Session Schedule

Find a specific presentation in the session by navigating to the timestamp indicated below.

0:00:00
Orexin as a key mechanism: Influence on comorbid and disease-immanent disorders in hypersomnolence
Jari Gool (Netherlands)

0:24:10
Narcolepsy and cardiovascular risk: Links between hypersomnolence and cardiovascular disease
Poul Jørgen Jennum (Denmark)

0:42:02
Mental comorbidities in narcolepsy: Depression, anxiety disorders and the impact of orexin on psychiatric health
Anna Heidbreder (Austria)

1:04:50
Therapeutic approaches in narcolepsy: New perspectives through orexin receptor agonists and their significance for the treatment of comorbidities
Lucie Barateau (France)

1:27:00
Question and answer

Summary

It is often difficult to differentiate whether diseases, symptoms or syndromes occurring alongside narcolepsy are a disease-specific phenomenon from the pathophysiology of the disease itself or an independent disease. This symposium will attempt to differentiate between the two and help to define questions that can be better differentiated pathophysiologically, diagnostically and thus therapeutically in the future.

The following questions will be addressed in this symposium:

1. to what extent are the comorbid symptoms directly caused by the central pathophysiologic cause of hypersomnolence (e.g., orexin deficiency), and to what extent are they independent of it?
This question aims to investigate whether the comorbid symptoms (e.g. depression, obesity, fatigue, restless legs) are primarily caused by the dysregulation of the orexin system or whether they occur independently and need to be treated as independent disorders. A deeper understanding of these interactions could influence therapeutic strategies.
2. how to distinguish clinically between the symptoms of the disorder (e.g. excessive daytime sleepiness, sleep disturbances) and the comorbid disorders (e.g. depression, anxiety disorders)?
This question is important to clarify the clinical distinction between the symptoms of the primary disorder (hypersomnolence) and the possible comorbid disorders. This is because it is often difficult to distinguish between the primary symptoms of hypersomnolence disorders and the associated secondary disorders, which can have an impact on diagnosis and treatment.
3. to what extent do comorbid conditions (e.g. depression, obesity, cardiovascular risk factors) contribute to the long-term course and quality of life of patients with hypersomnolence?
This question could be used to investigate the long-term impact of comorbidities on disease progression and treatment. A better understanding of the role of comorbidities in the course of the disease could lead to better predictions of disease progression and the development of preventive or complementary therapeutic approaches.
4. could the observed comorbidities (e.g. obesity, fatigue) possibly also be secondary symptoms due to the long suffering and stigmatization of the disease, rather than being directly caused by the primary hypersomnolence?
This question refers to the possibility that some comorbidities are not only due to the biological causes of hypersomnolence, but may also be due to the social and psychological stresses associated with the condition (e.g. social isolation, prolonged sleep deprivation, stigmatization). Understanding these psychosocial aspects could enhance the treatment approach.
Conclusion:
Distinguishing between causative and secondary factors in hypersomnolence disorders is crucial for correct diagnosis and treatment. By closely examining the interactions between the central mechanisms of the disorder and the comorbid disorders, new therapeutic approaches could be developed and the quality of life of affected patients could be significantly improved.