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Think of orexin as the brain's 'stay-awake, stay-out-of-REM' signal. When it fails, the switch that normally keeps REM sleep locked away during the day becomes leaky, so pieces of REM sleep — paralysis, vivid dreaming — leak into moments when the person is awake or falling asleep.

• Narcolepsy type 1 is caused by selective loss of orexin (hypocretin)-producing neurons in the lateral hypothalamusA small brain structure that controls basic functions like hunger, temperature, sleep and hormone release.Read more →, most likely through an autoimmune process.
• Orexin normally stabilises wakefulness and keeps REM-sleep mechanisms switched off during the day.
• Its loss lets REM-sleep phenomena — muscle atonia and dream imagery — intrude inappropriately into wakefulness and the sleep-wake transition.
• CSFCerebrospinal fluid, the fluid that cushions the brain and spinal cord.Read more → orexin-1 is markedly low or undetectable in narcolepsy type 1, supporting the diagnosis.
• Narcolepsy type 2 has the same daytime sleepiness but no cataplexy and usually normal orexin levels.

• A 22-year-old student describes recurrent episodes of falling asleep during lectures despite a full night's sleep, plus jaw-slackening when laughing, vivid falling-asleep experiences, and transient waking paralysis.
• A patient with narcolepsy reports that whenever he becomes very angry or excited, his knees suddenly buckle and he has to sit down, although he remains fully aware throughout.
• A 19-year-old man reports seeing a shadowy figure at the end of his bed just before falling asleep, alongside daytime sleepiness and cataplexy.
• A patient newly diagnosed with narcolepsy type 1 asks why he sometimes wakes up completely unable to move his limbs for around a minute.

• Cataplexy vs seizure — cataplexy preserves consciousness and is emotion-triggered; a seizure often impairs awareness and is not specifically emotion-triggered.
• Hypnagogic vs hypnopompic hallucinationSeeing, hearing, or otherwise sensing something that is not really there.Read more → — hypnagogic occurs falling asleep, hypnopompic occurs on waking; same phenomenon, different timing.
• Sleep paralysis vs conversion disorder — sleep paralysis has a stereotyped sleep-wake transition timing and resolves spontaneously within a minute or two, unlike a psychologically patterned conversion presentation.
• Narcolepsy vs obstructive sleep apnoea — both cause daytime sleepiness, but only narcolepsy produces cataplexy and the REM-intrusion phenomena.

• Assuming any 'jaw goes slack' or 'legs buckle' episode with preserved consciousness is a faint — cataplexy is preserved-consciousness muscle atonia specifically triggered by strong emotion.
• Confusing hypnagogic (falling asleep) with hypnopompic (waking) hallucinationsSeeing, hearing, or otherwise sensing things that are not really there.Read more → — the exam relies on this timing distinction.
• Forgetting that narcolepsy type 2 exists — daytime sleepiness without cataplexy does not exclude narcolepsy.
• Treating sleep paralysis as inherently pathological — it also occurs in healthy people, especially with sleep deprivation, and only forms part of the tetrad when it clusters with the other three features.

• Localise the clue to the relevant anatomical level, cell type, pathway or molecular process.
• Map that structure or process to its normal function.
• Predict the deficit or clinical sign produced when it is disrupted.
• Reject options that belong to a neighbouring structure, pathway or level of explanation.