Rapid triage and decision-making in the treatment of traumatic brain injury (TBI) present challenging dilemma in "resource poor" environments such as the battlefield and developing areas of the world. There is an urgent need for additional tools to guide treatment of TBI. The aim of this review is to establish the possible use of diagnostic TBI biomarkers in (1) identifying diffuse and focal brain injury and (2) assess their potential for determining outcome, intracranial pressure (ICP), and responses to therapy. At present, there is insufficient literature to support a role for diagnostic biomarkers in distinguishing focal and diffuse injury or for accurate determination of raised ICP. Presently, neurofilament (NF), S100β, glial fibrillary acidic protein (GFAP), and ubiquitin carboxyl terminal hydrolase-L1 (UCH-L1) seemed to have the best potential as diagnostic biomarkers for distinguishing focal and diffuse injury, whereas C-tau, neuron-specific enolase (NSE), S100β, GFAP, and spectrin breakdown products (SBDPs) appear to be candidates for ICP reflective biomarkers. With the combinations of different pathophysiology related to each biomarker, a multibiomarker analysis seems to be effective and would likely increase diagnostic accuracy. There is limited research focusing on the differential diagnostic properties of biomarkers in TBI. This fact warrants the need for greater efforts to innovate sensitive and reliable biomarkers. We advocate awareness and inclusion of the differentiation of injury type and ICP elevation in further studies with brain injury biomarkers.
Traumatic brain injury (TBI) treatment is now focused on the prevention of primary injury and reduction of secondary injury. However, no single effective treatment is available as yet for the mitigation of traumatic brain damage in humans. Both chemical and environmental stresses applied before injury, have been shown to induce consequent protection against post-TBI neuronal death. This concept termed “preconditioning” is achieved by exposure to different pre-injury stressors, to achieve the induction of “tolerance” to the effect of the TBI. However, the precise mechanisms underlying this “tolerance” phenomenon are not fully understood in TBI, and therefore even less information is available about possible indications in clinical TBI patients. In this review we will summarize TBI pathophysiology, and discuss existing animal studies demonstrating the efficacy of preconditioning in diffuse and focal type of TBI. We will also review other non-TBI preconditionng studies, including ischemic, environmental, and chemical preconditioning, which maybe relevant to TBI. To date, no clinical studies exist in this field, and we speculate on possible futureclinical situation, in which pre-TBI preconditioning could be considered.
Objective:Homonymous hemianopia due to damage to the optic radiations or visual cortex is a possible consequence of tumor resection involving the temporal or occipital lobes. The purpose of this review is to present and analyze a series of studies regarding the use of awake craniotomy (AC) to decrease visual field deficits following neurosurgery.Materials and Methods:A literature search was performed using the Medline and PubMed databases from 1970 and 2014 that compared various uses of AC other than intraoperative motor/somatosensory/language mapping with a focus on visual field mapping.Results:For the 17 patients analyzed in this study, 14 surgeries resulted in quadrantanopia, 1 in hemianopia, and 2 without visual deficits. Overall, patient satisfaction with AC was high, and AC was a means to reduce surgery-related complications and cost related with the procedure.ConclusionAC is a safe and tolerable procedure that can be used effectively to map optic radiations and the visual cortices in order to preserve visual function during resection of tumors infiltrating the temporal and occipital lobes. In the majority of cases, a homonymous hemianopia was prevented and patients were left with a quadrantanopia that did not interfere with daily function.
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