Neuronal damage secondary to traumatic brain injury (TBI) is a rapidly evolving condition, which requires therapeutic decisions based on the timely identification of clinical deterioration. Changes in S100B biomarker levels are associated with TBI severity and patient outcome. The S100B quantification is often difficult since standard immunoassays are time-consuming, costly, and require extensive expertise. A zero-length cross-linking approach on a cysteamine self-assembled monolayer (SAM) was performed to immobilize anti-S100B monoclonal antibodies onto both planar (AuEs) and interdigitated (AuIDEs) gold electrodes via carbonyl-bond. Surface characterization was performed by atomic force microscopy (AFM) and specular-reflectance FTIR for each functionalization step. Biosensor response was studied using the change in charge-transfer resistance (Rct) from electrochemical impedance spectroscopy (EIS) in potassium ferrocyanide, with [S100B] ranging 10–1000 pg/mL. A single-frequency analysis for capacitances was also performed in AuIDEs. Full factorial designs were applied to assess biosensor sensitivity, specificity, and limit-of-detection (LOD). Higher Rct values were found with increased S100B concentration in both platforms. LODs were 18 pg/mL(AuES) and 6 pg/mL(AuIDEs). AuIDEs provide a simpler manufacturing protocol, with reduced fabrication time and possibly costs, simpler electrochemical response analysis, and could be used for single-frequency analysis for monitoring capacitance changes related to S100B levels.

Point-of-Care (POC) testing for biomarker detection demands techniques that are easy to use, readily available, low-cost, and with rapid response times. This paper describes the development of a fully open-source, modular, wireless, battery-powered, smartphone-controlled, low-cost potentiostat capable of conducting electrochemical impedance spectroscopy for the electrochemical detection of the S100B protein captured in an ANTI-S100B functionalized thin-film gold interdigitated electrode platform to support traumatic brain injury diagnosis and treatment. EIS results from the developed potentiostat were validated with a commercial benchtop potentiostat by comparing impedance magnitude and phase values along the EIS frequency range. In addition, an experimental design was performed for detecting S100B in spiked human plasma samples with S100B concentrations of clinical utility, and a calibration curve was found for quantifying S100B detection. No statistically significant differences were found between EIS results from the developed potentiostat and the commercial potentiostat. Statistically significant differences in the changes in charge transfer resistance signal between each tested S100B concentration (p < 0.05) were found, with a limit of detection of 35.73 pg/mL. The modularity of the proposed potentiostat allows easier component changes according to the application demands in power, frequency excitation ranges, wireless communication protocol, signal amplification and transduction, precision, and sampling frequency of ADC, among others, when compared to state-of-the-art open-source EIS potentiostats. In addition, the use of minimal, easy acquirable open-source hardware and software, high-level filtering, accurate ADC, Fast Fourier Transform with low spectral leakage, wireless communication, and the simple user interface provides a framework for facilitating EIS analysis and developing new affordable instrumentation for POC biosensors integrated systems.

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The potential of early neurological inaccurate assessment of severity in patients with traumatic brain injury (TBI) has been highlighted; in some cases, for example, the severity of the injury is overestimated or underestimated. These findings have led to the search of biomarkers associated with early brain injury. Research in this field has exponentially increased over the past 20 years, with most publications on the subject in the last 10 years, whose results range from promising findings to other sometimes inconclusive one. An ideal biomarker should be able to demonstrate high sensitivity and specificity for brain injury, among other aspects. Literature has shown that there is not a single biomarker that predicts the patient's clinical decline with high sensitivity and specificity. Instead, it is required to use a panel of markers that reflect different aspects of head trauma. This chapter gives a review of the most promising biomarkers studied as predictors of severity of TBI, with a special focus on their nature, location, basal concentrations, and methods by which they can be quantified in blood samples.

Introducción. El trauma craneoencefálico es una de las principales causas de muerte y discapacidad en adultos jóvenes. Su gravedad se define según la escala de coma de Glasgow. Sin embargo, el deterioro neurológico agudo no siempre concuerda con la gravedad inicial indicada por la escala, lo que implica una subestimación de la magnitud real de la lesión.Objetivo. Estudiar la correlación entre la gravedad inicial del trauma craneoencefálico según la escala de coma de Glasgow y la condición final del paciente, en el contexto de diferentes variables clínicas y de los hallazgos de la tomografía.Materiales y métodos. Se analizó una cohorte retrospectiva de 490 pacientes con trauma craneoencefálico cerrado que requirieron atención en la unidad de cuidados intensivos de dos centros de tercer nivel de Barranquilla. La estimación del riesgo se estableció con la razón de momios (odds ratio, OR) y un intervalo de confianza (IC) del 95 %. Se utilizó un alfa de 0,05 como nivel de significación.Resultados. El 41,0 % de los pacientes requirió intubación endotraqueal; el 51,2 % había presentado traumas inicialmente clasificados como moderados y, el 6,0 %, como leves. El retraso en la implementación de un tratamiento agresivo afectó principalmente a aquellos con trauma craneoencefálico moderado, en quienes la letalidad aumentó al 100 % cuando no se detectó a tiempo el deterioro neurológico y, por lo tanto, el tratamiento agresivo se demoró más de 4 a 8 horas. Por el contrario, la letalidad fue de menos de 20 % cuando se brindó el tratamiento agresivo en el curso de la primera hora después del trauma.Conclusiones. El riesgo de letalidad del trauma craneoencefálico aumentó cuando el deterioro neurológico se detectó tardíamente y el tratamiento agresivo se inició después de transcurrida la primera hora a partir del trauma.