Adult ; Cerebral Angiography ; Female ; Humans ; Intracranial Aneurysm ; complications ; diagnostic imaging ; Lupus Erythematosus, Systemic ; complications ; diagnostic imaging ; Subarachnoid Hemorrhage ; diagnosis ; diagnostic imaging ; etiology ; Young Adult

Gastrodin is a phenolic glycoside that has been demonstrated to provide neuroprotection in preclinical models of central nervous system disease, but its effect in subarachnoid hemorrhage (SAH) remains unclear. In this study, we showed that intraperitoneal administration of gastrodin (100 mg/kg per day) significantly attenuated the SAH-induced neurological deficit, brain edema, and increased blood-brain barrier permeability in rats. Meanwhile, gastrodin treatment significantly reduced the SAH-induced elevation of glutamate concentration in the cerebrospinal fluid and the intracellular Ca overload. Moreover, gastrodin suppressed the SAH-induced microglial activation, astrocyte activation, and neuronal apoptosis. Mechanistically, gastrodin significantly reduced the oxidative stress and inflammatory response, up-regulated the expression of nuclear factor erythroid 2-related factor 2, heme oxygenase-1, phospho-Akt and B-cell lymphoma 2, and down-regulated the expression of BCL2-associated X protein and cleaved caspase-3. Our results suggested that the administration of gastrodin provides neuroprotection against early brain injury after experimental SAH.
Animals ; Apoptosis ; drug effects ; Astrocytes ; drug effects ; metabolism ; Benzyl Alcohols ; administration & dosage ; Blood-Brain Barrier ; drug effects ; metabolism ; Brain ; drug effects ; metabolism ; Brain Edema ; etiology ; prevention & control ; Calcium ; metabolism ; Glucosides ; administration & dosage ; Glutamic Acid ; metabolism ; Male ; Microglia ; drug effects ; metabolism ; Neurons ; drug effects ; Neuroprotective Agents ; administration & dosage ; Oxidative Stress ; drug effects ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage ; complications ; metabolism ; prevention & control

PURPOSE: Contrast-induced acute kidney injury (CI-AKI) is associated with poor outcomes after percutaneous coronary intervention. However, CI-AKI has rarely been evaluated within the neurovascular field. The aim of this study was to investigate the incidence and clinical implication of CI-AKI after coil embolization in patients with an aneurysmal subarachnoid hemorrhage (aSAH). MATERIALS AND METHODS: Between January 2005 and March 2016, 192 patients who underwent coil embolization were enrolled in this study. CI-AKI was defined as an increase from baseline serum creatinine concentration of >25% or >0.5 mg/dL within 72 hours after coil embolization. A poor clinical outcome was defined as a score of ≥3 on the modified Rankin Scale at one-year post-treatment. RESULTS: A total of 16 patients (8.3%) died as a result of medical problems within one year. CI-AKI was identified in 14 patients (7.3%). Prominent risk factors for one-year mortality included CI-AKI [odds ratio (OR): 16.856; 95% confidence interval (CI): 3.437–82.664] and an initial Glasgow Coma Scale (GCS) score ≤8 (OR: 5.565; 95% CI: 1.703–18.184). A poor clinical outcome was associated with old age (≥65 years) (OR: 7.921; 95% CI: 2.977–21.076), CI-AKI (OR: 11.281; 95% CI: 2.138–59.525), an initial GCS score ≤8 (OR 31.02; 95% CI, 10.669–90.187), and a ruptured aneurysm (p=0.016, OR: 4.278) in posterior circulation. CONCLUSION: CI-AKI seems to be an independent predictor of the overall outcomes of aSAH after endovascular treatment.
Acute Kidney Injury/chemically induced ; Acute Kidney Injury/diagnostic imaging ; Acute Kidney Injury/etiology ; Acute Kidney Injury/mortality ; Adult ; Aged ; Aged, 80 and over ; Aneurysm/complications ; Aneurysm/diagnostic imaging ; Aneurysm/therapy ; Angiography ; Contrast Media/adverse effects ; Embolization, Therapeutic/adverse effects ; Female ; Humans ; Incidence ; Male ; Middle Aged ; Subarachnoid Hemorrhage/complications ; Subarachnoid Hemorrhage/diagnostic imaging ; Subarachnoid Hemorrhage/therapy ; Treatment Outcome ; Young Adult

