Feline dysautonomia is characterized by widespread degeneration of the autonomic nervous system, leading to esophageal distension and/or dysfunction, gastric and bowel distension and hypomotility, urinary bladder distension, and pupillary dysfunction. 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 in Europe in the 1990s; sporadic cases have been seen in Dubai, New Zealand, and Venezuela; and a few cases have been reported in the USA, in eastern Kansas and western Missouri. The etiology is unknown, and most patients are euthanized.
Cats affected with feline dysautonomia may be of any breed or age, but younger cats may be more commonly affected. Initially, affected cats are anorectic and often have upper respiratory signs or transient diarrhea. The onset of more definite signs varies from peracute to chronic. Failure of the autonomic system of the GI and urinary tracts can cause esophageal distention and/or dysfunction, gastric and bowel distention and hypomotility, and urinary bladder distention.
Other common signs include:
In addition, dry oral mucous membranes, prolapse of the nictitating membrane, bradycardia, and urinary or fecal incontinence may be seen.
These signs reflect both sympathetic and parasympathetic dysfunction, and there is a wide range in the severity of presenting signs. A dilated anus is sometimes noted, but the underlying somatic lesion is undetermined. Clinical pathology findings are nonspecific.
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.
Neuronal chromatolysis and loss is marked in postsynaptic sympathetic and parasympathetic autonomic lower motor neurons in the 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 brain stem.
Very chronic feline cases may mainly show a paucity of neurons, with only a few chromatolytic or actively degenerating neurons evident.
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 reduced lacrimal secretion (<5 mm/min). 0.05% pilocarpine eye drops will induce miosis and retraction of third eyelid elevations in an affected animal but have no effect in healthy animals.
Although feline leukemia virus Feline Leukemia Virus and Related Diseases read more infection can cause both anisocoria and urinary incontinence, cats with dysautonomia usually show other clinical signs and are FeLV-negative.
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. 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 given orally is helpful for constipation but increases the risk of aspiration.
Parasympathomimetics, such as bethanechol (1–2.5 mg, PO, two to three times daily), 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, three times daily) 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.