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J Korean Neurosurg Soc. 1984 Mar;13(1):29-41. Korean. Original Article.
Choi CH , Lee YW .
Department of Neurosurgery, Busan National University School of Medicine, Busan, Korea.

This study was undertaken to identify acute changes and mechanism of traumatic brain edema in the rabit by measuring the regional specific gravities and water content with Evans blue dye staining. After delivery of brain injury on the frontal area, animals were sacrificed at 30 minutes, 2, 4 and 6 hours. Specific gravity data collection of regional brain tissue was taken in the serial copper sulfate gravity solution. The regions tested included frontal lobe, occipital lobe, basal ganglia, cerebellum, pons and medulla. Specific gravity data and Evans blue dye staining with spread were compared with those from similar areas in the uninjured anesthetized rabbits to test for brain edema. The results obtained were as follows: 1) Immediately following brain impact, almost all animals in this study demonstrated temporary respiratory arrest. The mean duration of respiratory arrest in experimental animals was 15+/-3 seconds. There was no correlation between length of respiratory arrest and either gross intracranial pathology or brain edema data. 2) The specific gravities in both hemispheres were same in control animals and were not affected by the duration of anesthesia. 3) Significant decrease of specific gravity was identified in the both supratentorial regions at 30 minutes, 2 and 4 hours after trauma. This finding was more prominent in the contused side. No significant changes occurred in the cerebellum but significant decrease of specific gravity occurred in medulla at 6 hours. 4) Almost brain water content was increased as the time course and arrived on peak value at 4 hours and decreased at 6 hours after trauma in the supratentorial regions. 5) Evans blue dye staining occurred in the contusion area at 30 minutes after trauma and spread to surrounding cortex and subcortex but dye density was decreased with time. These results suggest that traumatic brain edema may originate from vasogenic mechanism due to dysfunction of blood-brain barrier and this edema may spread to both cerebral hemispheres and brain stem.

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