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Sleepiness that cannot be overcome: narcolepsy and cataplexy.
1Department of Respiratory Medicine, The Peking University People's Hospital, Beijing, China. hanfang1@hotmail.com
Respirology (Carlton, Vic.)
|April 5, 2012
Summary
Narcolepsy-cataplexy involves excessive daytime sleepiness and is linked to hypocretin deficiency. Infections may trigger this autoimmune condition in genetically susceptible individuals, impacting breathing control.
Area of Science:
- Sleep Medicine
- Neuroimmunology
- Genetics
Background:
- Narcolepsy-cataplexy presents with excessive daytime sleepiness, cataplexy, and other sleep disturbances.
- The condition is strongly associated with the human leucocyte antigen (HLA) DQB1*06:02 genetic marker.
- Pathophysiology involves a deficit in the hypocretin/orexin system due to autoimmune-mediated neuronal degeneration.
Purpose of the Study:
- To explore the translation of basic science research into clinical practice for narcolepsy.
- To investigate recent advances linking respiratory medicine to narcolepsy-cataplexy.
- To understand the role of infections and sleep-disordered breathing in narcolepsy.
Main Methods:
- Review of scientific literature on narcolepsy pathophysiology and recent advances.
- Analysis of the association between hypocretin gene findings in animal models and human diagnostics.
- Examination of the interplay between infections, immune response, and hypocretin deficiency.
Main Results:
- Cerebrospinal fluid hypocretin measurements are now a diagnostic test for narcolepsy.
- Upper airway infections (H1N1, streptococcal) may trigger narcolepsy in susceptible individuals.
- Sleep-disordered breathing is more common in narcolepsy, potentially due to hypocretin deficiency or HLA DQB1*06:02 carriage.
Conclusions:
- Narcolepsy research has successfully translated basic science findings into clinical diagnostics.
- Infections and genetic susceptibility play a role in initiating the autoimmune process leading to hypocretin cell loss.
- Hypocretin deficiency and HLA DQB1*06:02 carriage are linked to neural dysfunction affecting both sleep-wake and respiratory control.
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