Central neuropathology and clinicopathological correlates in equine grass sickness

Equine Grass Sickness has traditionally been known as a dysautonomia, principally affecting parasympathetic neurons in the enteric nervous system. Studies of central neuropathology have been cursory and conflicting, examining different and occasionally poorly defined central structures in variable n...

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Bibliographic Details
Main Author: Hahn, Caroline Nora
Published: University of Edinburgh 2000
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Online Access:http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.651935
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Summary:Equine Grass Sickness has traditionally been known as a dysautonomia, principally affecting parasympathetic neurons in the enteric nervous system. Studies of central neuropathology have been cursory and conflicting, examining different and occasionally poorly defined central structures in variable numbers of cases and control animals. There was no agreement on the association or severity of clinical signs with the severity of central pathological changes. This study accurately describes the distribution of pathology in the brain of EGS cases. Chromatolytic neurons have a highly specific distribution which is unlike that reported in any other equine or human disease, but is apparently the same as in cats, dogs and hares with primary dysautonomias. The involvement of somatic efferent lower motor neurones suggests that EGS may be more correctly classified as a multisystem disease. This is a further incentive to search for a common aetiologic agent and may decrease the number of candidates under consideration. The nature of the pathological insult to the central neurons remains undetermined but, unlike peripheral neurons, central neurons do not appear to be dying; this study was unable to demonstrate evidence of apoptosis, axonal pathology or muscle fibre type grouping in muscles innervated by chromatolytic neurons. Phosphorylated neurofilament epitopes were labelled in the soma of somatic and visceral lower motor neurons indicating an axonal transport problem, but no consistent expression of the cell stress protein ubiquitin was evident. Smaller, CGRP-expressing dorsal root ganglia neurons are more likely to be chromatolytic than large neurons and may contribute to the observed rhinitis sicca. Electron microscopy revealed classical chromatolytic changes and no inclusion bodies. Electrodiagnostic examination of the blink reflex did not reveal a functional deficit of the facial nerve, and the characteristic ptosis of EGS cases was determined to be an expression of Horner's syndrome secondary to pathology to postganglionic sympathetic neurons. The response to the equine eyelid to alpha agonist eyedrops was defined and a significant difference found between control animals and EGS cases. The technique has been developed further as a useful non-invasive adjunct diagnostic test in Grass Sickness.