Fluid Biomarkers of Traumatic Brain Injury and Intended Context of Use

Abstract

Traumatic brain injury (TBI) is one of the leading causes of death and disability around the world. The lack of validated biomarkers for TBI is a major impediment to developing effective therapies and improving clinical practice, as well as stimulating much work in this area. In this review, we focus on different settings of TBI management where blood or cerebrospinal fluid (CSF) biomarkers could be utilized for predicting clinically-relevant consequences and guiding management decisions. Requirements that the biomarker must fulfill differ based on the intended context of use (CoU). Specifically, we focus on fluid biomarkers in order to: (1) identify patients who may require acute neuroimaging (cranial computerized tomography (CT) or magnetic resonance imaging (MRI); (2) select patients at risk for secondary brain injury processes; (3) aid in counseling patients about their symptoms at discharge; (4) identify patients at risk for developing postconcussive syndrome (PCS), posttraumatic epilepsy (PTE) or chronic traumatic encephalopathy (CTE); (5) predict outcomes with respect to poor or good recovery; (6) inform counseling as to return to work (RTW) or to play. Despite significant advances already made from biomarker-based studies of TBI, there is an immediate need for further large-scale studies focused on identifying and innovating sensitive and reliable TBI biomarkers. These studies should be designed with the intended CoU in mind.

Early Levels of Glial Fibrillary Acidic Protein and Neurofilament Light Protein in Predicting the Outcome of Mild Traumatic Brain Injury

“…7 In case of mTBI, blood biomarkers could be useful in evaluating the risk for prolonged problems. 8,9,10 S100 calcium binding protein (S100-B), which is principally expressed in glial cells, has been the most studied biomarker in mTBI. 11,12,13,14 Regrettably, it neither seems to be a useful prognosticator of TBI outcome, partly due to extracerebral expression; 15,16,17 nor has it been able to discriminate patients who will develop prolonged or persistent symptoms.…”

Modeling sports‐related mild traumatic brain injury in animals—A systematic review

“…TBI is a neurological episode whereby head trauma instigates molecular, cellular, and structural pathology, which may result in functional disturbance to the central nervous system (CNS) (Rehman, Ali, Tawil, & Yonas, ). TBI exists on a continuum, from asymptomatic mild injuries to severe TBI, involving high focal contact forces that can lead to fracturing of the skull, subdural hematoma, cerebral contusion, and hemorrhage within the hemispheres (Bogoslovsky, Gill, Jeromin, Davis, & Diaz‐Arrastia, ). This review will focus on mild traumatic brain injuries (mTBI), which account for three times the number of all other acquired brain injuries combined (Mannix & Meehan, ), and are typical of the contact forces that occur to athletes on the field of play.…”

Carbacetam effect on processes of neurodestruction in hippocampus during experimental traumatic brain injury.

“…В свою чергу в гіпокампі тварин з ЧМТ спостерігалися високі рівні експресії GFAP та S100, що свідчить про порушення нейрон-гліальних взаємодій та всіх процесів, які залежать від скоординованої роботи нейронів і астроцитів. В гіпокампі спостерігався високий рівень експресії NSE, що корелює з нормальним нейрональним метаболізмом [19]. Для гіпокампу також притаманні морфологічні та імуногістохімічні ознаки пошкодження, однак в цілому метаболічна активність нейронів знаходиться на високому рівні, на що вказує експресія маркера NSE.…”