Q: After I purchased my yearling Appaloosa filly, I noticed that she would pause in the middle of eating or being groomed, lie down and appear to go to sleep with her eyes open. Nothing fazed her—no temptations with food or pulling on the lead rope would get her attention. After a few minutes she would “check back in,” get up and appear to be fine. The veterinarian did bloodwork and the results were normal. As she has gotten older, the episodes have appeared to be less severe (she remains standing) and less frequent. Will my filly outgrow this? I was hoping to use her for breeding but this is a serious concern. — Name withheld upon request
A: Without direct observation, it can be difficult to distinguish seizures from episodes of sleep or cardiovascular collapse. The last of these is exceedingly rare in horses so it is more likely that your filly could be suffering from mild generalized seizures or, most probably, from abnormal sleep attacks. Benign epilepsy of foals can occur in youngsters up to about 12 months of age. It is seen in many breeds and family lines but most often appears in Arabian foals of Egyptian lineage. Episodes are usually characterized by abrupt recumbency with thrashing, but occasionally they can be quiet and passive events.
Your filly would more likely have a form of sleep disorder. These can be categorized into many groupings, including narcolepsy (sleep) with cataplexy (paralysis), narcolepsy without cataplexy, and idiopathic0 hypersomnia (daytime sleep attacks). These sleep disorders can be distinguished from one another by analyzing the individual brain-wave (EEG) activity, muscle activity (EMG) and eye movement (EOG), including the onset of rapid eye movement (REM) at the beginning instead of the middle of a sleep cycle.
Narcolepsy with cataplexy has been seen in foals from several breeds including Suffolk Punch, Miniature Horse, Fell Pony, Shetland Pony and Appaloosa. The syndrome tends to develop a variable but stable pattern of degrees of sleepiness and recumbency, depending on environmental stimuli. In the few cases that have been well documented, the condition persisted for life. Between typical cataplectic attacks there are no neurologic abnormalities. An episode may progress from buckling at the knees without falling, to sudden and total collapse and lack of reflex response (areflexia). Each recumbent episode may last from a few seconds to several hours if the foal is totally undisturbed, but the patient usually can be aroused from this state with varying degrees of difficulty and can regain his footing quietly and rapidly.
Juvenile-onset narcolepsy without cataplexy has been seen in warmblood, Icelandic and Thoroughbred foals. This syndrome probably has a familial basis but the role of genotype and/or immune response is debated. These foals intermittently remain standing in a trance-like state or stagger around, occasionally falling and injuring their knees or faces. Future neurochemical and genetic studies will be necessary to determine whether this truly is a genetic disorder and if and how it differs from narcolepsy with cataplexy and from idiopathic hypersomnia.
In conclusion, it would be reasonable to believe that your filly does suffer from a sleep disorder that may be familial narcolepsy with cataplexy. Only when a gene test is available will this be able to be determined and your question as to heritability be answered. Long-term therapy is inappropriate, although short-term responsiveness to some antidepressants and other drugs can alter the severity of the clinical syndrome. Time will tell if the condition will persist, but the odds are likely that it will in some form, even if subtle.
Joe Mayhew, BVSc, PhD
Palmerston North, New Zealand