Contrast extravasation mimicking intracerebral and intraventricular hemorrhage after intravenous thrombolytic treatment of ischemic stroke: a case report.

BACKGROUND: Although contrast extravasation on follow-up head computed tomography (CT) is frequently visualized after endovascular treatment, this phenomenon is rare after intravenous thrombolytic treatment in patients with acute ischemic stroke (AIS). Here, we report a case of contrast extravasation mimicking intracerebral hemorrhage (ICH) with intraventricular extension after intravenous thrombolytic treatment and computed tomography angiography (CTA). CASE PRESENTATION: A 52-year-old man presented with right-sided hemiparesis and hypoesthesia. Initial non-contrast head CT was negative for intracranial hemorrhage and acute ischemic changes. He received intravenous treatment with tenecteplase 3.8 h after the onset of stroke. CTA of the head and neck was performed at 4.3 h after stroke onset. It showed no stenosis or occlusion of the carotid and major intracranial arteries. At about 1.5 h after CTA, the right-sided hemiparesis deteriorated, accompanied by drowsiness, aphasia, and urinary incontinence. Immediate head CT showed hyperdense lesions with mild space-occupying effect in the left basal ganglia and both lateral ventricles. The hyperdense lesions were reduced in size on follow-up CT after 5 h. Two days later, CT showed that the hyperdense lesions in the lateral ventricles almost completely disappeared and only a small amount remained in the infarcted area. CONCLUSIONS: Contrast extravasation into the brain tissue and lateral ventricles, mimicking ICH with intraventricular extension, could occur after intravenous thrombolytic treatment and CTA in a patient with AIS, which might lead to misdiagnosis and wrong treatment of the patient. The rapid resolution of intracranial hyperdense lesions is key to differentiate contrast extravasation from ICH on serial non-enhanced CT.

Incidence and associated in-hospital mortality of myocardial injury characterised by elevated cardiac troponin in adult patients with traumatic brain injury: protocol for a systematic review and meta-analysis.

INTRODUCTION: Myocardial injury is a relatively common complication of traumatic brain injury (TBI). However, the incidence and clinical impact of myocardial injury characterised by elevated cardiac troponin (cTn) levels after TBI are still poorly known. The objective of our study is to assess the global incidence of myocardial injury characterised by elevated cTn in adult patients with TBI and its association with in-hospital mortality. METHODS AND ANALYSIS: The protocol of our systematic review and meta-analysis is performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols guidelines. We will search the Medline, Embase, Cochrane Library, Scopus and Web of Science databases from inception to 1 January 2024, for observational studies in any language that reported the incidence of elevated cTn and/or in-hospital mortality associated with elevated cTn among adult patients with TBI. Two reviewers will independently assess study eligibility, extract the data and assess the risk of bias. ORs and 95% CIs will be used with a random-effects or fixed-effects model according to the estimated heterogeneity among studies assessed by the I2 index. We will perform a quantitative synthesis for the incidence of elevated cTn and in-hospital mortality data. If sufficient data are available, we will perform subgroup analysis and meta-regression to address the heterogeneity. In addition, we will perform a narrative analysis if quantitative synthesis is not appropriate. ETHICS AND DISSEMINATION: Ethics approval was not required for this study. We intend to publish our findings in a high-quality, peer-reviewed journal. PROSPERO REGISTRATION NUMBER: CRD42023454686.

A case with a postoperative rapidly calcified subdural hematoma.

We report a rare case of a rapidly calcified subdural hematoma (SDH) occurring 15 days after craniotomy in an adolescent. It suggests that calcification of a SDH may occur not only in the chronic stage but also in the subacute stage and may appear in subdural hematomas (SDHs) after craniotomy.

Traumatic subdural hygroma and chronic subdural hematoma: A systematic review and meta-analysis.

