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

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

Narcolepsy Resources for Healthcare Professionals

Access tools and downloadable resources for you and your office.

Narcolepsy Tools and Resources

A Quick Guide for Evaluating the Impact of Narcolepsy

Understanding the impact of excessive daytime sleepiness and other symptoms on patient functioning and quality of life is important for improving clinical outcomes.

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A Quick Guide for Evaluating the Impact of Narcolepsy

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Clinical Assessment of Narcolepsy

Review these clinical interview strategies and see questions to ask your patients about their symptoms.

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Clinical Assessment of Narcolepsy

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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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Narcolepsy Assessment Tool

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A Guide to the Pathophysiology of Narcolepsy

A concise guide to understanding signs and symptoms that reflect sleep-wake state instability as well as the underlying neuronal processes behind stable wakefulness.

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A Guide to the Pathophysiology of Narcolepsy

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Epworth Sleepiness Scale (ESS)

An 8-item questionnaire to assess daytime sleepiness based on a person’s sleep propensity in common situations.

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Narcolepsy Severity Scale (NSS)

A 15-item scale that evaluates the frequency and impact of the five main narcolepsy symptoms.

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Functional Outcomes of Sleep Questionnaire-10 (FOSQ-10)

A 10-item questionnaire that assesses the impact of excessive daytime sleepiness on daily activities.

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Recent Publications

The Effects of the COVID-19 Pandemic on Patients With Narcolepsy

Ana Carolina Rodrigues Aguilar, Cristina Frange, Lucio Huebra, Ana Carolina Dias Gomes, Sergio Tufik, Fernando Morgadinho Santos Coelho

During quarantine, Brazilian patients with narcolepsy reported changes in their sleep-wake schedules, suggesting a tendency to circadian misalignment. There were strong associations found between changes in bedtime schedules and worsening excessive daytime sleepiness as well as a reduction in hallucinations.

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Narcolepsy Type 2: A Rare, Yet Existing Entity

Heide Baumann-Vogel, Lina Schreckenbauer, Philipp O. Valko, Esther Werth, Christian R. Baumann

The findings of this study suggest that the prevalence of narcolepsy type 2 may be up to 20-25 times lower than narcolepsy type 1. The authors emphasize the importance of excluding other potential causes of sleepiness when making a diagnosis of narcolepsy type 2.

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The Clinical Characteristics of Cataplectic Attack in Narcolepsy Type 1

Bei Huang, Tao Xu, Zongwen Wang, Ku Chen, Jihui Zhang, Zhongxin Zhao, Jianhua Zhuang, Huijuan Wu

The process of a cataplexy attack was found to occur in four stages: triggering, resisting, atonic, and recovering. The resisting stage was found to make up over half the duration of cataplexy episodes and may represent compensation efforts to avoid succumbing to full muscle atonia.

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Developing a Cognitive Behavioral Therapy for Hypersomnia Using Telehealth: A Feasibility Study

Jason C. Ong, Spencer C. Dawson, Jennifer M. Mundt, Cameron Moore

A novel cognitive behavioral therapy for hypersomnia (CBT-H) was shown to reduce depressive symptoms and improve self-efficacy in people with central disorders of hypersomnolence, including narcolepsy. Behavioral strategies included structured daytime schedule and scheduled naps and were customized based on disease-specific symptoms. Cognitive strategies were aimed at processing changes in self-identity or limitations and challenges relating to the disease (e.g. addressing anxiety with cataplexy for people living with narcolepsy type 1).

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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