Advancements in the understanding of narcolepsy are happening. Register for updates »

Advancements in the understanding of narcolepsy are happening. Register for updates »

The Impact of Narcolepsy on Patients

Narcolepsy can have functional, psychological, and social impact on patients.1

1 Biggest Impact

Biggest Impact of Narcolepsy


Scott shares why he believes narcolepsy changed the way his friends and family saw him and how the disorder set the course for his life today.

Neurocognitive Functioning

People living with narcolepsy must often allocate considerable attentional and cognitive resources to maintain alertness, which may impact neurocognitive functioning, such as the ability to concentrate, read, or remember important details.1,2 Studies have shown that about 40% of people living with narcolepsy report difficulty with concentration, and 40-50% report problems with memory.3

Psychological Impact

People living with narcolepsy can feel isolated, rejected, depressed, and anxious.1,2,4,5 Attention deficit/hyperactivity disorder (ADHD) symptoms are also reported more frequently and at a greater severity in people living with narcolepsy compared to the general population.6 Many people living with narcolepsy suffer from anxiety disorders, including social anxiety disorder, panic disorder, post traumatic stress disorder, or agoraphobia.7-9 It is thought that these disorders could evolve as a result of the debilitating nature of narcolepsy, but evidence suggests narcolepsy may share a pathophysiologic link with psychiatric disorders.10,11

Social Impact

People living with narcolepsy may unconsciously avoid or suppress emotions that might trigger their cataplexy. Individuals may gravitate away from or consciously avoid certain activities to prevent cataplexy attacks.9,12,13

Sean, living with narcolepsy

I didn’t look forward to my birthday because the attention and focus on me would make me have cataplexy.

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Know Narcolepsy Assessment Tool

Use this tool to help your patients assess how narcolepsy may be interfering with their lives. Encourage them to share their results at their next appointment.

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Know Narcolepsy Assessment Tool

Know Narcolepsy Assessment Tool
  1. 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.
  2. American Academy of Sleep Medicine. International Classification of Sleep Disorders. 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014.
  3. Bellebaum C, Daum I. Memory and cognition in narcolepsy. In: Goswami M, Thorpy MJ, Pandi-Perumal SR, eds. Narcolepsy. Springer; 2016:233-243.
  4. Maski K, Steinhart E, Williams D, et al. Listening to the patient voice in narcolepsy: diagnostic delay, disease burden, and treatment efficacy. J Clin Sleep Med. 2017;13(3):419-425.
  5. Kapella MC, Berger BE, Vern BA, Vispute S, Prasad B, Carley DW. Health-related stigma as a determinant of functioning in young adults with narcolepsy. PLoS One. 2015;10(4):1-12.
  6. Filardi M, Pizza F, Tonetti L, Antelmi E, Natale V, Plazzi G. Attention impairments and ADHD symptoms in adult narcoleptic patients with and without hypocretin deficiency. PLoS One. 2017;12(8):1-12.
  7. Black J, Reaven NL, Funk SE, et al. Medical comorbidity in narcolepsy: findings from the Burden of Narcolepsy Disease (BOND) study. Sleep Med. 2017;33:13-18.
  8. Ohayon MM. Narcolepsy is complicated by high medical and psychiatric comorbidities: a comparison with the general population. Sleep Med. 2013;14(6):488-492.
  9. Overeem S, Reading P, Bassetti C. Narcolepsy. Sleep Med Clin. 2012;7:263-281.
  10. Barateau L, Lopez R, Franchi JA, Dauvilliers Y. Hypersomnolence, hypersomnia, and mood disorders. Curr Psych Rep. 2017;19(2):13.
  11. Morse AM, Sanjeev K. Narcolepsy and psychiatric disorders: comorbidities or shared pathophysiology? Med Sci. 2018;6(1):16.
  12. Daniels E, King MA, Smith IE, Shneerson JM. Health-related quality of life in narcolepsy. J Sleep Res. 2001;10(1):75-81.
  13. Ahmed I, Thorpy M. Clinical features, diagnosis and treatment of narcolepsy. Clin Chest Med. 2010;31(2):371-381.

Performance of routine tasks without awareness.

Sudden and brief loss of muscle tone, often triggered by strong emotions or certain situations. Narcolepsy with cataplexy is known as narcolepsy type 1.

Complete collapse to the ground; nearly all skeletal muscles are involved.

Only certain muscle groups are involved.

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.

Frequent awakenings and inappropriate transitions between states of sleep and wakefulness during nighttime sleep.

The inability to stay awake and alert during the day.

A neurotransmitter in the brain that supports wakefulness.

Vivid, realistic, and sometimes frightening dream-like events that occur when falling asleep.

Also known as orexin. A neuropeptide that supports wakefulness and helps suppress non-REM sleep and REM sleep.

Primary brain region for regulating the timing of sleep-wake states.

Unintentionally falling asleep due to excessive daytime sleepiness. Also known as “sleep attacks.”

Brief, unintentional lapses into sleep or loss of awareness.

A validated objective measure of the tendency to fall asleep in quiet situations.

People living with narcolepsy type 1 have low levels of hypocretin.

Narcolepsy without cataplexy; the cause of narcolepsy type 2 is unknown.

A state of sleep characterized by slower-frequency, more synchronized neuronal activity and decreased muscle tone. Deep stages help to restore the body.

A multiparameter test that monitors physiologic signals during sleep; used as a diagnostic tool in sleep medicine.

A state of sleep characterized by fast-frequency, desynchronized activity on EEG, vivid dreams, and loss of muscle tone. Normally occurs 60-90 minutes after sleep onset. Also known as “paradoxical sleep.”

Brief loss of control of voluntary muscles with retained awareness at sleep-wake transitions.

Sleep-onset REM period.

The VLPO as well as the median preoptic nucleus (MnPO) are located in the hypothalamus and contain essential neurons for promoting non-REM sleep. These neurons project to all wake-promoting regions to inhibit wakefulness and promote non-REM sleep during the night.8,11 Neurons in the extended VLPO mediate the promotion of REM sleep by inhibiting certain wake-promoting neurons that suppress REM sleep.8