Background Stent-assisted coil embolization of ruptured wide-necked aneurysms is a controversial treatment modality due to concerns on the peri-procedural safety of anti-platelet therapy in the setting of acute subarachnoid hemorrhage. Our aim was to systematically review the literature on stent-assisted coil embolization of acutely ruptured wide-neck aneurysms to calculate the pooled prevalence of clinical outcome, thromboembolic and hemorrhagic complication rates and overall mortality. Methods We searched PubMed and Google Scholar for articles published between 2009 and 2019 and stratified selected articles based on risk of publication bias. Data on thromboembolic and hemorrhagic complications, clinical outcomes and mortality rates were analyzed using quality-effects model and double arcsine transformation. Results 24 articles were included featuring a total of 1582 patients. Thromboembolic and hemorrhagic complication rates were witnessed in 9.1% [95% CI: 6.0% – 12.7%; I2 = 72.8%] and 8.7% [95% CI: 5.4 – 12.6%; I2 = 77.2%] of patients, respectively. 245 patients received external ventricular drains, of which 33 (13.5%) had EVD-related hemorrhages. Total complication rate was 20.8% [95% CI: 14.2 – 28.1%; I2 = 87.0%]. 57% of aneurysms were completely occluded and a favorable clinical outcome was reported in 74.7% [95% CI: 66.4 – 82.2%; I2 = 86.0] of patients. Overall mortality rate came at 7.8% [95% CI: 4.8 – 11.6%; I2 = 76.9%]. Conclusion Stent-assisted coiling of ruptured intracranial aneurysm is a technically feasible procedure with controlled thromboembolic complication rate but may be associated with higher hemorrhagic and total complication rates compared to coiling alone. While stent-assisted coiling of ruptured wide-necked aneurysm seems to yield a lower rate of favorable clinical outcome, overall mortality is comparable to that of endovascular coiling alone.

Meningiomas are amongst the most commonly encountered intracranial tumors. The majority of these tumors arise intracranially, and the remaining incidents occur along the spinal cord. Meningiomas tend to grow gradually, with many tumors arising in inaccessible locations. Such sporadic behavior poses a therapeutic challenge to clinicians, causing incomplete tumor resections that often lead to recurrence. Therefore, ongoing research seeks to find alternative systematic treatments for meningiomas, with gene-based therapeutics of high interest. Subsequently, genetic studies characterized frequent somatic mutations in NF2, TRAF7, KLF4, AKT1, SMO, and PIK3CA. These genes are communally exhibited in 80% of sporadic meningiomas. In addition, other genes such as the DUSP family, the NR4 family, CMKOR, and FOSL2, have been identified as key players in spinal meningiomas. In this perspective, we aim to investigate current genetic-based studies, with the ongoing research mainly focused on the above NF2, TRAF7, KLF4, AKT1, SMO, and PIK3CA genes and their involved pathways. In addition, this perspective can serve as a potential cornerstone for future genetic analyses of meningioma cases.

Stroke is considered as the first cause of neurological dysfunction and second cause of death worldwide. Recombinant tissue plasminogen activator is the only chemical treatment for ischemic stroke approved by the US Food and Drug Administration. It was the only standard of care for a long time with a very narrow therapeutic window, which usually ranges from 3 to 4.5 h of stroke onset; until 2015, when multiple trials demonstrated the benefit of mechanical thrombectomy during the first 6 h. In addition, recent trials showed that mechanical thrombectomy can be beneficial up to 24 h if the patients meet certain criteria including the presence of magnetic resonance imaging/computed tomography perfusion mismatch, which allows better selectivity and higher recruitment of eligible stroke patients. However, magnetic resonance imaging/computed tomography perfusion is not available in all stroke centers. Hence, physicians need other easy and available diagnostic tools to select stroke patients eligible for mechanical thrombectomy. Moreover, stroke management is still challenging for physicians, particularly those dealing with patients with "wake-up" stroke. The resulting brain tissue damage of ischemic stroke and the subsequent pathological processes are mediated by multiple molecular pathways that are modulated by inflammatory markers and post-transcriptional activity. A considerable number of published works suggest the role of inflammatory and cardiac brain-derived biomarkers (serum matrix metalloproteinase, thioredoxin, neuronal and glial markers, and troponin proteins) as well as different biomarkers including the emerging roles of microRNAs. In this review, we assess the accumulating evidence regarding the current status of acute ischemic stroke diagnostic biomarkers that could guide physicians for better management of stroke patients. Our review could give an insight into the roles of the different emerging markers and micro-RNAs that can be of high diagnostic value in patients with stroke. In fact, the field of stroke research, similar to the field of traumatic brain injury, is in immense need for novel biomarkers that can stratify diagnosis, prognosis, and therapy.

No abstract

No abstract