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EQUINE VETERINARY EDUCATION / AE / OCTOBER 2014
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Fig 5: Discontinuity between the distal aspect of the right optic nerve (left side of the photomicrograph) and the optic chiasm. Between them is the collapsed leptomeninges. Notice in the chiasm there are numerous white pinpoint distinctly bordered optically vacant vacuoles (Wallerian degeneration and digestion chambers associated with chronic demyelination/axonal loss; arrows).
Fig 4: The gross specimen of the chiasmal region has segmental loss of the optic nerves and collapse of the leptomeninges (asterisks) at the beginning of the optic canals.
Light microscopy found NFL atrophy, decreased RGC
density, and moderate atrophy of the retinal neural and plexiform layers in the right eye. Similar but more extensive lesions were found in the left eye. Mildly dilated empty axonal sheaths were found longitudinally in both optic nerves. The right lamina cribrosa exhibited slight posterior displacement. The segmental loss of optic nerve neural tissue was replaced by collapsed leptomeninges (Fig 5). The meningeal area was hypercellular with fibroblast-like cells, haemorrhage, macrophages, opaque vacuoles and occasional haemosiderin material. The neural tissue at the edges of the lesion exhibited moderate Wallerian degeneration, axonal disruption and vacuolisation, and the presence of spheroids and gliosis. The occipital lobe of the brain had increased meningeal thickening and scattered haemorrhage.
Commentary
Veterinarians are frustrated because they do not know what to do in horses when apparently minor head trauma causes complete vision loss in a young healthy horse (Joseph 1995). The diagnosis of TON is made when a horse with head trauma develops acute vision loss and a dilated pupil that cannot be explained by injury to an apparently normal globe and intraocular optic nerve (Joseph 1995). Neuroimaging can be used following head trauma to document the extent, location and type of TBI and TON in these horses (Scrivani 2013). Knowledge concerning the pathophysiological mechanisms and therapy of traumatic optic neuropathy (TON) in horses is limited. The optic nerve is a tract of the brain. Therefore, the cellular and biochemical pathophysiology of brain and spinal cord trauma and ischaemia provide insight into mechanisms that may operate in traumatic optic neuropathy (Steinsapir et al. 1994). We know now that TON in
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most of the detailed reports of horse cases is intracranial and involves the optic chiasm (Martin et al. 1986; Blogg et al. 1990; Kullmann et al. 2014). We suspect that the intracranial metabolic changes noted in human and experimental studies are similar in the horse brain (Pieramici and Parver 1985; Wolf et al. 2001). The Kullman horse, the Martin horse and our colt had
chiasmal damage, which suggests brain shifting in response to trauma to the head. Is the intracranial optic nerve more at risk from head trauma in the horse than the intraocular and intraorbital optic nerves? In man, the intracanalicular optic nerve is most often damaged followed by the intracranial optic nerve, with the intraocular optic nerve the least often affected (Steinsapir and Goldberg 1994). Traumatic energy to the occipital bones of the horse causes shifting of the brain and damage to the axons at the fixated optic chiasm. The following is a possible scenario as to the cause of TON
in the horse following head trauma. Intracranial optic nerve stretching at the optic chiasm due to shifting of the brain following blunt trauma to the skull causes microvessel rupture and intraneuronal haemorrhage in or near the optic canal. This may or may not be associated with orbital or canalicular bone fractures. Disruption of the neural microcirculation results in ischaemia, free radical production, and breakdown of neuronal calcium homeostasis. Haemoglobin derived iron from the haemorrhage is also very neurotoxic and an important part of TON pathogenesis. Macrophages also play a role in post ischaemic central nervous system damage in man (Steinsapir et al. 1994) and were also found in the brain of our colt. The combination of these events appears to occur very quickly in the horse and man, and leads to rapid axonal dysfunction and axonal death. Clinical progress in the treatment of human cases of TON is
limited by small clinical studies lacking appropriate control groups. The Corticosteroid Randomization for Acute Head Trauma (CRASH) trial found an increased rate of death among human patients with acute head trauma treated with
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