Journal of neurotrauma
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Journal of neurotrauma · Feb 1996
Lesion volume, injury severity, and thalamic integrity following head injury.
Magnetic resonance (MR) scans of 63 traumatic brain injury (TBI) patients were analyzed to examine the relationship between injury severity, lesion volume (nonthalamic cortical/subcortical lesions), ventricle-to-brain ratio (VBR), and thalamic volume. For comparison, 33 normal control subjects were used. Patients with visible nonthalamic structural lesions showed significantly smaller thalamic volumes than patients without visible lesions or control subjects. ⋯ Patients with moderate-severe injuries had significantly smaller thalamic volumes and greater VBRs than patients with mild-moderate injuries. Although several variables related to thalamic volume, the presence of nonthalamic lesions was sufficient to result in smaller thalamic volume. Decreased thalamic volume following head injury suggests that subcortical brain structures may be susceptible to transneuronal degeneration following cortical lesions, and that this can be detected by in vivo MR-based volumetric analysis.
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Journal of neurotrauma · Feb 1996
The effect of lesion volume on cerebral vasomotor tone after focal brain injury and shock.
We have previously shown that the volume of a focal brain injury influences cerebral blood flow. We hypothesized that the cerebral vasomotor tone after traumatic brain injury and shock is related to lesion volume and that the size of the lesion would affect vasomotor reactivity. Swine were randomized to receive either a large or small cryogenic injury followed by shock, and were studied for 5 h postresuscitation. ⋯ A large brain injury and shock resulted in a significant decrease in the pial arteriolar diameter in the injured hemisphere. We also noted significant differences between and within groups in interhemispheric pial arteriolar diameter and pial arteriolar reactivity to acetylcholine and hypocarbia. These data suggest that the volume of injured tissue influences cerebral blood flow by a vascular mechanism, which may be due in part to an alteration in cerebral endothelial cell function.