The involvement of inflammation in the development and propagation of chronic subdural haematoma (CSH) was investigated by measuring the levels of inflammatory cytokines (tumour necrosis factor [TNF] alpha, interleukin [IL]-1 beta, IL-6, and IL-8). Peripheral venous blood and subdural fluid were obtained at the time of burr hole surgery from 34 patients with CSH and from 9 with subdural effusion. The levels of the inflammatory cytokines were analysed by enzyme-linked immunosorbent assay. The blood levels of TNF alpha, IL-1 beta, IL-6, and IL-8 in both CSH and subdural effusion groups were almost within the range of normal subjects, and no differences were observed between the two groups. IL-6 and IL-8 in the subdural fluid were much higher than in the blood of both groups, and the levels in CSH patients were significantly higher (10 times) than in subdural effusion patients. Local elevation of inflammatory cytokines in the subdural space of both CSH and subdural effusion without systemic change suggests the presence of local inflammation in the two diseases. The same behavioural patterns of cytokines for these and higher levels of cytokines in the CSH also suggest that inflammatory cytokines may be involved in the continuous development from subdural effusion to CSH and propagation of CSH.
A 4-year-old boy presented with a transorbital-transpetrosal penetrating head injury after a butter knife had penetrated the left orbit. The knife tip reached the posterior fossa after penetrating the petrous bone. Wide craniotomy and the pterional, subtemporal, and lateral suboccipital approaches were per formed for safe removal of the object. The patient was discharged with left-sided blindness, complete left ophthalmoplegia, and hypesthesia of the left face. Early angiography is recommended to identify vascular injury which could result in fatal intracranial hemorrhage.
The involvement of coagulation and fibrinolysis in the development of chronic subdural haematoma (CSH) from subdural effusion was investigated. Subdural fluid and venous blood samples were obtained from 34 patients with CSH and 9 patients with subdural effusion, and analyzed using enzyme-linked immunosorbent assays for thrombin-antithrombin III complex (TAT), prothrombin fragment F1 + 2 (F1 + 2), tissue factor, tissue factor pathway inhibitor (TFPI) and D-dimer. CSH was classified into the layering type, believed to be active, and other types according to x-ray computed tomography. All markers in the blood of both patient groups were similar to the values of normal subjects. Levels of TAT and F1 + 2 were much higher in the subdural fluid than in the blood of patients with CSH (P < 0.001, P < 0.001) and with subdural effusion (P < 0.05, P < 0.05). The level of D-dimer in the subdural fluid was significantly higher than in the blood (P < 0.001) in patients with CSH, but not in patients with subdural effusion. All markers in the subdural fluid of layering type CSH, except TFPI, were significantly higher than in the other types (P < 0.05). Local hypercoagulative activity in the subdural space is present in subdural effusion and precedes hyperfibrinolytic activity in CSH. Thrombin generation as indicated by TAT and F1 + 2 might be involved in the development of CSH. Propagation of CSH may be modulated by the coagulation system including the extrinsic pathway and fibrinolysis.
Cerebellar primordia of different ages (embryonic days of 14 to 20) were transplanted into cerebella of normal syngeneic adult rats (Fischer 344). After 1-12 months (mostly 5-6 months), the host brains were examined by light and electron microscopy. In about 80% of our successful experiments, grafted Purkinje and/or granule cells migrated into the host molecular layer. Some granule cells migrated down along host Bergmann glia, reminiscent of their normal developmental migration route. Other granule cells migrated along astroglial processes that ensheathed capillary walls. Some grafted Purkinje cells were also located ectopically in the host molecular layer. They were identified as graft origins autoradiographically. This migration seemed to be encouraged under conditions where the subjacent host Purkinje cells had been lost. Where the grafted Purkinje cells were located on top of the host molecular layer, their primary dendrites faced vertically downwards into the host molecular layer. However, the position of the apical poles of migrated Purkinje cell bodies in the deeper aspect of the molecular layer varied considerably, suggesting that the orientation of the Purkinje cell dendrites is probably determined by the availability of afferent fibers. Thus, the present study has demonstrated that Purkinje and granule cells can migrate from embryonic cerebellar grafts into the molecular layer of the normal, adult host rat cerebellum.
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