Pathophysiology of posttraumatic temporal lobe lesions

ArticleinSurgical Neurology 64 Suppl 1:S1:22-9; discussion S1:29 · February 2005with7 Reads
Impact Factor: 1.67 · DOI: 10.1016/j.surneu.2004.11.008 · Source: PubMed


    Posttraumatic parenchymal lesions in the temporal lobe may cause neurologic deterioration. An analysis was made of the natural evolution of this type of lesion, with emphasis on its 2 components: hemorrhage (hyperdense on computed tomography [CT]), and edema and necrosis (hypodense on CT). The clinical repercussions were studied, and the factors that might influence such evolution were investigated.
    Forty head-injured patients with temporal lobe lesions admitted within 12 hours after the injury were selected in a prospective manner. Computed tomography scans were systematically repeated within the first 36 hours and at 7 and 30 days postinjury. Factors such as interval between injury and the first CT scan, age, velocity of the injury, alcohol consumption, coagulation abnormalities, and the presence of decompressive measures were compared between the patients that had enlargement of the hemorrhage and those who did not. Increase in hypodensity was compared with that in hyperdensity.
    Fourteen patients showed enlargement of the hemorrhage. In all cases but one, the interval between injury and admission was 3 hours or less. Other factors had no statistical significance as predisposing causes for such enlargement. In approximately half of the cases, the hypodense component increased in the first 36 hours and continued increasing until the end of the first week. Evolution of the hypodense component was not dependent on behavior of the hemorrhage, surgical drainage, or diameter of the hemorrhagic lesion.
    The natural evolution of the hyperdense component of temporal lobe lesions was to enlarge within the first few hours after the injury. Edema and necrosis developed more slowly and with no significant clinical manifestations.