The exact cause of narcolepsy is unclear, although in many cases the condition occurs as an autoimmune response.
In autoimmune disorders, the body’s own antibodies target healthy cells and tissues. In the case of narcolepsy, regions of the brain are attacked that usually release a neurotransmitter involved in sleep regulation called orexin. This leads to a deficiency in orexin and the symptoms of narcolepsy start to develop. In other cases of narcolepsy, however, orexin levels are found to be normal and the cause of narcolepsy remains unclear.
Autoimmune response in narcolepsy
In 2010, narcolepsy research showed that the areas of the brain that release orexin are attacked by an antibody called trib 2. The resulting decrease in orexin leads to narcolepsy, and in particular narcolepsy accompanied by cataplexy or temporary muscle weakness.
The research showed that individuals with narcolepsy had significantly higher levels of the trib 2 antibodies than individuals without the condition and that the increase in trib 2 was directly related to the decreased orexin level in those with narcolepsy. Furthermore, the higher the trib2 levels, the greater the degree of damage to the brain areas responsible for orexin release. However, the research could not explain why some people with narcolepsy have near-normal levels of orexin.
Our sleep pattern is usually made up of two cycles of brain activity which include:
- Non-rapid eye movement (NREM) sleep
- Rapid eye movement (REM)
Usually, sleep begins with NREM sleep, which is divided into four stages. This is followed by a short period of REM sleep, when the brain becomes more active and a person may dream. In the case of narcolepsy, the REM sleep occurs much earlier on in the cycle than usual and a person may start to dream as they fall into a nap, for example. The dreaming or paralysis that usually occurs in REM sleep may also occur while a person is awake.