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Background: The reported prevalence of unruptured cerebral aneurysms (UCAs) varies widely. Objective: To measure the prevalence of UCAs by using 3-dimensional time-of-flight magnetic resonance angiography in adults aged 35 to 75 years. Design: Cross-sectional study done between June 2007 and June 2011. Setting: Two communities chosen at random from 2 districts (1 urban and 1 suburban) in Shanghai, China. Participants: 4813 adults aged 35 to 75 years. Measurements: Three-dimensional time-of-flight magnetic resonance angiography, interpreted by 3 observers blinded to the participants' information, was used to identify the location and size of UCAs and to estimate the overall, age-specific, and sex-specific prevalence. Results: 369 UCAs were found in 336 participants (130 men and 206 women); 4477 participants had no evidence of UCAs. The prevalence was 7.0% overall (95% CI, 6.3% to 7.7%), with 5.5% for men (CI, 4.6% to 6.4%) and 8.4% for women (CI, 7.3% to 9.5%). The overall prevalence of UCAs was higher in women than in men (P < 0.001) and peaked at ages 55 to 64 years in men and women. The UCAs were mostly located in the internal carotid artery (81%), and 90.2% had a maximum diameter less than 5 mm. Mean diameter was larger in women than in men (3.7 mm vs. 3.2 mm; P < 0.009). Limitation: Participants were from 2 communities selected from 2 districts in Shanghai, and adults older than 75 years were not studied. Conclusion: The overall prevalence of UCAs was 7.0% in Chinese adults aged 35 to 75 years, and most lesions had a diameter less than 5 mm. Primary Funding Source: National Natural Science Foundation of China. [ABSTRACT FROM AUTHOR]

PTEN (phosphatase and tensin homologue deleted on chromosome 10) is a dual-specificity lipid and protein phosphatase. The loss of PTEN was originally discovered in numerous human cancers. PTEN inhibition by bisperoxovanadium (bpV) reduces neurological damage after ischemic brain injury. The purpose of this study was to identify the optimal neuroprotective dose of bpV when administrated after focal ischemia/reperfusion (I/R) injury in rats. Focal I/R injury was induced using the middle cerebral artery occlusion method. bpV at doses of 0.25, 0.50 and 1.0 mg/kg were injected intraperitoneally just after reperfusion, with saline serving as a vehicle control. A maximal reduction in brain injury was observed with 1.0 mg/kg bpV. This dose of bpV also significantly blocked apoptosis in the penumbral cortex of rats. This beneficial effect was associated with the increasing levels of Akt phosphorylation in the penumbral cortex. These results demonstrate that the pharmacological inhibition of PTEN protects against I/R injury in a dose-dependent manner and the protective effect might be induced through upregulation of the phosphoinositide-3 kinase/Akt pro-survival pathway, suggesting a new therapeutic strategy to combat ischemic brain injury. [ABSTRACT FROM AUTHOR]

Posttraumatic cerebral infarction (PTCI) is a severe secondary insult of head injury and often leads to a poor prognosis. Hemocoagulation disorder is recognized to have important effects on hemorrhagic or ischemic damages. We sought to assess if posttraumatic hemocoagulation disorders were associated with cerebral infarction, and evaluate their influence on outcome among patients with moderate or severe head trauma. In this study, PTCI was observed in 28 (10.57%) of the 265 patients within the first week after injury. In multivariate analysis, the thrombocytopenia (odds ratio (OR) 2.210, 95% confidence interval (CI) 1.065-4.674), abnormal prothrombin time (PT) (OR 3.241, 95% CI 1.090-7.648), D-dimer (>2mg/L) (OR 7.260, 95% CI 1.822-28.076), or disseminated intravascular coagulation (DIC) scores (≥5) (OR 4.717, 95% CI 1.778-12.517) were each independently associated with an increased risk of PTCI. Admission Glasgow Coma Scale (GCS) score, abnormal activated partial thromboplastin time (APTT) and fibrinogen, and D-dimer (>2 mg/L) and DIC scores (≥5) showed an independent predictive effect on poor outcome. In conclusion, recognition of this important treatable cause of PTCI and the associated risk factors may help identify the group at risk and tailor management of patients with TBI. [ABSTRACT FROM AUTHOR]

