Thrombomodulin (TM), which is located in the surface of the endothelium in the arteries, veins, and capillaries of major organs such as the brain, lungs, liver, kidneys, skeletal muscles, and gastrointestinal tract, is one of several indicators of endothelial injury. Von Willebrand factor (vWf), which is synthesized by endothelial cells, is also an endothelial specific glycoprotein. The serum level of vWf increases in response to various stimuli without endothelial injury. An elevated serum level of vWf may suggest endothelial activation in severe head injury. We hypothesize that the degree of cerebral endothelial activation or injury depends on the type of head injury and that measuring the TM and vWf is useful for predicting delayed traumatic intracerebral hematoma (DTICH), produced by weakness of the vessel wall, occuring either as a direct or indirect effect of head injury. The values of vWf in focal brain injury (ranging from 332.5 +/- 52.8% to 361.7 +/- 86.2%) were significantly higher than those in diffuse axonal injury from 2 h to 7 days after the injury occurred (ranging from 201.6 +/- 59.5% to 242.5 +/- 51.7%). The serum level of TM in focal brain injury (ranging from 3.84 +/- 1.54 to 4.12 +/- 1.46 U/mL) was higher than that in diffuse axonal injury (ranging from 2.96 +/- 0.63 to 3.67 +/- 1.70 U/mL), but these differences were not statistically significant. In patients with DTICH, TM was significantly higher than in patients without DTICH (p < 0.01). The results of our study demonstrate that the degree of endothelial activation in focal brain injury was significantly higher than in diffuse brain injury. In addition, the serum level of TM in patients with DTICH was significantly higher than in patients without DTICH. These findings suggest that cerebral tissue injury is often accompanied by cerebral endothelial activation, and that these two phenomena should be distinguished from each other. The levels of serum TM and vWf appear to be good indicators of the cerebral endothelial injury and of endothelial activation in severe head injury.

Even immediately following resuscitation, absence of cortical activity in SSEP indicates unlikelihood of recovering consciousness, while the preservation of such activity suggests that consciousness is improved. The result promises further accumulation of patients to validate the predictive ability of SSEP in managing postresuscitated patients.

Metabolic depression reflecting neural injury was apparent in subjacent normal-appearing white matter at 1 week after cortical contusion; this had normalized substantially at 1 month.

One hundred and seventy patients with ruptured cerebral aneurysms were treated by coil embolization from September 1997 to December 2002. After January 2000, coil embolization was selected as the first-choice treatment for ruptured aneurysms. During this period, the authors investigated the number of aborted cases, the number of complications, and how many patients could be treated by coil embolization according to the locations of ruptured cerebral aneurysms. One hundred and ninety-five sessions were performed on 170 patients, and 13 sessions (6.7%) were aborted mainly because of the difficulty of the approach and the wide necks of the aneurysms. In four patients, although procedural perforation and haemorrhage occurred, the outcome was good or excellent. Eight poor-grade patients experienced haemorrhage after coil embolization and seven patients died. The volume embolization ratios of small and large aneurysms were 27% and 21%, and the recanalization of small and large aneurysms occurred in 9% and 38% of patients, respectively. From January 2000 to December 2002, 119 (66%) of 180 ruptured cerebral aneurysms were treated by coil embolization. According to the location of aneurysms, 89% vertebrobasilar, 87% anterior cerebral, 65% internal carotid and 24% middle cerebral artery aneurysms could be treated by coil embolization. Because the tight packing of large aneurysms was difficult, the recanalization rate of large aneurysms was high. However, the results of small aneurysms were satisfactory. Almost 90% of vertebrobasilar and anterior cerebral artery aneurysms could be treated by coil embolization.

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