Hallucinations hypnagogic

The sleep disorder narcolepsy, which affects around 1 in every 2000 people, is characterized by a tetrad of symptoms excessive daytime sleepiness, cataplexy (loss of muscle tone triggered by emotional arousal), hypnagogic hallucinations,... 

The essential features are sleep attacks, cataplexy, hypnagogic hallucinations, and sleep paralysis. Individuals with narcolepsy complain of excessive daytime sleepiness, sleep attacks that last up to 30 minutes, fatigue, impaired performance, and disturbed nighttime sleep. They have multiple arousals during the night. 

Sodium oxybate (yhydroxybutyrate a potent sedative-hypnotic) improves excessive daytime sleepiness and decreases episodes of sleep paralysis, cataplexy, and hypnagogic hallucinations. It is taken at bedtime and repeated 2.5 to 4 hours later. Side effects include nausea, somnolence, confusion, dizziness, and incontinence. 

Granek M, Shalev A, Weingarten AM. (1988). Khat-induced hypnagogic hallucinations. Acta Psychiatr Scand. 78(4) 458-61. 

Einally, patients with narcolepsy may experience very vivid visual or auditory hallucinations, called hypnagogic hallucinations, while falling asleep. Similar to sleep paralysis, hypnagogic hallucinations occasionally occur in the absence of narcolepsy, but the patient with narcolepsy may experience them several times a week. 

Recurrent intrusions of elements of rapid eye movement (REM) sleep into the transition between sleep and wakefulness, as manifested by either hypnopompic or hypnagogic hallucinations or sleep paralysis at the beginning or end of sleep episodes... 

Narcolepsy can usually be distinguished from insomnia by the presence of one of the auxiliary symptoms (cataplexy, sleep paralysis, hypnagogic hallucinations). When the diagnosis remains unclear, then a sleep study is necessary. 

Antidepressants. In addition to increasing alertness, the psychostimulants also mildly suppress the REM phase of sleep. Because the auxiliary symptoms of narcolepsy (cataplexy, hypnagogic hallucinations, and sleep paralysis) are basically... 

Narcolepsy (ICD G47.4) and other types of hypersomnia are severe disturbances of vigilance expressed as a sudden and irresistible requirement for sleep during the day, so-called sleep attacks (Aldrich. 1990). Apart from sleep attacks, the classical tetrad of narcolepsy includes cataplexy (sudden loss of muscular tone), sleep paralysis (waking from sleep with the feeling of not being able to move) and hypnagogic hallucinations (linages or sequences of... 

Hypnagogic hallucinations—Bizarre and often frightening dreams and sounds that occur during the onset or waking up from cataplexy. 

Examples of dissociations of consciousness that often divide the waking mind into two compartments include microsleeps, attentional lapses, and fantasy states. At the edges of sleep are hypnagogic hallucinations and sleep paralysis. Within sleep are sleep walking, sleep talking, and lucid dreaming. In all of these conditions, consciousness has some features characteristic of one state mixed with features characteristic of another. 

One of the most instructive examples of state boundary crossing is the tendency to experience dreamlike visuomotor sensations at sleep onset. These are called hypnagogic hallucinations if the subject is still awake enough to notice or be aroused by them. Apparently, one need only carry waking brain activation over the sleep boundary and dreaming will im-... 

In order for a sleep onset dream to become a hypnagogic hallucination, the internal stimulus strength has only to achieve a momentary advantage over the diminished force of external stimuli to generate emotionally salient perceptions. Because the prevalent emotion is anxiety, the salient imagery is fearsome, as befits the evolutionary theory advanced above. Better safe than sorry, and Forewarned is fore-armed, as we say. 

This normalizing account of hypnagogic hallucinations lends itself nicely to explanation in terms of AIM and hence to integration with those spontaneous and induced alterations in conscious state that interest us most. For example, an exaggeration of the normal tendency to hallucinate at sleep onset is seen in narcolepsy, as well as with the use of clinical and recreational drugs that alter the M axis of the AIM model in ways that promote REM sleep phenomena, including the intense dreaming often associated with it. 