Recently, a relationship between traumatic subdural hygroma (SDG) and chronic subdural hematoma (CSDH) has been proposed. However, the role of traumatic SDG in development of CSDH has not been well characterized. This systematic review aimed to estimate the rate of evolution of traumatic SDG to CSDH, and to identify risk factors associated with traumatic SDG evolution to CSDH. We searched MEDLINE, EMBASE, and Cochrane Library databases from inception to May 26, 2021, using the combination of the terms "subdural hygroma" and "chronic subdural hematoma." Using a random-effects model, we calculated a pooled estimate of rate of evolution of traumatic SDG to CSDH. In addition, we conducted a systematic review of studies of risk factors for traumatic SDG evolution to CSDH. Nineteen studies with 1,335 patients met the inclusion criteria for meta-analysis. The pooled estimate of evolution rate was 25.0 % (95 % CI, 19.3 %-30.7 %; I2 = 85.6 %), with significant heterogeneity among studies (P < 0.01). Age ≥ 60 years was associated independently with traumatic SDG evolution to CSDH, after adjustment for study design using multivariate meta-regression. Risk factors associated with evolution of traumatic SDG to CSDH were radiological characteristics such as thicker SDG and higher SDG CT value. The rate of traumatic SDGs evolution to CSDH is approximately 25 %. Patients aged 60 or older with traumatic SDGs are at increased risk of CSDH development. Thicker SDG and higher SDG CT value, are commonly reported risk factors for traumatic SDG evolution to CSDH. However, higher quality studies are needed.

Reduction of Autophagosome Overload Attenuates Neuronal Cell Death After Traumatic Brain Injury.

Previous studies have shown that alterations in autophagy-related proteins exist extensively after traumatic brain injury (TBI). However, whether autophagy is enhanced or suppressed by TBI remains controversial. In our study, a controlled cortical impact was used to establish a model of moderate TBI in rats. We found that a significant increase in protein levels of LC3-II and SQSTM1 in the injured cortex group. However, there were no significant differences in protein levels of VPS34, Beclin-1, and phosphor-ULK1, which are the promoters of autophagy. Lysosome dysfunction after TBI might lead to autophagosome accumulation. In addition, the highly specific autophagy inhibitor SAR405 administration reduced TBI-induced apoptosis-related protein cleaved caspase-3 and cleaved caspase-9 levels in the ipsilateral cortex, as well as brain edema and neurological defects accessed by mNSS. Furthermore, chloroquine treatment reversed the beneficial effects of SAR405 by increasing the accumulation of autophagosomes. Finally, our data showed that autophagy inhibition by VPS34 gene knockout method attenuated cell death after TBI. Our findings indicate that impaired autophagosome degradation is involved in the pathological reaction after TBI, and the inhibition of autophagy contributes to attenuate neuronal cell death and functional defects.

ß-Blockers for traumatic brain injury: A systematic review and meta-analysis.

BACKGROUND: Paroxysmal sympathetic hyperactivity (PSH) and catecholamine surge, which are associated with poor outcome, may be triggered by traumatic brain injury (TBI).ß Adrenergic receptor blockers (ß-blockers), as potential therapeutic agents to prevent paroxysmal sympathetic hyperactivity and catecholamine surge, have been shown to improve survival after TBI. The principal aim of this study was to investigate the effect of ß-blockers on outcomes in patients with TBI. METHODS: For this systematic review and meta-analysis, we searched MEDLINE, EMBASE, and Cochrane Library databases from inception to September 25, 2020, for randomized controlled trials, nonrandomized controlled trials, and observational studies reporting the effect of ß-blockers on the following outcomes after TBI: mortality, functional measures, and cardiopulmonary adverse effects of ß-blockers (e.g., hypotension, bradycardia, and bronchospasm). With use of random-effects model, we calculated pooled estimates, confidence intervals (CIs), and odds ratios (ORs) of all outcomes. RESULTS: Fifteen studies with 12,721 patients were included. Exposure to ß-blockers after TBI was associated with a significant reduction in adjusted in-hospital mortality (OR, 0.39; 95% CI, 0.30-0.51; I2 = 66.3%; p < 0.001). ß-Blockers significantly improved the long-term (≥6 months) functional outcome (OR, 1.75; 95% CI, 1.09-2.80; I2 = 0%; p = 0.02). Statistically significant difference was not seen for cardiopulmonary adverse events (OR, 0.91; 95% CI, 0.55-1.50; I2 = 25.9%; p = 0.702). CONCLUSION: This meta-analysis demonstrated that administration of ß-blockers after TBI was safe and effective. Administration of ß-blockers may therefore be suggested in the TBI care. However, more high-quality trials are needed to investigate the use of ß-blockers in the management of TBI. LEVEL OF EVIDENCE: Systematic review and meta-analysis, level III.

