RATIONALE/OBJECTIVE

Aneurysmal subarachnoid hemorrhage (aSAH) may be associated with meteorologic factors in temperate countries. The authors aimed to investigate the relationship between meteorologic factors and aSAH admissions in the Philippines, a tropical country with two seasons: rainy and dry.

A census review of aSAH admissions from 2015 to 2019 at a tertiary hospital was performed. Meteorologic data were collected for the same time period, and statistical analysis was performed.

A total of 660 patients were admitted for aSAH, 275 and 385 during the rainy and dry seasons, respectively. August and October had the greatest number of mean admissions (13.2) while February had the least (6.2). There was a moderate positive correlation between aSAH admissions and mean temperature. Negligible to weak negative correlations were seen between aSAH admissions and humidity, barometric pressure and precipitation. However, there was no correlation on regression analysis.

There were no significant differences in aSAH admissions between rainy and dry seasons. The authors found an increase in aSAH admissions during months with higher temperatures and HI, and weak to negligible negative correlations between aSAH admissions and humidity, barometric pressure, and precipitation. These findings may inform health care facilities in terms of readiness for aSAH admissions.

We present a 66-year-old male presenting with sudden onset of headache. Medical decompression was done and neuroimaging of plain cranial CT angiogram (CTA) and CT venogram (CTV) showed components of subarachnoid hemorrhage, intracerebral hemorrhage and hyperdense appearance of the superior sagittal sinus and proximal left transverse sinus. The following were done to look for etiologic factors: 1. fungal swab to determine the cause of the intracerebral hemorrhage secondary to venous thrombosis as the patient presented with a chronic history of sinusitis, 2. coagulopathy workup to look for a hypercoagulable state, and 3. workup for systemic disease of autoimmune in etiology. Anticoagulation was safely initiated within several days given the regression of the intracerebral hemorrhage along with stable findings of subarachnoid hemorrhage. Here we report cerebral venous sinus thrombosis rarely presenting as acute subarachnoid hemorrhage and intracerebral hemorrhage.
Subarachnoid Hemorrhage ; Cerebral Hemorrhage

OBJECTIVE

This study aims to determine the clinical outcome of patients diagnosed with aneurysmal subarachnoid hemorrhage and their association with grading scores.

The authors conducted a single-center cross- sectional study involving patients diagnosed with aneurysmal subarachnoid hemorrhage admitted at Vicente Sotto Memorial Medical Center, Cebu City, Philippines from January 2015 to December 2020.

Out of 240 patients diagnosed with ruptured aneurysms, 215 underwent definitive treatment. The average age was 56 years old, predominantly female with a ratio of 2:1. Most patients were classified with admitting Hunt and Hess grading scale of 2-3 and Fisher grading scale of 3. Females had increased incidence of multiple aneurysms (ratio 3:1) compared to male sex. Among patients, 197 underwent clipping while 18 underwent coiling. Clinical Outcome revealed that 84% had good outcome while 16% had poor outcome. The association between Hunt and Hess grading scale and patient outcome was statistically significant (p < 0.001) as well as for Fisher grading scale and patient outcome (p < 0.001). Fisher grading scale and incidence of clinical vasospasm were also significant (p =0.004).

Higher scores for Hunt and Hess grading scale and Fisher grading scale were associated with poor outcome. Higher Fisher grading scale was associated with the occurrence of clinical vasospasm among patients with ruptured aneurysm. Female sex also had higher aneurysm incidence with complex and more multiple aneurysms as compared to male sex.

