The clinical and neuroradiological features of patients of coexisting atraumatic convexity subarachnoid hemorrhage and large artery atherosclerosis stroke: A retrospective observational study.

ABSTRACT: Atraumatic convexity subarachnoid hemorrhage (c-SAH) concomitant with large artery atherosclerosis (LAA) stroke has been rarely discussed in the literature. Our aim in this study is to characterize the clinical and neuroradiological features of patients with LAA stroke and c-SAH.A retrospective study from a single institution was performed between January 2016 and June 2020. Only patients diagnosed with c-SAH and LAA stoke were included in this study. The clinical presentation and neuroimaging finding were summarized by our experienced neurologists.In total, 12 patients (8 men, 4 women), ranging in age from 45 to 75 years, were identified. All of them had cardiovascular risk factors and hypertension was the commonest (50%). Almost all patients presented hemiparesis (91.7%). Other clinical presentations included, dysarthria (41.7%), hemianesthesia (33.3%), facial palsy (33.3%), aphasia (16.7%), and cognitive impairment (8.3%). Internal border-zone (IBZ) infarction and cortical border-zone (CBZ) infarction occurred in 12 and 3 patients, respectively. c-SAH might occurred in different cortical sulcis. Percentages of frontal lobe, parietal lobe and fronto-parietal lobe were 41.7% (n = 5), 25% (n = 3) and 25% (n = 3), respectively. All ischemic lesions were ipsilateral to the sites of c-SAH. High-grade atherosclerotic stenosis of large artery was detected in all patients. The M1 segment of middle cerebral artery (MCA) is the second most common atherosclerotic artery after internal carotid artery (ICA).Our data suggest that LAA stroke is always ipsilateral to the site of c-SAH. Severe atherosclerotic changes can also been seen in the M1 segment of MCA apart from extracranial ICA. Moreover, border zone infarction may be a specific form of infarct when c-SAH is confronted with LAA stroke.

Atorvastatin Pretreatment Attenuates Ischemic Brain Edema by Suppressing Aquaporin 4.

BACKGROUND: Cerebral edema, a serious complication of acute cerebral infarction, has a crucial impact on morbidity and mortality in the early stage of cerebral infarction. And aquaporin 4 (AQP4), a bidirectional water transporting protein, plays a pivotal role in edema formation. At experimental model, it has proven that atorvastatin could exert pleiotropic neuroprotection on acute cerebral infarction independent of its cholesterol-lowering action. It was a common protective manifestation that atorvastatin can reduce the infarct volume and cerebral edema. However, little is known about atorvastatin improving ischemic brain edema by regulating AQP4 expression. This study intended to investigate the neuroprotection effects of atorvastatin pretreatment in rats with cerebral ischemia and further explore the potential relationship between atorvastatin and AQP4 expression. METHODS: Fifty-one adult male Sprague Dawley rats were randomly divided into 3 groups: sham, middle cerebral artery occlusion (MCAO), and atorvastatin pretreatment (Ator) group. For Ator group, 20 mg/kg of atorvastatin injectable suspension was administered once for 7days by gavage before operation, whereas the others were administered the same volume of saline matching. Except for sham group, MCAO and Ator groups were subjected to permanent MCAO by modified intraluminal suture method. Infarct volume, neurological deficit, brain water content (BWC), immunohistochemistry, western blot, and polymerase chain reaction (PCR) were measured at 24 hours after MCAO. RESULTS: Compared with sham group, the mNSS, infarct volume, and BWC of ischemic hemisphere were significantly increased (P < 0.001) in MCAO group. Positive cells and protein levels of p-p38MAPK and AQP4 in peri-infarction were significantly increased (P < 0.01). The mRNA levels of p38MAPK and AQP4 were also prominently upregulated (P < 0.01). Interestingly, preadministration of atorvastatin dramatically decreased infarct volume and the BWC of ischemic hemisphere compared with MCAO group (P < 0.05). The overexpressions of p-p38MAPK and AQP4 in peri-infarction were significantly decreased (P < 0.05) and their mRNA levels were downregulated by atorvastatin pretreatment (P < 0.05). Neurological deficits were also dramatically improved (P < 0.001). CONCLUSION: To the best of our knowledge, this is the first study that demonstrates an effect of atorvastatin on expression of AQP4, and we propose that decreased AQP4 expression through a p38MAPK-suppression pathway may be the mechanism of atorvastatin alleviating ischemic cerebral edema.

Bilateral wallerian degeneration of the middle cerebellar peduncles secondary to pontine infarction: A case series.

OBJECTIVE: Wallerian degeneration (WD) of middle cerebellar peduncles (MCPs) secondary to pontine infarction is rarely reported in the literature. Our aim in this study is to characterize its clinical and neuroradiological features. METHODS: A retrospective review of 7 patients from a single institution was conducted. Only patients with pontine infarction and subsequent degeneration of the MCPs were included in the analysis. The features of clinical presentation and neuroimaging finding were summarized by our experienced neurologists. RESULTS: Seven patients (5 male, 2 female), ranging in age from 50 to 77 years, satisfied the inclusion criteria. All patients had cardiovascular risk factors and hypertension was the most common one. Almost all of the patients had hemiparesis and dysarthria, and could achieved good clinical outcome. On the initial scan, hyperintense on T2- and diffusion-weighted images suggested the acute pontine infarction. On the follow-up scan, however, hyperintensities of bilateral MCPs on T2-weight and FLAIR images were apparently demonstrated in all patients. The specific lesions in the MCPs were attributed to bilateral WD of the pontocerebellar fibres secondary to pontine infarction. CONCLUSION: WD should be taken into account when patients are initially diagnosed with paramedian pontine infarction and follow-up MRI manifest as symmetrical hyperintense in the MCPs.

Association between restless legs syndrome and hypertension: a meta-analysis of nine population-based studies.

Previous population-based studies evaluating the association between restless legs syndrome (RLS) and cardiovascular risk factors have showed inconsistent results, especially for the relationship between RLS and hypertension. We, therefore, aimed to meta-analyze to assess the association between RLS and hypertension. PubMed and Embase databases were systematically searched to identify eligible studies. Nine population-based cross-sectional studies were selected for inclusion, involving 102,408 individuals. Overall, the prevalence of hypertension in RLS subjects was higher than those without RLS (OR = 1.36, 95% CI, 1.18-1.57, P = 0.043). Our findings indicate that RLS is associated with increased blood pressure. More large-scale and prospective studies are warranted to further clarify the relationship and its potential mechanism.