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A 4-year study (Japan Neurotrauma Data Bank) of the medical treatment of 1002 cases of traumatic brain injuries in Japan was conducted from 1998 to 2001 at 10 emergency medical centers. Patients with severe head injury were eligible for entry with a Glasgow Coma Scale score of 8 or less at admission. Patients who underwent craniotomy were also included. Children under 5 years old were excluded. An original data sheet with 392 items from multi-focal viewpoints, such as etiology of injury, pre-hospital care, initial treatment including neuro-intensive care unit, and surgical treatment, was created. The results show that the patient's age and mechanism of injury are the most important factors in the outcome.

A case of multiple intracranial epidermoids is reported. A 38-year-old woman who had a three-year history of hemihypesthesia on the right side of her body, diplopia, gait disturbance, dysarthria, and visual field defect, was admitted. Neurological examination revealed right hemiparesis, bilateral abducens palsies, and cerebellar dysfunction. A computed tomography (CT) scan demonstrated a huge low density area in the left middle cranial fossa and heterogeneous density area in the brain stem. She was diagnosed tentatively as epidermoid in the middle fossa and intraaxial mass of the brain stem. Surgery was performed twice. In the first operation, the temporal mass was removed subtotally. Secondarily, only suboccipital craniectomy was performed. After the second operation, her condition deteriorated due to recurrent aseptic meningitis and aspiration pneumonia. She died three months later. Autopsy revealed that an epidermoid was situated in the brain stem intraaxially and another epidermoid was located in the temporal region independently. An intraaxial epidermoid is a rare entity, especially in the brain stem. There is no report of multiple intracranial epidermoids in the literature. The authors emphasize the necessity to rule out epidermoid, when CT shows a high or heterogeneous density area, even if multiple and/or contrast enhanced.

This study was carried out to clarify the biochemical changes in the cold injured brain and their relationship to pathological changes. The cold lesion was produced by application of a cryoprobe containing liquid nitrogen to the exposed left temporal surface for 1 minute in rats anesthetized with a halothane and oxygen gas mixture. The brain edema developed by this procedure was localized in one hemisphere. The animals were guillotined at scheduled times after the cold injury. The brains were rapidly removed and divided exactly between the two hemispheres. Changes in specific gravity of the brain tissue were measured by the dry-weight method until 4 weeks after the injury. Hematoxylin-eosin and Kliiver-Barrera stains were applied to pathological specimens. Free amino acid and uric acid levels were measured chronologically by using Iriyama's method. Catecholamine levels were analyzed by using high-performance liquid chromatography with electrochemical detection. Water content in the injured hemisphere reached a peak level at 12 hours after the injury, then decreased gradually, and entered the normal range at 1 week after the injury. This results was similar to the previous report. Multiple small hemorrhagic lesions were disclosed 2 hours after the injury. This suggests that a mechanism similar to hemorrhagic infarction might play a role in the development of cold injury. Essential amino acids were increased in the injured hemisphere, while those in the contralateral side remained within normal ranges. This result suggests that, in the injured hemisphere, there was not only nonutilization of the essential amino acids but also disturbance of the blood brain barrier, and that the aerobic glycolytic pathway was maintained normally in the contralateral hemisphere. Norepinephrine and dopamine were lowered, while tyrosine was increased in the early stage of cold injury. This suggests impairment of the catecholamine synthesis followed by nonutilization of catecholamine precursors. Uric acid level was increased immediately after the injury, especially on the injured side, and lowered to near baseline level at 4 weeks after the insult. Although biosynthesis of uric acid in the brain is not fully understood, it seems to be a fine parameter of brain damage.