Diffuse axonal injury and traumatic coma in the primate
ABSTRACT Traumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impairment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. All 15 concussioned animals had good recovery, and none had DAI. Conversely, coma lasting more than 6 hours occurred in one of the sagittal or oblique injury groups but was present in 20 of the laterally injured animals, all of which were severely disabled afterward. All laterally injured animals had a degree of DAI similar to that found in severe human head injury. Coma lasting 16 minutes to 6 hours occurred in 2 of 13 of the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group, these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in sever head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.
SourceAvailable from: Kwong Ming Tse[Show abstract] [Hide abstract]
ABSTRACT: Head injury, being one of the main causes of death or permanent disability in everyday life, continues to remain as a major health problem with significant socioeconomic costs. Therefore, there is a need for biomechanical studies of head injury, its mechanisms and its tolerance to external loading. Throughout the decades, finite element head models (FEHMs) have been used to assess the biomechanics of head injury mechanism. Given the fact that some of the internal biomechanical responses of the brain can neither be measured easily nor in-vivo by experimental techniques, FEHM offers a cost-effective alternative to experimental method in estimating the internal biomechanical responses of human head. This review paper aims to provide researchers in this field with some background information about head injury. A thorough literature review has been done to summarize the essential details in terms of modeling, material properties and boundary conditions of various FEHMs. The outline of this review is divided into two main sections. The first section consists of definitions, epidemiology, mechanism and classifications of head injury as well as some basic anatomy of human head. Beginning with the history of FEHMs and their revolution in geometry and complexity, the second section would be focusing on the various mechanical aspects of the FEHMs. Various boundary conditions and validations used by the FEHMs are also included in the review article. In addition, important findings and head injury criteria from these FEHMs are summarized.
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ABSTRACT: CT is the frontline imaging modality for diagnosis of acute traumatic brain injury (TBI), involving the detection of fresh blood in the brain (contrast of 30–50 HU, detail size down to 1 mm) in a non-contrast-enhanced exam. A dedicated point-of-care imaging system based on cone-beam CT (CBCT) could benefit early detection of TBI and improve direction to appropriate therapy. However, flat-panel detector (FPD) CBCT is challenged by artifacts that degrade contrast resolution and limit application in soft-tissue imaging. We present and evaluate a fairly comprehensive framework for artifact correction to enable soft-tissue brain imaging with FPD CBCT. The framework includes a fast Monte Carlo (MC)-based scatter estimation method complemented by corrections for detector lag, veiling glare, and beam hardening.The fast MC scatter estimation combines GPU acceleration, variance reduction, and simulation with a low number of photon histories and reduced number of projection angles (sparse MC) augmented by kernel de-noising to yield a runtime of ~4 min per scan. Scatter correction is combined with two-pass beam hardening correction. Detector lag correction is based on temporal deconvolution of the measured lag response function. The effects of detector veiling glare are reduced by deconvolution of the glare response function representing the long range tails of the detector point-spread function. The performance of the correction framework is quantified in experiments using a realistic head phantom on a testbench for FPD CBCT.Uncorrected reconstructions were non-diagnostic for soft-tissue imaging tasks in the brain. After processing with the artifact correction framework, image uniformity was substantially improved, and artifacts were reduced to a level that enabled visualization of ~3 mm simulated bleeds throughout the brain. Non-uniformity (cupping) was reduced by a factor of 5, and contrast of simulated bleeds was improved from ~7 to 49.7 HU, in good agreement with the nominal blood contrast of 50 HU. Although noise was amplified by the corrections, the contrast-to-noise ratio (CNR) of simulated bleeds was improved by nearly a factor of 3.5 (CNR = 0.54 without corrections and 1.91 after correction). The resulting image quality motivates further development and translation of the FPD-CBCT system for imaging of acute TBI.Physics in Medicine and Biology 02/2015; 60(4). DOI:10.1088/0031-9155/60/4/1415 · 2.92 Impact Factor
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ABSTRACT: Traumatic brain injury (TBI) is linked to several pathologies for which there is a lack of understanding of disease mechanisms and therapeutic strategies. To elucidate injury mechanisms, it is important to consider how physical forces are transmitted and transduced across all spatial scales of the brain. Although the mechanical response of the brain is typically characterized by its material properties and biological structure, cellular mechanotransduction mechanisms also exist. Such mechanisms can affect physiological processes by responding to exogenous mechanical forces directed through sub-cellular components, such as extracellular matrix and cell adhesion molecules, to mechanosensitive intracellular structures that regulate mechanochemical signaling pathways. We suggest that cellular mechanotransduction may be an important mechanism underlying the initiation of cell and sub-cellular injuries ultimately responsible for the diffuse pathological damage and clinical symptoms observed in TBI, thereby providing potential therapeutic opportunities not previously explored in TBI. Copyright © 2015 Elsevier Inc. All rights reserved.Neuron 03/2015; 85(6):1177-1192. DOI:10.1016/j.neuron.2015.02.041 · 15.98 Impact Factor