Many narcoleptic patients show a marked intensification of sleep onset REM physiology, making the enhancement of hypnagogic hallucinations easily understandable. Because narcolepsy is also associated with the occurrence of hallucinations on awakening from REM sleep, I will defer discussion of the clinical aspects of the disorder until we have considered these hypnopompic extensions of dreaming into the wake state. 

Sleepiness is a primary symptom of narcolepsy, often preceding the onset of the other well-known symptoms of the disease, namely cataplexy, sleep paralysis, and hypnagogic hallucinations (44). Evaluation of the MSLT of narcoleptic patients has demonstrated a short sleep latency (<5 min) and multiple sleep-onset REM periods (SOREMPs). The more specific finding in the MSLT of narcoleptic patients is more than 2 SOREMPs, shown to reach a specificity of 99% by Amira et al. (45), which further increased to 99.2% if 3 SOREMPs were recorded (46). On the other hand, more than one SOREMP can occur in nonnarcoleptic patients, such as those with sleep apnea, sleep deprivation, depression, periodic limb movements, circadian rhythm disruption, or withdrawal from REM-suppressing medications (5,47). Thus, the findings of the MSLT, which is always performed for suspected narcoleptic patients, must be interpreted in view of the clinical history and nocturnal PSG. 

The word narcolepsy refers to a syndrome of unknown origin that is characterized by abnormal sleep tendencies, including excessive daytime sleepiness and often disturbed nocturnal sleep and pathological manifestations of REM sleep. The REM sleep abnormalities include sleep onset REM periods and the dissociated REM sleep inhibitory processes, cataplexy and sleep paralysis. Excessive daytime sleepiness, cataplexy, and less often sleep paralysis and hypnagogic hallucinations are the major symptoms of the disease [12]. 

Narcoleptic individuals experience EDS, usually associated with REM sleep phenomena, such as sleep paralysis, cataplexy (emotion-induced weakness), and hypnagogic hallucinations (visual, tactile, kinetic, and auditory phenomena occurring during sleep onset) [37], Dismpted nocturnal sleep occurs frequently. Sleepiness is usually the first symptom to appear, followed by cataplexy, sleep paralysis and hypnagogic hallucinations [6,37 40]. Cataplexy onset occurs within five years after the occurrence of daytime somnolence in approximately two thirds of the cases [38, 40], The mean age of onset of sleep paralysis and hypnagogic hallucinations is also 2-7 years later than that of sleepiness [39, 41], In most cases, EDS and irresistible sleep episodes persist throughout the lifetime. 

At the present time, there is no cure for narcolepsy, and treatment goals include control of EDS, cataplexy, hypnagogic hallucinations, and sleep paralysis improvement of nocturnal sleep and reduction of psychosocial problems. 

Takahashi Y, Jimbo M (1963) Polygraphic study of narcoleptic syndrome with special reference to hypnagogic hallucinations and cataplexy. Folia Psychiatr Neurol Jpn 7 (Suppl) 343-347... 

Narcolepsy genetic characteristics. Rare, disabling sleep disorder of unknown origin. Characterized by sudden attacks of flaccid paralysis (cataplexy), extensive daytime sleepiness, sleep paralysis, hypnagogic hallucinations and rapid onset of rapid eye movement (REM) phase of sleep. 

In a double-blind, randomized, placebo-controlled, crossover study in 24 patients with narcolepsy, gammahydroxybutyrate 60 mg/kg in a single night-dose for 4 weeks reduced the daily number of hypnagogic hallucinations, daytime sleep attacks, and the severity of subjective daytime sleepiness, and tended to reduce the number of daily attacks of cataplexy (2). It reduced the percentage of wakefulness during REM sleep and the number of awakenings out of REM sleep, and tended to increase slow wave sleep. Adverse events were few and mild. 

Khat has amphetamine-like effects and can cause psychoses (132-138), including mania (139) and hypnagogic hallucinations (140). Two men developed relapsing short-lasting psychotic episodes after chewing khat leaves the psychotic symptoms disappeared without any treatment within 1 week (141). 

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