Although much research has occurred over the last century to determine the cause(s) of narcolepsy, no exact cause can be identified. However, there are various theories concerning the cause, including narcolepsy's relationship with the dysfunction of rapid-eye-movement (REM) sleep.
Since the 1970s, Stanford University has been studying narcolepsy mainly in Doberman Pinschers. These dogs have served as an animal model of the condition. The sympotoms of narcolepsy in canines closely resembles the symptoms of human narcolepsy. The four major symptoms of narcolepsy are present in both humans and dogs (that have already been diagnosed with narcolepsy). Both excessive daytime sleepiness and cataplexy can be observed in both humans and dogs. Recently, researchers have discovered the withering away of axons in the brains of the narcoleptic dogs. Still, they have not found a clear link between this sympotom and narcolepsy in humans. One suggestion given for the lack of evidence in the human brain is that the axon degeneration could have disappeared by the time the patient dies. This would explain why no evidence of the disorder has been found during autopsies of narcoleptics. Many researchers are skeptical of this finding.
Narcolepsy has also been linked to genetics. In 1983, Honda, Asaka, Tanaka, and Juji, discovered a link between a class II antigen of the major histocompatibility complex (MHC) known as DR2 and found that 100% of the narcoleptic patients in Japan are DR2 positive (as cited in Guilleminault, 1994). Mamelak (1991) also reported the "strong, almost 100%" association between the disease and the class II MHC antigens HLA-DR2 and HLA DQw1. These findings have been confirmed by Langdon, Welch, & Dam (1984) and Guilleminault & Grumet (1986) in the British, French, Canadian, and US. It is also noted that a specific genetic substrate is almost always present in narcoleptic families (Aldrich, 1990).