Narcolepsy is not a rare disease. Age of onset varies from childhood to the 5th decade. Evidence for a genetic basis stems from the overall rate of narcolepsy and/or disorder of excessive somnolence among first degree relatives. The clinical features include overwhelming episodes of sleep, excessive daytime somnolence, hypnagogic hallucinations, disturbed nocturnal sleep; manifestations of dissociated REM sleep inhibitory process, cataplexy and sleep paralysis; and a special polygraphic pattern: the sleep onset REM episode. Not all symptoms are necessarily present at the onset or even during the course of narcolepsy. Excessive daytime somnolence never disappears completely while other symptoms may. Narcolepsy is a disabling condition. Its aetiology is still poorly understood but the use of natural animal models, namely dogs and horses, has been an important contribution in the areas of genetic, pharmacological and direct neurochemical analysis. Treatment of excessive daytime somnolence is still primarily based upon CNS stimulants while treatment of cataplexy and other related symptoms rests on chlorimipramine. However, new treatments are being tested, which could be of significant value.