Recent studies have suggested that endogenous angiogenesis inhibitor endostatin/collagen XVIII might play an important role in the secondary brain injury following traumatic brain injury (TBI). In this study, we measured endostatin/collagen XVIII concentrations serially for 1 week after hospitalization by using the enzyme-linked immunosorbent assay method in the cerebrospinal fluid (CSF) of 30 patients with TBI and a Glasgow Coma Scale (GCS) score of 8 or less on admission. There was a significant trend toward increased CSF levels of endostatin after TBI versus control from 72 h after injury. In patients with GCS score of 3-5, CSF endostatin concentration was substantially higher at 72 h after injury than that in patients with GCS score of 6-8 (P < 0.05) and peaked rapidly at day 5 after injury, but decreased thereafter. The CSF endostatin concentration in 12 patients with an unfavorable outcome was significantly higher than that in 18 patients with a favorable outcome at day 5 (P = 0.043) and day 7 (P = 0.005) after trauma. Receiver operating characteristic curve analysis suggested a reliable operating point for the 7-day CSF endostatin concentration predicting poor prognosis to be 67.29 pg/mL. Our preliminary findings provide new evidence that endostatin/collagen XVIII concentration in the CSF increases substantially in patients with sTBI. Its dynamic change may have some clinical significance on the judgment of brain injury severity and the assessment of prognosis. [ABSTRACT FROM AUTHOR]

Progressive epidural hematoma (PEDH) after head injury is often observed on serial computerized tomography (CT) scans. Recent advances in imaging modalities and treatment might affect its incidence and outcome. In this study, PEDH was observed in 9.2% of 412 head trauma patients in whom two CT scans were obtained within 24 hours of injury, and in a majority of cases, it developed within 3 days after injury. In multivariate logistic regression, patient gender, age, Glasgow Coma Scale (GCS) score at admission, and skull fracture were not associated with PEDH, whereas hypotension (odds ratio (OR) 0.38, 95% confidence interval (CI) 0.17-0.84), time interval of the first CT scanning (OR 0.42, 95% CI 0.19-0.83), coagulopathy (OR 0.36, 95% CI 0.15-0.85), or decompressive craniectomy (DC) (OR 0.46, 95% CI 0.21-0.97) was independently associated with an increased risk of PEDH. The 3-month postinjury outcome was similar in patients with PEDH and patients without PEDH (χ2 = 0.07, P = 0.86). In conclusion, epidural hematoma has a greater tendency to progress early after injury, often in dramatic and rapid fashion. Recognition of this important treatable cause of secondary brain injury and the associated risk factors may help identify the group at risk and tailor management of patients with TBI. [ABSTRACT FROM AUTHOR]

Aims: The advent of three-dimensional (3D) rotational angiography (3D DSA) challenged the role of digital subtraction angiography (DSA) as a "gold standard" in the diagnosis of intracranial aneurysms. In this study, we report our experiences in diagnosing intracranial aneurysms by using 3D DSA with volume rendering (VR) technique, particularly focusing on its role in depicting additional aneurysms missed by 2D DSA. Materials and Methods: One hundred and thirty-eight consecutive patients with known or suspected aneurysms (54 men, 84 women; median age, 55 years; age range, 18-83 years) underwent both conventional DSA and 3D DSA with VR examination simultaneously. The images of 2D DSA or 3D DSA with VR were evaluated by two observers independently for the presence of aneurysms. Then additional aneurysms were decided and depicted. Results: 3D DSA with VR showed 146 aneurysms in 123 (89.1%) of 138 patients and no aneurysms in 15 patients. 2D DSA showed 115 aneurysms in 110 of 137 patients, with one aneurysm in 106 patients each, 2 in 3 patients each and 3 in 1 patient. After reaching a consensus, there were 31 additional aneurysms detected by 3D DSA with VR. 30 aneurysms were <3 mm in maximum diameter with 3 aneurysms ruptured. These additional aneurysms were located in internal carotid artery (ICA, n = 28, 90.32%), anterior cerebral artery (ACA, n = 3, 9.68%). No additional aneurysms were found in either middle cerebral artery (MCA) or vertebrobasilar and posterior cerebral artery (PCA) systems. Conclusions: 3D DSA, especially VR images, not only clearly reveals aneurysms and aneurysmal morphology, but also detects additional aneurysms missed by 2D DSA, especially small aneurysms less than 3 mm. [ABSTRACT FROM AUTHOR]

