Recurrence of chronic subdural hematoma after burr-hole craniostomy and closed system drainage is not uncommon. We sought to identify risk factors for recurrence. In 121 patients, various factors including age, initial neurologic status, hematoma thickness, computed tomographic density of the hematoma, midline shift, multiplicity, systemic disease, and drainage volume were compared retrospectively between nonrecurring cases and recurring cases. Recurrence was noted in 10 cases (8.3%). In recurring cases, the drainage volume was significantly larger than in nonrecurring cases, and the recurrence rate increased in proportion to drainage volume. Other factors significantly influencing recurrence were hematoma thickness and associated diabetes mellitus. Drainage contents mainly derived from either exudate within the subdural membrane or cerebrospinal fluid leakage. Entry of cerebrospinal fluid into the hematoma cavity or continuing leakage of serum components through opened endothelial gap junctions are considered to be major causes of increased drainage volume, leading in turn to recurrence of the hematoma.

The synthetic pyrazolopyrimidine, 4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP1) is a novel, potent, and selective inhibitor of Src family tyrosine kinases. Vascular permeability appears to be mediated by vascular endothelial growth factor (VEGF), which requires the activation of downstream Src family kinases to exert its function. This study investigates the effects of PP1 on vascular permeability and inflammatory response in a rat spinal cord compression model. Ten minutes after compression, PP1 (PP1 group) or the vehicle only (control group) was administered. On days 1, 3, and 7 after compression, the spinal cords were removed and examined histopathologically to determine the expression of VEGF and the extent of edema and inflammation. The dryweight method was used to measure the water content of the spinal cords. The mRNA levels of tumor necrosis factor a (TNFalpha) and interleukin 1beta (IL-1beta), which is related to inflammatory responses, were measured with a real-time polymerase chain reaction (RT-PCR) system 6 h after compression. Although VEGF expression was similar in both groups, the extent of contusional lesion in the PP1 group was reduced by approximately 35% on day 3. Moreover, the water content on days 1, 3, and 7 was significantly reduced and macrophage infiltration on days 3 and 7 was dramatically reduced in the PP1 group. TNF and IL-1beta mRNA expression in the PP1 group were also significantly reduced. These results indicate that PP1 reduces secondary damage after spinal cord injury.

By use of this method, reoperation was avoided and the patients were mobile early in the postoperative period. This method was suitable for refractory chronic subdural hematoma accompanied by severe disease that adversely influenced the clinical course.

Apolipoprotein E (ApoE) is a major apolipoprotein in the central nervous system (CNS) that plays an important role in Alzheimer's disease. It may also be involved in other CNS disorders including ischemic injury. We investigated the changes of ApoE protein and mRNA expression in the brain with middle cerebral artery occlusion (MCAO) to clarify its origin after focal ischemia in rats. Increased ApoE immunoreactivity was recognized in astrocytes 3-14 days after MCAO in the affected side of cortex, and in neurons 4-14 days after MCAO in the same area. ApoE immunoreactivity was also detected in macrophages in the ischemic core 3-14 days after MCAO. In contrast, ApoE mRNA was expressed in astrocytes and macrophages, but not in neurons. These results suggested that neuronal ApoE was not synthesized in neurons, but derived from astrocytes.