Preoperatively recorded short-latency somatosensory evoked potentials (SSEP) and brain stem auditory evoked potentials (BAEP) were studied in 8 surgical cases of cerebral hemorrhage. The patients were comatose with clinical signs of transtentorial herniation. Six of the 8 cases regained consciousness after the emergency surgery, but the other 2 cases did not. In recordings of SSEP, the interpeak latency (IPL) of Erb's potential-P14, P14-N16 and N16-N20 were measured. The N20 of SSEP recorded by stimulating the median nerve contralateral to the supratentorial lesion was absent in all cases. In recordings of BAEP, the IPL of waves I-III and III-V were measured. Components of P14 and N16 in SSEP, and of waves III and V in BAEP, are considered to be generated in the brain stem. The interval between onset and recording of evoked potentials was 5±6 hours. The interval between onset and hematoma evacuation by craniotomy was 7±6 hours. Four of the 6 cases who regained consciousness after surgery showed anisocoria with light-reactive pupils, but the other 2 cases showed anisocoria with light-fixed pupils. Thus in the latter, preoperative prediction of postoperative recovery of consciousness was difficult. However, in all of the 6 cases who regained consciousness after surgery, the IPL of Erb's potential-P14, P14-N 16, I-III and III-V were within 3 SD from the normal mean value. Two cases who did not regain consciousness after surgery showed anisocoria with light-fixed pupils. Their SSEP were recorded by stimulating the median nerve contralateral to the supratentorial lesion. The IPL of P14-N16 were over +3 SD of the normal mean value. Of the 4 cases with light -fixed pupils, 2 cases (with normal latencies of the brain stem components of SSEP and BAEP) regained consciousness after surgery. Therefore, in comatose cases with transtentorial herniation due to supratentorial hematoma, records of SSEP and BAEP were valuable to predict postoperative consciousness and recovery after emergency surgery.

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The management of acute brain infarction consists of emergency supportive care, treatment of medical and neurological complications (including brain edema, hemorrhagic transformation and brain herniation), and prevention of early recurrence. Acute management in a stroke care unit can reduce the short-term and long-term mortality, and may improve the functional outcome. The NINDS rt-PA Stroke Study Group recently demonstrated that treatment with intravenous t-PA within 3 hours of the onset of ischemic stroke improved clinical outcome at 3 months. Diffusion MRI enables demonstration not only of irreversibly damaged but also of penumibral brain tissues within minutes or hours after a stroke. Many neuroprotective agents, and hypothermia, are now under the clinical evaluation. To obtain the maxum benefits from these promising diagnostic and therapeutic tools, the education of the public and health-care workers will be needed. The establishment of emergency transfer centers and management systems will also be required.

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We have investigated the correlation between spinal cord blood flow and artery diameter following acute spinal cord injury in rats. In the acute stage after the spinal cord injury, remote post-traumatic ischemia was apparent. From direct measurement of the artery caliber, it is highly likely that arterial vasoconstriction may contribute to the immediate decrease of blood flow in the area surrounding the injury site in the spinal cord. An hour after the injury autoregulation and responses to CO_2, especially in the spinal cord rostral to the injury site, were also disturbed. Extension of the pathological area may partly depend on arterial constriction following the spinal cord injury, and on the severity of impairment of autoregulation and CO_2 responsiveness. We have studied the overall results of cervical spinal cord injury between 1986 and 1996. Thirty-two of the cases were treated surgically and 27 cases conservatively. Although there was no statistically significant difference between the follow-up results of the 2 groups, a 2 step improvement in Frankel grading was observed in 6 cases in the surgically-treated group while no improvement was noticed in the conservative group. The interval from injury to operation ranged from 2 hours to 6 months, resulting in a wide therapeutic window for surgical intervention. There is still debate about the management of spinal cord injury with respect to the timing of the surgery, and use of instrumentation.

