The Biomechanics of Indirect Traumatic Optic Neuropathy Using a Computational Head Model With a Biofidelic Orbit

Abstract

Indirect traumatic optic neuropathy (ITON) is an injury to the optic nerve due to head trauma and usually results in partial or complete loss of vision. In order to advance a mechanistic understanding of the injury to the optic nerve, we developed a head model with a biofidelic orbit. Head impacts were simulated under controlled conditions of impactor velocity. The locations of impact were varied to include frontal, lateral, and posterior parts of the head. Impact studies were conducted using two types of impactors that differed in their rigidity relative to the skull. The simulated results from both the impactors suggest that forehead impacts are those to which the optic nerve is most vulnerable. The mode and location of optic nerve injury is significantly different between the impacting conditions. Simulated results using a relatively rigid impactor (metal cylinder) suggest optic nerve injury initiates at the location of the intracranial end of the optic canal and spreads to the regions of the optic nerve in the vicinity of the optic canal. In this case, the deformation of the skull at the optic canal, resulting in deformation of the optic nerve, was the primary mode of injury. On the other hand, simulated results using a relatively compliant impactor (soccer ball) suggest that primary mode of injury comes from the brain tugging upon the optic nerve (from where it is affixed to the intracranial end of the optic canal) during coup countercoup motion of the brain. This study represents the first published effort to employ a biofidelic simulation of the full length of the optic nerve in which the orbit is integrated within the whole head.

Biomechanical analysis of ocular diseases and its in vitro study methods

“…Foletti et al [ 79 ] used a modified 3D FE human head, which is the most complex model developed to date, to advance the understanding of the mechanics of optic nerve injury. Singman et al [ 80 ] developed a model of the head with a biofiber-mesh eye socket. This study represented the first published biological neural simulation using the full length of the optic nerve, in which the eye socket is integrated with the entire head.…”

Oxidative stress in the brain and retina after traumatic injury

“…Li et al (2020) conducted a study in which they modeled different blunt force head injuries to determine how iTON may be induced. From their study they determined a blunt force impact to the center of the forehead (0 • ) and a blunt force impact to the right frontal region of the forehead (45 • ) resulted in injury to the optic nerve via a shearing form of injury (Li et al, 2020). They determined blunt force impact to the head can result in stress wave propagation through the orbital rim to the optic canal (Li et al, 2020).…”

“…From their study they determined a blunt force impact to the center of the forehead (0 • ) and a blunt force impact to the right frontal region of the forehead (45 • ) resulted in injury to the optic nerve via a shearing form of injury (Li et al, 2020). They determined blunt force impact to the head can result in stress wave propagation through the orbital rim to the optic canal (Li et al, 2020). In their model they observed the translation of impact energy propagated along the orbital ceiling to the top rim of the optic canal, which lead to optic canal diameter reduction (Li et al, 2020).…”

Mild-to-Moderate Traumatic Brain Injury: A Review with Focus on the Visual System

“…The optic nerve and tracts can be damaged from transmitted forces during TBI, even when the impact is minor, and can result from either the primary or secondary injury. The mechanism of traumatic optic neuropathy is not fully understood, but may result from tension on the nerve or nerve compression and involve damage to the axons and/or reduction of the blood supply to the nerve [76][77][78]. The visual impairment from optic nerve damage in TBI generally occurs at the time of injury and may vary from a deficit in color vision to loss of visual acuity to sudden, complete visual loss [79,80].…”