Observations on Neuronal Changes in Grass Sickness of Horses

Gilmour, J.S.

doi:10.1016/s0034-5288(18)33828-1

Cited by 62 publications

(61 citation statements)

References 2 publications

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“…Damage to the peripheral nervous system in EGS has been known to occur for some time 36 , 46 and involves: paravertebral ganglia (stellate, cranial cervical, caudal cervical, thoracic sympathetic chain); prevertebral ganglia (coeliaco‐mesenteric, 40 , 48 , 49 , 132 cranial mesenteric, caudal mesenteric); dorsal root ganglia 3 , 7 (but not 38 , thoracic root 10 DRG, but only neurones with small diameter‐perikarya); ciliary ganglia; and enteric nervous system (myenteric and submucous plexuses 49 ). These nervous elements are not always affected to the same degree 9 .…”

Section: Neuropathologymentioning

confidence: 99%

“…Equine grass sickness (EGS, equine dysautonomia) is a polyneuropathy affecting the central, peripheral and enteric nervous system of horses 1 –9 with particularly serious consequences for alimentary function in the acute form of the disease, which is rapidly fatal. It affects 2–4% of the equine population in all breeds throughout the British Isles 5 , 10 , 11 and appears sporadically elsewhere in Continental Europe, 12 –15 Australia 16 and the Falkland Islands 17 .…”

Section: Introductionmentioning

confidence: 99%

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The neurology and enterology of equine grass sickness: a review of basic mechanisms

Cottrell

McGorum

Pearson

1999

Neurogastroenterology Motil

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Autonomic dysfunction constitutes a prominent clinical feature of equine grass sickness (EGS). Significant injury to the nervous control of the alimentary system is life threatening, partly because of dysphagia but also because of the failure of the unique regulatory mechanisms in equine digestion involving water and electrolyte balance. The neuropathology also indicates the presence of a somatic polyneuropathy. The morphological features of EGS are similar to those of excitotoxic neuronal degeneration, which resembles neuronal apoptosis. It is difficult to ascertain from published accounts the degree of damage to central neurones: the distribution is well documented and selective but the proportion of damage is poorly quantified. If lesions involve a significant number of regulatory neurones they should produce functional deficits. Any clinical assessment of horses, especially those with chronic EGS, should include a thorough neurological examination. Although this will not necessarily improve the outcome of the case, it may enable the rational selection of animals with a reasonable prognosis for recovery which is partly determined by the extent of CNS lesions. The evidence supports the following pathogenesis. There is an initial lesion in the enteric nervous system of susceptible horses. In the acute form of EGS, massive enteric neuronal damage occurs first functionally, then structurally leading to generalized alimentary smooth muscle atony, enhanced secretions and altered fluid fluxes. Severe distension of the stomach and small intestines rapidly develops, which augments the intestinal ileus by intersegmental inhibitory reflexes and causes colic and dehydration. In subacute cases, failure of intestinal bicarbonate buffer together with alimentary stasis rapidly reduces caecal-colonic fermentation. Thus the osmolality of large intestinal digesta reduces and water travels out of the bowel along osmotic gradients. Water returns to the circulation, but is eventually lost in the gastric and small intestinal secretions. The observation that pathological lesions may not be seen in the prevertebral ganglia within the first few days of acute cases supports the view that a functional deficit precedes structural lesions which may be secondary to a retrograde degeneration. It is therefore possible to resolve the observations that less damage may be seen in prevertebral ganglia and elsewhere in peracute and acute cases with the more common finding that greater neuronal damage is present in acute than in chronic cases. These different observations are probably time dependent. Chronic EGS occurs when there is less initial enteric nerve damage which may lead to less secondary prevertebral ganglionic pathology, and more time for functional and structural compensatory mechanisms to develop. Denervation hypersensitivity develops at target sites both in the gut and in peripheral somatic nerves which may account, in part, for the clinical signs of patchy sweating and muscle tremors. Raised circulating adrenaline levels may also ac...

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Section: Neuropathologymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The neurology and enterology of equine grass sickness: a review of basic mechanisms

Cottrell

McGorum

Pearson

1999

Neurogastroenterology Motil

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“…83 Histologic lesions of neuronal degeneration are most evident in the autonomic ganglia, gut wall nerve plexuses, brain, and spinal cord. [96][97][98] There is chromatolysis, nuclear eccentricity, nuclear degenerative changes, cell death and neuronophagia, cytoplasmic vacuolation, and spheroid formation. 99 Lesions are most evident in prevertebral (celiacomesenteric, cranial mesenteric, caudal mesenteric) and paravertebral (stellate, cranial cervical, caudal cervical, thoracic sympathetic chain) ganglia of the autonomic nervous system and enteric neurons (myenteric and submucous plexuses).…”

Section: Necropsy Findingsmentioning

confidence: 99%

Neurodegenerative Disorders

MacKay¹

2007

Equine Neurology

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“…Foci of myocarditis were found in one case (Obel 1955) and slight oedema of the myocardium was recorded in two cases (Holman and others 1974). Histopathological changes typical of those observed in other autonomic ganglia are found in the cervical, thoracic, cervicothoracic and vertebral ganglia, the sites of synapse of cardiac sympathetic preganglionic neurons (Gilmour 1973). The possible involvement of the parasympathetic terminal cardiac ganglia has not been investigated previously.…”

mentioning

confidence: 97%

Functional and histopathological evidence of cardiac parasympathetic dysautonomia in equine grass sickness

Perkins

Bowen²,

Else³

et al. 2000

Veterinary Record

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The parasympathetic terminal cardiac ganglia were examined in three normal horses and in five horses with grass sickness. Histopathological changes, consistent with those observed in other ganglia of horses with grass sickness, were identified in the terminal cardiac ganglia of the affected horses. A functional analysis of cardiac autonomic control by time domain analysis (TDA) of heart rate variability was applied to eight horses with grass sickness, and double-paired to 16 normal horses on the basis of their age, sex and breed, and the time of day at which the electrocardiographs were obtained. There were statistically significant differences between the normal and the affected horses in terms of the triangular index (P=0.01), a geometric method of TDA, the sNN100 index (P=0.009), a statistical method of TDA, and the R to R interval (P<0.0005). These results indicate that there is a pathological and functional parasympathetic decentralisation to the heart in equine grass sickness.

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Observations on Neuronal Changes in Grass Sickness of Horses

Cited by 62 publications

References 2 publications

The neurology and enterology of equine grass sickness: a review of basic mechanisms

The neurology and enterology of equine grass sickness: a review of basic mechanisms

Neurodegenerative Disorders

Functional and histopathological evidence of cardiac parasympathetic dysautonomia in equine grass sickness

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