title: Pathophysiology of posttraumatic temporal lobe lesions.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Neurosurgery, Hospital das Clínicas, Federal University of Minas Gerais, Belo Horizonte, Brazil. agjg@zaz.com.br
authors.forename: Alexandre Varella
authors.initials: AV
authors.lastname: Giannetti
authors.forename: Mirto Nelso
authors.initials: MN
authors.lastname: Prandini
authors.forename: Audrey Beatriz
authors.initials: AB
authors.lastname: Santos Araujo
authors.forename: Lina Márcia
authors.initials: LM
authors.lastname: de Araujo Herval
mesh_terms: D000367:Age Factors; D000368:Aged; D000428:Alcohol Drinking / Q000009:adverse effects; D001778:Blood Coagulation Disorders / Q000503:physiopathology; D001929:Brain Edema / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D020201:Brain Hemorrhage, Traumatic / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D001930:Brain Injuries / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D018450:Disease Progression; D006801:Humans; D009336:Necrosis / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D012189:Retrospective Studies; D013702:Temporal Lobe / Q000000981:diagnostic imaging / Q000293:injuries* / Q000503:physiopathology*; D013997:Time Factors; D014057:Tomography, X-Ray Computed