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Granulocyte-colony stimulating factor (G-CSF) was administered to 18 patients with malignant gliomas (6 glioblastoma multiforme and 12 anaplastic astrocytoma) who developed neutropenia after receiving chemotherapies with 2.67±0.49 (mean.±SD) of ACNU (3-[(4-amino-2-methyl-5-pyrimidynyl]-1-(2-chloroethyl)-1-nitrosourea hydrochloride) mg/kg administration. The nadir of neutrophils of the 18 cases was 910±373/mm^3, which was not significantly different from the nadir of the 18 control glioma cases (1,086±537) who were administered ACNU 2.58±0.62mg/kg without G-CSF. However, the number of days in which neutrophils were lower than 1,000/mm^3 was significantly smaller in the 18 cases (2.4±2.7 days) than that of the control group (5.4±3.4 days) . In addition, administration of G-CSF for 5 consecutive days decreased significantly the number of days in which the thrombocytes were lower than 105/mm^3, which suggests that the effect of G-CSF is recovery from the myelosuppression by ACNU administration. The mere effect of G-CSF decreasing the neutropenia level after chemotherapies is in itself, not clinically valuable. It should increase the dose-intensity of chemotherapeutic agents, as well as improve the therapeutic results. From this point of view, It is significant that among the 18 malignant glioma patients treated by ACNU ccmbined with G-CSF, radiation in 15 patients and IFN-β in 17 patients, 9 (50%) of the patients showed more than 50% regression of the tumor mass although among the control patients treated by ACNU without G CSF, with radiation in 15 patients and IFN-β in 3 patients, only 16.7% of the patients showed tumor regression.

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We report a case of dural arteriovenous fistulae (AVF) of the transverse sigmoid sinus associated with sinus occlusion stenosis. A 72-year-old male was presented who had had repeated episodes of intraventricular hemorrhage. We failed to obliterate the fistulae by transarterial embolization due to the recruitment of other feeding vessels and recanalization of embolized vessels. The transvenous embolization or resection of dural AVF seemed to be dangerous since the venous drainage system was not compensated by cortical veins. Although balloon angioplasty from the stenotic sinus gave temporary relief of venous congestion, this case, in the end, had an unfavorable outcome. We feel, this suggests that the treatment of dural AVF without compensatory venous drainage system can be very difficult.

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Malignant optic glioma in adulthood is a rare tumor which causes early loss of vision and usually leads to death within a year. We describe an adult case of malignant optic glioma and a review of past literatures. A 62-year-old man complained of rapidly deteriorating vision in his left eye. His visual acuity of the left eye was 0.07 (0.3) and that of the right eye was 1.2. Magnetic resonanse imaging (MRI) showed contrast enhancing masses in the left temporal lobe, left optic nerve, and chiasma. His visual loss of the left eye progressed, resulting in blindness within 4 weeks. A craniotomy was performed at the left pterion. Macroscopically, the left optic nerve was hyperemic and diffusely swollen. The temporal lesion was distinguished from the normal region,infiltrating into the subarachnoid space, having no apparent connection. A small biopsy of the left optic nerve and partial removal of the temporal lesion were performed. The histological diagnosis was anaplastic astrocytomas. Next, he received radiotherapy and chemotherapy consisting of carboplatin, etoposide, MCNU and vincristine. His visual acuity improved slightly after these therapies. However, 2 months later, he became blind in both eyes and showed right hemiparesis. An MRI exhibited the tumor infiltrating into the the left basal ganglia, the left internal capsule, as well as the right optic nerve. Nine months after the initial symptoms, he became comatose and died.

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It is a relatively well known complication that extracranial-intracranial bypass provokes the conversion of an intracranial arterial stenosis to a occlusion. We report a 57-year-old patient who deteriorated after bypass surgery which was attributable to this phenomenon. Postoperative cerebral blood flow decreased further in the whole cortical area as well as in the basal ganglia. One should bear in mind the possibility of this complication and should be cautious for performing bypass surgery in patients with intracranial arterial stenosis.

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