Clinical and imaging features of vertebrobasilar dolichoectasia combined with posterior circulation infarction: A retrospective case series study.

This study aims to analyze the clinical and imaging features of vertebrobasilar dolichoectasia (VBD) combined with posterior circulation infarction, and to explore risk factors for the occurrence of posterior circulation infarction in VBD patients.VBD patients were divided into 2 groups, according to the results of the imaging examination: posterior circulation infarction group and nonposterior circulation infarction group. The demographics, vascular risk factors, imaging, and other clinical data of the VBD patients were collected and retrospectively compared, and the risk factors for the occurrence of posterior circulation infarction in VBD patients were analyzed. The relationship between imaging features of the VBD blood supply artery and the infarct site was also analyzed.A total of 56 VBD patients were included into the analysis. Among these patients, 26 patients had posterior circulation infarction. Infarction occurred in the blood supply area of the posterior cerebral artery in 14 patients. The difference in the height of the basilar artery bifurcation between patients with vertebrobasilar artery blood supply area infarction and patients with posterior cerebral artery supply area infarction was statistically significant. Hypertension and posterior circulation intracranial atherosclerosis were the risk factors for posterior circulation infarction in VBD patients.Elevated basilar artery bifurcation is a risk factor for infarction in the posterior cerebral artery supply area in VBD patients. Posterior circulation infarction in VBD may be the comprehensive result of multiple factors, such as congenital defects of the basilar artery wall, hypertension, and atherosclerotic lesions.

Epidermal growth factor receptor inhibitor ameliorates excessive astrogliosis and improves the regeneration microenvironment and functional recovery in adult rats following spinal cord injury.

BACKGROUND: Astrogliosis is a common phenomenon after spinal cord injury (SCI). Although this process exerts positive effects on axonal regeneration, excessive astrogliosis imparts negative effects on neuronal repair and recovery. Epidermal growth factor receptor (EGFR) pathway is critical to the regulation of reactive astrogliosis, and therefore is a potential target of therapeutics to better control the response. In this report, we aim to investigate whether blocking EGFR signaling using an EGFR tyrosine kinase specific inhibitor can attenuate reactive astrogliosis and promote functional recovery after a traumatic SCI. METHOD: The astrocyte scratch injury model in vitro and the weight-drop SCI model in vivo were used as model systems. PD168393 was used to inhibit EGFR signaling activation. Astrocytic activation and phosphorylated EGFR (pEGFR) were observed after immunofluorescence staining and Western blot analysis. The rate of proliferation was determined by immunofluorescence detection of BrdU-incorporating cells located next to the wound. The levels of TNF-α, iNOS, COX-2 and IL-1ß in the culture medium under different conditions were assayed by ELISA. Western blot was performed to semi-quantify the expression of EGFR/pEGFR, glial fibrillary acid protein (GFAP) and chondroitin sulfate proteoglycans (CSPGs). Myelin was stained by Luxol Fast Blue Staining. Cresyl violet eosin staining was performed to analyze the lesion cavity volume and neuronal survival following injury. Finally, functional scoring and residual urine recording were performed to show the rats' recovery. RESULTS: EGFR phosphorylation was found to parallel astrocyte activation, and EGFR inhibitor PD168393 potently inhibited scratch-induced reactive astrogliosis and proinflammatory cytokine/mediator secretion of reactive astrocytes in vitro. Moreover, local administration of PD168393 in the injured area suppressed CSPGs production and glial scar formation, and resulted in reduced demyelination and neuronal loss, which correlated with remarkable hindlimb motor function and bladder improvement in SCI rats. CONCLUSIONS: The specific EGFR inhibitor PD168393 can ameliorate excessive reactive astrogliosis and facilitate a more favorable environment for axonal regeneration after SCI. As such, EGFR inhibitor may be a promising therapeutic intervention in CNS injury.