The term 'neurasthenia' was popularized by Dr. George Miller Beard in 1869 as a condition to describe women who had the sudden onset of weakness, fatigue, pain, and passing out. They were thought to have a "weak nervous system".
But to look at the term 'dysautonomia' proper, one turns to the Veterinary literature, where the term is well entrenched. In the early 1900's, dysautonomia was first described as affecting horses in the United Kingdom. The major symptoms of the clinical syndrome included dysphagia and gastric dysmotility, with horses becoming severely cachetic and malnourished. Horses grazing in particular fields seemed prone to dysautonomia, and the term, "grass sickness" was coined. In 1928, Grieg described a Veterinary account of horse dysautonomia. The prognosis for horses was poor, with most horses suffering death or euthanasia. Survivors were rare and there was no effective treatment.
In 1949, Familial Dysautomomia (FD) was discovered by Drs. Conrad Riley and Richard Day, hence 'Riley-Day' Syndrome. From 1949-1959, a series of clinical markers were determined: two clinical tests, to include the Histamine Test and Tongue Markers; and two physiologic studies, to include urine and plasma catecholamine levels and a lack of compensation for conditions of low oxygen and high carbon-dioxide levels.
From 1969-1979, Drs. Aguayo and Pearson used electron microscopy to show that the FD defect was a decreased number of small, unmyelinated neurons.
In 1982, feline dysautonomia was reported in the veterinary literature by Key and Gaskell, from the University of Bristol. The diagnosis was prevalent, with hundreds of cases reported around 1985. Cats displayed dry mucous membranes, pupillary dilation, and protrusion of the third eyelid. Only about one-quarter of the cases survived. In 1983, canine dysautonomia was first described in Britain, then subsequently in Europe and America. In 1991, the United Kingdom reported dysautonomia in wild hares.
In 1993, the FD defect was located on Chromosome 9. In 1995, patients with FD participated in clinical trials that formed the basis of pharmacologic agent midodrine being FDA approved.
Symptomatic orthostatic intolerance is a presenting complaint of mostly young women who are subsequently diagnosed with Postural Orthostatic Tachycardia Syndrome (POTS). In 1997, Grubb et al. defined the criteria which impose an increase in heart rate to 30 beats/min or an increased heart rate of 120 beats/min or greater when changing from a supine to the standing position (1, 2). From 1997-1999, additional neurophysiologic invesigations were described to further assess FD: Cold Face Stimulation, laser doppler Flowmeter, and temperature assessment as correlated with cardiac risk.
In 1999, precise mapping of the FD gene was performed to show that the site was 9q31, and dysautonomia was reported in the llama of the Netherlands. At the same time, Schondorf et al. estimated the prevalence of orthostatic intolerance in patients with chronic fatigue syndrome was 40% (Schondorf).
For Images of Animals with Dysautonomia, Click Here.
Images of Animals with Dysautonomia