OBJECTIVE: To determine whether CSF amyloid beta 1-42 (Abeta-42) and tau have predictive value for prognosis after head injury. METHODS: CSF samples were collected from 29 patients with severe head trauma between 1 and 284 days post-trauma. Abeta-42 and tau levels were measured using sandwich ELISA techniques and compared with CSF levels in patients with cognitive disorders and headache. RESULTS: At all time points, concentrations of Abeta-42 were significantly lower in patients with traumatic brain injury (TBI) than in control groups. A significant correlation existed for Abeta-42 levels and outcome of patients. Below a cutoff of 230 pg/mL, the sensitivity of Abeta-42 to discriminate between good outcome (Glasgow Outcome Score 4 and 5) and poor outcome (Glasgow Outcome Score 1 through 3) was 100% at a specificity of 82%. CSF tau levels were significantly higher in patients with TBI than in any control group. In patients with multiple CSF samples collected at various time points between 1 and 32 days after the trauma, tau levels increased early after TBI, peaked in the second week post-trauma, and slowly decreased thereafter. Independent of outcome, all patients had normal tau levels when CSF was collected more than 43 days post-trauma. CONCLUSIONS: Abeta-42 and tau may play a potential role in the pathophysiology of TBI. Furthermore, the results of this study suggest that Abeta-42 may be a supportive early predictor for recovery after severe head injury.
OBJECTIVE: To determine whether CSF amyloid beta 1-42 (Abeta-42) and tau have predictive value for prognosis after head injury. METHODS:CSF samples were collected from 29 patients with severe head trauma between 1 and 284 days post-trauma. Abeta-42 and tau levels were measured using sandwich ELISA techniques and compared with CSF levels in patients with cognitive disorders and headache. RESULTS: At all time points, concentrations of Abeta-42 were significantly lower in patients with traumatic brain injury (TBI) than in control groups. A significant correlation existed for Abeta-42 levels and outcome of patients. Below a cutoff of 230 pg/mL, the sensitivity of Abeta-42 to discriminate between good outcome (Glasgow Outcome Score 4 and 5) and poor outcome (Glasgow Outcome Score 1 through 3) was 100% at a specificity of 82%. CSFtau levels were significantly higher in patients with TBI than in any control group. In patients with multiple CSF samples collected at various time points between 1 and 32 days after the trauma, tau levels increased early after TBI, peaked in the second week post-trauma, and slowly decreased thereafter. Independent of outcome, all patients had normal tau levels when CSF was collected more than 43 days post-trauma. CONCLUSIONS:Abeta-42 and tau may play a potential role in the pathophysiology of TBI. Furthermore, the results of this study suggest that Abeta-42 may be a supportive early predictor for recovery after severe head injury.
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