Characterization of axonal injury produced by controlled cortical impact.
Axonal injury and behavioral changes were evaluated 3-7 days after traumatic brain injury. Previous research from this laboratory demonstrated that clinical central nervous pathology is produced by dynamic brain compression using a stroke-constrained impactor. We wanted to determine if the technique also would produce diffuse axonal injury after recovery from the procedure. The experiments were performed at Wayne State University School of Medicine using aseptic techniques while assuring analgesic care. Impacts were performed at 4.3 m/sec or 8.0 m/sec, with congruent to 10% compression (2.5 mm). Extensive axonal injury was observed at 3 and 7 days postinjury using both velocity-compression combinations. Regions displaying axonal injury were the subcortical white matter, internal capsule, thalamic relay nuclei, midbrain, pons, and medulla. Axonal injury also was evident in the white matter of the cerebellar folia and the region of the deep cerebellar nuclei. Behavioral assessment showed functional coma lasting up to 36 h following 8.0 m/sec impacts, with impaired movement and control of the extremities over the duration of the postinjury monitoring time. These experiments confirm that the cortical impact model of traumatic brain injury mimics all aspects of traumatic brain injury in humans and can be used to investigate mechanisms of axonal damage and prolonged behavioral suppression.
Lighthall
J W
JW
Biomedical Science Department, General Motors Research Laboratories, Warren, Michigan.
Goshgarian
H G
HG
Pinderski
C R
CR
D000818:Animals; D001369:Axons / Q000473:pathology*; D001930:Brain Injuries / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D002335:Carnivora / Q000502:physiology*; D003128:Coma / Q000209:etiology* / Q000503:physiopathology; D004195:Disease Models, Animal; D005289:Ferrets / Q000502:physiology*; D008297:Male; D009069:Movement Disorders / Q000209:etiology* / Q000503:physiopathology