OBJECTIVES: Stroke has become the leading cause of death and disability among adults in China. This study aims to analyze the disease burden based on gender and age and the risk factors for stroke subtypes in China 2019, and to provide reference for targeted stroke prevention and control. METHODS: Based on 2019 data of the Global Burden of Disease (GBD), the gender and age in patients with different stroke subtypes (ischemic stroke, intracranial hemorrhage, subarachnoid hemorrhage) in China 2019 was described by using disability-adjusted life years (DALY), and attributable burden of related risk factors was analyzed. RESULTS: In 2019, the burden of intracranial hemorrhage was the heaviest one in China, resulting in 22.210 6 million person years of DALY, following by ischemic stroke and subarachnoid hemorrhage, resulting in 21.393 9 and 2.344 7 million person years of DALY, respectively. Among them, except the 0-14 age group, the disease burden of different subtypes of stroke in men was higher than that in women. The disease burden of ischemic stroke was increased with age in both men and women, with the heaviest disease burden in ≥70 years group. The disease burden of intracranial hemorrhage and subarachnoid hemorrhage was the heaviest in males aged 50-69 years old, and in females aged ≥70 years and 50-69 years, respectively. Metabolic factors were the main risk factors in all ages of different stroke subtypes, and the most important risk factor was high systolic blood pressure. Other risk factors were different between men and women. Smoking, high body mass index, high low-density lipoprotein, and outdoor particulate matter pollution were the main risk factors for stroke in men, while high body mass index, outdoor particulate matter pollution, and high fasting blood glucose were the main risk factors of stroke in women. The main risk were different among different age groups. CONCLUSIONS The burden and attributable risk factors for different stroke subtypes are discrepancy in different gender and age groups. Targeted interventions should be conducted in the future to reduce the burden of stroke.
Male ; Adult ; Humans ; Female ; Infant, Newborn ; Infant ; Child, Preschool ; Child ; Adolescent ; Middle Aged ; Aged ; Subarachnoid Hemorrhage/epidemiology* ; Quality-Adjusted Life Years ; Cost of Illness ; Stroke/etiology* ; Risk Factors ; China/epidemiology* ; Particulate Matter ; Ischemic Stroke ; Intracranial Hemorrhages/etiology*

Headaches are a common presentation in the emergency department (ED). Even though not all are potentially serious, some such as subarachnoid hemorrhage (SAH) can be more dangerous than others. SAH is a medical emergency with an almost 50% mortality rate. It is crucial not to miss the diagnosis of SAH, as a missed or delayed diagnosis can be severely detrimental. It classically presents as thunderclap headache, a severe, sudden-onset headache. There are various approaches in diagnosing or excluding SAH, which is classically done by performing a computed tomography (CT) scan followed by a lumbar puncture (LP). But with the improved sensitivity of more modern diagnostic tools, more physicians are in support of changing this classical teaching. The aim of this case report is to review the advantages and disadvantages of LP in diagnosing SAH, along with other diagnostic tools commonly used.
Subarachnoid Hemorrhage ; Spinal Puncture ; Cerebrospinal Fluid

OBJECTIVES: Subarachnoid hemorrhage (SAH) is a serious cerebrovascular disease. Early brain injury (EBI) and cerebral vasospasm are the main reasons for poor prognosis of SAH patients. The specific inhibitor of histone deacetylase 6 (HDAC6), tubastatin A (TubA), has been proved to have a definite neuroprotective effect on a variety of animal models of acute and chronic central nervous system diseases. However, the neuroprotective effect of TubA on SAH remains unclear. This study aims to investigate the expression and localization of HDAC6 in the early stage of SAH, and to evaluate the protective effects of TubA on EBI and cerebral vasospasm after SAH and the underlying mechanisms. METHODS: Adult male SD rats were treated with modified internal carotid artery puncture to establish SAH model. In the first part of the experiment, rats were randomly divided into 6 groups: a sham group, a SAH-3 h group, a SAH-6 h group, a SAH-12 h group, a SAH-24 h group, and a SAH-48 h group. At 3, 6, 12, and 24 h after SAH modeling, the injured cerebral cortex of rats in each group was taken for Western blotting to detect the expression of HDAC6. In addition, the distribution of HDAC6 in the cerebral cortex of the injured side was measured by immunofluorescence double staining in SAH-24 h group rats. In the second part, rats were randomly divided into 4 groups: a sham group, a SAH group, a SAH+TubA_L group (giving 25 mg/kg TubA), and a SAH+TubA_H group (giving 40 mg/kg TubA). At 24 h after modeling, the injured cerebral cortex tissue was taken for Western blotting to detect the expression levels of HDAC6, endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase (iNOS), terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining to detect apoptosis, and hematoxylin and eosin (HE) staining to detect the diameter of middle cerebral artery. RESULTS: The protein expression of HDAC6 began to increase at 6 h after SAH (P<0.05), peaked at 24 h (P<0.001), and decreased at 48 h, but there was still a difference compared with the sham group (P<0.05). HDAC6 is mainly expressed in the cytoplasm of the neurons. Compared with the sham group, the neurological score was decreased significantly and brain water content was increased significantly in the SAH group (both P<0.01). Compared with the SAH group, the neurological score was increased significantly and brain water content was decreased significantly in the SAH+TubA_H group (both P<0.05), while the improvement of the above indexes was not significant in the SAH+TubA_L group (both P>0.05). Compared with the sham group, the expression of eNOS was significantly decreased (P<0.01) and the expressions of iNOS and HDAC6 were significantly increased (P<0.05 and P<0.01, respectively) in the SAH group. Compared with the SAH group, the expression of eNOS was significantly increased, and iNOS and HDAC6 were significantly decreased in the SAH+TubA group (all P<0.05). Compared with the SAH group, the number of TUNEL positive cells was significantly decreased and the diameter of middle cerebral artery was significantly increased in the SAH+TubA group (both P<0.05) . CONCLUSIONS HDAC6 is mainly expressed in neurons and is up-regulated in the cerebral cortex at the early stage of SAH. TubA has protective effects on EBI and cerebral vasospasm in SAH rats by reducing brain edema and cell apoptosis in the early stage of SAH. In addition, its effect of reducing cerebral vasospasm may be related to regulating the expression of eNOS and iNOS.
Rats ; Male ; Animals ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage/drug therapy* ; Vasospasm, Intracranial/metabolism* ; Histone Deacetylase Inhibitors/therapeutic use* ; Neuroprotective Agents/therapeutic use* ; Histone Deacetylase 6/pharmacology* ; Apoptosis ; Brain Injuries/drug therapy*

