Perhaps nothing transcends medical disciplines these days as does the concept of defining “biomarkers.” The desire to determine measures that correlate with diagnosis, treatment response, or the presence or absence of active disease resides in all physicians. As either a serological test or some other measure, a useful biomarker could prove to be of great value. Research grants that aim to determine such markers are being prioritized. Indeed, biomarkers, if validated, could decrease health care costs by improving clinical management decision making. In the study that follows, the authors attempt to determine the role of 2 putative markers, S100B and neuron-specific enolase (NSE), in traumatic brain injury, particularly for help in determining the use of brain CT scanning.1 The reviewers of this article all felt that the work was carefully performed and well documented. The reviewers did have differing opinions on the eventual value of these tests, particularly since they may not be readily available, can be more time consuming than a quickly obtained CT scan, and do not provide the specific information that brain imaging gives the surgeon. Nevertheless, the authors note that there are numerous published guidelines or “rules” for CT imaging in cases of milder traumatic brain injury. These include failure to return to a normal neurological condition within a short period of time, suspected open or stable skull fracture, repeated vomiting episodes, an older patient age, drug or alcohol intoxication, memory deficits, and seizures. In addition, assessment tools used in sportsor military-related injuries may help to clarify the need for further diagnostic testing. In this study, the authors hypothesized that the combination of an increase in S100B and NSE together with other defined risk factors would be associated with a “pathological finding” on CT scanning. It is a prospective study of 107 patients between the ages of 18 and 97 years, and samples were obtained within 3 hours of trauma. The authors included only those patients who were evaluated within 3 hours of injury, with a Glasgow Coma Scale score between 13 and 15 and blunt head trauma. There were specific exclusion criteria. They obtained CT studies in all patients, usually within 30 minutes of the initial evaluation. They found that patients with an intracranial hemorrhage had significantly higher levels of S100B and NSE and more often had nausea and vomiting. For some reason, NSE values were missing in 47 patients, and yet intracranial hemorrhage remained significantly associated with the presence of nausea, unconsciousness, and elevated S100B. The authors do not tell us how long it took for the serum tests to be returned to the doctor. The S100B concentration was elevated to the greatest extent in patients with subarachnoid hemorrhage, followed by levels in patients with intracerebral and subdural hematomas. It was also elevated in patients with a negative CT scan, ostensibly due to soft-tissue trauma. The authors do not overstate the value of their findings. They conclude that a combination of serum biomarkers together with symptoms showed good concordance with CT-positive patients who had evidence of brain hemorrhage. The authors did not provide detail as to the volumes of blood in the brain, what actually constituted a hemorrhage (CT positive vs CT negative), or the fact that other measures were somewhat subjective. Is nausea without vomiting important? Does a small white dot on a CT scan indicate an intracerebral hemorrhage or would it be considered negative? In different parts of the world and in different health care environments, brain imaging may not be readily available. The value of the clinical examination perhaps together with simply obtained serum biomarkers may direct patients more appropriately to hospitals with brain imaging capability, should that not be available at the original evaluation site. The authors’ report may serve as a foundation for additional work in this area. (http://thejns.org/doi/abs/10.3171/2012.10.JNS121942)
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