A 30-year-old male clinico-pathological case survived for 1 year and 9 months after being hit by a truck while riding on his motorbike on Aug. 21, 1988. On admission, his consciousness level was 5 according to the Glasgow Coma Scale, and a traumatic intraventricular hemorrhage and cerebral contusion were revealed by CT scanning. He underwent immediately an operation in order to drain blood from the ventricles at which time a right side dominant quadriplegia was noted. He made a gradual improvement and by January 1989 was able to tell us his name and address correctly. However, he remained incontinent and bedridden owing to the contracture of joints. He was put on rehabilitation exercises in March 1989 which trained him to operate a wheelchair. In April 1990 he regained urinary control, but was remarkably devoid of will power, perseverance and memory. He expired of pneumonia on May 11, 1990. At autopsy, his brain weighed 1180 g. The cerebral convexity was discolored, especially the rectal gyri and bilateral olfactory bulbs were brownish-yellow. Old gross contusional scars were observed on the left rectal and orbital gyri, and the 3rd ventricle and inferior horns of the lateral ventricles were enlarged. Holzer's method revealed fibrillary gliosis in the corpus callosum, fornix, cingulate gyrus and a part of the caudate nucleus adjacent to the thalamus. Microscopically, axons were seen to be disrupted in the corpus callosum as well as in the anterior commissure, having the appearance of macrophages. A myelin pallor was noted in the bilateral pyramidal tracts below the level of the midbrain, and there was a slight myelin pallor in the deep cerebral white matter. The medial part of the cerebrum was almost exclusively affected, whereas the damage of the superficial part was relatively minimal. Such a distribution of lesions suggests that the brain had sustained injury by revolving acceleration at the time of the accident. However, a mild change of white matter without any axonal disruption prevented us from concluding that this was a DAI (diffuse axonal injury) case. In the hitherto reported cases of DAI, including the authors' cases, a variety of white matter lesions were seen: mild myelin pallor as in this case, little or dense gliosis, widespread axonal disruption, gliding contusion, etc. The degree of intensity of gliosis might depend upon intracranial pressure or the functional state of the astrocytes. The protracted comatous state and the absence of fracture suggest clinically Diffuse Brain Injury (DBI), but it is important to distinguish the "clinical" DBI and the "histological" DAI. Furthermore, it would be worth re-examining whether all the white matter lesions seen in so-called DAI occur at the time of injury.
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