Normal Sleep and Sleep-Wake Mechanisms
Core physiology
Sleep is generated by the interaction of a circadian alerting signal (the suprachiasmatic nucleus, entrained by light via the retinohypothalamic tract) and a homeostatic sleep drive that accumulates with wakefulness. In the two-process model these are Process C and Process S; sleep propensity is greatest when circadian low and high homeostatic pressure coincide. The ascending arousal system includes cholinergic laterodorsal/pedunculopontine nuclei, noradrenergic locus coeruleus, serotonergic raphe, and histaminergic tuberomammillary nucleus; the ventrolateral preoptic area promotes sleep by inhibiting these. Orexin (hypocretin) neurons in the lateral hypothalamus stabilize wakefulness.
Sleep architecture
NREM sleep progresses N1 to N3; N3 (slow-wave sleep) predominates in the first third of the night, while REM periods lengthen toward morning. REM features low-voltage mixed-frequency EEG, rapid eye movements, and atonia from medullary inhibition of spinal motor neurons.
Ontogeny
Neonates enter sleep through active (REM-like) sleep; sleep cycles are short (~50-60 min) and lengthen with age. Slow-wave sleep declines across the lifespan, and older adults show earlier sleep timing and more fragmented sleep.
Question traps
Distinguish circadian (Process C) from homeostatic (Process S) contributions. Do not confuse the circadian nadir with sleep inertia. Remember that melatonin is suppressed by light and that core temperature minimum occurs in the second half of the night.
Rule of thumb: If a stem describes a person who cannot sleep at the desired time but sleeps fine when allowed to follow their own schedule, think circadian misalignment rather than insomnia.