versus 11.2 per 100,000 population), and similar results were seen on age-adjusted analysis. The unadjusted all-cause inpatient mortality rate for SAH admissions was higher in maintenance dialysis versus the general population (38.4% versus 21.9%; P<0.001). Maintenance dialysis was an independent predictor of mortality (odds ratio, 2.48; 95% confidence interval, 1.85-3.34), although other significant predictors of mortality were similar in both subgroups. Incidence of SAH hospitalizations has been relatively stable during the study period, but mortality seems to be decreasing. SAH hospitalizations are more common and associated with higher mortality in patients on maintenance dialysis than in the general population. Although being on maintenance dialysis is an independent predictor for mortality in patients with SAH, other predictors of mortality evaluated in this study are not necessarily different between the 2 groups.

Trends in the mortality of non-traumatic subarachnoid hemorrhage in Colombia: a 10-year analysis of a nationwide registry

To assess trends in mortality from 1999 to 2008 resulting from non-traumatic subarachnoid hemorrhage (SAH) in the Colombian population. This population-based study analyzed all deaths by assuming a Poisson model. Subarachnoid hemorrhage-related deaths showed a statistically significant increase of 1.6% per year (p<0.001). The age-standardized analysis demonstrated an increased mortality trend of 3.3% per year (p<0.001) in people older than 70 years, but a decreased mortality trend in people younger than 50. It remained stable in patients 50-69 years old. The overall SAH-related mortality rate in Colombia has increased because increased mortality among the elderly has been counterbalanced by reduced mortality rates in younger age groups. These disparities may reflect epidemiologic transition, treatment inequities, or a less favorable comorbid profile.

Frequency of Unruptured Cerebral Aneurysms in Chinese Patients

Cerebral aneurysms are the leading cause of nontraumatic subarachnoid hemorrhage. Identifying and, in selected cases, treating unruptured aneurysms

Nontraumatic Convexity Subarachnoid Hemorrhage: Different Etiologies and Outcomes

Nontraumatic convexity subarachnoid hemorrhage (cSAH) is a rarely reported condition with multiple etiologies. We report the clinical presentation, imaging findings, etiologies, and long-term outcomes of a case series of cSAH. We retrospectively analyzed consecutive cases of cSAH, admitted at a Stroke Unit of a tertiary hospital (January 2006 to March 2012). Recorded variables were demographics, clinical presentation, complementary investigation, etiology, and outcome. We included 15 patients (9 men, median age of 65years), 7% of the 210 nontraumatic SAH patients in this period. The most common clinical manifestation was a focal neurologic deficit. Predominant location of the cSAH was frontal. In 5 cases, there was a clinical significant internal carotid artery (ICA) atheromatous stenosis, ipsilateral to cSAH. Two patients had a possible cerebral amyloid angiopathy (CAA) at presentation. There were 2 cases of reversible cerebral vasoconstriction syndrome, 1 cerebral venous thrombosis, 2 dural fistulae, and 3 undetermined. Short-term outcomes were good in most patients. At follow-up (24.3months), 2 of the patients with undetermined etiology had a lobar hematoma conferring a severe disability, and the diagnosis of CAA was made. There were no other relevant events or added disability in the other patients. Significant ICA atherosclerotic stenosis was the most frequent cause of cSAH in our series, reinforcing that cSAH should prompt vascular imagiological evaluation including cervical vessels. Outcomes in cSAH seem to be related to etiology. Patients with undetermined etiology should be followed up because cSAH may be the first manifestation of CAA.