Purpose of review
To describe the multiple clinical aspects of hypersomnias of central origin. Emphasis is given to the new pathophysiological pathways and treatment options described in the current literature.
Narcolepsy is the most recognized of the hypersomnias of central origin. Hypocretin deficiency appears to underlie narcolepsy with cataplexy, and infections and vaccinations have been associated with disease onset. Targeted therapeutic approaches are currently underway. A putative naturally occurring constituent in the cerebrospinal fluid of patients with non-narcoleptic primary hypersomnias, able to stimulate γ-aminobutyric acid alpha receptors and induce sleep, has recently been postulated. Neuroimaging has also provided more insight into the pathophysiology of Kleine–Levin syndrome. Sleep deprivation is currently recognized as a major differential diagnosis.
Excessive daytime sleepiness is the cardinal symptom of the hypersomnias of central origin, with major impact on the quality of life. It is important that clinicians be able to recognize these conditions, so that appropriate management or onward referral is expedited.