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To investigate the association between subarachnoid hemorrhage-induced delayed cerebral vasospasm (DCVS) and oxidative stress, an oxidation product, hydroperoxide, was measured in 3 specimens: peripheral arterial blood, cerebrospinal fluid (CSF), and internal jugular venous blood (IJVB).Hydroperoxide was measured using the diacron reactive oxygen metabolites (d-ROMs) test. The hydroperoxide levels were evaluated based on the rate of change in the d-ROMs test value on day 6 relative with that on day 3 (d-ROMs change rate).The subjects were 20 patients. The d-ROMs change rate in IJVB was significantly higher in patients with DCVS on day 6 than in those without it (P.01). When the patients were classified into the following 3 groups: Group A (no DCVS occurred throughout the clinical course); Group B (DCVS occurred, but no cerebral infarction [CI] was induced); and Group C (DCVS occurred and caused CI), the d-ROMs change rate in IJVB was the highest in Group C, followed by Group B then A (P.01). The d-ROMs change rates in peripheral arterial blood and CSF were not related to the development of DCVS.It was concluded that the more severe DCVS occurs and is more likely to progress to CI as the IJVB hydroperoxide level rises early after the development of subarachnoid hemorrhage.

Aims: Neurointensive care has reduced the mortality and improved the outcome of patients for severe brain damage, over recent decades, and made it possible to perform this therapy in safety. However, we have to understand the complications of this therapy well. The purpose of our study was to determine the systemic circulation disturbance during the initiation of therapeutic hypothermia by using this continuous neurointensive monitoring system. Materials and Methods: Ten severe brain damage patients treated with hypothermia were enrolled. All patients had Glasgow Coma Scale (GCS) less than or equal to 8, on admission. Results: We verified that heart rate, cardiac output, and oxygen delivery index (DO2I) decreased with decreasing core temperature. We recognized that depressed cardiac index (CI) was attributed to bradycardia, dehydration, and increased systemic vascular resistance index (SVRI) upon initiation of hypothermia. Conclusion: Although the hypothermia has a therapeutic role in severe brain damage patients, we have to carry out this therapy while maintaining their cardiac output using multimodality monitoring devices during hypothermia period.

Subarachnoid hemorrhage (SAH) causes dynamic changes in cerebral blood flow (CBF), and results in delayed ischemia due to vasospasm, and early perfusion deficits before delayed cerebral vasospasm (CVS). The present study examined the severity of cerebral circulatory disturbance during the early phase before delayed CVS and whether it can be used to predict patient outcome. A total of 94 patients with SAH underwent simultaneous xenon computed tomography (CT) and perfusion CT to evaluate cerebral circulation on Days 1-3. Cerebral blood flow (CBF) was measured using xenon CT and the mean transit time (MTT) using perfusion CT and calculated cerebral blood volume (CBV). Outcome was evaluated with the Glasgow Outcome Scale (good recovery [GR], moderate disability [MD], severe disability [SD], vegetative state [VS], or death [D]). Hunt and Hess (HH) grade II patients displayed significantly higher CBF and lower MTT than HH grade IV and V patients. HH grade III patients displayed significantly higher CBF and lower MTT than HH grade IV and V patients. Patients with favorable outcome (GR or MD) had significantly higher CBF and lower MTT than those with unfavorable outcome (SD, VS, or D). Discriminant analysis of these parameters could predict patient outcome with a probability of 74.5%. Higher HH grade on admission was associated with decreased CBF and CBV and prolonged MTT. CBF reduction and MTT prolongation before the onset of delayed CVS might influence the clinical outcome of SAH. These parameters are helpful for evaluating the severity of SAH and predicting the outcomes of SAH patients.

Traumatic brain injury (TBI) is widely known to cause dynamic changes in cerebral blood flow (CBF). In particular, secondary brain insults have been reported to decrease CBF. The purpose of this study was to clarify the cerebral circulation in different types of TBI.Sixty-nine patients with TBI were divided into four groups, the subdural hematoma group, the contusion/intracerebral hematoma group, the diffuse axonal injury group, and the diffuse brain swelling group. In these patients, we simultaneously performed Xe-CT and perfusion CT to evaluate the cerebral circulation on post-injury days 1-3. We measured CBF using Xe-CT and mean transit time using perfusion CT and calculated the cerebral blood volume using the AZ-7000 W98 computer system.There were no significant differences in the Glasgow Coma Scale score on arrival or the Glasgow Outcome Scale score between the groups. The patients who had suffered focal TBI displayed more significant cerebral circulation disturbances than those that had suffered diffuse TBI. We were able to evaluate the cerebral circulation of TBI patients using these parameters.Moderate hypothermia therapy, which decreases CBF, the cerebral metabolic rate oxygen consumption (CMRO2), and intracranial pressure might be effective against the types of TBI accompanied by cerebral circulation disturbance. We have to use all possible measures including hypothermia therapy to treat severe TBI patients according to the type of TBI that they have suffered.

Introduction: Traumatic brain injury (TBI) is widely known to cause dynamic changes in cerebral blood flow (CBF). In particular, secondary brain insults have been reported to decrease CBF. The purpose of this study was to clarify the cerebral circulation in different types of TBI.

The trans-sylvian approach is one of the most frequently employed neurosurgical procedures, but it is difficult for medical students to understand the approach stereoscopically. A three-dimensional model equipped with an arachnoid membrane and sylvian vein was developed which can be repeatedly used to simulate surgery for the education of medical students and residents in the trans-sylvian approach. The model was prepared using existing models of the skull bone, brain, and cerebral artery. Polyvinylidene chloride film, commonly used as plastic wrap for food, was adopted for the arachnoid membrane, and wetted water-insoluble tissue paper for the arachnoid trabeculae. The sylvian vein was prepared by ligating woolen yarn with cotton lace thread at several sites. Students and residents performed the trans-sylvian approach under a microscope, and answered a questionnaire survey. Using this model, simulation of division of the arachnoid membrane and arachnoid trabeculae, and dissection of the sylvian vein was possible. In the questionnaire, the subjects answered 8 questions concerning understanding of the stereoscopic anatomy of the sylvian fissure, usefulness of the simulation, and interest in neurosurgical operation using the following ratings: yes, very much; yes; somewhat; not very much; or not at all. All items rated as ‘yes, very much’ and ‘yes’ accounted for more than 70% of answers. This model was useful for medical students to learn the trans-sylvian approach. In addition, repeated practice is possible using cheap materials, which is advantageous for an educational model.

ATF5 is a member of the CREB/ATF family of transcription factors. In the current study, using a transient transfection system to express FLAG epitope fusion proteins of ATF5, we have shown that CdCl{sub 2} or NaAsO{sub 3} increases the protein levels of ATF5 in cells, and that cadmium stabilizes the ATF5 protein. Proteasome inhibitors had a similar effect to cadmium on the cellular accumulation of ATF5. Proteasome inhibition led to an increase in ubiquitinated ATF5, while cadmium did not appear to reduce the extent of ATF5 ubiquitination. ATF5 contains a putative nuclear export signal within its N-terminus. We demonstrated that whereas deletion of N-terminal region resulted in a increase of ATF5 levels, this region does not appear to be involved in the ubiquitination of ATF5. These results indicate that ATF5 is targeted for degradation by the ubiquitin-proteasome pathway, and that cadmium slows the rate of ATF5 degradation via a post-ubiquitination mechanism.