ABSTRACT
Sleep paralysis (SP), hypnagogic=hypnopompic hallucinations (HH), and cataplexy, classic symptoms of narcolepsy, have been considered dissociated manifestations of rapid eye movement (REM) sleep (1,2). Although primarily examined in clinical narcolepsy (3) or other sleep disordered patient populations (4-6), these symptoms have also been reported outside of clinical settings and across various countries. For instance, cataplexy-like episodes have been reported in army draftees, and SP in undergraduates, medical students, and shift workers (7-11). While these phenomena have been described in several non-clinical settings, they have been described only rarely in population-based samples (12-15). Moreover, few epidemiologic studies have focused on individual symptoms (13,14), as compared to narcolepsy prevalence estimations. This chapter thus characterizes distributions and correlates of SP, HH, cataplexy, and automatic behavior (AB)—an auxiliary narcolepsy symptom-in adults from a community-based sample. SP, HH, and AB might constitute narcolepsy without cataplexy. Its recent prevalence, based on patients diagnosed with narcolepsy, was estimated at 0.02% (16). To explore the viability of a narcolepsy spectrum, this chapter examines the prevalence of these phenomena and their relationships to narcolepsy’s diagnostic and biological markers-sleepiness, nocturnal sleep disruption (3,17), and HLA DQB10602, its genetic marker related to a higher risk of developing narcolepsy (18). Along with the tendency to fall directly into REM sleep from wakefulnessexpressed as SP, hypnagogic hallucinations, or cataplexy, the unremitting propensity to fall into sleep is a fundamental disturbance of narcolepsy (1). Daytime sleepiness, a key narcolepsy symptom, has been reported in 100% of narcoleptics (3). Disturbed nocturnal sleep (e.g., awakenings) and increased parasomnias (nightmares included) have also been commonly reported in narcoleptics (3,17,19-21), with parasomnias found to co-occur with HH and SP (21). To date, investigations of HLA alleles’ relationships to the individual symptoms of SP and=or HH have been limited to clinically-derived (including narcolepsy multiplex families) or specific (e.g., college student) samples (20,22-24). The influence of HLA susceptibility alleles on cataplexy
and other narcolepsy symptoms was evaluated presently to consider these symptoms as constituting a possible narcolepsy spectrum in a population-based sample.
