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insomnia vs. normal sleep (What is insomnia? (Types) (Psychophysiological:…
insomnia vs. normal sleep
What is insomnia? (Types)
Psychophysiological: excessive worrying, focused on not being able to fall asleep, accurate estimation of sleep, conditioned by sleep-related stimuli eg. bedroom, stimuli are associated with anxiety/frustration -> increased arousal levels
Paradoxical: severe type, without objective evidence of sleep disturbance (sleep state misperception)
Comorbid: occurs with condition such as anxiety or depression
Idiopathic/ Childhood onset: starting before age of 10, show less distress than paradoxical insomniacs, probably resignation/coping mechanisms developed over life time
Chronic: longterm pattern of difficulty sleeping (at least 3 nights per week for 3 months or longer)
Main Definition:
complaint of prolonged sleep latency (sleep onset insomnia)
difficulties in maintaining sleep (sleep maintenance insomnia)
waking up too early in the morning (terminal insomnia)
mix of different sleep complaints (mixed insomnia)
experience of non-restorative sleep
Acute: brief episode of difficulty sleeping, usually caused by a life event
diagnosis relies on subjective reports, it doesn't require an objective confirmation
Why did comorbid insomnia replace the secondary insomnia?
Because diretion of causality isn't always easy to identify when insomnia is present in the context of other cconditions. Insomnia could also cause anxiety & depression.
Common consequences of insomnia
fatigue, sleepiness, mood disruption, impaired attention, memory deficits -> people seek treatment not due to sleep difficulties per se but due to the daily consequences
Neuropsychological complaints based on neuropsychological assessment (only subtle deficits)
concentration & memory deficits -> score higher on cognitive failures questionnaire
complaints about mistakes related to work demands
score higher on questionnaires measuring fatigue & depressive/anxiety symptoms -> also lower quality of life
During NP testing:
deficits in tasks measuring attention, reaction time, semantic memory storage, working memory, verbal fluency, problem solving
studies on vigilance yield ambiguous results]- more sleepiness at pretest before a cognitive task than good sleepers but the difference disappeared at posttest
compensation: give more effort to perform, their expectations towards their performance increase when they had a bad night
good night is associated with better performance
perceived sleep quality is more important than sleep duration
Normal Human Sleep
Length of sleep: highly variable
volitional control as critical factor
depends on genetic determinants
length of prior waking
sleep onset:
EMG: rarely indicates sleep onset because EMG of a relaxed person is similar to that of sleep, may show diminished muscle tonus
EOG: slow & asynchronous eye movements
EEG: changes from alpha to low-voltage/mixed frequency pattern (stage 1)
--> difficult to accept a single variable as marking sleep onset. It isn't a unitary event.
REM: ca. 25% of total night sleep, desynchronized EEG, muscles are atonic (paralyzed body), dreaming (active brain), episodic bursts of rapid eye movements
Behavioral changes at sleep onset:
Auditory response: series of tones are played & the subject needs to respond when the tone is heard -> RTs become longer close to stage 1
Olfactory response: depends on sleep state & odorant -> responses to graded strengths of peppermint (pleasant) & pyridine (unpleasant) were maintained during stage 1
Visual response: bright light placed in front of subject's eyes and the subject responds when a light flash is seen --> perceptual disengagement from environment, no response in stage 1/2
Meaningful stimuli: We have a lower arousal threshold for our names -> sensory processing at some level does continue
Simple Behavioral Task: tap two switches alternately at a steady pace -> automatic behavior can persist several seconds past sleep onset
Memory impairment: in the 30 second condition, people could recall the entire session but in the 10 minutes condition they only recalled the words from LTM but bot the ones from STM heard close to sleep onset
NREM: variably synchronous EEG pattern, sleep spindles & K complexes & slow waves (high voltage), movable body
stage 1: 5%, lowest arousal threshold
stage 2: 50%, sleep spindles & K complexes
stage 3&4: 15-20%, SWS, highest arousal threshold
K-complexes: in stage 2, large waves that react to external stimuli
Sleep begins with NREM. The first REM occurs 80-100 minutes later. Then, REM & NREM cycle with a period of ca. 90 minutes.
REM episodes lengthen across the night (linked to circadian rhythm of body temperature)
SWS gets shorter across the night (linked to initiation of sleep & length of time awake)
also brief episodes of wakefulness that are usually not remembered in the morning
Sleep spindles: in stage 2, sudden bursts of oscillatory activity, follow K-complexes -> protective mechanisms?
Hypnic Myoclonia: generalized or localized muscle contraction, associated with vivid visual imagery (not a pathological event but occurs more often with stress & unusual/irregular sleep schedules)
What factors could modify the sleep stage distribution?
