Flexible endoscopically assisted evacuation of acute and subacute subdural hematoma through a small craniotomy: preliminary results.

BACKGROUND: The first choice to treat acute subdural hematoma (SDH) is a large craniotomy under general anesthesia. However, increasing age or comorbid burden of the patients may render invasive treatment strategy inappropriate. These medically frail patients with SDH may benefit from a combination of small craniotomy and endoscopic hematoma removal, which is less invasive and even available under local anesthesia. Although hematoma evacuation with a rigid endoscope for acute or subacute SDHs has been reported in the literature, use of a flexible endoscope may have distinct advantages. In this article, we attempted to clarify the utility of small craniotomy evacuation with a flexible endoscope for acute and subacute SDH in the elderly patients. METHOD: Between November 2013 and September 2016, a total of 17 patients with acute SDH (15 patients), subacute SDH (1 patient), or acute aggravation of chronic SDH (1 patient) underwent hematoma evacuation with a flexible endoscope at our hospital and were enrolled in this retrospective study. Either under local or general anesthesia, the SDH was removed with a flexible suction tube with the aid of the flexible endoscope through the small craniotomy (3 × 4 cm). Hematoma evacuation rate, improvement of clinical symptoms, and procedure-related complications were evaluated. RESULTS: Hematoma evacuation rate was satisfactory, and statistically significant clinical improvement was observed in postoperative Glasgow Coma Scale in all cases compared to the preoperative assessment. No procedure-related hemorrhagic complications were observed. CONCLUSIONS: The results reported here suggest that small craniotomy evacuation with a flexible endoscope is a safe, effective, and minimally invasive treatment for acute and subacute SDH in selected cases.

Nifedipine inhibits the progression of an experimentally induced cerebral aneurysm in rats with associated down-regulation of NF-kappa B transcriptional activity.

Cerebral aneurysm (CA) causes a life-threatening subarachnoid hemorrhage. However, no effective medical treatment to prevent the growth of CA is available. Nifedipine, a widely used calcium antagonist, was shown to improve endothelial function in various cardiovascular diseases. We examined whether nifedipine has a protective effect on CA progression. CAs were experimentally induced in Sprague-Dawley rats followed by intraperitoneal injection of either 10mg/kg of nifedipine per day or vehicle. The size and media thickness of CAs were measured one month after aneurysm induction. NF-kappa B (NF-kappaB) activity in aneurysmal walls was assessed by immunohistochemistry for activated NF-kappaB p65 subunit and electrophoretic mobility shift assay (EMSA). Expression of monocyte chomoattractant protein-1 (MCP-1) and matrix metalloproteinase (MMP) -2 in aneurysmal walls was examined by RT-PCR and immunohistochemistry. To examine whether nifedipine has a suppressive effect on preexisting CAs, nifedipine administration started at one month after aneurysm induction and pathological changes were assessed at two months after aneurysm induction. Aneurysm size was smaller and the media was thicker in the nifedipine-treated group even though blood pressure was not different between groups. Nifedipine inhibited DNA binding of NF-kappaB in aneurysmal walls. As regards MCP-1 expression and macrophage, which is the main inflammatory cell in the aneurysmal walls, infiltration into aneurysmal walls was decreased by nifedipine. Immunohistochemistry and gelatin zymography showed that the expression and activity of MMP-2 was also reduced by nifedipine. Furthermore, nifedipine significantly prevented the enlargement and degeneration of aneurysmal walls of preexisting CAs. Nifedipine may be useful as a medical drug for patients with CAs.