Dysautonomia in dogs
Contributed by Dennis P. O’Brien DVM PhD
Professor of Veterinary Neurology
Department of Veterinary Medicine and Surgery
College of Veterinary Medicine
University of Missouri, Columbia, MO

Dysautonomia is characterized by degeneration of neurons in the autonomic ganglia with associated failure of sympathetic and parasympathetic functions. Neurons are diminished or absent in the ganglia of affected dogs and replaced by gliosis. There is little inflammation present. The cause is unknown. Since the 1980's, the disease has become endemic in the midwest United States. This article will describe the diagnostic and therapeutic approaches we have applied to these cases at the University of Missouri, Veterinary Medical Teaching Hospital.

Dysautonomia has been diagnosed primarily in young adult dogs (median age 14 months with a range from 8 weeks to 10 years of age). Although Labrador retrievers were slightly over-represented, a wide variety of breeds have been affected, and the disease occurs occasionally in cats as well. The most common presenting complaints in affected dogs have been dysuria, regurgitation, purulent nasal discharge, photophobia, anorexia, and weight loss (Table 1). The duration of clinical signs averaged about 2 weeks.

Figure 1. Normal autonomic
ganglia are packed with neurons (left). In dysautonomia, the
neurons die and are replaced
with scar tissue (right).

Clinical Signs
Physical exam findings reflected primarily loss of parasympathetic functions although sympathetic dysfunction was also present. Pupillary light responses were absent with normal vision, and the pupils varied from maximally dilated to midrange. Ocular and oral mucous membranes lacked normal secretion. The dogs would frequently posture to urinate, but they produced little urine. On abdominal palpation, the bladder was distended, and pain was occasionally noted.

Sympathetic dysfunction was often less obvious. Loss of sympathetic as well as parasympathetic innervation of the iris may have contributed to the midrange pupils seen in some dogs. Other signs of Horner’s syndrome such as elevated third eyelids, ptosis and enophthalmos were often present. The distended bladder was easily expressed suggesting diminished sphincter tone. Heart rate and blood pressure were generally in the low end of the normal range, but did not increase with stress or excitement.

The only sign of somatic motor system involvement was decreased anal sphincter tone; this was present in most dogs. Myotatic and withdrawal reflexes, sensory perception, and postural reactions were normal. Secondary effects of the autonomic dysfunction such as aspiration pneumonia and lethargy soon developed. Rhinitis secondary to dry mucous membranes and/or regurgitation was a common finding. Weight loss was often dramatic with many of the dogs presenting cachexic. No consistent changes were observed in the complete blood counts, urinalyses, serum chemistries, or cerebrospinal fluid analyses.

Figure 2. Nasal discharge,
elevated third eyelid & dilated
pupils are typical of

Figure 3. Affected dogs lose
weight dramatically. The
bladder is distended and
easily expressed.

Diagnostic Tests
Confirming a diagnosis of dysautonomia depends on documenting diffuse sympathetic and parasympathetic dysfunction without significant somatic nervous system involvement or sensory loss. A complete neurologic exam will be necessary to rule out somatic involvement. For example, a dog with a sacral cord lesion due to canine distemper may have urinary retention and loss of anal tone, but he should also have other signs such as loss of sensation to the perineum and loss of tail movements. In cases with limited signs initially (e.g. dysuria or photophobia alone), more common causes of the signs (e.g. cystitis or corneal ulcer respectively) must be ruled out. Cases that present initially with only gastrointestinal signs can be particularly challenging since the radiographic changes can de difficult to distinguish from a foreign body. Since parasympathetic dysfunctions predominate in dysautonomia, cholinergic blockade with toxins or drugs (e.g. atropine) must be ruled out. Necropsy confirmation of autonomic ganglia degeneration without inflammation provides the definitive diagnosis, but a variety of tests can be used to support an antemortem diagnosis of dysautonomia.

Pharmacologic testing of the pupils is probably the best single test for confirming the diagnosis. Pilocarpine ophthalmic solution (Isopto Carpine 1%, Alcon) is diluted to 0.05% with normal saline and 1-2 drops placed in one eye. Pupil size is then observed every 15 minutes. Dogs with dysautonomia generally show a rapid constriction of the pupils. Even at the 0.05% dilution, some normal dogs may show some constriction of the pupils, but it will take >60 minutes. Rapid constriction to such a low dose of pilocaprine occurs due to denervation supersensitivity which confirms a loss of the post-ganglionic neurons. If no response is seen 90 minutes after instilling the 0.05% solution, the test is repeated with full strength (1-2%) pilocarpine. Since drugs such as atropine produce their effects by blocking cholinergic receptors, dogs who have parasympathetic signs due to such drugs or toxins should not respond to even the full strength pilocarpine solutions.

