Feline dysautonomia is characterized by widespread degeneration of the autonomic nervous system, leading to esophageal distention and/or dysfunction, gastric and bowel distention and hypomotility, urinary bladder distention, and pupillary dysfunction.
Feline dysautonomia was first reported in 1982 (under the name Key-Gaskell syndrome) and initially became widespread in the UK. The incidence has declined considerably; however, multiple cases of feline dysautonomia have been reported in Europe, New Zealand, the United Arab Emirates, and the US.
The etiology is unknown, but several suggestions of toxic damage such as from Clostridium botulinum (type C/D) neurotoxin involvement have been made (1). A 2020 study of 34 cases showed an 80% mortality rate (2).
Clinical Findings of Feline Dysautonomia
Cats of any age can be affected by feline dysautonomia, but it is more common in younger cats (median age 3.9 years). Affected cats may commonly have clinical signs that reflect both sympathetic and parasympathetic dysfunction, such as the following:
anorexia or hyporexia
vomiting or regurgitation along with megaesophagus and intestinal dilation and ileus
constipation
nasal discharge or crusting
lower urinary tract clinical signs
Less commonly, cats may develop respiratory clinical signs, bradycardia, altered anal tone, and diarrhea.
Specific ocular clinical signs also occur in cats with dysautonomia, including decreased lacrimation, absent or delayed pupillary light reflex, mydriasis, and third eyelid protrusion (see feline dysautonomia image). Clinicopathological findings are nonspecific.
Courtesy of Dr. Caroline Hahn.
Lesions
Necropsy of cats with feline dysautonomia may show megaesophagus, diphtheritic mucous membranes, an atonic bladder, and retention of fecal material.
During the first few weeks after onset, chromatolysis and neuronal degeneration of pre- and postganglionic sympathetic and parasympathetic neurons is typical. These changes are evident within ganglia as well as presynaptic autonomic lower motor neurons in the brain and spinal cord. A specific characteristic is finding chromatolytic somatic lower motor neurons in the ventral horn of the spinal cord and in nuclei of somatic cranial nerves in the brainstem.
Chronic feline cases may mainly show a paucity of neurons, with only a few chromatolytic or actively degenerating neurons evident.
Diagnosis of Feline Dysautonomia
Physical examination findings
Radiological evaluation
Pharmacological testing
Diagnosis of feline dysautonomia is typically based on physical examination findings, radiological findings, and pharmacological testing, such as a pilocarpine test with a 0.05% solution.
Definitive diagnosis depends on histological examination of autonomic ganglia.
Radiographic abnormalities suggestive of feline dysautonomia include aspiration pneumonia, megaesophagus, dilated stomach, diffuse ileus, and a distended urinary bladder. A Schirmer tear test may disclose decreased lacrimal secretion (< 5 mm/min). Pilocarpine eye drops (0.05%–0.1%) will induce miosis and retraction of third eyelid elevations in ~80% of cases within 45 minutes but have no effect in healthy animals.
Although feline leukemia virus (FeLV) infection can cause both anisocoria and urinary incontinence, cats with dysautonomia usually show other clinical signs and test negative for FeLV.
Treatment and Prognosis of Feline Dysautonomia
Supportive care
There is no effective treatment for feline dysautonomia; however, supportive nursing care may enable mildly affected cases to survive.
The main aim of treatment is to rehydrate the cat and then to maintain adequate fluid balance. Total parenteral nutrition is useful initially but later can be replaced by gastrostomy or nasogastric tube feeding when regurgitation resolves. Maintaining an upright posture after oral intake is important because the main complication of this condition is aspiration pneumonia.
Expression of the bladder three times a day, provision of warmth, use of artificial tears, steam inhalation, and assistance with grooming are all important nursing considerations. Liquid paraffin administered orally is helpful for constipation but increases the risk of aspiration.
Parasympathomimetics, such as bethanechol (1–2.5 mg per cat, PO, every 8–12 hours), may be of use; however, their effect is crude, and overdosage requires treatment with atropine. Prokinetic medications such as metoclopramide (0.1 mg/kg, IV, or 0.3 mg/kg, SC, every 8 hours) may improve gastric emptying.
A small proportion of cats have recovered, and others are able to cope with residual autonomic deficits, particularly megaesophagus. Such improvements often require up to 1 year. In general, the prognosis is poor for severely affected cats.
Key Points
Feline dysautonomia is a rare disease of unknown etiology that is characterized by degeneration of autonomic neurons resulting in autonomic nervous system dysfunction.
The prognosis is guarded, and treatment is limited to supportive care.
For More Information
Černá P, Botts MM, Watson A, Carr SV. Dysautonomia in two littermate kittens. JFMS Open Rep. 2023;9(1). doi:10.1177/20551169231164579
Also see pet health content regarding dysautonomia in cats.
References
Nunn F, Poxton IR, Cave TA, Knottenbelt C. Association between Key-Gaskell syndrome and infection by Clostridium botulinum type C/D. Vet Rec. 2004;155(4):111-115. doi:10.1136/vr.155.4.111
Clarke KE, Sorrell S, Breheny C, et al. Dysautonomia in 53 cats and dogs: retrospective review of clinical data and outcome. Vet Rec. 2020;187(12):e118. doi:10.1136/vr.105258
