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Equine polysaccharide storage myopathy (EPSM, PSSM, EPSSM) is a hereditary glycogen storage disease of horses that causes exertional rhabdomyolysis.It is currently known to affect the following breeds American Quarter Horses, American Paint Horses, Warmbloods, Cobs, Dales Ponies, Thoroughbreds, Arabians, New Forest ponies, and a large number of Heavy horse breeds.
LATE is a term that describes a prevalent medical condition with impaired memory and thinking in advanced age, often culminating in the dementia clinical syndrome. [1] In other words, the symptoms of LATE are similar to those of Alzheimer's disease. The acronym LATE stands for Limbic-predominant Age-related TDP-43 Encephalopathy.
However, any horse that can store excess amounts of glycogen, usually genetic, can develop this form of ER. [1] Recurrent Exertional Rhabdomyolysis (RER) is commonly found in breeds that are high strung such as Arabians and thoroughbreds. However, any horse can develop this type of ER if it displays abnormal muscle contractions. [1]
Hypokalemic periodic paralysis (hypoKPP), also known as familial hypokalemic periodic paralysis (FHPP), [1] is a rare, autosomal dominant channelopathy characterized by muscle weakness or paralysis when there is a fall in potassium levels in the blood (hypokalemia).
Within hours of first symptoms horse may be unable to stand and in 72 hours of the onset of signs mortalities may occur. [16] [13] [1] The mortality rate of atypical myopathy is high; only 30-40% of affected horses survive. [9] EAM affected horse’s urine is dark red or brown. Sweating and muscle trembling can be observed while moving.
Patients with type 2 RTA are also typically hypokalemic due to a combination of secondary hyperaldosteronism, and potassium urinary losses - though serum potassium levels may be falsely elevated because of acidosis. Administration of bicarbonate prior to potassium supplementation might lead to worsened hypokalemia, as potassium shifts ...
Cerebellar abiotrophy in horses was originally thought to be a form of cerebellar hypoplasia (CH) and was described as such in older research literature. However, it was discovered that in horses, the die-off of purkinje cells began after the animal was born, rather than occurring in utero .
Apparent mineralocorticoid excess is a rare form of monogenic hypertension that is transmitted as an autosomal recessive trait. The clinical symptoms of AME were first reported in 1974 by a Professor from Switzerland; Edmond A Werder in a 3-year-old girl with low birth weight, delayed growth, polydipsia, polyuria, and hypertension.