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Background: Early neurological deterioration is common in the acute phase after stroke. We sought to investigate the correlation between the progression of microembolic signal (MES), ischemic infarcts and the neurological deficits in the acute phase of stroke patients with large artery occlusive disease. Methods: Transient ischemic attack or stroke patients with relevant significant large artery stenosis (≧50% diameter reduction) and admitted within 7 days of the symptom onset were recruited in this study. MES, infarcts on diffusion-weighted imaging and National Institutes of Health Stroke Scale (NIHSS) score were assessed on days 1 and 7 of recruitment. Results: Among 67 patients, 50.7% (34 of 67) had MES on day 1. Presence of MES correlated with both a higher number of infarcts (p = 0.006) and the incidence of multiple infarcts (χ² test, p = 0.002), but not with the NIHSS score. On day 7, MES was detected in 25.4% of the patients (17 of 67), 11.8% of them (2 of 17) displayed new or extended infarct on DWI (p = 0.14) and 29.4% (5 of 17) showed neurological improvement (p = 0.039). Among the patients with positive MES at baseline, NIHSS reduction was positively correlated with disappearance of MES on day 7 (MES disappearance vs. persistence group, 2.05 vs. 0.73, p = 0.023). Conclusions: Neither the disappearance of MES nor the changes in NIHSS score correlated with the progression of infarct. Disappearance of MES indicated better neurological improvement in the acute phase.

Cardiovascular autonomic function is impaired in patients with ischemic stroke, but patients with carotid stenosis show more severely impaired parasympathetic and sympathetic functions.

Objective To investigate the effect of water extract of Gastrodiae Rhizoma (GR) on the development of acquired temporal lobe epilepsy (TLE) and on regulating the expression of the mammalian target of rapamycin (mTOR) and semaphorin 3F (SEMA3F). Methods A pilocarpine‐induced status epilepticus (SE) model was adopted to precipitate injury in the limbic systems. GR and carbamazepine (CBZ) treatments were given to mice for 14 days prior to SE induction to demonstrate the antiepileptic effects and continued for 5 more days to illustrate the effects on histologic studies. Results Our results consolidated that GR treatment (92.1 minutes) could delay the SE onset in comparison with the control group (61.5 minutes, P = .041). Fewer mice had reached SE with GR treatment (41.7%) when compared with the control group (83.3%, P = .044). GR treatment (2.1 hours/mouse) could suppress the number of acute seizures in post‐SE survival mice when compared with the control group (4.5 hours/mouse, P < .001). The effects of GR treatment were elucidated with the mechanism of actions. GR treatment reduced the overexpression of mTOR (0.27 vs 0.67 AU/mg protein, P = .047). GR treatment increased the underexpression of SEMA3F (0.51 vs 0.16 µg/mg protein, P = .034). In the histochemical study of microtubule‐associated protein 2 (MAP2) staining, our results showed that GR prevented neuronal loss in the GR treatment group (64.8% positively stained pixel area) as compared with the control group (59%, P = .014) in the hippocampus. In glial fibrillary acidic protein (GFAP) staining, the severity of astrogliosis was mitigated by the GR treatment (4.1% positively stained pixel area) when compared to the control group (5.6%, P = .047) in the hippocampus. Significance These results provide preclinical evidence to support the use of GR, which could suppress acute seizures and relieve pathological changes in pilocarpine‐induced TLE mice. We demonstrated that the antiepileptic effects of GR could be accompanied by mTOR reduction and astrogliosis attenuation.

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Background and Purpose: Vasa vasorum, which constitutes a network of microvasculature, plays a nutritive and drainable role in vessel walls of arteries. The existence of vasa vasorum within brain vasculature is rarely reported. Based on a series of cerebral artery specimens, we aimed to describe the distribution features of vasa vasorum among intracranial arteries, including middle cerebral arteries (MCAs), basilar arteries (BAs) and vertebral arteries (VAs) and potential effects of vasa vasorum on atherosclerosis morphology. Methods: One hundred and fifty- seven arteries (64 MCAs, 32 Bas and 61 VAs) were obtained from consecutively recruited 32 autopsy cases aged 45 years or above. Routine histology and immunostaining processing were performed to identify the presence of adventitial vasa vasorum and to study the phenotypes and specific components of intracranial atherosclerotic lesions. Results: Among 157 intracranial cerebral arteries, adventitial vasa vasorum were present most frequently in the vertebral arteries (77%), followed by basilar arteries (44%) and middle cerebral arteries (20%). Arteries with adventitial vasa vasorum had greater thickness of tunica adventitia (0.10±0.06 mm vs. 0.06±0.03 mm, p &lt 0.001) and larger size in diameters (3.41± 0.73 mm vs. 2.97± 0.66 mm, p &lt 0.001). The occurrence of adventitial vasa vasorum correlated with high frequency of complicated plaques and higher rate of concentric atherosclerotic lesions (70% vs. 36%, p &lt 0.001). Conclusion: For the first time, our study demonstrated the presence of adventitial vasa vasorum within brain vasculature, especially at vertebral arteries. The correlations between adventitial vasa vasorum and intraplaque hemorrhage, inflammation and calcification suggest that adventitial vasa vasorum may serve as a predictor of unstable atherosclerotic lesions. Further studies are required to explore the biological behavior of adventitial vasa vasorum within cerebral arteries.

Introduction: In the face of population ageing and contemporary cardiovascular risk factor control, understanding the evolution of ischemic stroke mechanisms may inform stroke prevention strategy and guide resources allocation. Method: Through a registry-based observational study in a regional hospital in Hong Kong, we studied the evolution of stroke mechanisms by TOAST classification over a 15-year period (2004-2018). We retrieved demographic data, pre-defined cardiovascular risks, use of medications, intensity of risk factor control and clinical outcomes (2-year recurrence and 3-month mortality and disability) from the stroke registry. We defined stroke mechanisms by clinical signs and symptoms, cardiovascular risk profile and infarct topography. We compared the trends of stroke mechanisms by Chi-square test for trend and continuous variables by one-way ANOVA test with post-hoc Bonferroni test. Interobserver reliability was assessed by kappa statistics. Results: We included 5982 patients over the 15-year period. The number of atrial fibrillation (AF)-related stroke increased by 213% (p<0.001) and large-artery-disease (LAD)-related stroke decreased by 47.7% (p<0.001). AF-related stroke had the highest mean age (77.4±11, p<0.001) and National Institute of Health Stroke Scale on admission (14.8±10.8, p<0.001). Within the AF-related stroke patients, the number of strokes as first presentation of AF increased by 200%. 2-year recurrence of stroke or transient ischemic attack of patients with symptomatic intracranial atherosclerosis (ICAS) decreased from 20.7% to 9.3%. Conclusion: We observed a huge increase in AF-related stroke and newly diagnosed AF at presentation. Our results demanded an enhanced surveillance in detecting AF, primary prevention and thrombectomy facilities given the high morbidity and mortality associated with AF-related strokes. The decline in ICAS-related stroke and its recurrence may underscore the importance of intensive risk factor management in the Asia-Pacific region where ICAS remained prevalent.