Kleine–Levin syndrome (KLS) is a rare neurological disorder characterized by persistent episodic hypersomnia accompanied by cognitive and behavioral changes.

These changes may include disinhibition (failure to inhibit actions or words), sometimes manifested through hypersexuality, hyperphagia or emotional lability, and other symptoms, such as derealization.

The onset of the condition usually follows a viral infection (72% of patients); several different viruses have been observed to trigger KLS.

[2] It is generally only diagnosed after similar conditions have been excluded; MRI, CT scans, lumbar puncture, and toxicology tests are used to rule out other possibilities.

The condition is named after Willi Kleine and Max Levin,[4] who described cases of the disease in the early 20th century.

Patients with Kleine–Levin syndrome (KLS) experience recurring episodes of prolonged sleep (hypersomnia).

[9][7] Several other symptoms usually accompany the syndrome, including marked changes in mood and cognitive ability.

[6] Sleep studies of KLS show varying results based on the period the patient is observed.

Studies also show that stage one and three non-rapid eye movement sleep becomes more efficient when the episodes end.

[14] The Multiple Sleep Latency Test has yielded inconsistent results when given to KLS patients.

[9][14] Lifestyle habits such as alcohol abuse, lack of sleep and stress have also been proposed as possible triggers.

[17] The condition generally disrupts the social lives and academic or professional obligations of those with KLS.

[6] In patients with KLS, MRI and CT scans show normal brain morphology.

[5] Specifically, the medial temporal regions of the thalamus may be involved,[22] although examinations of KLS patients have not consistently found abnormalities in this area.

[8] The temporal lobe also appears to play a role in the condition, possibly causing cognitive difficulties.

The apathy and disinhibition found in some with KLS suggest that the condition may include frontal lobe dysfunction as well.

[16] Androgen might (indirectly) block melatonin receptors, possibly through vasodilation, and cause cholinergic abnormalities in some cases of Kleine–Levin syndrome.

[citation needed] Because KLS occurs at a much higher rate in Jews and some families, there is likely some genetic component in addition to environmental factors.

[21] Genetic studies hold promise for understanding the disease, but they have yielded inconsistent results[20] and few patients are available for testing.

[23] KLS can be diagnosed when there is confusion, apathy, derealization, and frequent bouts of extreme tiredness and prolonged sleep.

[5] Several drug therapies have been used on patients with KLS, but none of them have been subject to randomized controlled trials.

[5] In several cases, stimulants, including modafinil,[8] have been reported to have a limited effect on patients, often alleviating sleepiness.

[5] They can cause behavioral problems,[20] but they may pose fewer issues if used in older patients with mild symptoms.

[9] The median duration of KLS episodes is about ten days, but some last several weeks or months.

First-degree relatives of people who have the syndrome are much more likely than the general population to have it, although only in about one percent of cases do family members contract it.

[11] In 1815, there was a report of a young man who showed excessive appetite and prolonged sleep after experiencing a fever; this may have been an early description of the condition.

This report was followed four years later by details of a similar case by New York-based psychiatrist Max Levin.

He named the condition Kleine–Levin syndrome and noted four common traits: hypersexuality, adolescent onset, spontaneous resolution, and compulsive eating.

[22] Diagnostic criteria for KLS were established by Schmidt in 1990, and the International Classification of Sleep Disorders further refined them.