Albuminuria excretion rate, calculated as urinary albumin-to-creatinine ratio (UACR), is used clinically to evaluate albuminuria. There are different attitudes to whether high UACR predicts higher risk of stroke. The aim of this study was to evaluate the relationship between UACR and stroke. Two investigators independently searched MEDLINE, EMBASE, Cochrane Controlled Trials Register Database, Scopus and Google Scholar from January 1966 through June 2021 were screened. In addition, a manual search was conducted using the bibliographies of original papers and review articles on this topic. Two blinded reviewers abstracted the data independently to a predefined form. Among the 10,939 initially identified studies, 7 studies with 159,302 subjects were finally included. It is demonstrated that UACR predicted an increased risk of stroke using cutoff value of either 0.43 (HR, 2.39; 95% CI: 1.24 - 4.61; P <0.01), 10 mg/g (HR, 1.60; 95% CI: 1.30 - 1.97; P < 0.01) or 30 mg/g (HR, 1.84; 95% CI: 1.49 - 2.28; P < 0.01). The overall analysis confirmed that high UACR was associated with an increased rate of stroke (HR, 1.81; 95% CI: 1.52 - 2.17; P < 0.01). Furthermore, High UACR predicted higher risk of stroke in local inhabitants (HR, 1.67; 95% CI: 1.17 – 2.37; P = 0.04), adults (HR, 2.21; 95% CI: 2.07 – 2.36; P < 0.01) or elderly adults (HR, 1.96; 95% CI: 1.56 – 2.46; P < 0.01). Whereas, high UACR was unable to predict stroke in patients with either T2DM (HR, 2.25; 95% CI: 0.55 – 9.17; P = 0.26) or hypertension (HR, 0.95; 95% CI: 0.28 – 3.22; P = 0.93). Another subgroup analysis revealed that high UACR was associated with increased risk of ischemic stroke (HR, 1.60; 95% CI: 1.43 - 1.80; P < 0.01), as well as hemorrhagic stroke (HR, 1.76; 95% CI: 1.22 - 1.45; P < 0.01). In conclusion, UACR is associated with an increased risk of hemorrhagic and ischemic stroke. UACR may be used as an indicator to predict stroke in non-diabetic and non-hypertensive subjects.

An isolated or trapped fourth ventricle is a relatively rare, although serious, adverse effect of hemorrhagic, infectious, or inflammatory processes that involve the central nervous system. This entity usually occurs after successful shunting of the lateral ventricles and may become clinically evident with the development of delayed clinical deterioration. This decline of the neurological status of the patient is evident after an initial period of improvement of the relevant symptoms. Surgical treatment options include cerebrospinal fluid shunting procedures, along with open surgical and endoscopic approaches. Complications related to its management are common and are related with obstruction of the fourth ventricular catheter, along with cranial nerve or brainstem dysfunction. We used the keywords: “isolated fourth ventricle,” and “trapped fourth ventricle,” in PubMed^® and Web of Science^®. Treatment of the trapped fourth ventricle remains a surgical challenge, although the neurosurgical treatment armamentarium has broadened. However, prompt recognition of the clinical and neurological findings that accompany any individual patient, in conjunction with the relevant imaging findings, is mandatory to organize our treatment plan on an individual basis. The current experience suggests that any individual intervention plan should be mainly based on the underlying pathological substrate of hydrocephalus. This could help us to preserve the patient's life, on an emergent basis, as well as to ensure an uneventful neurological outcome, maintaining at least the preexisting level of neurological function.

Dissecting intracranial pseudoaneurysms (IPs) are associated with a high incidence of rupture and poor neurologic outcomes. Lesions in the posterior circulation are particularly malignant and pose even greater management challenges. Traditional management consists of microsurgical vessel sacrifice with or without bypass. Flow diversion (FD) in the setting of subarachnoid hemorrhage (SAH) represents a reconstructive treatment option and can be paired with coil embolization to promote more rapid thrombosis of the lesion. We report a case of a ruptured dissecting vertebral artery (VA) IP successfully acutely treated with coil-assisted FD. A 53-year-old male presented with a right V4 dissection spanning the origin of the posterior inferior cerebellar artery and associated ruptured V4 IP. The patient was treated with coil-assisted FD. Oral dual-antiplatelet therapy (DAPT) was initiated during the procedure, and intravenous tirofiban was used as a bridging agent. Immediate obliteration of the IP was achieved, with near-complete resolution of the dissection within 48 h. The patient made a complete recovery, and angiography at 6 weeks confirmed total IP obliteration, reconstruction of the VA, and a patent stent. The use of FD and DAPT in the setting of acute SAH remains controversial. We believe that coil-assisted FD in carefully selected patients offers significant advantages over traditional microsurgical and endovascular options. The risks posed by DAPT and potential for delayed thrombosis with FD can be effectively mitigated with planning and the development of protocols. We discuss the current literature in the context of our case and review the challenges associated with treating these often devastating lesions.

