Richard P Knudsen MD CNP (

Dr. Knudsen of the Pacific Sleep Tech in Aiea, Hawaii has no relevant financial relationships to disclose.

Antonio Culebras MD FAAN FAHA FAASM, editor. (

Dr. Culebras of SUNY Upstate Medical University at Syracuse received an honorariums from Jazz Pharmaceuticals for a speaking engagements.

Originally released January 22, 2001; last updated December 18, 2020; expires December 18, 2023


Hypersomnolence is deleteriously prevalent, especially in modern society. The common medical complaint has various underpinnings. Sleep medicine, as a growing field or subspecialty, can evaluate the nature of the problem and improve life and longevity with a myriad of scientifically effective interventions. The cost to society, if sleepiness is left unaddressed, is profound given the negative effects on health and on education and on work-related issues, including workableness and propensity toward accidents and clashes. Fitness to drive is a challenging dilemma given an aging and senior population. The socioeconomic burden of disabling excessive daytime sleepiness is vast and is best addressed by all (Jennum 2009).

Hypersomnolence, or excessive daytime sleepiness, is a frequent complaint of patients and a symptom associated with many medical conditions, including intrinsic sleep disorders, such as narcolepsy and obstructive sleep apnea or insufficient nighttime sleep. Though a nearly universal experience, sleepiness is often ignored or minimized by patients, often increasing their risk for industrial or motor vehicle accidents. In this article, the author discusses the differential diagnosis, evaluation, and treatment of this often overlooked symptom complex. Information from the International Classification of Sleep Disorders (3rd edition) is highlighted. Newer therapeutic agents, deemed somnolytics, are reviewed.

Key points


• Hypersomnolence or excessive daytime sleepiness (EDS) is a common clinical complaint.


• Causes frequently include underlying, coexistent medical disorders.


• Consequences include impaired job performance, diminished intellectual acuity, curbed psychosocial functioning, risk of serious accidents, and grave physical and medical health consequences.


• The diagnostic evaluation, including the administration of the Multiple Sleep Latency Test (MSLT), can lead to a diagnosis of narcolepsy or idiopathic hypersomnia.


• Stimulant therapy may be prescribed to overcome sleepiness.

Historical note and terminology

Hypersomnolence is 1 of the most common complaints that patients make to their physicians. However, investigation of underlying physiologic causes did not begin in earnest until the 1930s (von Economo 1930). After rapid eye movement sleep was identified in the 1950s (Aserinsky and Kleitman 1953), and careful neurophysiologic studies separated non-REM sleep into 3 stages (N1, N2, and N3, based on progressive trending toward delta or SWS/slow wave sleep), a new awareness arose that sleep was a diverse and functionally important mechanism in the maintenance of homeostasis. Sleep medicine developed substantially as a discipline in the 1960s and 1970s, fueled by new interest in the diagnosis and treatment of narcolepsy and of obstructive sleep apnea (Yoss and Daly 1959; Rechtschaffen et al 1963).

The term hypersomnolence describes excessive sleepiness, a persistently increased need for sleep, and an abnormally high likelihood of drowsiness when sleep is not desired or anticipated. Other terms sometimes used synonymously include excessive daytime somnolence, excessive daytime sleepiness, or hypersomnia, although hypersomnia is best used to denote excessive amounts of sleep. Hypersomnolence can be assessed by subjective or by objective measures. Physiologic functions that reflect hypersomnolence include pupillometry, other autonomic functions, and EEG activity. The most commonly utilized objective measure of hypersomnolence is the Multiple Sleep Latency Test. This clinical test is performed in a sleep laboratory, where recordings of EEG, surface EMG, and eye movements aid in the identification of time taken to fall asleep during several daytime nap attempts.

As an overview, the classifications of hypersomnia (not due to a sleep-related breathing disorder), according to ICSD-3 (International Classification of Sleep Disorders-3) and DSM-IV-TR (Diagnostic and Statistical Manual of Mental Disorders), include:


• Narcolepsy type 1 (NT1) (with cataplexy – THE pathognomonic feature)
• Narcolepsy type 2 (NT2) (without cataplexy)
• Idiopathic hypersomnia


- Kleine-Levin syndrome (recurring hypersomnia)

• Hypersomnia due to a medical disorder
• Hypersomnia due to a medication or substance
• Hypersomnia associated with a psychiatric disorder


- Insufficient sleep syndrome

In 2014, the American Academy of Sleep Medicine released the ICSD-3, which is an adaptation of nomenclature and diagnostic criteria previously in the field (American Academy of Sleep Medicine 2014). For example, narcolepsy with cataplexy is now alluded to as narcolepsy type 1, also known as hypocretin deficiency syndrome. The previous criterion of “daily periods of irrepressible need to sleep or daytime lapses into sleep occurring for at least three months” remains in place; however, now either cataplexy with multiple sleep latency test (MSLT) less than 8 minutes and 2 sleep onset REM periods (SOREMPs) or CSF Hcrt-1 measured concentrations less than 110 pg/mL are valid as qualifying criteria. REM onset within 15 minutes of sleep onset during the preceding polysomnogram may replace 1 of the SOREMPs during the MSLTs. Also, among the changes, narcolepsy type 2 can be reclassified to type 1 if cataplexy develops over time.

Briefly, on a historical note, the milestones of narcolepsy are:


1880 - Narcolepsy first described by the neurologist, Gelineau. Gelineau described the cataplectic falls as “astasias.”


1930 - Daniels noted the association of daytime sleepiness with cataplexy, hypnagogic hallucinations, and sleep paralysis.


1960 - Yoss and Daly noted SOREMPs during sleep in narcoleptic patients.


1975 - First International Symposium on Narcolepsy.


1999 - Hypocretin mutations discovered to cause narcolepsy in mice and dogs.


2000 - Human narcolepsy realized to be stemming from hypocretin (orexin) deficiency.


2013 - Epitope (antigenic determinant) of hypocretin (orexin) uncovered.


2014 - FDA approval of a dual orexinergic receptor antagonist in the clinical treatment of insomnia; novel somnogenic agent.

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