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Traumatic brain injury (TBI) is a multiphasic disease. Following the initial impact, secondary injury, including oxidative stress and inflammation, is thought to contribute significantly to death and disability. This ongoing damage in the penumbra of the brain leads to the demise of neuronal populations, and ultimately decreased brain function. Identification of various neural markers such as neuronal specific enolase (NSE) at various time points following TBI may help us better understand the magnitude of secondary injury following TBI, and may help predict outcome in these patients.
Early serial cerebrospinal fluid (CSF) samples were collected from patients with severe TBI (GCS 3 to 8) who required placement of a therapeutic ventriculostomy. Following ventriculostomy placement, CSF samples were obtained every 4 hours for the first 24 hours post-injury, then every 8 hours for post-injury days 2 to 5. The levels of NSE were then measured using the ELISA method.
Following sample analysis in 11 patients, we found that in TBI patients that had a good neurological outcome, the levels of NSE in the CSF rose early (between 25 and 60 ng/ml) within 12 to 16 hours following the initial injury. The NSE levels then rapidly decreased to normal levels (~5 ng/ml) at approximately 20 hours following injury, with these levels persisting until day 5 (day of final sample collection). Patients with a poor outcome (lack of ability to return to pre-injury activities or death) showed significantly higher levels of NSE persisting out to 5 days post injury, with late levels ranging from 35 to 50 ng/ml.
In TBI patients with a good outcome, there was an increase in NSE levels in the CSF noted at early time points (~16 hours), which abated at approximately 20 hours after injury. In TBI patients with a poor clinical outcome, CSF levels of NSE were significantly elevated at later time points over the first 5 days post injury.