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activation of two hypocretin receptors reproduces narcolepsy In both humans and animals, hypocretin-containing neurons in the hypothalamus send projections widely through the brain and particularly to structures implicated in control of sleep: the locus coeruleus (noradrenergic), the tuberomammillary nucleus (histaminergic), the raphe nucleus (serotonergic), and the ventral tegmental area (dopaminergic) A number of compelling data implicate hypocretin and its receptors in human narcolepsy First, a narcoleptic patient has been described with a mutation in the gene encoding human hypocretin Second, hypocretin-secreting neurons are depleted in the brains of human narcoleptics, and CSF hypocretin levels are reduced or absent in affected patients; low CSF levels of hypocretin have also been reported after head trauma (Ripley) In some studies, the absence of CSF hypocretin distinguished narcoleptic individuals from patients with other categories of sleep disorders Somewhat suprisingly, several lines of evidence suggest an autoimmune causation for narcolepsy For example, it has long been known that there is an almost universal association with speci c alleles of the histocompatibility antigen HLA-DQ (B1-0602) (Neely et al; Kramer et al) Because the mode of inheritance of narcolepsy is not clearly mendelian (Kessler et al), it has been proposed that the disease re ects a genetic predisposition, possibly with a superimposed autoimmune reaction that impairs the function of hypocretin neuronal systems or damages the neurons that secrete the peptide As mentioned earlier, a secondary or symptomatic narcolepsy syndrome on occasion results from cerebral trauma, multiple sclerosis, craniopharyngioma, or other tumors of the third ventricle or upper brainstem, or a sarcoid granuloma within the hypothalamus (Servan et al) Our understanding of narcolepsy was greatly advanced by the demonstration by Dement and his group that this disorder is associated with a reversal in the order of the two states of sleep, with REM rather than NREM sleep occurring at the onset of the sleep attacks Not all the sleep episodes of the narcoleptic begin with REM sleep, but almost always a number of sleep attacks with such an onset can be identi ed in narcoleptic-cataplectic patients in the course of a polygraphic sleep study The hypnagogic hallucinations (which in this formulation are viewed as dream phenomena), cataplexy, and sleep-onset paralysis (inhibition of anterior horn cells) all coincide with the REM period These investigators have also shown that the night sleep pattern of patients with narcolepsycataplexy may begin with a REM period This also occurs in normal subjects, though infrequently Furthermore, the nocturnal sleep pattern is altered in narcoleptics, who have frequent body movements and transient awakenings and a decrease in sleep stages 3 and 4 as well as in total sleep Another important nding in narcoleptics is that sleep latency (the interval between the point when an individual tries to sleep and the point of onset of EEG sleep patterns), measured repeatedly in diurnal nap situations, is greatly reduced Thus, narcolepsy is not simply a matter of excessive diurnal sleepiness (essential daytime drowsiness) or even a disorder of REM sleep but a generalized disorganization of sleep-wake function Diagnosis The greatest dif culty in diagnosis relates to the problem of separating narcolepsy from the daytime sleepiness of certain sedentary, obese adults who, if unoccupied, doze readily after meals, while watching television, or in the theater (Many of these patients prove to have obstructive sleep apnea) A more serious form of recurrent daytime sleepiness, referred to as independent.

