Proceedings of a Workshop on - The Havemeyer Foundation

Equine Recurrent Laryngeal Neuropathy
groups <strong>of</strong> atrophied fibres adjacent to
hypertrophied fibres with central nuclei (Duncan
and Griffiths 1974; Duncan et al. 1991). The first
muscle groups affected appear to be the adductor
muscles and within the adductor group the
cricoarytenoideus lateralis is among the earliest
and most severely affected muscles (Lopez Plana
et al. 1993). The chronic, repetitive nature <strong>of</strong> the
disease is further exemplified by the presence <strong>of</strong>
muscle fibre type grouping, as muscle fibre type is
controlled by the innervating neuron.
Together, these pathological changes have
been classified as a distal axonopathy, with the
greater pathology in the left recurrent laryngeal
nerve being explained by its greater length. One
hypothetical cause <strong>of</strong> distal axonopathy is a defect
in the neuronal soma, as the axon depends on the
cell body for metabolic support and sustaining or
trophic influences. Indeed, many <strong>of</strong> the peripheral
nerve lesions that are typical in equine motor
neuron disease, a disease primarily affecting the
cell body, are also observed in RLN including
axonal atrophy, proliferated Schwann cell cords
(Büngner’s bands), loss <strong>of</strong> myelinated fibres and
an increase in endoneurial collagen.
HYPOTHETICAL AETIOLOGIES
Despite years <strong>of</strong> work we appear to be no closer to
clarifying the aetiology <strong>of</strong> this common equine
disease. Hypotheses range from mechanical
causes such as tension and stretch to the recurrent
laryngeal nerve and its blood supply during neck
movement, growth, or the caudal shift <strong>of</strong> the heart
during embryonic development, to environmental
factors, including toxins (reviewed by Cahill and
Goulden 1987). The latter have been viewed as
unlikely causes <strong>of</strong> RLN as the neuropathological
changes are limited to the recurrent laryngeal
nerves.
Myelinopathies and the inherited and
metabolic primary axonopathies affect multiple
nerves and in other species would be expressed as
part <strong>of</strong> a polyneuropathy and be progressive.
Comparable pathology has indeed been noted in
foals (Duncan 1992; Harrison et al. 1992) and
clinical signs <strong>of</strong> left-sided hemiplegia have been
demonstrated to be clinically progressive (Dixon
et al. 2002). Interestingly, however, there have
been no reports <strong>of</strong> left hemiplegic horses
progressing to develop right-sided clinical signs
(Dixon, personal communication). On the other
hand, it is clear that horses affected with RLN do
not show classical clinical signs <strong>of</strong>
polyneuropathy such as megaoesophagus,
tetraparesis and muscle atrophy. Notwithstanding,
involvement <strong>of</strong> other long peripheral nerves
(common, deep and superficial peroneal and tibial
nerves) has been reported by some workers (Cahill
and Goulden 1986a; Kannegieter 1989), but was
not found by Duncan et al. 1978). Similarly,
neurogenic muscle changes have been reported to
exist in the extensor digitorum longus (Cahill and
Goulden 1986d) in 3 out <strong>of</strong> 4 horses suffering
from RLN. The above observations however have
been isolated, uncontrolled and have not taken into
account that age-related pathological changes can
be demonstrated in distal limb nerves <strong>of</strong> horses
(Wheeler and Plummer 1989). A detailed study <strong>of</strong>
the peripheral nerves in RLN affected and control
animals has not been undertaken.
It should be remembered that axonal
degeneration, characterised by distal degeneration
that spreads proximally (‘dying back’), is the most
common pathology seen in peripheral nerve
diseases caused by a wide variety <strong>of</strong> toxic,
metabolic, and infectious insults. Some <strong>of</strong> these
processes affect the cell body, and it may be that
the axonal dying back process may be initiated in
order to conserve energy. How a cell can eliminate
part <strong>of</strong> itself while leaving the rest intact is
unknown. Localised axonal degeneration that
resembles dying back can also occur in cell culture
if the distal portion <strong>of</strong> the axon is deprived <strong>of</strong>
nerve growth factor, and a similar process may be
involved in disease states. Other forms <strong>of</strong> axonal
degeneration that seem distinct from typical dying
back occur in various human neurodegenerative
diseases such as Alzheimer’s, Parkinson’s and
Huntington’s diseases.
Pathological changes <strong>of</strong> the recurrent
laryngeal nerve in RLN has been described in
great detail using light and electron microscopy
but the tools <strong>of</strong> the burgeoning science <strong>of</strong>
molecular pathology have not been utilised. A
detailed examination <strong>of</strong> changes in gene
regulation and cytokine expression will have to be
applied if further details <strong>of</strong> the pathogenesis are to
be uncovered.
REFERENCES
Cahill, J.I. and Goulden, B.E. (1986a) Equine laryngeal
hemiplegia. I. A light microscopic study <strong>of</strong>
peripheral nerves. N. Z. vet. J. 34, 161-169.
Cahill, J.I. and Goulden, B.E. (1986b) Equine laryngeal
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