Pressure Aberrations inside the Spinal Canal During Rear-End Impact

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Abstract

Minor soft tissue injuries of the cervical spine increasingly pose problems in public health. Such injuries are conveyed particularly often in rear-end automobile collisions at low impact speeds and it has been established that they may be associated with long-term impairment. As a possible cause for this type of injury it has been hypothesized that pressure pulses induced in cervical fluid compartments during the impact could damage the membrane of spinal nerve cells. To date, animal as well as cadaver experiments performed support this hypothesis. A theoretical analysis has been undertaken in order to investigate the pressure and flow pulse emerging in a cervical fluid compartment under conditions representing rear-end impacts with a äv of 15 km/h. Using the finite element (FE) method, a three-dimensional model of the cervical spine was developed. The model consists of eight vertebrae (C1-T1), the intervertebral discs, the intervertebral joints, all the major ligaments, most of the neck muscles and the head. Additionally, a typical venous blood vessel was included. To determine the pressure behaviour inside the blood vessel, fluid-structure interaction was taken into account. For the time interval including the development of the S-shape, the pressure pulses were calculated and found to be in qualitative agreement with the reported measurements. The shear stresses acting on the vessel wall can be determined from the associated flow pulses. An extrapolation of the results into the interstitial space where nerve cells are located at this stage does not allow assessment of whether a damage threshold may be reached.

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Computer simulation of local blood flow and vessel mechanics in a compliant carotid artery bifurcation model.

Karl Perktold, Gerhard Rappitsch (1995)

To investigate the effect of the distensible artery wall on the local flow field and to determine the mechanical stresses in the artery wall, a numerical model for the blood flow in the human carotid artery bifurcation has been developed. The wall displacement and stress analysis use geometrically non-linear shell theory where incrementally linearly elastic wall behavior is assumed. The flow analysis applies the time-dependent, three-dimensional, incompressible Navier-Stokes equations for non-Newtonian inelastic fluids. In an iteratively coupled approach the equations of the fluid motion and the transient shell equations are numerically solved using the finite element method. The study shows the occurring characteristics in carotid artery bifurcation flow, such as strongly skewed axial velocity in the carotid sinus with high velocity gradients at the internal divider wall and with flow separation at the outer common-internal carotid wall and at the bifurcation side wall. Flow separation results in locally low oscillating wall shear stress. Further strong secondary motion in the sinus is found. The comparison of the results for a rigid and a distensible wall model demonstrates quantitative influence of the vessel wall motion. With respect to the quantities of main interest, it can be seen, that flow separation and recirculation slightly decrease in the sinus and somewhat increase in the bifurcation side region, and the wall shear stress magnitude decreases by 25% in the distensible model. The global structure of the flow and stress patterns remains unchanged. The deformation analysis shows that the tangential displacements are generally lower by one order of magnitude than the normal directed displacements. The maximum deformation is about 16% of the vessel radius and occurs at the side wall region of the intersection of the two branches. The analysis of the maximum principal stresses at the inner vessel surface shows a complicated stress field with locally high gradients and indicates a stress concentration factor of 6.3 in the apex region.

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A new model for rapid stretch-induced injury of cells in culture: characterization of the model using astrocytes.

K Willoughby, Angela E. Ellis, S. Liang … (1995)

The purpose of this study was to develop a simple, reproducible model for examining the morphologic, physiologic, and biochemical consequences of stretch-induced injury on tissue-cultured cells of brain origin. Rat cortical astrocytes from 1- to 2-day-old rats were cultured to confluency in commercially available 25-mm-diameter tissue culture wells with a 2-mm-thick flexible silastic bottom. A cell injury controller was used to produce a closed system and exert a rapid positive pressure of known amplitude (psi) and duration (msec). The deformation of the membrane, and thus the stretch of the cells growing on the membrane, was proportional to the amplitude and duration of the air pressure pulse. Extent of cell injury was qualitatively assessed by light and electron microscopy and quantitatively assessed by nuclear uptake of the fluorescent dye propidium iodide, which is excluded from cells with intact membranes. Lactate dehydrogenase (LDH) enzyme release was measured spectrophotometrically. Cell injury was found to be proportional to the extent of the silastic membrane deformation. Increasing cell stretch caused mitochondrial swelling and vacuolization as well as disruption of glial filaments. Stretching also caused increased dye uptake, with maximum dye uptake occurring with a 50 msec pressure pulse duration, whereas deformations produced over longer periods of time (seconds) caused little dye uptake. With increasing postinjury survival fewer cells took up dye, implying cell repair. LDH release was also proportional to the amplitude of cell stretch, with maximum release occurring within 2 h of injury. In summary we have developed a simple, reproducible model to produce graded, strain-related injuries in cultured cells. Our continuing experiments suggest that this model can be used to study the biochemistry and physiology of injury as well as serve as a tool to examine the efficacy of therapeutic agents.

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In vitro central nervous system models of mechanically induced trauma: a review.

T McIntosh, D Meaney, Alexandra Morrison … (1998)

Injury is one of the leading causes of death among all people below the age of 45 years. In the United States, traumatic brain injury (TBI) and spinal cord injury (SCI) together are responsible for an estimated 90,000 disabled persons annually. To improve treatment of the patient and thereby decrease the associated mortality, morbidity, and cost, several in vivo models of central nervous system (CNS) injury have been developed and characterized over the past two decades. To complement the ability of these in vivo models to reproduce the sequelae of human CNS injury, in vitro models of neuronal injury have also been developed. Despite the inherent simplifications of these in vitro systems, many aspects of the posttraumatic sequelae are faithfully reproduced in cultured cells, including ultrastructural changes, ionic derangements, alterations in electrophysiology, and free radical generation. This review presents a number of these in vitro systems, detailing the mechanical stimuli, the types of tissue injured, and the in vivo injury conditions most closely reproduced by the models. The data generated with these systems is then compared and contrasted with data from in vivo models of CNS injury. We believe that in vitro models of mechanical injury will continue to be a valuable tool to study the cellular consequences and evaluate the potential therapeutic strategies for the treatment of traumatic injury of the CNS.