Terms and phrases to help know narcolepsy.
Performance of routine tasks (e.g., writing, cooking) without awareness or memory.1-3
Sudden and brief loss of muscle strength or tone (e.g., knees buckling, jaw sagging) with retained awareness, often triggered by strong emotions.1-5 Specific to narcolepsy, but not every person with narcolepsy has cataplexy. Narcolepsy with cataplexy is known as type 1 narcolepsy.1,2,4
Complete collapse to the ground; usually takes several seconds to develop and nearly all skeletal muscles are involved.1.4.5
Only certain muscle groups are involved; facial, head, or neck weakness is common.1
Biological clock mechanism that regulates the 24-hour cycle in the physiological processes of living beings. It is controlled in part by the SCN in the hypothalamus and is affected by the daily light-dark cycle.6,7
The inability to maintain a continuous nocturnal sleep.1 Frequent inappropriate transitions between different states of sleep and wakefulness that occur at night, causing poor quality sleep. These disruptions significantly decrease restorative sleep stages.1,8
The inability to stay awake and alert during the day, resulting in an intense need for sleep or unintentional lapses into drowsiness or sleep. The primary symptom of narcolepsy.1
A monoaminergic neurotransmitter that supports wakefulness. The hypothalamic tuberomammillary nucleus (TMN) is the only neuronal source of histamine in the brain, and histamine is its main transmitter.6,9,10
Vivid, realistic, and usually frightening dream-like events that occur when falling asleep (hypnagogic). When they occur while waking up, they are called hypnopompic hallucinations.1,3,11
Vivid, realistic, and frightening dream-like events that occur when falling asleep.
A neuropeptide that supports wakefulness and helps control non-REM sleep and REM sleep. Low levels of hypocretin cause the boundaries between sleep and wakefulness to become unstable, leading to symptoms of narcolepsy.6,9,11
Primary brain region for regulating the timing of sleep-wake states.7,12,13
A manifestation of excessive daytime sleepiness.1 Unintentionally falling asleep due to excessive daytime sleepiness. Also known as "sleep attacks."1
Only location in the brain where hypocretin-producing neurons originate.13 Hypocretin neurons promote wakefulness by activating neurons in the cortex, thalamus, histamine neurons in the TMN of the hypothalamus and regions containing wake-promoting neurons (e.g., norepinephrine, acetylcholine, serotonin, dopamine neurons).6,11,13 Hypocretin neurons also inhibit non-REM sleep–promoting neurons and REM sleep–promoting neurons to stabilize wakefulness during the day.6,9
Brief, unintentional lapses into sleep or loss of awareness.14
A validated objective measure of the physiologic ability or tendency to fall asleep in quiet situations. The test consists of 5 20-minute nap opportunities 2 hours apart, following an overnight sleep study.1,15 The test measures brain waves, EEG, muscle activity, and eye movements. Narcolepsy diagnostic criteria require a mean sleep latency of ≤8 minutes and 2 or more SOREMPs on MSLT.1,14
A state of sleep when muscle tone or tension is decreased.6 People usually wake up more easily from light non-REM sleep than from deep non-REM sleep.6,15 Slower-frequency more synchronized neuronal activity ranges from light to deep stages of non-REM sleep. Deep stages help to restore the body.6,15
Overnight study used to diagnose sleep disorders by monitoring sleep stages and cycles to detect disruptions of a normal sleep pattern.15 The test measures brain waves (EEG), eye movements, muscle activity, and heart rhythm.14
Rapid eye movement sleep; normally occurs at night and includes dreams.6 Most muscles are paralyzed to prevent people from acting out their dreams.6,16 Fast-frequency, desynchronized activity on EEG with distinct features. Also known as "paradoxical sleep."6,15
Daytime and evening habits and routines to help improve nighttime sleep.16
Brief loss of control of voluntary muscles with retained awareness. Occurs before falling asleep or while waking up and can be frightening.1,11,17
An abnormal sleep phenomenon characterized by REM sleep occurrence within 15 minutes of sleep onset; may occur during nighttime sleep or daytime napping.18
Located in the hypothalamus and coordinates circadian timing (in addition to other circadian rhythms) in order to align sleep and wakefulness to the daily light-dark cycle.6
Located in the hypothalamus, it is the only region of the brain where histamine neurons originate.6,10 Histamine neurons promote wakefulness by activating neurons in the cortex, thalamus, and regions containing wake-promoting neurons (e.g., norepinephrine, acetylcholine, serotonin, dopamine neurons).10,19 Histamine neurons also suppress non-REM sleep–promoting neurons and REM sleep–promoting neurons to help stabilize wakefulness during the day.6,10,20
Also called narcolepsy with cataplexy, although cataplexy is not always present or obvious; people with type 1 narcolepsy have low levels of hypocretin.1
Narcolepsy without cataplexy; the cause of type 2 narcolepsy is not well understood.1 Patients with type 2 narcolepsy may have undetectable to normal hypocretin levels.1
The VLPO as well as the median preoptic nucleus (MnPO) are located in the hypothalamus and contain essential neurons for promoting non-REM sleep.6,9 These neurons project to all wake-promoting regions to inhibit wakefulness and promote non-REM sleep during the night.6,9 Neurons in the extended VLPO mediate the promotion of REM sleep by inhibiting certain wake-promoting neurons that suppress REM sleep.6
- American Academy of Sleep Medicine. International Classification of Sleep Disorders. 3rd ed.; 2014.