Introduction: Spontaneous acute subdural hematoma (ASDH) is rare and comprises 2.6% of all ASDH. In one recent study, only 178 spontaneous ASDH were documented. However, only 1 case was attributed to dural arteriovenous fistula (dAVF). Vascular malformations cause less than 10% of subarachnoid hemorrhage (SAH). Spontaneous ASDH and SAH occurring together are extremely rare. Literature is scarce on cases with dAVF of the occipital lobe as a cause of simultaneous spontaneous ASDH and SAH. Objective: This paper aims to present a case of a spontaneous acute subdural hematoma and subarachnoid hemorrhage caused by a dural arteriovenous fistula of the occipital lobe, along with its clinical presentation, diagnosis, and treatment. Case Summary: A 44-year-old Filipino male with no history of trauma presented with severe headache, vomiting, and decreasing sensorium – CT scan revealed acute parenchymal bleed in the left occipital lobe with subarachnoid extension and subdural hematoma in the left fronto-parieto-temporal convexity along the tentorium cerebelli and posterior interhemispheric falx. Due to the location of the lesion seen on the CT scan and the gender distribution, Arteriovenous malformation (AVM) was initially considered, thus proceeded to computed tomography angiogram (CTA) to establish the diagnosis of vascular anomaly, however, revealed dAVF instead. Four-vessel angiogram was done to assess the tributaries of the dAVF and confirmed the diagnosis. Complete obliteration of dAVF of the occipital lobe was done with Onyx Embolization in one session. Conclusion This is the first case of Borden type II, Cognard type IIa+IIb dAVF, as reported in this institution. Although extremely rare as a cause of SAH and ASDH, dAVF should be considered a differential diagnosis in patients with no identifiable common cause of the new onset of severe headache and poor neurologic status.
Subarachnoid Hemorrhage

Insufficient remyelination due to impaired oligodendrocyte precursor cell (OPC) differentiation and maturation is strongly associated with irreversible white matter injury (WMI) and neurological deficits. We analyzed whole transcriptome expression to elucidate the potential role and underlying mechanism of action of lipocalin-2 (LCN2) in OPC differentiation and WMI and identified the receptor SCL22A17 and downstream transcription factor early growth response protein 1 (EGR1) as the key signals contributing to LCN2-mediated insufficient OPC remyelination. In LCN-knockdown and OPC EGR1 conditional-knockout mice, we discovered enhanced OPC differentiation in developing and injured white matter (WM); consistent with this, the specific inactivation of LCN2/SCl22A17/EGR1 signaling promoted remyelination and neurological recovery in both atypical, acute WMI due to subarachnoid hemorrhage and typical, chronic WMI due to multiple sclerosis. This potentially represents a novel strategy to enhance differentiation and remyelination in patients with white matter injury.
Mice ; Animals ; Remyelination/physiology* ; Oligodendrocyte Precursor Cells/metabolism* ; White Matter ; Subarachnoid Hemorrhage/metabolism* ; Lipocalin-2/metabolism* ; Early Growth Response Protein 1/metabolism* ; Oligodendroglia/metabolism* ; Mice, Knockout ; Cell Differentiation/physiology* ; Brain Injuries/metabolism*

