Unlike narcolepsy with cataplexy, which has a known cause (autoimmune destruction of hypocretin-producing neurons), the cause of IH is largely unknown. , researchers have identified a few abnormalities associated with IH, which with further study may help to clarify the etiology. Destruction of noradrenergic neurons has produced<unk>  in experimental animal studies, and injury to adrenergic neurons has also been shown to lead to<unk> . IH has also been associated with a malfunction of the norepinephrine system and decreased cerebrospinal fluid (CSF) histamine levels. Researchers have recently found an abnormal hypersensitivity to GABA (the major brain chemical responsible for sedation) in a subset of patients with central<unk>  i.e.: IH, narcolepsy without cataplexy and long sleepers. They have identified a small (500 to 3000 daltons) naturally occurring bioactive substance (most likely a peptide as it is trypsin-sensitive) in the CSF of afflicted patients. Although this substance requires further identification of its chemical structure, it is currently referred to as a "somnogen" because it has been shown to cause hyper-reactivity of GABAA receptors, which leads to increased sedation or somnolence. In essence, it is as though these patients are chronically sedated with a benzodiazepine (medication which acts through the GABA system) such as Versed or Xanax, even though they do not take these medications.
Idiopathic hypersomnia
Strephosymbolia
Psychoorganic syndrome
Nightmare disorder
Erotolepsy
Interictal dysphoric disorder
Narcolepsy
Klazomania