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termed traumatic optic neuropathy (TON). Energy transmitted to the head or globe from blunt force can cause direct damage at the site of impact (coup injury), but also release shock waves that move the brain or rotate the globe to cause damage opposite the site of impact (‘contrecoup injury’) (Pieramici and Parver 1985). Diffuse axonal injury is one of the most common and
important pathologies resulting from the mechanical deformation of the brain during TBI (Maxwell et al. 1997; Wolf et al. 2001). A key component of both mild and severe TBI diffuse axonal injury results at least partially from stretching of neural tissue (Ma et al. 2012). Axonal stretch injury is characterised by early cytoskeletal proteolysis, axoplasmic flow transport disruption, and secondary axotomy. Calpains, a family of Ca2+-dependent proteases, play a causal role in transport disruption after in vivo axonal stretch injury. Traumatic axonal deformation induces abnormal sodium influx through mechanically sensitive Na+ channels, which subsequently trigger an increase in intra-axonal calcium via the opening of voltage gated calcium channels (Wolf et al. 2001). Rapid acceleration-deceleration of an infant’s head
during intentional shaking can exert severe mechanical strain to result in stretching or shearing forces upon the optic nerves sufficient to cause axonal injury (Le Fanu 2005). Beta-amyloid precursor protein immunohistochemistry of the optic nerve has been shown to be a highly effective method for identifying diffuse axonal injury in the brains of infants with shaken baby syndrome (Gleckman et al. 2000). A stroke is the loss of brain function due to a lack of blood
flow (arterial thrombosis or embolism) or to a haemorrhage. Intracerebral haemorrhage (ICH) is a subtype of stroke with very high mortality in man. Clot formation and lysis, and haemoglobin derived iron toxicity play an important role in ICH-induced brain injury. Intracerebral iron from haemorrhage causes brain oedema, lipoperoxidation and neuronal death. Deferoxamine, an iron chelator, is an approved drug for the treatment of acute iron intoxication and chronic iron overload due to transfusion-dependent anaemia. It can rapidly penetrate the blood-brain barrier and accumulate in the brain tissue in significant concentration after systemic administration to reduce ICH-induced brain oedema, neuronal death, brain atrophy, and neurological deficits (Hua et al. 2007). Iron chelation with deferoxamine appears to be an effective therapy for ICH (Hua et al. 2008). Calcium ions also move intracellularly in cerebral ischaemia to cause neuronal death (Steinsapir et al. 1994). Iron and calcium chelators may have an important role in TBI and TON therapy.
Traumatic optic neuropathy
Traumatic optic neuropathy appears to be a compartment syndrome with impact injury to the optic nerve, haemorrhage and oedema in the confined space of the optic canal leading to pronounced ischaemia and irreversible neural damage. Optic nerve dysfunction can be partial or complete and permanent or temporary. Injury can occur anywhere along the length of the optic nerve. In the absence of a penetrating wound, TON is presumed to be an indirect injury that occurs when the force of impact is transmitted to the nerve through the bones or by motion of the globe. The bony orbit protects against direct optic nerve injury (Steinsapir et al. 1994). Traumatic optic neuropathy can be anterior or posterior in
animals. Anterior TON in man involves the intraocular portion of the nerve and posterior TON involves the canalicular portion of
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the nerve. Anterior optic nerve injuries occur when the globe is suddenly rotated or displaced anteriorly from blunt force to the frontal bones in man resulting in avulsion of the intraocular optic nerve at the lamina cribrosa (Pieramici and Parver 1985). Dimensional changes in the eye also occur following blunt force to the anterior segment. The eye shortens in the anteroposterior dimension and expands equatorially. Tractional forces at the point of maximum equatorial expansion occur in the vitreous and peripheral retina as the vitreous body and lens diaphragm are directed posteriorly (Pieramici and Parver 1985). Posterior optic nerve involvement at the optic chiasm is the
most common manifestation of TON in man, and is a result of movement of the brain in relation to the tethered intracanalicular optic nerve such that avulsion of the intracanalicular or intracranial optic nerve occurs. Brain movement at the time of impact could also cause chiasmal trauma (Steinsapir and Goldberg 1994). Contusion and ischaemic injury to the intracanalicular optic nerve in this confined space occur from force applied to the frontal bone that is transferred and concentrated in the area of the bones forming the optic foramen and along the optic canal to the neural tissue and nutrient vessels to cause deformation of these bones. Oxygen free radical production and a macrophage response also occur (Pieramici and Parver 1985). The human intraorbital optic nerve is not usually affected in blunt force trauma as it is not tethered to the globe or orbit allowing it to move when external forces are applied (Pieramici and Parver 1985). Sphenoid bone fractures in man with involvement of the
optic canal may exacerbate blunt anterior segment trauma but are not essential for posterior optic neuropathy. Swelling of the optic nerve in the optic canal can cause necrosis such that optic canal decompression or high dose corticosteroid administration has been recommended (Pieramici and Parver 1985).
Clinical and experimental studies have concluded that the mechanisms of the optic nerve damage due to blunt head trauma in TON are both mechanical and biochemical (Matsuzaki et al. 1982). Blunt trauma to the head results in optic nerve injury from the sudden force of impact being transmitted through the frontal or occipital bones, and/or by rotational motion of the globe. Several mechanisms for this ‘contrecoup injury’ opposite the coup injury have been proposed for TON. Blunt trauma to the forehead and globe anterior segment could cause summation of multiple waves of force reflected from within the globe wall to a single point opposite the blunt force to result in traumatic contrecoup optic nerve injury (Pieramici and Parver 1985). Force to the skull and globe could also be transmitted in a single wave or block of force toward the posterior globe and optic nerve with subsequent TON injury resulting in the path of the force vector (Pieramici and Parver 1985). Brain movement at the time of initial impact could also cause chiasmal trauma and the posterior form of TON (Steinsapir and Goldberg 1994). Traction or pressure does little to cause optic nerve
damage. Stretching by itself does little to cause optic nerve injury. Other factors are involved to cause TON. Ligation of the central retinal artery does cause immediate and permanent blindness (Matsuzaki et al. 1982). Axonal straining and shearing of the optic nerve or chiasm at the moment of impact cause contusion necrosis of the optic nerve and chiasmal tissue. Irreversible ischaemic injury to the neural membrane of axons
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