Large Animal Neurology. Joe Mayhew

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      The role of sleep in mammalian biology is somewhat of an enigma.¹ Adult herbivores spend a substantial proportion of time foraging, and only a few hours daily are spent in stages of sleep, a small proportion of which is rapid eye movement (REM) sleep with accompanying somatic hypotonia or atonia and recumbency.^1–3 For adult cattle and horses, this amounts to 3–5 h per day in sleep states and about 0.5 h per day in REM sleep.^3–6 Some horses appear to be able to perform REM sleep while standing² and to tolerate weeks of being unable to lie down to sleep, whereas others experience great difficulties in being cross‐tied for several days. The latter appear to go into a deep sleep state but stagger as not being able to remain upright, and some can injure themselves. Thus, the concept of sleep deprivation in horses may well be an individual phenomenon.^3,7

Without observing episodes, it can be difficult to distinguish seizures from normal and abnormal episodes of sleep and from cardiovascular collapse or syncope in otherwise perfectly healthy patients. The last of these show multiple episodes of collapse but with apparent normalcy between is incredibly rare in our experience, but seizures and sleep disorders can be quite distinguishable if observed. In this regard, 24‐h video monitoring and recording can be useful to capture suspected episodes of sleep and seizures when they are not overt.⁸ However, intermittent paralysis or cataplexy can pose as syncope, epileptic seizures (particularly pseudocataplexy or atonic seizures), hyperekplexia, and vestibular drop attacks.⁹

      In the context of sudden and unexpected collapse, there are many systemic issues that can mediate an abrupt loss of body support,¹⁰ but the majority result in other progressive signs such as weakness and obtundation or are associated with other factors such as trauma, diarrhea, or drug usage.¹¹ In about half the cases of episodic collapse, it may be possible to arrive at a final diagnosis with most having signs other than collapse being evident. Such diagnoses include cardiac arrhythmia, right‐sided heart failure, hypoglycemia, neurocardiogenic syncope, and exercise‐induced pulmonary hemorrhage. For most other cases, there will be a strong suspicion of epilepsy (Chapter 6) and sleep disorders.¹²

Sleep disorders in humans^313–15 can be categorized into many groupings, but these usually include narcolepsy with cataplexy (narcolepsy type‐1, NT‐1) (Figure 7.1), narcolepsy without cataplexy (NT‐2), and idiopathic hypersomnia (see Chapter 31 for further readings on narcolepsy in large animals).^316–23 Narcolepsy occurs in 0.02–0.15% of the population, and patients typically demonstrate excessive diurnal sleep, flaccid paralysis with somatic areflexia that constitutes cataplexy, sleep paralysis, sleep‐onset hallucinations, and nocturnal disrupted sleep. Strict EEG and EOG criteria, including the early onset of rapid eye movement at the beginning instead of the middle of a sleep cycle, are in place for confirming the diagnosis and for distinguishing narcolepsy with cataplexy from narcolepsy without cataplexy and from idiopathic hypersomnia. A familial form of narcolepsy with cataplexy occurs in dogs and humans, and in the latter it is strongly associated with the genetic allele HLA‐DQβ1*0602. An autoimmune basis to at least some forms of narcolepsy thus seems likely.¹³ Narcolepsy without cataplexy shares the same electrophysiological abnormalities and associated signs, but there is no demonstrable cataplexy. Purely excessive daytime sleep attacks, also referred to as unwanted siestas (a well‐appreciated term!), occur in idiopathic hypersomnia.