EQUINE VETERINARY EDUCATION / AE / OCTOBER 2014
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not damaged by the initial impact can occur to a large degree due to release of oxygen free radicals from lipoperoxidation of axonal membranes in response to partial ischaemia and reperfusion (Steinsapir et al. 1994). Ligation of the optic nerve, traction to the optic nerve, or meningeal sheath removal alone in animal studies of traumatic optic nerve damage found little effect on nerve conduction (Matsuzaki et al. 1982). In man, vision loss from optic nerve trauma is usually instantaneous with forehead impact, and permanent in half of the cases. There is no known ideal therapy although current concepts of therapy for brain and spinal cord injury may eventually benefit TON cases (Steinsapir et al. 1994). The results of the International Optic Nerve Trauma Study provide some evidence to conclude that neither corticosteroids nor optic canal decompression surgery should be considered the standard of care for human patients with traumatic optic neuropathy. There was also no indication that the dosage or timing of corticosteroid treatment or the timing of the surgery was associated with an increased probability of visual improvement (Levin et al. 1999). Some humans recover without therapy (Steinsapir et al. 1994).
Traumatic optic neuropathy in the horse
In 400 BCE, Hippocrates noted the association between injuries to the brow and forehead and delayed vision loss in man (Hippocrates 1928; Iwamoto & Bstaendig 1995). Amaurosis or blindness with apparently normal eyes was also noted by early veterinarians in horses following head trauma from ‘falling over backwards’ (Percival 1876; Law 1923; Nicolas 1925). Trauma to the occipital region of the horse skull was associated with optic nerve stretching, rupture or avulsion, and blindness in a later series of 4 horses (Martin et al. 1986). Fractures of the medial and ventral orbital wall, mandible, zygomatic process of the temporal bone, palatine bone, basisphenoid bone, maxillary bone and vomer bone caused blindness and extensive atrophy of the right retina and optic nerve in a horse (Blogg et al. 1990). The paper by Kullmann et al. (2014) in this journal found basisphenoid bone fracture and bilateral optic nerve avulsion with irreversible blindness in a horse after it fell over backwards. In other horse cases, the optic nerve injury may result from
rapid deceleration and stretching. The redundancy of the orbital optic nerve allows the globe to travel forward but is ultimately tethered by the optic nerve. The optic nerve then is stretched to initiate the process of haemorrhage from meningeal vessels, oedema and necrosis (Joseph 1995). Brain movement at the time of impact appears responsible for the chiasmal trauma in TON of the horse. Like human cases of TON, equine TON is immediate and irreversible.
Additional case report
Acute blindness and epistaxis occurred following trauma to the side of the head in a one-year-old Thoroughbred colt. Examination 10 days later found an absence of hand motion, no light perception and fixed dilated pupils. There was subtle optic disc pallor bilaterally (Fig 2). The remainder of the general and neurological examination was normal at that time. Magnetic resonance imaging found the optic nerves to be bilaterally small and flattened posteriorly anterior to the chiasm (Fig 3). The horse was subjected to euthanasia due to concern for poor quality of life 6 weeks following injury.
Fig 3: Magnetic resonance imaging of the colt’s brain found the optic nerves to be bilaterally small and flattened anterior to the chiasm (the asterisks are adjacent to optic nerves).
A necropsy was performed. No significant lesions noted in
spleen, lymph nodes, upper respiratory tract, lungs or digestive tract. The globes were grossly unremarkable. Examination of the brain found that anterior to the optic chiasm there was a segmental loss of the optic nerve and collapse of the leptomeninges (Fig 4).
© 2014 EVJ Ltd
Fig 2: The optic nerve exhibits pale colour, and slight retinal vessel attenuation one month following injury.
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