Aim: The potential causes of the optic nerve injury as a result of blunt object trauma, were investigated using a computer model. Methods: A finite element model of the eye, the optic nerve, and the orbit with its content was constructed to simulate blunt object trauma. We used a model of the first phalanx of the index finger to represent the blunt body. The trauma was simulated by impacting the blunt body at the surface between the globe and the orbital wall at velocities between 2-5 m/s, and allowing it to penetrate 4-10 mm below the orbital rim. Results: The impact caused rotations of the globe of up to 5000˚/s, lateral velocities of up to 1 m/s, and intraocular pressures (IOP) of over 300 mm Hg. The main stress concentration was observed at the insertion of the nerve into the sclera, at the side opposite to the impact. Conclusions:The results suggest that the most likely mechanisms of injury are rapid rotation and lateral translation of the globe, as well as a dramatic rise in the IOP. The strains calculated in the study should be sufficiently high to cause axonal damage and even the avulsion of the nerve. Finite element computer modelling has therefore provided important insights into a clinical scenario that cannot be replicated in human or animal experiments.A nterior traumatic optic neuropathy and optic nerve avulsion may result from a blunt injury where a foreign object intrudes between the globe and the orbital wall.

The dynamics of the movement of the cerebrospinal fluid (CSF) may play an important role in the genesis of pathological neurological conditions such as syringomyelia, which is characterized by the presence of a cyst (syrinx) in the spinal cord. In order to provide sound theoretical grounds for the hypotheses that attribute the formation and growth of the syrinx to impediments to the normal movement of the CSF, it is necessary to understand various modes through which CSF pulse in the spinal column propagates. Analytical models of small-amplitude wave propagation in fluid-filled coaxial tubes, where the outer tube represents dura, the inner tube represents the spinal cord, and the fluid is the CSF, have been used to that end. However, so far, the tendency was to model one of the two tubes as rigid and to neglect the effect of finite thickness of the tube walls. The aim of this study is to extend the analysis in order to address these two potentially important issues. To that end, classical linear small-amplitude analysis of wave propagation was applied to a system consisting of coaxial tubes of finite thickness filled with inviscid incompressible fluid. General solutions to the governing equations for the case of harmonic waves in the long wave limit were replaced with the boundary conditions to yield the characteristic (dispersion) equation for the system. The four roots of the characteristic equation correspond to four modes of wave propagation, of which the first three are associated with significant motion of the CSF. For the normal range of parameters the speeds of the four modes are c(1)=13 ms, c(2)=14.7 ms, c(3)=30.3 ms, and c(4)=124.5 ms, which are well within the range of values previously reported in experimental and theoretical studies. The modes with the highest and the lowest speeds of propagation can be attributed to the dura and the spinal cord, respectively, whereas the remaining two modes involve some degree of coupling between the two. When the thickness of the spinal cord, is reduced below its normal value, the first mode becomes dominant in terms of the movement of the CSF, and its speed drops significantly. This suggests that the syrinx may be characterized by an abnormally low speed of the CSF pulse.

A finite element model of the eye and the orbit was used to examine the hypothesis that the orbital fat provides an important mechanism of eye stability during head trauma. The model includes the globe, the orbital fat, the extra-ocular muscles, and the optic nerve. MRI images of an adult human orbit were used to generate an idealized geometry of the orbital space. The globe was approximated as a sphere 12 mm in radius. The optic nerve and the sclera were represented as thin shells, whereas the vitreous and the orbital fat were represented as nearly incompressible solids of low stiffness. The orbital bone was modelled as a rigid shell. Frontal head impact resulting from a fall onto a hard floor was simulated by prescribing to the orbital bone a triangular acceleration pulse of 200 g (1962 m/s(2)) peak for a duration of 4.5 ms. The results show that the fat provides the crucial passive mechanism of eye restraint. The mechanism is a consequence of the fact that the fat is incompressible and that its motion is restricted by the rigidity of the orbital walls. Thus, the acceleration loads of short duration cannot generate significant distortion of the fat. In contrast, the passive muscles provide little support to the globe. When the connection between the orbital fat and the eye is absent the eye is held mainly by the optic nerve. We discuss the possible role that this loss of contact may have in some cases of the evulsion of the eye and the optic nerve.

The role of the cerebral venous bed in the cranial volume-pressure test was examined by means of a mathematical model. The cerebral vascular bed was represented by a single arterial compartment and two venous compartments in series. The lumped-parameter formulation for the vascular compartments was derived from a one-dimensional theory of flow in collapsible tubes. It was assumed in the model that the cranial volume is constant. The results show that most of the additional volume of cerebrospinal fluid (deltaV(CSF)) was accommodated by collapse of the cerebral venous bed. This profoundly altered the venous haemodynamics and was reflected in the cranial pressure P(CSF). The cranial volume-pressure curve obtained from the model was consistent with experimental data; the curve was flat for 0 < or = deltaV(CSF) < or = 20 ml and 35 < or = deltaV(CSF) < or = 40 ml, and steep for 20 < or = deltaV(CSF) < or = 35 ml and deltaV(CSF) > or = 40 ml. For deltaV(CSF) > 25 ml and P(CSF) > 5.3 kPa (40 mmHg), cerebral blood flow dropped. When P(CSF) was greater than the mean arterial pressure, all the veins collapsed. The conclusion of the study was that the shape of the cranial volume-pressure curve can be explained by changes in the venous bed caused by various degrees of collapse and/or distension.

BackgroundSyringomyelia is a pathological condition in which fluid-filled cavities (syringes) form and expand in the spinal cord. Syringomyelia is often linked with obstruction of the craniocervical junction and a Chiari malformation, which is similar in both humans and animals. Some brachycephalic toy breed dogs such as Cavalier King Charles Spaniels (CKCS) are particularly predisposed. The exact mechanism of the formation of syringomyelia is undetermined and consequently with the lack of clinical explanation, engineers and mathematicians have resorted to computer models to identify possible physical mechanisms that can lead to syringes. We developed a computer model of the spinal cavity of a CKCS suffering from a large syrinx. The model was excited at the cranial end to simulate the movement of the cerebrospinal fluid (CSF) and the spinal cord due to the shift of blood volume in the cranium related to the cardiac cycle. To simulate the normal condition, the movement was prescribed to the CSF. To simulate the pathological condition, the movement of CSF was blocked.ResultsFor normal conditions the pressure in the SAS was approximately 400 Pa and the same applied to all stress components in the spinal cord. The stress was uniformly distributed along the length of the spinal cord. When the blockage between the cranial and spinal CSF spaces forced the cord to move with the cardiac cycle, shear and axial normal stresses in the cord increased significantly. The sites where the elevated stress was most pronounced coincided with the axial locations where the syringes typically form, but they were at the perimeter rather than in the central portion of the cord. This elevated stress originated from the bending of the cord at the locations where its curvature was high.ConclusionsThe results suggest that it is possible that repetitive stressing of the spinal cord caused by its exaggerated movement could be a cause for the formation of initial syringes. Further consideration of factors such as cord tethering and the difference in mechanical properties of white and grey matter is needed to fully explore this possibility.Electronic supplementary materialThe online version of this article (10.1186/s12917-018-1410-7) contains supplementary material, which is available to authorized users.