Most likely, it is caused by less severe injury to the hypocretin neurons, resulting in fewer and less severe symptoms. Though much has been learned about narcolepsy with cataplexy, considerably less is known about the cause of narcolepsy without cataplexy. In fact, REM sleep can become so poorly regulated that the paralysis or dreaming that normally occurs only in REM sleep can mix into wakefulness, causing cataplexy and dreamlike hallucinations. The consequent lack of hypocretins results in lasting sleepiness and poor control of REM sleep. In people who have narcolepsy with cataplexy, most of the hypocretin-producing neurons die off. In individuals without narcolepsy and whose sleep is well regulated, hypocretins are released during wakefulness and increase activity in target neurons that promote wakefulness and suppress rapid-eye-movement (REM) sleep. (This website uses the term “hypocretins,” as this name is preferred by clinicians.) 1, 2 One group named them hypocretin-1 and -2, and the other group named them orexin-A and -B. Hypocretins were first discovered in 1998 when two research groups independently identified them in the brain.
Hypocretins are released from these neurons during wakefulness and bind to specific hypocretin receptors on target neurons, which increases the activity of these neurons. Of the billions of neurons in the brain, only about 100,000–200,000 produce hypocretins.
Hypocretins are only produced by a small cluster of neurons in the hypothalamus, a brain region located roughly behind the eyes and between the ears. Hypocretins are neurotransmitters, chemicals that transmit signals from a neuron to a target neuron. Recent research has revealed that narcolepsy with cataplexy is caused by a lack of hypocretins, key brain chemicals that help sustain alertness and prevent REM sleep from occurring at the wrong times.
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