Feline dysautonomia is characterized by widespread dysfunction of the autonomic nervous system. All breeds and age groups are susceptible. Feline dysautonomia was first reported in 1982 and initially became widespread in the UK (under the name Key-Gaskell syndrome); the incidence has declined considerably, but a few cases were recorded more recently in Europe, a few have been documented in North America, and sporadic cases have been seen in Dubai, New Zealand, and Venezuela. The etiology is unknown. Dysautonomias in horses, dogs, rabbits, and hares share striking similarities to the condition in cats.
Affected cats initially are anorectic and often have upper respiratory signs or transient diarrhea. The onset of more definite signs varies from peracute to chronic. The most common of these signs are dilated, nonresponsive pupils, ptosis, and third eyelid protrusion; a dry rhinarium; reduced lacrimal secretion; esophageal dysfunction with regurgitation; and constipation. Other signs include dry oral mucous membranes, prolapse of the nictitating membrane, bradycardia, and urinary or fecal incontinence. These signs reflect both sympathetic and parasympathetic dysfunction, and there is a wide range in the severity of presenting signs. Somatic signs include anal areflexia. Pelvic limb proprioceptive deficits have been reported but should be carefully differentiated from paresis—ataxia is not a feature of dysautonomia in other species. Clinical pathology findings are nonspecific.
Necropsy 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. A very specific distribution of chromatolytic autonomic and somatic lower motor neurons is found in the brain stem and spinal cord. The central lesions are identical to those found in the equivalent disease in dogs, horses, rabbits, and hares. Chronic cases can be difficult to confirm because surviving neurons appear normal, and diagnosis depends on an assessment of their numbers relative to surrounding stromal cells.
Definitive diagnosis depends on histopathologic examination of autonomic ganglia. Clinical confirmation may be aided by contrast radiography (including fluoroscopy) of the esophagus and by reduced lacrimal secretion (<5 mm/min when measured by the Schirmer tear test). Pilocarpine (0.1%) applied to the cornea causes profound miosis within 10–15 min due to denervation hypersensitivity but has no effect on a healthy cat. Dilute (0.5%) phenylephrine reverses the ptosis and protruding third eyelid. Although feline leukemia virus (FeLV, see Feline Leukemia Virus and Related Diseases) infection can cause both anisocoria and urinary incontinence, cats with dysautonomia usually show other clinical signs and are FeLV-negative.
Treatment and Prognosis
The main aim of therapy is first 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 inhalation pneumonia. Thrice daily evacuation of the bladder, provision of warmth, use of artificial tears and steam inhalation, and assistance with grooming are all important nursing considerations. Liquid paraffin PO is helpful for constipation but increases the risk of aspiration. Other parasympathomimetics, such as bethanechol (1.0–2.5 mg, PO, bid-tid), may be of use; however, their effect is crude, and overdosage requires treatment with atropine. Metoclopramide (0.1 mg/kg, IV, or 0.3 mg/kg, SC, tid) may improve gastric emptying.
A small proportion of cats have recovered, and others are able to cope with residual autonomic deficits. Such improvements often require up to 1 yr. In general, the prognosis is poor for severely affected cats.
Last full review/revision July 2011 by Caroline N. Hahn, DVM, MSc, PhD, DECEIM, DECVN, MRCVS