Fluoxetine, an anti-depressant drug, has recently been shown to provide neuroprotection in central nervous system injury, but its roles in subarachnoid hemorrhage (SAH) remain unclear. In this study, we aimed to evaluate whether fluoxetine attenuates early brain injury (EBI) after SAH. We demonstrated that intraperitoneal injection of fluoxetine (10 mg/kg per day) significantly attenuated brain edema and blood-brain barrier (BBB) disruption, microglial activation, and neuronal apoptosis in EBI after experimental SAH, as evidenced by the reduction of brain water content and Evans blue dye extravasation, prevention of disruption of the tight junction proteins zonula occludens-1, claudin-5, and occludin, a decrease of cells staining positive for Iba-1, ED-1, and TUNEL and a decline in IL-1β, IL-6, TNF-α, MDA, 3-nitrotyrosine, and 8-OHDG levels. Moreover, fluoxetine significantly improved the neurological deficits of EBI and long-term sensorimotor behavioral deficits following SAH in a rat model. These results indicated that fluoxetine has a neuroprotective effect after experimental SAH.
Animals ; Apoptosis ; drug effects ; Blood-Brain Barrier ; drug effects ; Brain Edema ; drug therapy ; etiology ; Cytokines ; genetics ; metabolism ; Disease Models, Animal ; Fluoxetine ; pharmacology ; therapeutic use ; In Situ Nick-End Labeling ; Male ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Pain Measurement ; Psychomotor Performance ; drug effects ; RNA, Messenger ; metabolism ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage ; complications ; drug therapy ; pathology ; Time Factors ; Vasospasm, Intracranial ; drug therapy ; etiology

OBJECTIVEWe aim to explore the potential association between serum gamma-glutamyl transferase levels and functional outcome after aneurysmal subarachnoid hemorrhage in a Chinese population.

METHODSA total of 386 aneurysmal subarachnoid hemorrhage patients were included in the study from September 2007 to February 2015. Baseline serum gamma-glutamyl transferase levels and 6-month follow-up functional outcomes were determined. A poor outcome was defined as a modified ranking scale score of ⋝ 3. The multivariable logistic model was used to analyze the relationship between serum gamma-glutamyl transferase and clinical outcomes after aneurysmal subarachnoid hemorrhage.

RESULTSThe adjusted poor outcome rates of patients with gamma-glutamyl transferase levels of < 30 U/L, 30-50 U/L and ⋝ 50 U/L were 16.7%, 19.6%, and 34.4%, respectively (P < 0.01). The age-sex and multivariable adjusted odds ratios (95% confidence intervals) of poor prognosis comparing the top group (⋝ 50 U/L) with the lowest group (< 30 U/L) were 5.76 (2.74-12.13), 6.64 (2.05-21.52), and 6.36 (1.92-21.02). A significant linear trend existed between gamma-glutamyl transferase level and aneurysmal subarachnoid hemorrhage prognosis. This association was also observed among nondrinkers.

CONCLUSIONPatients with higher gamma-glutamyl transferase levels were more likely to have a poor prognosis. Serum gamma-glutamyl transferase can be considered to be an independent predictor of functional outcomes after aneurysmal subarachnoid hemorrhage.

Aged ; Female ; Follow-Up Studies ; Gene Expression Regulation, Enzymologic ; Humans ; Male ; Middle Aged ; Predictive Value of Tests ; Subarachnoid Hemorrhage ; blood ; complications ; gamma-Glutamyltransferase ; blood

Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). This study investigated the role of glucose-regulated protein 78 (GRP78) in EBI after SAH. Male Sprague-Dawley rats (n=108) weighing 260±40 g were divided into control, sham-operated, and operated groups. Blood was injected into the prechiasmatic cistern of rats in the operated group. Neurological scores, ultrastructures of neurons, apoptosis, and GRP78 expression in the hippocampus were examined using Garcia scoring system, transmission electron microscopy, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling, and Western blotting at 1, 6, 12, 24, 48, and 72 h after SAH, respectively. The results showed that neurological scores were significantly decreased in the operated group as compared with those in control and sham-operated groups at 12, 24, 48, and 72 h. Metachromatin, chromatin pyknosis at the edge, endoplasmic reticulum swelling, and invagination of nuclear membrane were observed at 24 h in the operated group, indicating the early morphological changes of apoptosis. The number of apoptotic cells was significantly increased in the operated group as compared with that in control and sham-operated groups at 6, 12, 24, 48, and 72 h. The GRP78 protein expression levels in the operated group were significantly elevated at all time points and reached the peak at 12 h. GRP78 expression was positively associated with apoptosis cells and negatively with neurological scores. In conclusion, EBI was demonstrated to occur after SAH and GRP78 was involved in the development of EBI after SAH.
Animals ; Apoptosis ; Brain Injuries ; complications ; metabolism ; pathology ; Chromatin ; pathology ; Endoplasmic Reticulum Stress ; Heat-Shock Proteins ; genetics ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage ; etiology ; metabolism ; pathology

OBJECTIVETo investigate the risk factors of progressive brain contusion and to evaluate their impact on patients' outcome.

METHODSOne hundred and thirty two patients with traumatic brain contusion were enrolled in the study, including 70 cases with progressive contusion and 62 cases with non-progressive contusion. The risk factors were investigated with univariate and multivariate Logistic regression analysis.

RESULTSThe univariate analysis showed that Glasgow Coma Score (GCS) at admission, contusion volume at the first brain CT scans, midline shift, combined with skull fracture, subarachnoid hemorrhage, epidural hematoma, subdural hematoma, location of brain contusion, D-dimer levels, combined with type 2 diabetes were associated with progressive brain contusion. Multivariate Logistic regression analysis showed that GCS at admission, contusion volume at the first CT scans, combined with subarachnoid hemorrhage, combined with type 2 diabetes were the independent risk factors for disease progression. The outcome in the progressive group was more aggravated than that in non-progressive group (P = 0.001).

