Burr hole and craniotomy in the treatment of subdural hematoma: A comparative study.

Aim: This article aims to study the clinical outcomes in patients with chronic subdural hematoma (CSDH) who underwent burr hole drainage or craniotomy. Patients and Methods: The length of hospitalization, Glasgow outcome scales (GOS) of patients undergoing burr-hole drainage or craniotomy, were evaluated and compared statistically. In this study, we also evaluated the relationship by receiver operating characteristic (ROC) analysis. Results: The sex and age distribution and specific clinical parameters of the patients were investigated. In this study, we provide the evidence of the GOS and length of hospitalization findings of the patients and the superiority of burr hole drainage over craniotomy. Conclusions: Chronic subdural hematoma responds better to burr hole drainage with shorter hospitalization and improved Glasgow score.

Histopathological changes in the choroid plexus after traumatic brain injury in the rats: a histologic and immunohistochemical study.

BACKGROUND: Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analysed the histopathological changes in E-cadherin and vascular endothelial growth factor (VEGF) expression after TBI in rats. MATERIALS AND METHODS: The rats were divided into two groups as the control and the trauma groups. Sprague-Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight-height impact. After 5 days of TBI, blood samples were taken under ketamine hydroxide anaesthesia and biochemical analyses were performed. The control and trauma groups were compared in terms of biochemical values. RESULTS: There was no change in glutathione (GSH) levels and blood-brain barier permeability. However, malondialdehyde (MDA) and myeloperoxidase (MPO) activity levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricle, near the pia mater membrane, was removed. In the traumatic group, some of epithelial cells were hyperplasic. Some of them were peeled off the apical surface and had local degeneration. CONCLUSIONS: In addition, we observed congestion in capillary vessels and mononuclear cell infiltration around the vessels. After TBI, the increase in VEGF levels, vascular permeability, and interaction with VEGF receptors in endothelial cells lead to oedema of the vessel wall. On the other hand, E-cadherin expression decreased in the tight-junction structures between epithelial cells and basal membrane, resulting in an increase in cerebrospinal fluid in the intervillous area.