After the introduction of shunt treatment for the management of childhood hydrocephalus, a wide variety of complications related to this treatment modality have been recognized. The entity of slit ventricle syndrome (alternatively, symptomatic ventricular coaptation) is one of them, is frequently encountered in the pediatric population and its symptom complex resembles that of shunt failure. We conducted research on PubMed®, MEDLINE®, and Web of Science®, using the keywords: “slit ventricles,” “slit ventricle syndrome,” “SVS” and “ventricular coaptation.” The aim of our review was to trace the advances made through the past decades, concerning our knowledge about the clinical characteristics, pathophysiology, and treatment options of this entity. The discrepancy among researchers about the offending etiology and the optimum treatment algorithm of this entity, as well as the necessity of an updated concept regarding shunt over drainage is analyzed. The multiple treatment modalities proposed and pathophysiologic mechanisms implicated for the treatment of slit ventricle syndrome illustrate the complexity of this entity. Consequently, the issue requires more detailed evaluation. In this review, we comment on all the main facets related to shunt over drainage and the resultant slit ventricle syndrome.

Physical exercise is a promising rehabilitative strategy for acute ischemic stroke. Preclinical trials suggest that exercise restores cerebral blood circulation and re-establishes the blood–brain barrier's integrity with neurological function and motor skill improvement. Clinical trials demonstrated that exercise improves prognosis and decreases complications after ischemic events. Due to these encouraging findings, early exercise rehabilitation has been quickly adopted into stroke rehabilitation guidelines. Unfortunately, preclinical trials have failed to warn us of an adverse effect. Trials with very early exercise rehabilitation (within 24 h of ischemic attack) found an inferior prognosis at 3 months. It was not immediately clear as to why exercise was detrimental when performed very early while it was ameliorative just a few short days later. This review aimed to explore the potential mechanisms of harm seen in very early exercise administered to acute ischemic stroke patients. To begin, the mechanisms of exercise's benefit were transposed onto the current understanding of acute ischemic stroke's pathogenesis, specifically during the acute and subacute phases. Then, exercise rehabilitation's mechanisms were compared to that of remote ischemic conditioning (RIC). This comparison may reveal how RIC may be providing clinical benefit during the acute phase of ischemic stroke when exercise proved to be harmful.

BACKGROUND: Inflammation is increasingly recognized as a target to reduce residual cardiovascular risk. Colchicine is an anti-inflammatory drug that was associated with improved cardiovascular outcomes. However, its effect on stroke reduction was not consistent across studies. Therefore, the aim of this study-level meta-analysis was to evaluate the influence of colchicine on stroke in patients with coronary artery disease (CAD). METHODS: Electronic databases were searched through October 2020, to identify randomized controlled trials using colchicine in patients with CAD. The incidence of clinical endpoints such as stroke, death, myocardial infarction (MI), study-defined major adverse cardiovascular events (MACE), and atrial fibrillation (AF) was compared between colchicine and placebo groups. RESULTS: A total number of 11,594 (5,806 in the colchicine arm) patients from 4 eligible studies were included in the final analysis. Stroke incidence was lower in the colchicine arm compared to placebo (rate ratio [RR] 0.48 [95% confidence interval [CI], 0.29–0.78], P = 0.003) whereby no significant difference was observed in the incidence of AF (odds ratio [OR] 0.86 [95% CI, 0.69–1.06], P = 0.16). Furthermore, a significant effect of colchicine on MACE [RR 0.65 (95% CI, 0.51–0.83), P = 0.0006] and MI (RR 0.65 (95% CI, 0.54–0.95], P = 0.02) was detected, with no influence on all-cause mortality (RR 1.04 [95% CI, 0.61–1.78], P = 0.88). CONCLUSIONS: This meta-analysis confirms a significant influence of colchicine on stroke in CAD patients. Despite its neutral effect on AF occurrence, other mechanisms related to plaque stabilization are plausible. The concept seems to be supported by contemporaneous MI reduction and posits that anti-inflammatory properties of colchicine may translate into a reduction of stroke risk.