CONCLUSIONPatients with disturbance of consciousness, the larger contusion volume, combined with subarachnoid hemorrhage and diabetes are at risk for progressive brain contusion and unfavorable outcome.

Brain Injuries ; complications ; pathology ; Diabetes Mellitus, Type 2 ; complications ; Disease Progression ; Fibrin Fibrinogen Degradation Products ; metabolism ; Glasgow Coma Scale ; Hematoma, Epidural, Cranial ; complications ; Hematoma, Subdural ; complications ; Humans ; Risk Factors ; Subarachnoid Hemorrhage ; complications ; Tomography, X-Ray Computed

OBJECTIVETo investigate risk factors for the occurrence of shunt-dependent hydrocephalus in patients with aneurysmal subarachnoid hemorrhage (aSAH).

METHODSA cohort of 136 consecutive patients who were treated for ruptured aneurysms within 72 h after onset of aSAH from January 2011 to January 2013 were retrospectively analyzed. Lumbar drainage was performed during the surgery in all patients. The risk factors of shunt-dependent hydrocephalus were analyzed.

RESULTSOf 136 patients, 23 (16.91%) underwent shunt operation to treat shunt-dependent hydrocephalus. Univariate analysis showed that Hunt-Hess grade at admission (P<0.01), Fisher grade (P<0.01), the presence of intraventricular hemorrhage (P<0.01), location of ruptured aneurysm (P=0.001), and the average daily volume of cerebrospinal fluid drainage (CSF) (P=0.047) were associated with shunt-dependent hydrocephalus.

CONCLUSIONThe aSAH patients with poor Hunt-Hess grade at admission, high Fisher grade, the presence of intraventricular hemorrhage, ruptured aneurysm in posterior circulation, and abnormal average daily volume of CSF are more likely to develop shunt-depended hydrocephalus.

Adult ; Aged ; Aneurysm, Ruptured ; complications ; Arteriovenous Shunt, Surgical ; adverse effects ; Female ; Humans ; Hydrocephalus ; etiology ; prevention & control ; Intracranial Aneurysm ; complications ; Male ; Middle Aged ; Retrospective Studies ; Risk Factors ; Subarachnoid Hemorrhage ; etiology ; surgery

A 58-year-old Indian woman presented with asystole after an episode of haemetemesis, with a patient downtime of 20 mins. After initial resuscitation efforts, computed tomography of the brain, obtained to evaluate neurological injury, demonstrated evidence of severe hypoxic ischaemic brain injury. The imaging features of hypoxic ischaemic brain injury and the potential pitfalls with regard to image interpretation are herein discussed.
Adolescent ; Brain Ischemia ; diagnosis ; diagnostic imaging ; Cerebellum ; diagnostic imaging ; Critical Care ; Female ; Heart Arrest ; diagnosis ; diagnostic imaging ; Humans ; Male ; Middle Aged ; Shock, Cardiogenic ; complications ; Subarachnoid Hemorrhage ; diagnosis ; diagnostic imaging ; Tomography, X-Ray Computed

OBJECTIVE: To investigate the relation between the expression of tPA, MMP-2, MMP-9 and AEG-1 in the human brain tissue and the ethanol concentration under the acute alcohol poison, and to analyze the role of alcohol and trauma in the mechanism of death of subarachnoid hemorrhage. METHODS: Fifteen real cases were collected in this study. The brain tissues were researched by histological examination and the concentration of ethanol in heart blood were detected. The tPA, MMP-2, MMP-9 and AEG-1 in brainstem, brain and cerebellum were observed respectively by immunohistochemistry. RESULTS: In alcohol poisoning groups with or without trauma, the acute alcohol toxicity resulted in the swelling of brain tissues. The tPA, MMP-2, MMP-9 and AEG-1 of brainstem, brain and cerebellum showed high expression in alcohol victims, and the tPA in cerebellum showed no difference. The expression of the MMP-2, MMP-9 and AEG-1 showed good relation with the ethanol concentration in blood (P < 0.05, r > 0.6). CONCLUSION The expressions of tPA, MMP-2, MMP-9 and AEG-1 are significant higher in alcohol victims, and expressions of MMP-2 and MMP-9 and AEG-1 have positive correlation with the alcohol concentration. The alcohol has acute toxicity to brain cells.
Alcohol Drinking/adverse effects* ; Brain ; Cell Adhesion Molecules/metabolism* ; Craniocerebral Trauma/etiology* ; Death ; Ethanol/poisoning* ; Heart/drug effects* ; Humans ; Matrix Metalloproteinase 2/metabolism* ; Matrix Metalloproteinase 9/metabolism* ; Membrane Proteins ; RNA-Binding Proteins ; Subarachnoid Hemorrhage/complications*