Dysautonomia

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Nasal discharge, elevated third eyelid and dilated pupils are typical of dysautonomia[1]
Affected dogs lose weight dramatically. The bladder is distended and easily expressed[1]

Dysautonomia is an idiopathic neurological disease of dogs characterized by degeneration of neurons in the autonomic ganglia with associated failure of sympathetic and parasympathetic functions.

This condition resembles the human disease, Key-Gaskell syndrome[2].

In this disease, which affects many breeds of young adult dogs, neuronal function is diminished or absent in the ganglia and replaced by a noninflammatory gliosis. There is little inflammation present. The cause is unknown. More recently an increasing number of cases of canine dysautonomia have been diagnosed in the midwest United States[3].

Dysautonomia has been diagnosed primarily in the mid-west United States[4].

Clinically affected dogs present with a brief history of rapid weight loss, dysuria, urinary bladder distension, reduced anal sphincter tone, regurgitation, Horner's syndrome[5], lack of salivary secretions, purulent nasal discharge, photophobia, anorexia, and weight loss[6].

Blood tests, urinalysis and CF tests are usually unremarkable. Radiography usually show varying degrees of megaesophagus and aspiration pneumonia, as well as urinary bladder distension and ileus.

An antemortem diagnosis is often one of exclusion of other disease and testing pupillary reflex response to topical pilocarpine. Dogs with dysautonomia generally show a rapid constriction of the pupils.

Additionally, bladder contractility can be tested with low dose bethanecol at 0.0375 mg/kg given subcutaneously, followed by bladder volume re-assessment with ultrasonography. Emptying of the bladder with low-dose bethanechol would suggest denervation hypersensitivity. Some affected dogs have not responded to bethanechol, presumably due to secondary detrusor atony.

Histological examination of the autonomic ganglia usually shows degeneration without inflammation of neurones with accompanying gliosis[7].

Treatment can be problematic, but use of bethanacol and pilocarpine may alleviate clinical symptoms. Gastrointestinal motility can be improved by the use of prokinetic drugs such as metoclopramide. Parenteral nutrition may be necessary to prevent the development of cachexia[8].

The prognosis in most cases is considered grave but some dogs recover after 1 - 3 months with aggressive supportive therapy.

References

  1. 1.0 1.1 Missouri University
  2. Pollin M, Sullivan M (1986) A canine dysautonomia resembling the Key-Gaskell syndrome. Veterinary Record 118:402-403
  3. O'Brien, DP (2010)
  4. Schrauwen E, et al (1991) Canine dysautonomia: a case report. Veterinary Record '128:524-525
  5. Longshore RC, et al (1996) Dysautonomia in dogs: a retrospective study. J Vet Intern Med 10:103-109
  6. Edney ATB, Gaskell CJ, and Sharp NJH (1987) Feline dysautonomia - an emerging disease. J Small Animal Practice 28:333-416
  7. O'Brien DP, Longshore RC (2000) Diagnosis and management of dysautonomia in dogs. In Bonagura, JD ed. Kirk's Current Veterinary Therapy XIII, WB Saunders Co, Philadelphia, pp:957-959
  8. Presthus J, Bjerkas (1987) Canine dysautonomia in Norway. Veterinary Record 120:463-464