Thoracic radiographs can confirm the presence of megaesophagus and detect secondary aspiration pneumonia. Abdominal radiographs may demonstrate a distended urinary bladder and occasionally ileus. Alternatively, ultrasound can be used to document the distended bladder, ileus and lack of normal gastrointestinal motility. Attempts to urinate will have little effect on bladder volume. The dog can then be tested with a low dose (0.0375 mg/kg SQ) of bethanechol (Urecholine, Merck Sharp & Dome) and bladder volume re-evaluated with ultrasound. Emptying of the bladder with low-dose bethanechol would suggest denervation supersensitivity. Some affected dogs have not responded to bethanechol, presumably due to secondary detrusor atony.

Confirming sympathetic involvement is more problematic. Blood pressure and hearth rate are usually at the low end of normal limits, but do not increase as expected with stress or excitement. Provocative challenges with drugs that affect heart rate and blood pressure are not recommended due to the risk of deleterious effects. Recent studies have shown that dogs with dysautonomia have diminished systolic function on echocardiograms. The wheel and flair response to histamine depends upon normal sympathetic innervation of the blood vessels. Thus dogs with dysautonomia do not respond normally to intradermal histamine with some having no response while others develop the wheel but not the flair.

Since the cause of dysautonomia is still unknown, we are limited to symptomatic therapy. Cholinergic drugs can help relieve some of the signs of parasympathetic dysfunction. Bethanechol (1.25-5 mg q 12 h) given orally provided some improvement in secretion and urination, but better results have been seen with subcutaneous administration (started at 0.0375 mg/kg q 12 h and slowly increased as necessary). Frequent expressing of the bladder will be necessary if the bladder does not empty adequately with the bethanechol. Pilocarpine eye drops will stimulate tear production and relieve photophobia. Use of artificial tears is also beneficial. Gastrointestinal motility can be improved by the use of prokinetic drugs such as metaclopramide (Sidmack Laboratories). Humidifying the air can help relieve some of the dryness to the oral and nasal mucous membranes. Parenteral nutrition may be necessary to prevent the development of cachexia.

The prognosis in dysautonomia is grave. In the feline epidemic, mortality was about 70% and our experience to date with the canine disease suggests a similar high mortality. Animals who survived have been largely left with permanent dysfunction and require intensive nursing care. In contrast to the situation in England where the incidence of dysautonomia declined over time, the disease has shown no signs of decreasing in the midwest, but also has not become prevalent in other areas of the country. Research to identify the cause is still desperately needed so that preventative measures and effective therapies can be developed.


Figure 4. Dilation of the
esophagus (arrows) can be
seen on thoracic radiographs

Table 1
Historical and physical examination findings in 11 dogs with necropsy confirmed dysautonomia (Longshore et al 1996).
Historical and/or physical finding Number of dogs affected/
Number in which evaluation was recorded
Dysuria 11/11
Distended urinary bladder 10/10
Mydriasis 11/11
Absent pupillary light reflex 11/11
Dry mucous membranes 10/11
Weight loss 8/10
Decreased Schirmer tear test (<15mm/min) 8/10
Decreased anal reflex 7/9
Decreased appetite 7/10
Vomiting/Regurgitation 6/9
Lethargy 7/11
Elevated third eyelid 5/11
Constipation 3/9
Dysphagia 3/9
Diarrhea 3/9
Weakness 2/9
Abdominal pain 1/10

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54 (4):291- 300, 2002.

R. D. Berghaus, D.P O'Brien, G.C. Johnson, and J.G Thorne. Risk factors for development of dysautonomia in dogs. J Am Vet Med Assoc 218:1285-1292, 2001.

K.R Harkin, G.A Andrews, and J.C Nietfeld. Dysautonomia in dogs: 65 cases (1993-2000). J Am Vet Med Assoc. 220 (5):633-639, 2001.

K.R. Harkin, B. J Bulmer, and D.S Biller. Echocardiographic evaluation of dogs with dysautonomia.
J Am Vet Med Assoc 235 (12):1431-1436, 2009.

A.C Kidder, C. Johannes, D.P O'Brien, K.R Harkin, and T. Schermerhorn. Feline dysautonomia in the Midwestern United States: a retrospective study of nine cases. J Feline Med Surg 10 (2).130-136, 2008.

R. C. Longshore, D.P O'Brien, G.C Johnson, A. M. Grooters, and R.A Kroll. Dysautonoia in dogs - a retrospective study. J Vet Int Med 10 (3):103-109, 1996.

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