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  • Updated 05.14.2023
  • Released 01.22.2001
  • Expires For CME 05.14.2026




Hypersomnolence is deleteriously prevalent, especially in modern society. This common medical complaint has various causative underpinnings. Sleep medicine, as a growing subspecialty field, can evaluate the nature of the problem and improve life and longevity with a great number 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 behind-the-wheel is a challenging dilemma given an aging and senior population with alertness issues. The socioeconomic burden of disabling excessive daytime sleepiness is vast and is best addressed by all (57).

Hypersomnolence, or excessive daytime sleepiness, is a frequent complaint of patients and is 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 mishaps. In this article, discussion will focus on 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 symptomatic 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

EDS is a public health issue. However, it remains largely undervalued, scarcely diagnosed, and poorly supported. Variations in the definition of EDS and limitations in clinical assessment lead to difficulties in its epidemiological study, but the relevance of this symptom from a socioeconomic perspective is inarguable. EDS might be a consequence of several behavioral issues leading to insufficient or disrupted sleep, as well as a consequence of sleep disorders including sleep apnoea syndrome, circadian disorders, central hypersomnolence disorders (narcolepsy and IH), other medical or psychiatric conditions, or medications. Furthermore, EDS can have implications for health as it is thought to act as a risk factor for other conditions, such as cardiovascular and neurodegenerative disorders. Because of the heterogeneous causes of EDS and the complexity of its pathophysiology, management will largely depend on the cause, with the final aim of making treatment specific to the individual using precision medicine and personalized medicine.


Hypersomnolence is one of the most common complaints that patients raise to their physicians. However, investigation of underlying physiologic causes did not begin in earnest until the 1930s (148). After rapid eye movement sleep was identified in the 1950s (11), 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 (154; 120).

The term “hypersomnolence” describes excessive sleepiness, a persistently increased debt toward sleep, and an abnormally high likelihood of drowsiness when sleep is not desired or anticipated. Dauvilliers accurately states, “Hypersomnolence is not just characterized by daily episodes of an irrepressible need to sleep or daytime lapses into sleep. The term usually harbors much more in the way of disabling symptoms. Accordingly, it often includes impaired vigilance or sustained attention; automatic behaviors; cognitive complaints, especially linked to poor memory; and it can be accompanied by increased need for sleep and severe sleep inertia” (41). 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 formal and 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 latency 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 (IH)

- 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

A reappraisal by European experts and led by Dauvilliers and colleagues stresses the importance of creating a new consistent, complaint driven, hierarchical classification for central disorders of hypersomnolence, containing levels of certainty, and giving diagnostic tests, particularly the MSLT, a weighting based on its specificity (41; 71).

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 (06). For example, narcolepsy with cataplexy is now alluded to as narcolepsy type 1, also known as hypocretin (orexin) 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 two 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 one of the SOREMPs during the succeeding 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 (DORA) in the clinical treatment of insomnia; novel somnogenic agent.

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