Proceedings of a Workshop on - The Havemeyer Foundation

Havemeyer Foundation Monograph Series No. 11
laryngeal paralysis. Older pet dogs with unilateral
laryngeal paralysis are seldom presented with
clinical signs but working or racing dogs with
unilateral paralysis may present with clinical signs
that interfere with their work (Greenfield 1987).
Greenfield et al. (1997) showed that clinical
signs and measurable airflow changes associated
with bilateral laryngeal paralysis did not develop in
dogs until a median <strong>of</strong> 38 days following bilateral
denervation <strong>of</strong> the recurrent laryngeal nerves. The
reason for such a delay is unclear. It has been
suggested that slow development <strong>of</strong> clinical signs in
many naturally occurring cases <strong>of</strong> canine idiopathic
laryngeal paralysis is due to progressive
deterioration <strong>of</strong> the recurrent laryngeal nerve.
However, progressive anatomical changes in the
laryngeal structures may also be necessary for
development <strong>of</strong> severe clinical signs.
Canine idiopathic laryngeal paralysis can be
confirmed by ultrasonography in the conscious
dog or laryngoscopy in the lightly anaesthetised
subject (deeper anaesthesia will cause immobility
<strong>of</strong> even the normal larynx), taking care to
distinguish passive laryngeal abduction associated
with deep expiration from normal active laryngeal
abduction that occurs during inspiration.
Most publications on idiopathic canine
laryngeal paralysis report the diagnosis and
treatment <strong>of</strong> this disorder, or the use <strong>of</strong> dogs as
models to treat human laryngeal paralysis. Few
comment on the pathogenesis or epidemiology.
Early work suggested involvement <strong>of</strong> a neurogenic
or denervation atrophy <strong>of</strong> the laryngeal muscles
(such as occurs in horses) and this has become
widely accepted as the most likely aetiopathogenesis
(O’Brien et al. 1973). Most studies have either used
retrospective case analysis (O’Brien et al. 1973);
have been restricted to congenital laryngeal
paralysis (van Haagen et al. 1978, 1981) or have
analysed laryngeal innervation in normal dogs
(Braund et al. 1988 a,b), and so their data and
conclusions can be difficult to extrapolate to
idiopathic canine laryngeal paralysis. For example,
van Haagen et al. (1978, 1981) have described
histological evidence <strong>of</strong> neurogenic axonal
degeneration <strong>of</strong> the right and left recurrent laryngeal
nerves in cases <strong>of</strong> congenital laryngeal paralysis
Biopsies <strong>of</strong> intrinsic laryngeal muscles in cases
<strong>of</strong> idiopathic canine laryngeal paralysis have shown
evidence <strong>of</strong> neurogenic atrophy (O’Brien et al.
1973; Love et al. 1987). A comparative study <strong>of</strong> the
neuropathology <strong>of</strong> canine and equine ‘RLN’ could
provide much useful information for both species.
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Morphologic and morphometric studies <strong>of</strong> the vagus
and recurrent laryngeal nerves in clinically normal
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Braund, K.G., Steiss, J.E., Marshall A.E., Mehta, J.R.
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