South African Equine Veterinary Association Congress 2015 Protea Hotel Stellenbosch
are of pes cavus (a foot deformity) due to neurogenic muscle atrophy of foot muscles that are
supplied by the longest motor axons. Unlike in humans, the nerves to the limbs of horses are not
the longest in the body; indeed, in horses, nerves to the distal limb are predominantly sensory
(motor nerves mainly innervate muscles proximal to the carpus and tarsus). Motor nerves to the
distal limb muscles are considerably shorter than the recurrent laryngeal nerves, which might
explain why RLN seems clinically to affect only intrinsic laryngeal musculature; nonetheless,
evidence for neuropathy of other long motor nerves is provided by several early studies (Cahill
and Goulden 1986a,b) though not in a more recent study in which there was no evidence for
generalized neuropathy in distal limb nerves and muscles and phrenic nerve and diaphragm in 3
RLN-affected horses (Hahn et al 2008). Since axonopathy might be both length- and usedependent, it is conceivable that the axonal death might only occur in the longest, and most
commonly used nerves - perhaps therefore, the long motor (recurrent laryngeal) nerves that are
active during breathing. Intriguingly, many primary neuropathies in humans affect both sensory
and motor nerves; loss of sensory innervation to the larynx has not been closely examined in RLN
horses, however evidence for involvement of long sensory axons is provided by a study that
reported more axonal spheroids in the lateral cuneate nuclei of RLN-affected horses in
comparison with controls (Cahill and Goulden 1986c).
Which motor units are predominantly affected in RLN?
The motor unit is defined as the combination of the motor nerve and the muscle fibres that it
innervates. Large motor units (i.e. where many muscle fibres are innervated by a single axon) are
typically found in locomotor muscles, whereas small motor units are found associated with
muscles that have fine movements (such as the extra-ocular muscles). When a motor axon dies,
the fibres that it innervates start to atrophy; they send out paracrine signals (such as nerve growth
factors) that induce re-innervation via the nearby sprouting of surviving axons. Since fibre types
in the same vicinity will tend to be reinnervated by the same axon, and since muscle fibre type is
largely dependent on its axonal supply, muscles that have undergone cycles of denervation and
renervation (as in RLN) typically have considerable fibre type grouping. Consequently, a loss of
specific fibre types over time in the disease, or differences in loss of specific fibre types in horses
with varying severity of disease, might indicate whether fast motor units or slow motor units are
preferentially involved. Although our data, and that of others (Rhee at al. 2009), supports a loss of
the fastest (type 2X) motor units, there appears to be considerable variation between horses. Since
the motor unit size in equine laryngeal muscles is unknown, such variation might be influenced by
differences in size of fast to slow motor units, and to the degree to which each motor unit type is
utilised (i.e. more active motor units will have a greater metabolic load, and therefore might be
more susceptible to disease). Such a difference in motor unit susceptibility, might therefore
account for the more severe histopathological changes that are detectable in the cricoarytenoideus
lateralis muscle in comparison with the dorsalis muscle, since the former has a higher proportion
of fast motor units (Lopez-Plana et al. 1993, Duncan 1973, Cahill and Goulden 1986d). Available
evidence from our group and that of others however, suggests that RLN affects predominantly fast
motor units earlier in the disease course, similar to many human motor neuropathies or their
models, such as Amyotrophic lateral sclerosis (Hegedus et al. 2008).
Mechanism of disease
Whilst evidence for the disease has been identified in fetuses (Gunn 1973) and in a few young
(draught horse) foals (Harrison et al. 1992, Duncan 1992) the disorder is typically recognized as
racehorses go into training. There is some evidence supporting disease progression (Dixon et al.
2002), however such work is likely compromised by difficulties in performing longitudinal
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