GASTRO-ENTEROLOGY
Sialoadenosis has a major clinical impact and is often
misdiagnosed as nausea. The following two articles
aim to demystify the condition
Sialoadenosis
and Limbic
Epilepsy
Liesel van der Merwe BVSc MMed Vet (Med) Small
Animals
Senior Lecturer, Outpatients OVAH
[email protected]
Sialoadenosis is a bilateral, persistent, painless,
soft, non-neoplastic, non-inflammatory swelling
usually involving the parotid and sometimes also the
mandibular salivary glands.
Salivary gland enlargement is an uncommon
condition in dogs. In a review of 245 salivary gland
biopsies from animals, salivary glands accounted
for only 0.3% of all biopsies received. The majority
of these biopsies (65%) were obtained from dogs
and demonstrated neoplasia (30%), inflammation
(29%), sialocoele formation (11%), infarction (9%),
with the remainder showing miscellaneous changes.
Hypersialosis or ptyalism is excessive secretion of
saliva (true hypersialosis) or inability to contain saliva
within the oral cavity, as may occur with dysphagia.
Ptyalism also occurs secondary to both stimulation
of salivary secretion caused by other disorders
(e.g. dysphagia) and primary disease of the salivary
gland (e.g. sialadenosis). Sialorrhoea, ptyalism or
hypersialosis are synonyms used to describe the
excessive production of saliva. Sialoadenosis causes
clinical signs of retching, gulping, anorexia, nausea,
vomiting and sialorrhoea with firm palpable, often
enlarged salivary glands in dogs.
If endoscopic evaluation of the stomach and
oesophagus reveals no lesions and there is no
histological evidence of gastritis or oesophagitis, and
thoracic imaging reveal no extraluminal oesophageal
pathology, a diagnosis of idiopathic phenobarbitone-
responsive hypersialosis can be made. The terrier
breeds, especially fox terriers and Jack Russell
terriers, are over-represented in the literature for both
secondary and idiopathic sialorrhoea.
It is suggested that all forms of human sialoadenosis
are caused by degenerative changes demyelinating
polyneuropathy,in the autonomic nervous system.
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Salivary gland enlargement may be a secondary
reactive change because of over-stimulation by the
parasympathetic system. Three publications reported
that surgical resection of the affected salivary glands,
failed to stop the hypersalivation and dysphagia until
phenobarbitone was administered to the patients. This
finding supports the theory that the sialorrhoea is part
of a multifactorial parasympathetic response to an
underlying stimulus or condition.
It has been suggested that the idiopathic form of
the disease may be a form of epilepsy, namely
limbic epilepsy.The sialorrhoea and oral discomfort
(odynophagia) exhibited by these patients responds
well to phenobarbitone. There is no direct evidence
linking phenobarbitone to saliva production but it
does reduce small intestinal motility and could have
local effects on the salivary glands The effectiveness
of the phenobarbitone may indicate that the primary
cause of the condition is parasympathetic activation
of salivary gland secretion.
The exact mechanism of action of phenobarbitone
is unknown, but is likely to involve inhibition of
excitatory neurotransmitters, such as glutamate, and a
gamma aminobutyric acid mimetic effect. Successful
therapeutic intervention using anticonvulsants for
sialoadenosis in dogs was first demonstrated in 1979
by Kelly et al. using phenytoin and primidone and
subsequently, phenobarbitone was successfully used
in several small case series. Most dogs improved within
48 h and all improved within 4 days. In the largest case
series described, a starting oral dose of 1 mg/kg PO
q12h was effective, although others have used higher
doses (2–3 mg/ kg PO q12h), suitable for control of
idiopathic epilepsy, with and without a loading dose.
In one-quarter of the cases, tapering and cessation of
phenobarbitone therapy was possible after a variable
length of time (6–12 months until cessation).
References
1.
Boydell, P., Pike, R., Crossley, D. & Whitbread, T., 2000a, ‘Sialadeno-
sis in dogs’, Journal of the American Veterinary Medical Association
216, 872–874.
2.
Brooks, D.G., Hottinger, H.A. & Dunstan, R.W., 1995, ‘Canine nec-
rotizing sialometaplasia: A case report and review of the literature’,
Journal of the American Animal Hospital Association 31, 21–25.
3.
Chapman, B.L. & Malik, R., 1992, ‘Phenobarbitone-responsive
hypersialism in two dogs’, Journal of Small Animal Practice 33,
549–552.
4.
Cooke, M.M. & Guilford, W.G., 1992, ‘Salivary gland necrosis in a
wire-haired fox terrier’, New Zealand Veterinary Journal 40, 69–72.
5.
Gibbon, K.J., Trepanier, L.A. & Delaney, F.A., 2004, ‘Phenobarbitone
responsive ptyalism, dysphagia and apparent esophageal spasm
in a German shepherd puppy’, Journal of the American Animal
Hospital Association 40, 230–237.
6.
Kelly, D.F., Lucke, V.M., Denny, H.R. & Lane, J.G., 1979, ‘Histology
of salivary gland infarction in the dog’, Veterinary Pathology 16,