This study sought to describe and evaluate any relationship between D-dimer values and progressive hemorrhagic injury (PHI) after traumatic brain injury (TBI). In patients with TBI, plasma D-dimer was measured while a computed tomography (CT) scan was conducted as soon as the patient was admitted to the emergency department. A series of other clinical and laboratory parameters were also measured and recorded. A logistic multiple regression analysis was used to identify risk factors for PHI. A cohort of 194 patients with TBI was evaluated in this clinical study. Eighty-one (41.8%) patients suffered PHI as determined by a second CT scan. The plasma D-dimer level was higher in patients who demonstrated PHI compared with those who did not ( P < 0.001. Using a receiver–operator characteristic curve to predict the possibility by measuring the D-dimer level, a value of 5.00 mg/L was considered the cutoff point, with a sensitivity of 72.8% and a specificity of 78.8%. Eight-four patients had D-dimer levels higher than the cut point value (5.0 mg/L); PHI was seen in 71.4% of these patients and in 19.1% of the other patients ( P < 0.01). Factors with P < 0.2 on bivariate analysis were included in a stepwise logistic regression analysis to identify independent risk factors for TBI coagulopathy. Logistic regression analysis showed that the D-dimer value was a predictor of PHI, and the odds ratio (OR) was 1.341 with per milligram per liter ( P = 0.020). The stepwise logistic regression also identified that time from injury to the first CT shorter than 2 h (OR = 2.118, P = 0.047), PLT counts lesser than 100 × 109/L (OR = 7.853, P = 0.018), and Fg lower than 2.0 g/L (OR = 3.001, P = 0.012) were risk factors for the development of PHI. When D-dimer values were dichotomized at 5 mg/L, time from injury to the first CT scan was no longer a risk factor statistically while the OR value of D-dimer to the occurrence of PHI elevated to 11.850( P < 0.001). The level of plasma D-dimer after TBI can be a useful prognostic factor for PHI and should be considered in the clinical management of patients in combination with neuroimaging and other data. [ABSTRACT FROM AUTHOR]

We examined the incidence and timing of posttraumatic cerebral infarction (PTCI) and provide predictive factors for the development of PTCI in patients with moderate or severe traumatic brain injury. Three hundred and fifty-three consecutive patients with moderate or severe head trauma were retrospectively reviewed to determine the incidence and timing of PTCI and to evaluate the effects of age, gender, admission Glasgow Coma Scores (GCS), decompressive craniectomy, brain herniation, and low systolic blood pressure (BP) on the development of cerebral infarction. Risk factors for posttraumatic cerebral infarction were evaluated using logistic regression analysis. PTCI was observed in 36 (11.96%) of the 353 patients, and in a majority of cases, cerebral infarction developed within 2 weeks after injury. Poor admission GCS ( P < 0.01), low systolic BP ( P < 0.01), brain herniation ( P < 0.05), and decompression craniotomy ( P < 0.05) were significantly associated with the development of PTCI. No relationship was found between PTCI and gender or increased age. Posttraumatic cerebral infarction is a relatively common complication in patients with head trauma that develops early in the clinical course. Low GCS, low systolic BP, brain herniation, and decompression craniotomy may be risk factors for PTCI in patients with moderate or severe traumatic brain injury. [ABSTRACT FROM AUTHOR]