- Thorpy M, Morse AM. Reducing the clinical and socioeconomic burden of narcolepsy by earlier diagnosis and effective treatment. Sleep Med Clin. 2017;12(1):61-71.
- Ahmed I, Thorpy M. Clinical features, diagnosis and treatment of narcolepsy. Clin Chest Med. 2010;31(2):371-381.
- Dauvilliers Y, Siegel JM, Lopez R, Torontali ZA, Peever JH. Cataplexy—clinical aspects, pathophysiology and management strategy. Nat Rev Neurol. 2014;10(7):386-395.
- Overeem S. The clinical features of cataplexy. In: Baumann CR, Bassetti CL, Scammell TE, eds. Narcolepsy: Pathophysiology, Diagnosis, and Treatment. Springer-Verlag New York; 2011:283-290.
- Scammell TE, Arrigoni E, Lipton JO. Neural circuitry of wakefulness and sleep. Neuron. 2017;93(4):747-765.
- Saper CB, Scammell TE, Lu J. Hypothalamic regulation of sleep and circadian rhythms. Nature. 2005;437(7063):1257-1263.
- Roth T, Dauvilliers Y, Mignot E, et al. Disrupted nighttime sleep in narcolepsy. J Clin Sleep Med. 2013;9(9):955-965.
- España RA, Scammell TE. Sleep neurobiology from a clinical perspective. Sleep. 2011;34(7):845-858.
- Haas HL, Sergeeva OA, Selbach O. Histamine in the nervous system. Physiol Rev. 2008;88(3):1183-1241.
- Scammell TE. Narcolepsy. N Engl J Med. 2015;373(27):2654-2662.
- Schwartz JRL, Roth T. Neurophysiology of sleep and wakefulness: basic science and clinical implications. Curr Neuropharmacol. 2008;6:367-378.
- Scammell TE. The neurobiology, diagnosis, and treatment of narcolepsy. Ann Neurol. 2003;53(2):154-166.
- Overeem S, Reading P, Bassetti C. Narcolepsy. Sleep Med Clin. 2012;7:263-281.
- Brown RE, Basheer R, McKenna JT, Strecker RE, McCarley RW. Control of sleep and wakefulness. Physiol Rev. 2012;92(3):1087-1187.
- Plazzi G, Serra L, Ferri R. Nocturnal aspects of narcolepsy with cataplexy. Sleep Med Rev. 2008;12(2):109-128.
- Dauvilliers Y, Lopez R. Parasomnias in narcolepsy with cataplexy. In: Baumann CR, Bassetti CL, Scammell TE, eds. Narcolepsy: Pathophysiology, Diagnosis, and Treatment. Springer-Verlag New York; 2011:291-299.
- Kim CY, Ong A, Chung SA, Shapiro CM. SOREMs in sleep clinic patients: association with sleepiness, alertness, and fatigue. Sleep and Hypnosis. 2012;14(1-2):20-28.
- Torrealba F, Riveros ME, Contreras M, Valdes JL. Histamine and motivation. Front Syst Neurosci. 2012;6(51):1-14.
- Williams RH, Chee MJ, Kroeger D. Optogenetic-mediated release of histamine reveals distal and autoregulatory mechanisms for controlling arousal. J Neurosci. 2014;34(17):6023-6029.