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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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