sleep: reversible behavioral state of perceptual disengagement from an unresponsiveness to the environment. It is a mixture of physiological and behavioral processes.

NREM: it is subdivided into 4 stages: 1, 2, 3 and 4. Roughly parallel a depth-of-sleep continuum, with a arousal threshold generally lowest in age 1 and highest in stage 4 sleep. NREM sleep is usually associated with minimal or fragmentary mental activity.

REM: defined by EEG activation, muscle atonia, and episodic bursts of rapid eye movements. It is not divided into stages, although tonic and phasic types of REM can be distinguish for study. In the first cycle, is very short and then extends.

Simplified sequence: NREM sleep => REM sleep after 80 minutes or longer => NREM sleep => REM sleep (alternate through th night, with an aprox. 90 min cycle). In normal sleep, the sleep onset is through NREM sleep

Stage 2: signalled by sleep spindles or K-complexes in the EEG, follows this brief episode of stage 1 and continues for aprox. 10 to 25 minutes. A more intense stimulus is required to produce arousal. 45% of total sleep.

Stage 3: lasts only a few minutes in the first cycle and is transitional to stage 4 as more and more high-voltage slow-wave activity occurs. Deltha waves - deepest sleep -below 4 hz (slowest frequency but highest amplitude) 25%

Stage 1 : usually persists for only a few (1 to 7) minutes at the onset of sleep. It is usually discontinued during this stage and is associated with a low arousal threshold. Role in initial wake to sleep transition and it occurs as a transitional stage throughout the night. - 4-8 hz theta waves (in the transition to sleep, alpha waves 9-13 hertz) 5% of total sleep

Nrem sleep - lasts approx, 20-40 mins in the first cycle. An incrementally larger stimulus is usually required to produce an arousal from stage 3 or 4 sleep than from stage 1 o 2 sleep. stag 4?

NREM- REM cycle: NREM sleep and REM sleep continue to alternate through the night in cyclic fashion. REM sleep become longer across the night. Stage 3 and 4 sleep occupy less time in the second cycle and might disappear altogether from later cycles, as stage sleep 2 expands to occupy the NREM portion of the cycle. Average length of first NREM-REM sleep is approx. 70-100.

stages across the night: In young adults stages 3 + 4 NREM dominates the NREM portion of the sleep cycle toward the beginning of the night. REM sleep episodes are longest in the last one third of the night. Brief episodes of wakefulness tend to intrude later in the night, usually near REM sleep transitions.

From neurocognitve perspective: Medication decreases sleep latency and increases sleep time, the magnitude of these effects are moderate. Sleep latency is reduced by 15 minutes and total sleep time is increased by about 30 minutes. This patients overestimate this effect because of diminish ability to process information and promoting mesograde amnesia.

explains that insomnia occurs acutely in relation to both trait and precipitating factors (stressful life events) => an individual may be vulnerable to insomnia because of trait characteristics, but experience an episode because of precipitating factors. Acute insomnia becomes chronic because it is reinforced by maladaptive coping strategies. These strategies result in conditioned arousal and insomnia.

maladapatative strategies that make it chronic: (1) excessive time in bed => to increase opportunities to sleep, they go to bed very early or get out of the bed. This results in a conditioned arousal during the traditional sleep period and chronic insomnia. (2) staying in bed while awake: increase the opportunity to get more sleep. You associate bed and bedroom with arousal, not sleepiness and sleep. Also elicits arousal via classical condition when confronted with stimuli associated with sleep.

Trait factors: biological (hyperarousal and hyperactivity), psychological factors (worry or tendency to be excessively ruminative), social factors (bed partnes, social pressure)

Classical conditioning: High frequency EEG activity is elicited in response to the visual and/or temporal cues usually associated with sleepiness and sleep, and this occur in the abscence of stressors (as oppose to acute insomnia).

High EEG activity: allows for increased sensory processing, information processing and formation of long-term memory This capacities should be attenuated in sleep.

(2) High frequency EEG and Insomnia: transition from wakefulness to sleep entails a shift in the frequency spectrum of the EEG from high frequency to low frequency. Subjects with insomnia exhibit increased high frequency EEG activity prior to sleep onset, for a period to be as long as 15 min into the first NREM cycle.

(1) Cortical arousal:high frequency EEG activity in beta and gamma is associated with cognitive function.

Enhanced information processing: at around sleep-onset may be directly related to the perception of sleep and wakefulness. The perception of perturbing environmental stimuli may blur the distinction between sleep and wakefulness. (asleep but capable of information processing, trouble recognising if they were awake or asleep). For that reason, insomnia patients can judge PSG sleep was wakefulness. Hypnotic medication block sensory processing, thus the patient would be less aware of environment, and conclude being asleep.

Enhanced long-term memory function: normally subjects can recall information from periods immediately prior to sleep, during sleep, or from brief arousals which occur during the night. If the ability to encode is intact in arousal, this can influence judgement of sleep onset and sleep duration => tendency to overestimate retrospectively: (1) amount of time that takes to sleep and the amount of time awake during the night. => hypotics may be able to produce amnesia.

From neurocognitive perspectives: sleep state misperception occurs as a result of high-frequency EEG related increases in information processing. Perception of perturbing environmental stimuli serves to blur the phenomenologiclal distinction between sleep and wakefulness.

From neurocognitve perspectives: high-frequency EEG is associated with increased information processing and long-term memory formation, then the patient is correctly estimating the amount of time required to disengage from the environment (p)

From neurocognitve perspective: the sleep EEG effect of hypnotics appears to be in strong contradiction to the neurocognitive model. How can the hypnotics be effective but speed up sleep EEG? they are faster than delta but slower than beta and gamma.

The pyschobiological model: The inability to disengage from active active wake processes interferes with normal sleep processes. Higher cortical arousal might be present at any time before sleep onset and during the night, and there is an inability to lower arousal.

General concepts: (1) consciousness: requires activity in: Reticular formation, thalamus, and cerebral cortex. Reduced neuronal activity in any of these structures that may disrupts an integration that apparently must be present among the 3 structures to maintain conscious./(2) sedation: a state of reduced alertness, decreased motor activity, and relaxation. Consciousness with burst of sleep-like electrical activity, person is neither sleep nor aroused/ hypnosis: state of drowsiness that leads to sleep from which an individual is readily aroused (3) hypnosis: state of drowsiness that leads to sleep, general slowness of EEG activity in comparison to wake state.