Ommaya A K, Goldsmith W, Thibault L
Department of Neurosurgery, George Washington University Medical Center, Washington DC, USA.
Br J Neurosurg. 2002 Jun;16(3):220-42. doi: 10.1080/02688690220148824.
The objective of this study was to understand the biomechanics in age-related primary traumatic brain injuries (TBI) causing initial severity and secondary progressive damage and to develop strategy reducing TBI outcome variability using biomechanical reconstruction to identify types of causal mechanisms prior to clinical trials of neuro-protective treatment. The methods included the explanation of TBI biomechanics and physiopathological mechanisms from dual perspectives of neurosurgery and biomechanical engineering. Scaling of tolerances for skull failure and brain injuries in infants, children and adults are developed. Diagnostic assumptions without biomechanical considerations are critiqued. Methods for retrospective TBI reconstruction for prevention are summarized. Mechanisms of TBI are based on the differences between the mechanical properties of the head and neck related to age. Skull fracture levels correlate with increasing cranial bone thickness and in the development of the cranial sutures in infants and in adults. Head injury tolerance levels at three age categories for cerebral concussion, skull fracture and three grades of diffuse axonal injuries (DAI) are presented. Brain mass correlates inversely for TBI caused by angular head motions and locations of injurious stresses are predictable by centripetal theory. Improved quantitative diagnosis of TBI type and severity levels depend primarily on age and biomechanical mechanisms. Reconstruction of the biomechanics is feasible and enables quantitative stratification of TBI severity. Experimental treatment has succeeded in preventing progressive damage in animal TBI models. In humans this has failed, because the animal model received biomechanically controlled TBI and humans did not. Clinical similarities of human TBI patients do not necessarily predict equivalent biomechanics because such trauma can be produced in various ways. We recommend 'reverse engineering' for in-depth reconstruction of the TBI injury mechanism for qualitative diagnoses and reduction of outcome variability.
本研究的目的是了解与年龄相关的原发性创伤性脑损伤（TBI）中的生物力学，这些损伤会导致初始严重程度和继发性进行性损伤，并制定策略以减少TBI结果的变异性，通过生物力学重建在神经保护治疗的临床试验之前识别因果机制的类型。方法包括从神经外科和生物力学工程的双重角度解释TBI生物力学和生理病理机制。制定了婴儿、儿童和成人颅骨骨折及脑损伤的耐受性标度。对没有生物力学考虑的诊断假设进行了批判。总结了用于预防的回顾性TBI重建方法。TBI的机制基于与年龄相关的头颈部力学特性差异。颅骨骨折水平与颅骨厚度增加以及婴儿和成人颅骨缝的发育相关。给出了三个年龄组脑震荡、颅骨骨折和三级弥漫性轴索损伤（DAI）的头部损伤耐受水平。脑质量与角向头部运动引起的TBI呈负相关，损伤应力的位置可由向心力理论预测。TBI类型和严重程度水平的改进定量诊断主要取决于年龄和生物力学机制。生物力学重建是可行的，能够对TBI严重程度进行定量分层。实验性治疗已成功预防动物TBI模型中的进行性损伤。在人类中这一方法失败了，因为动物模型接受了生物力学控制的TBI，而人类没有。人类TBI患者的临床相似性不一定预示着等效的生物力学，因为这种创伤可以通过多种方式产生。我们建议进行“逆向工程”，以深入重建TBI损伤机制，用于定性诊断并减少结果变异性。