OBJECTIVE: To determine whether Schisandrin B (Sch B) attenuates early brain injury (EBI) in rats with subarachnoid hemorrhage (SAH). METHODS: Sprague-Dawley rats were divided into sham (sham operation), SAH, SAH+vehicle, and SAH+Sch B groups using a random number table. Rats underwent SAH by endovascular perforation and received Sch B (100 mg/kg) or normal saline after 2 and 12 h of SAH. SAH grading, neurological scores, brain water content, Evan's blue extravasation, and terminal transferase-mediated dUTP nick end-labeling (TUNEL) staining were carried out 24 h after SAH. Immunofluorescent staining was performed to detect the expressions of ionized calcium binding adapter molecule 1 (Iba-1) and myeloperoxidase (MPO) in the rat brain, while the expressions of B-cell lymphoma 2 (Bcl-2), Bax, Caspase-3, nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated specklike protein containing the caspase-1 activator domain (ASC), Caspase-1, interleukin (IL)-1β, and IL-18 in the rat brains were detected by Western blot. RESULTS: Compared with the SAH group, Sch B significantly improved the neurological function, reduced brain water content, Evan's blue content, and apoptotic cells number in the brain of rats (P<0.05 or P<0.01). Moreover, Sch B decreased SAH-induced expressions of Iba-1 and MPO (P<0.01). SAH caused the elevated expressions of Bax, Caspase-3, NLRP3, ASC, Caspase-1, IL-1β, and IL-18 in the rat brain (P<0.01), all of which were inhibited by Sch B (P<0.01). In addition, Sch B increased the Bcl-2 expression (P<0.01). CONCLUSION Sch B attenuated SAH-induced EBI, which might be associated with the inhibition of neuroinflammation, neuronal apoptosis, and the NLRP3 inflammatory signaling pathway.
Animals ; Apoptosis ; Brain/pathology* ; Brain Injuries/pathology* ; Caspase 3/metabolism* ; Cyclooctanes ; Evans Blue ; Inflammasomes/metabolism* ; Interleukin-18/metabolism* ; Lignans ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism* ; Polycyclic Compounds ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage/drug therapy* ; Water ; bcl-2-Associated X Protein/metabolism*

OBJECTIVE: To investigate the impact of postoperative serious cardiovascular adverse events (CAE) on outcomes of patients undergoing craniotomy for intracranial aneurysm clipping. METHODS: This retrospective cohort study was conducted among the patients undergoing craniotomy for intracranial aneurysm clipping during the period from December, 2016 to December, 2017, who were divided into CAE group and non-CAE group according to the occurrence of Clavien-Dindo grade ≥II CAEs after the surgery. The perioperative clinical characteristics of the patients, complications and neurological functions during hospitalization, and mortality and neurological functions at 1 year postoperatively were evaluated. The primary outcome was mortality within 1 year after the surgery. The secondary outcomes were Glasgow outcome scale (GOS) score at 1 year, lengths of postoperative hospital and intensive care unit (ICU) stay, and Glasgow coma scale (GCS) score at discharge. RESULTS: A total of 361 patients were enrolled in the final analysis, including 20 (5.5%) patients in CAE group and 341 in the non-CAE group. No significant differences were found in the patients' demographic characteristics, clinical history, or other postoperative adverse events between the two groups. The 1-year mortality was significantly higher in CAE group than in the non-CAE group (20.0% vs 5.6%, P=0.01). Logistics regression analysis showed that when adjusted for age, gender, emergency hospitalization, subarachnoid hemorrhage, volume of bleeding, duration of operation, aneurysm location, and preoperative history of cardiovascular disease, postoperative CAEs of Clavien-Dindo grade≥II was independently correlated with 1-year mortality rate of the patients with an adjusted odds ratio of 3.670 (95% CI: 1.037-12.992, P=0.04). The patients with CEA also had a lower GOS score at 1 year after surgery than those without CEA (P=0.002). No significant differences were found in the occurrence of other adverse events, postoperative hospital stay, ICU stay, or GCS scores at discharge between the two groups (P > 0.05). CONCLUSION Postoperative CAEs may be a risk factor for increased 1-year mortality and disability in patients undergoing craniotomy for intracranial aneurysms.
Craniotomy/adverse effects* ; Humans ; Intracranial Aneurysm/surgery* ; Postoperative Period ; Retrospective Studies ; Subarachnoid Hemorrhage/surgery* ; Treatment Outcome