Subperiosteal versus Subdural Drain After Burr Hole Drainage for Chronic Subdural Hematomas: A Systematic Review and Meta-Analysis.

BACKGROUND: The use of drains has been considered to be superior to no drains after burr hole drainage of chronic subdural hematomas (CSDHs). Therefore, routine placement of a subdural drain (SDD) is supported by most neurosurgeons. However, whether the drain location after CSDH burr hole evacuation influences patient outcomes is unclear. Therefore, we compared the efficacy and safety of subperiosteal drains (SPDs) with those of SDDs for patients with CSDHs. METHODS: Using the PRISMA (preferred reporting items for systematic reviews and meta-analyses) guidelines, eligible studies reported up to September 2019 were identified through a search of MEDLINE, EMBASE, and Cochrane Central. Pooled estimates, confidence intervals (CIs), and odds ratios (ORs) were calculated for all outcomes. RESULTS: Ten studies with 3169 patients were included. The use of a SPD after CSDH burr hole drainage resulted in a significant decrease in recurrences compared with the use of a SDD (OR, 0.73; 95% CI, 0.58-0.92; I2, 14%; P = 0.007). No significant differences were identified between the SPD and SDD groups in the favorable outcomes (OR, 1.29; 95% CI, 1-1.68; I2, 0%; P = 0.05). Adverse event rates, including mortality, seizures, and surgical infection, were not significantly different between the 2 groups. However, the use of SPDs was associated with a lower risk of parenchymal injuries compared with SDDs (OR, 0.29; 95% CI, 0.11-0.76; I2, 0%; P = 0.01). CONCLUSIONS: The results from the present meta-analysis suggest that the use of an SPD is safer and might be more effective than an SDD in the treatment of CSDH. However, more large randomized controlled trials are needed to investigate the use of SPDs in the management of CSDH.

Recurrent Acute Subdural Hematoma Due to Middle Meningeal Artery Bleeding Treated by Embolization.

BACKGROUND: Recurrent acute subdural hematomas (ASDHs) are a common complication of neurosurgical operations. However, ASDHs associated with middle meningeal artery (MMA) injury are extremely rare. We encountered a rare case of recurrent ASDH due to MMA bleeding after craniotomy for a nontraumatic ASDH and successfully performed MMA embolization for treatment of it. CASE DESCRIPTION: A 56-year-old woman was admitted to our department with progressively worsening headache and vomiting approximately 1 week. She had no history of head trauma and illness. A head computed tomography (CT) scan revealed an ASDH on the right hemisphere. The patient underwent a right-sided craniotomy for evacuation of the hematoma. Two days later, she exhibited impaired consciousness and a repeat CT scan showed a recurrent ASDH. To clarify the cause, we performed cerebral digital subtraction angiography for the patient. Obvious contrast extravasation from the anterior branch of the right MMA was noticed. It was considered to be related to the recurrent ASDH. Embolization of the MMA was performed using Onyx 18 (Micro Therapeutics, Inc., Irvine, California, USA). Follow-up CT scans showed progressive resolution of the ASDH and no recurrence. The patient was discharged without any neurologic deficits. CONCLUSIONS: In our case, the relationship between the recurrent ASDH and MMA was observed via angiography and MMA embolization was successfully performed to avoid surgery for reevacuation, suggesting that active bleeding of MMA may be a cause of recurrent ASDH after neurosurgical operations and endovascular exploration, and possible treatment is necessary for an unexplained ASDH.