The delayed-sleep-phase syndrome is a chronic inability to fall asleep and to arise at conventional clock times. Sleep onset is delayed until 3 to 6 a.m.; the subject then sleeps normally until 11 a.m. to 2 p.m. An imposed sleep period from 11 p.m. to 7 a.m. leads to a prolonged sleep latency and daytime sleepiness. By contrast, the advanced-sleep-phase syndrome is characterized by an early evening sleep onset (8 to 9 p.m.) and early morning awakening (3 to 5 a.m.). Simply delaying the onset of sleep usually fails to prevent early morning awakening. This pattern is not uncommon among healthy elderly persons (and also among college students), in whom it should probably not be defined as an insomnia syndrome. Still other persons show a completely irregular sleep–wake pattern; sleep consists of persistent but variable short or long naps throughout the night and day, with a nearly normal 24-h accumulation of sleep.
Several interesting and distressing sleep disturbances are known in completely blind persons, the most troubling being the lack of entrainment to the day-night cycle. As a result of the absence of retinal-hypothalamic entrainment of the circadian rhythm, there is an innate cycle that is just longer than 24 hours, resulting in bouts of insomnia as hypothalamic function moves in and out of phase with the day. In clinical trials, the melatonin receptor agonist tasimelteon has helped entrain the sleep cycle in blind individuals (Lockley et al).
Although new classifications have rearranged the nosology of these phenomena, included under this title are several diverse disorders: somnolescent starts, sensory paroxysms, sleep paralysis, night terrors and nightmares, somnambulism, and REM sleep behavior disorder.
Somnolescent (Sleep, Hypnic, Myoclonic) Starts
As sleep comes on, certain motor centers may be excited to a burst of insubordinate activity. The result is a sudden “start” or myoclonic bodily jerk of large amplitude, which rouses the incipient sleeper. It may involve one or both legs or the trunk, less often, the arms. If the start occurs repeatedly during the process of falling asleep and is a nightly event, it may become a matter of great concern to the patient. The starts are more apt to occur in individuals in whom the sleep process develops slowly; they are especially frequent under conditions of tension and anxiety. Polysomnographic recordings have shown that these bodily jerks occur at the moment of falling asleep or during the early stages of sleep. Sometimes they appear as part of an arousal response to a faint external stimulus and are then associated with a frontal K complex in the EEG. These bodily jerks are not variants of epilepsy.
A small proportion of otherwise healthy infants exhibit rhythmic jerking of the hands, arms, and legs or abdomen, both at the onset and in the later stages of sleep (benign neonatal myoclonus). The movements begin in the first days of life and disappear within months. There may be a familial tendency toward these movements. Coulter and Allen differentiate this state from myoclonic epilepsy and neonatal seizures by the absence of EEG changes, and its occurrence only during sleep.
Sensory centers may be disturbed in a similar way to the earlier-described sleep starts, either as an isolated phenomenon or in association with motor phenomena. The patient, dropping off to sleep, may be roused by a sensation that darts through the body, a sudden flash of light, or a sudden crashing sound or thunderclap of head pain—cephalgia fugax, or “the exploding head syndrome” (Pearce). Sometimes there is a sensation of being turned or lifted, and dashed to the ground; conceivably, these are sensory paroxysms involving the labyrinthine-vestibular mechanism. Though obvious causes for concern by patients, these sensory paroxysms are benign.