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narcolepsy or essential narcolepsy, is described further on However, both of these forms of daytime drowsiness are isolated disturbances, lacking the other sleep and motor disturbances that characterize the narcolepsy syndrome The distinguishing features of narcolepsy are the imperative need for sleep, even under unusual circumstances, and the tendency of the sleep attacks to recur, sometimes abruptly, several times each day When cataplexy is conjoined with daytime sleepiness, the diagnosis becomes certain The brief attacks of automatic behavior and amnesia of the narcoleptic must be distinguished from hysterical fugues and complex partial seizures Excessive daytime somnolence, easily mistaken for idiopathic narcolepsy, may attend sleep apnea syndromes (the most frequent cause), obesity, heart failure, hypothyroidism, excessive use of barbiturates and other anticonvulsants, abuse of alcohol, cerebral trauma, and certain brain tumors (eg, craniopharyngioma; see Table 19-1) Interestingly, excessive daytime sleepiness is not a frequent part of the chronic fatigue syndrome, although there may be prolonged periods of sleepiness if the illness begins with a mononucleosis-like syndrome Cataplexy must also be distinguished from syncope, drop attacks (page 329), and atonic seizures; in the latter, consciousness is temporarily abolished The careful documentation of narcolepsy by laboratory techniques is imperative when the diagnosis is in doubt, in part because of the potential for abuse of stimulant drugs used for treatment Overnight polysomnography followed by a standardized multiple sleep latency test, in which the patient is afforded opportunities for napping at 2-h intervals permit the quanti cation of drowsiness and increase the probability of detecting short-latency REM activity (within 10 min from the onset of each sleep period) According to some investigators, a reduced level (below 110 pg/mL) of hypocretin in the spinal uid is virtually diagnostic of narcolepsy in the proper clinical circumstances (see Mignot et al) We would comment, however, that it is rarely necessary to resort to any of these studies in clinically typical cases Treatment No single therapy will control all the symptoms The narcolepsy responds best to (1) strategically placed 15- to 20-min naps (during lunch hour, before or after dinner, etc); (2) the use of stimulant drugs moda nil (Provigil), dextroamphetamine sulfate (Dexedrine), methylphenidate hydrochloride (Ritalin), or pemoline (Cylert) to heighten alertness; and (3) a tricyclic antidepressant (protriptyline, imipramine, or clomipramine) for control of cataplexy All these drugs are potent suppressants of REM sleep Monoamine oxidase (MAO) inhibitors also inhibit REM sleep and can be used if they are tolerated The timing and frequency of the scheduled naps has to be individualized, depending on the pattern of hypersomnolence and the patient s work and social demands for full wakefulness Similarly, the medication schedule should be adjusted to the patient s study or work habits Until now the drug of choice has been methylphenidate, because of its prompt action and relative lack of side effects It is usually, given in doses of 10 to 20 mg three times daily on an empty stomach Alternatively, amphetamine 5 to 10 mg may be given three to ve times a day; this is ordinarily well tolerated and does not cause wakefulness at night Pemoline (50 to 75 mg daily) and mazindol (1 mg thrice daily) may also be useful in reducing daytime sleep episodes These drugs have rather little effect on cataplexy (They are partially effective in the KleineLevin syndrome) Moda nil (200 mg daily, up to 600 mg in divided doses) may prove to be the safest of the stimulants (Fry), but experience with this agent is still being acquired Protriptyline (Vi-.

vactil), 5 to 15 mg in the morning; imipramine (Tofranil), in doses of 25 mg three to four times a day; and clomipramine, 10 mg daily are effective in preventing cataplexy Sodium oxybate, whose active agent is gamma hydroxybutyrate, is bene cial for cataplexy and narcolepsy in some individuals The combined use of these stimulant and tricyclic antidepressant drugs is often indicated A problem with the stimulant drugs is the development of tolerance over a 6- to 12-month period, which requires the switching and periodic discontinuation of drugs Excessive amounts of amphetamines may induce a schizophreniform psychosis The stimulant drugs and the tricyclic antidepressants increase catecholamine levels; their chronic administration may produce hypertension Narcoleptics must be warned of the dangers of falling asleep and lapses of consciousness while driving or during engagement in other activities that require constant alertness The earliest feeling of drowsiness should prompt the patient to pull off the road and take a nap Long-distance driving should probably be avoided completely

By selecting Toggle at runtime, you switch the module from Active to Inactive or vice versa TABLE 6-11

Idiopathic Hypersomnia (Essential Hypersomnolence; Independent Narcolepsy)