INTRODUCTION: Brain tissue was adversely affected by renal ischemia-reperfusion injury (renal IRI) in several studies. Moreover, we are awareness that kidney diseases are gender dependent, but there is not enough evidence of the impact of gender on renal IRI-induced brain injury. Hence, this study was designed to investigate gender differences in renal IRI-induced brain tissue injury in adult rats. MATERIALS AND METHODS: Forty Wistar rats (four groups) include two main groups (20 male and 20 female). Each of them was divided into two subgroups including 1 and 2: male and female sham-operated groups and 3and 4: male and female ischemia (ISC) groups were exposed to renal ischemia for 45 min and then 24 h reperfusion (male and female ISC 24 h). Sham groups were exposed to surgery without ischemia process. After reperfusion time, blood samples were obtained for the renal function measurements. The kidney and brain were removed and were fixed in a 10% formalin solution for pathological assessment. The left kidney was used to measure malondialdehyde (MDA) and nitrite. RESULTS: Renal IRI increased significantly levels of creatinine, blood urea nitrogen, kidney weight, and damage score in both genders (P < 0.05). Furthermore, brain injuries were significantly higher following 24 h of reperfusion in male and female groups. Serum nitrite level and MDA concentration of female rats decreased significantly in ISC 24 h group (P < 0.05) but not in male rats. CONCLUSION: The brain tissue of both genders, male and female, is affected by renal IRI as a remote organ. Female sex hormones may indicate a protective role against IR by the nitric oxide pathway and antioxidant signaling.

INTRODUCTION: Prior retrospective and case-control studies have shown that the use of general anesthesia (GA) during endovascular therapy (EVT) for acute ischemic stroke with large vessel occlusion (AIS-LVO) was independently associated with poor clinical outcomes compared with cases performed under conscious sedation (CS). Conversely, recent small randomized clinical trials (RCT) demonstrated a trend toward better outcome in cases performed under GA. METHODS: We submitted an online survey to 193 Society of Vascular Interventional Neurology and 78 American Association of Neurological Surgeons and Congress of Neurological Surgeons – Cerebrovascular Section neuroendovascular practitioners. Questions were aimed at understanding the current state of anesthesia practice during EVT, and to determine if there is clinical equipoise for a large multicenter RCT comparing GA versus CS during EVT. RESULTS: Between March and May of 2017, we received 116 (43%) responses. Anesthesiologists were responsible for managing 96% of the GA cases as compared to only 51% of the CS cases (P < 0.0001). Notable 56% of providers reported performing less than a quarter of their cases under GA. Only 7% performed all cases under GA compared with 17% who used solely CS (P = 0.048). More than half of respondents thought a new RCT was necessary, of whom 61% were interested in participating. Among interested responders, 59% were located in centers with 3 or more neurointerventionalists. CONCLUSION: The significant variation among neuroendovascular providers, added with the lack of consensus among recent trials and meta-analyses, demonstrate clinical equipoise for further studies to explore the effects of anesthesia during EVT in AIS-LVO.

Cerebral ischemia following clipping of cerebral aneurysms constitutes major cause of morbidity and mortality. Clip-related injury to vessel, postoperative clip rotation, prolonged temporary occlusion, intraoperative rupture, and vasospasm are some etiological factors compromising forward flow in parent or branch vessel. On suspicion of compromised forward flow, immediate intraoperative evaluation is done to detect the cause of vascular compromise and further management is done by microsurgical or endovascular means. We describe a case of ruptured distal anterior cerebral artery (ACA) aneurysm complicated by occlusion of ACA after surgical clipping. The patient was managed by endovascular means by combined technique of intra-arterial nimodipine, antiplatelet infusion, and mechanical clot disruption using J-tip microwire.

Tentorium is a rare location of the brain dural arteriovenous fistulae (DAVF) consisting <4% of cases. Hemorrhagic clinical presentation is common, as cortical venous reflux consists a usual characteristic of tentorial DAVF's angioarchitecture. We present a case of transvenous, transjugular embolization of a ruptured huge venous ectasia of a Cognard IV tentorial middle-line DAVF, as a first step life-saving procedure. Initially, a transarterial antegrade embolization attempt was performed but failed due to the tortuous course of arterial feeders. Subsequently, the internal jugular vein (IJV) was directly catheterized under ultrasound (U/S) guidance and a 6F guiding catheter was placed at the ipsilateral transverse sinus. A microcatheter was navigated inside the venous ectasia and eventually, coils were deployed inside causing complete occlusion of the huge venous ectatic aneurysm. In this way, initial occlusion of the venous ectatic ruptured point has been achieved as a first-stage lifesaving treatment. Subsequently, the patient underwent stereotactic radiosurgery for the DAVF 4 months after embolization. Angiographic control with digital subtraction angiography 2 years after embolization and additional stereotactic radiosurgery revealed complete occlusion of the tentorial DAVF. The patient experienced complete neurological recovery. Direct puncture of the IJV under U/S guidance may assist transvenous embolization of ruptured venous ectasia in case of complex tentorial middle-line DAVFs type IV when the ecstatic venous aneurysm is recognized as the bleeding source.