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transmitted from the skull to the optic nerve. These forces produced by the posterior movement of the brain against the 3 cm intracranial portion of the optic nerve may have caused stretching, shearing, and ultimately avulsion of the optic nerve (Sisson 1914; Martin et al. 1986; Rebhun 1992; Davis 2011; Irby 2011).
Both uni- and bilateral blindness have been described
Fig 3: Gross post mortem sagittal section of the skull (cranial to the right) showing the fracture of the basisphenoid bone (solid arrow) ventral to the ethmoid turbinates (open arrow) on the right side.
previously in horses following head trauma as a consequence of optic nerve atrophy (Martin et al. 1986; Blogg et al. 1990; Reppas et al. 1995). Unilateral and bilateral mydriasis and absence of menace, direct and indirect light responses were reported in these cases. Post mortem examination of the optic nerves showed distinct areas of nerve thinning (Martin et al. 1986) and extensive Wallerian neuronal degeneration (Blogg et al. 1990). Optic nerve injury and subsequent atrophy may result from shearing, contusive and concussive forces, and interrupted vascular supply including infarction (Blogg et al. 1990). Alternatively the optic chiasm and associated nerves can also be compressed by haemorrhage secondary to basilar fractures or by direct bony compression from fracture fragments (Irby 2011). Immediately following head or ocular trauma, ophthalmic examination may identify optic disc hyperaemia, haemorrhage or oedema (Millichamp 1992; Nell and Walde 2010). Normal fundic examination in conjunction with vision loss and pupillary light reflex deficits, may indicate retrobulbar optic nerve injury (Rebhun 1992), as was noted in the reported case. Three to 4 weeks following nerve injury, optic disc pallor and decreased retinal vasculature may be evident on fundic evaluation and this would support optic neuropathy (Martin et al. 1986; Millichamp 1992). Traumatic nerve avulsion causing optic neuropathy has
100 µm
Fig 4: Histological section of right optic nerve stained with haematoxylin and eosin (2×) shows extensive haemorrhage (solid arrows) and fibrin (open arrows).
of haemorrhage and fibrin (Fig 4). Sections of the optic chiasm (nearest the avulsion site) were also characterised by locally extensive regions of haemorrhage, fibrin, as well as prominent endothelium surrounded by numerous macrophages. Longitudinal sections of the optic nerve at the level of the optic chiasm contained multiple 5–10 m in diameter, round, eosinophilic bodies with moderate vacuolation. In the most severely damaged regions, vessels contained and were surrounded by increased numbers of lymphocytes, plasma cells, neutrophils, and macrophages, referred to as gitter cells.
Discussion
This report describes the evaluation, treatment, and pathological findings of a horse with blindness following cranial trauma. Blindness in this horse was caused by bilateral optic nerve avulsion. The dural sheath that encases the equine optic nerve is fused with the periosteum of the optic canal. Forces created during head trauma were presumed to have been
also been described in cats, dogs and man (Gilger 1995; Buchwald et al. 2003; Paya et al. 2012). In 2 human case reports blunt trauma to the face induced unilateral avulsion of the optic nerve from the globe at the level of the disc and the lamina cribrosa, respectively, without rupture of the dural sheath. These case reports stress the importance of advanced imaging diagnostics such as computed tomography and magnetic resonance imaging to identify the location and extent of the lesion accurately. Further emphasis for the use of advanced imaging techniques vs. plain radiographs alone is the poor detection rate of skull fractures on radiographs. Fifty percent of skull fractures are reported to be evident on survey radiographs, with subtle nondisplaced basilar fractures, (Stick et al. 1980; Feary et al. 2007). Unlike the fracture in this mature horse, fractures of the basilar bones in horses aged <5 years are more common at the junction of basisphenoid and basioccipital bones, due to the open spheno-occipital suture (Butler et al. 2008). Visual function may progressively deteriorate for the first
24 h as a result of secondary injury despite supportive care and anti-inflammatory therapy (Mackay 2004). Poor prognostic indicators for return of vision in blind horses include bilateral mydriasis with nonresponsive pupils (Martin et al. 1986; Magdesian 2000). The lack of improvement 72 h after injury and failure to restore or improve pupillary and visual function, as noted in the horse in this report, is indicative of permanent optic nerve damage (Rebhun 1992).
Authors’ declaration of interests No conflicts of interest have been declared.
© 2014 EVJ Ltd
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