Narcolepsy—A Neuropathological Obscure Sleep Disorder: A Narrative Review of Current Literature
Abstract
:1. Introduction
2. Epidemiology
3. Genetic and Non-Genetic Associations with Narcolepsy
3.1. HLA Genes: HLADQB1 as Risk Factor of Narcolepsy Type 1
3.2. Non-HLA Genetic Associations
3.3. Environmental Factors
4. Inflammatory Response
4.1. Autoimmune Hypothesis
4.2. Autoantibody and T Cell Laboratory Findings
5. Narcolepsy and Neuromediator Systems
5.1. Hypocretinergic System
5.2. Dopaminergic System
5.3. Histaminergic System
6. Clinical Features
7. Pathophysiology and Links with Other Diseases
7.1. Narcolepsy and Diabetes
7.2. Narcolepsy and Ischemic Stroke
7.3. Narcolepsy and Alzheimer’s Disease (AD)
7.4. Narcolepsy and Parkinson’s Disease
8. Diagnosis and Treatment
8.1. Future Therapeutics
8.2. Prospects for Future Research
Sr No. | Class | Drug Candidate | Mode of Action | Improve Narcolepsy Symptoms |
---|---|---|---|---|
1 | Stimulants [189,190,191,192,193] | Modafinil | Blocks several monoaminergic transporters and inhibits dopamine reuptake transporter. | Potential to cause fatal hepatotoxicity; no longer recommended. |
- | - | Armodafinil | (R)-enantiomer of modafinil more-potent and long-lasting | Treats excessive daytime sleepiness. |
- | - | Methylphenidate | Non-competitive dopamine reuptake blocker and, to a lesser degree, a serotonin–noradrenaline reuptake blocker. | Second-line treatment for excessive daytime sleepiness. |
- | - | Dextro-amphetamine sulfate | Competitive dopamine transporter blocker that also blocks the vesicular mono amine transporter. | Third-line treatment for excessive daytime sleepiness. |
- | - | Pemoline | Selectively blocks dopamine reuptake. | |
- | - | Solriamfetol (JZP-11) | Inhibits norepinephrine-dopamine reuptake. | Treats impaired wakefulness and excessive sleepiness. |
2 | Sodium salt of γ-hydroxybutyrate (GHB; a neurotransmitter that related to γ-aminobutyric acid (GABA) [194] | Sodium oxybate | GABAB receptor agonist that activates the GABA type B receptor and possibly its own specific GHB receptor. | First-line treatment for cataplexy. Improves “qualitative wakefulness”—fewer nightly awakenings, reduces NREM stage 1 sleep and increases slow-wave sleep, decreases arousals, and has a variable effect on latency and amount of REM sleep. Alleviates sleep paralysis, hypnagogic hallucinations. |
3 | Antidepressant [16,162,195,196,197,198,199] | Venlafaxine, duloxetine, reboxetine, and viloxazine (SNRI), atomoxetine (SNRI) | Blocks serotonin–noradrenaline reuptake pumps. | First-line off-label to treat cataplexy. Improves excessive daytime and night-time sleepiness. Second line to treat cataplexy. |
Clomipramine, imipramine (TCA) | Mono-aminergic reuptake inhibition, inhibit the reuptake of catecholamines. | It increases muscle tone and suppresses REM sleep. Second line to treat cataplexy. | ||
Selegiline (MOAI) | Monoamine oxidase type B inhibitor. | Preferred initial choice for treatment of excessive daytime sleepiness. Can be used to treat cataplexy. | ||
Fluoxetine, Femoxetine, Citalopram (SSRI) | Blocks serotonin reuptake pumps. | Second line or third line to treat cataplexy. | ||
4 | Psychoactive drugs [200,201] | Benzodiazepines and hypnotics, Triazolam, Ambien, clonazepam | Enhances the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABAA receptor. | Second-line disrupted nocturnal sleep. Decreases arousal at night and sleep fragmentation. It improves cataplexy and sleep paralysis. |
5 | H3 blockers [202] | Pitolisant | histamine H3 receptor antagonists (inverse agonist). | Improves excessive daytime sleepiness. Not recommended in the newest guidelines. |
6 | Hypocretin replacement therapy or hypocretin receptor agonists [203] | - | HCRTR2 agonist-YNT-185, trace amine-associated receptor 1 (TAAR1) agonist. | Improves cataplexy, excessive daytime sleepiness, sleep paralysis and hypnagogic/hypnopompic hallucinations and suppress REM sleep. |
7 | Non-pharmacological therapy [203] | Sleep–wake schedules | - | Single scheduled daytime nap (of about 2 h) reduces the total amount of involuntary daytime sleep. Combined with stimulant treatment, two 15 min naps per day, and regular night-time sleep schedules, it has been shown to reduce subjective drowsiness and involuntary daytime sleep. Intensity of night-time NREM sleep is improved by daytime sleep restriction. |
8 | - | Psychosocial guidance | - | Helps in awareness and improves social problems associated with narcolepsy |
9 | - | Slow-wave sleep-enhancing treatments | - | Improves sleep |
9. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Conflicts of Interest
References
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Chavda, V.; Chaurasia, B.; Umana, G.E.; Tomasi, S.O.; Lu, B.; Montemurro, N. Narcolepsy—A Neuropathological Obscure Sleep Disorder: A Narrative Review of Current Literature. Brain Sci. 2022, 12, 1473. https://doi.org/10.3390/brainsci12111473
Chavda V, Chaurasia B, Umana GE, Tomasi SO, Lu B, Montemurro N. Narcolepsy—A Neuropathological Obscure Sleep Disorder: A Narrative Review of Current Literature. Brain Sciences. 2022; 12(11):1473. https://doi.org/10.3390/brainsci12111473
Chicago/Turabian StyleChavda, Vishal, Bipin Chaurasia, Giuseppe E. Umana, Santino Ottavio Tomasi, Bingwei Lu, and Nicola Montemurro. 2022. "Narcolepsy—A Neuropathological Obscure Sleep Disorder: A Narrative Review of Current Literature" Brain Sciences 12, no. 11: 1473. https://doi.org/10.3390/brainsci12111473