Prior sleep history:
if sleep deprived -> sleep pattern favors SWS during recovery
recovery sleep is usually deeper, with higher arousal threshold, a bit prolonged
preferential rebound of the stage that was deprived, even REM
chronic restriction of sleep, irregular sleep schedule, disturbance of sleep -> premature REM
delayed onset of REM during first night in the lab
Circadian Rhythms (especially REM influenced):
especially during jet lag or phase shift
eg. if sleep onset is delayed until the peak REM phase of the circadian rhythm (early morning), REM tends to predominate and can even occur at sleep onset
Age:
Newborns: enter REM before NREM, have shorter sleep cycle ca. 50 minutes
young children: SWS is maximal
Adolescents: SWS decreases by 40 %
Elderly: SWS might no onger be present, arousals increase, extended wake episodes increase
Temperature: extremes disrupt sleep
REM is more sensitive to disruption because mammals can't well thermoregulate during REM
in NREM we are sweating or shivering
Drug Ingestion:
Benzodiazepines: suppress SWS
Tricyclic Antidepressants, SSRIs: suppress REM
Acute presley alcohol intake: SWS & REM suppression early in the night
Other pathologies
Narcolepsy: abnormally short delay to REM (abnormal sleep onset pattern), hypnagogic hallucinations, sleep paralysis, cataplexy (sudden muscle weakness)
Sleep Apnea Syndromes: breathing issue, may be associated with suppression of SWS or REM
Treatment
Non-pharmacological:
Cognitive Behavioral Treatment (known short & longterm gains, positive impact on EEG frequency, decrease in hyperarousal)
behavioral: stimulus control (reassociating the bedtime stimuli with sleepiness rather than with frustration/anxiety) & sleep restriction (limiting the time spent in bed to the actual time sleeping)
cognitive therapy: identifying, challenging & altering dysfunctional beliefs & attitudes about sleep
sleep hygiene & education about environmental factors eg. light, noise
other components: relaxation, biofeedback, bright light exposure, body temperature manipulations, exercise
Pharmacological: Benzodiazepines or other hypnotic agents (sedative hypnotics or anxiolytics)
little known about long term efficacy, useful in short term
possible issues with dependence, tolerance, withdrawal
adverse effects: memory impairments, altered sleep schedules (reduced SWS)
General actions of sedative hypnotics
Motor Incoordination: maybe due to depressed cerebellar function due to GABAa, even slurred speech, nystagmus, hyporeflexia
Cognitive effects: judgment, concentration, insight, planning -> all blurred
Muscle Relaxation: at higher doses even motor weakness, Gamma motor neuron activity in the spinal cord is reduced
Disinhibition release: mild euphoria, paradoxical excitement, mood elevation, enhanced motivation, behavior less inhibited (can even be antisocial, aggressive)
Respiratory depression (not benzodiazepines): breathing is compromised, especially during tolerance
Anterograde amnesia (especially Benzos)
Sedation: reduce the time needed to fall asleep, extend the time in sleep, reduce intermittent arousals, reduce the amount of movement during sleep, reduce the time spent in SWS & REM, increase time in stage 2 (doesn't mimic normal sleep)
Drug Hangovers
What are CNS depressants and how do they affect consciousness?
They reduce electrical activity in the brain
to facilitate sleep, reduce anxiety, produce anesthesia, promote muscle relaxation, treat seizures
Consciousness requires electrical activity in: reticular formation, thalamus, cerebral cortex
What is the drug hangover effect of Benzodiazepines?
Most benzos are enterohepatically recirculated & this extends their duration of action
Becuase of their lipid solubility, they are also redistributed to skeletal muscle & then to body fat
Their deposition in muscle & body fat & later slow release back into circulation contribute to hangover effects next day
Benzodiazepines:
benzene ring fused with diazepine ring
affect GABA a receptor (allosteric effect on GABA)
Why are not all Benzos the same?
All are moderately lipid soluble but their lipophilicity varies -> they differ in their rates of absorption (this determines their onset of action & their redistribution)
depends on their method of biotransformation, lipid solubility & half lives: classified as short, intermediate & long acting
eg. if a patient needs a fast acting drug to induce sleep because of situational anxiety -> short acting agent is best
Side effects:
tolerance when chronic use, reduced ability to enhance Cl- conductance (that's why they aren't used as aniepileptics) -> leads to higher dosage
light-headedness, tiredness, increased RT, ataxia, confusion, dry mouth, anterograde amnesia, paradoxical anxiety, euphoria, hallucination
overdose is extremely rare
How do they work?
GABA r receptor forms the Cl- ionophore (by combining subunits from alpha, beta, gamma)
Benzos enhance the action of GABA at GABAa receptors by binding to a regulatory site on the ionophore (ligand-gated channel)
influence the frequency at which the Cl- channel opens -> potentiated GABA inhibition, GABA activates the channel more frequently
-> excitatory activity is reduced throughout the brain because GABA is widely distributed
also inhibition of Adenosine reuptake (potentiation of adenosine effect): Adenosine reduces ACh release
Berbiturates:
lack CNS depressant activity
predominantly used as anticonvulsant & anesthetic
How do they work?
increased Cl- conductance because they enhance GABAa activity
increase the amount of time the Cl- channel remains open
can also increase Cl- conductance in the absence of GABA (GABA-independent action which is responsible for their toxicity)
Consequences/Side effects:
depress respiration dose-dependently (can induce coma & fatal respiratory depression at high doses)
drug automatism due to overdose: patients take drugs unnecessarily
state-independent action: no ceiling effect (even when GABA release is reduced, a barbiturate will continue to open Cl- gates & produce further CNS depression)
dependence, tolerance -> can lead to addiction
Sleep/Insomnia Measures
Cyclic Alternating Pattern (arousal-related events follow odd time organization)
CAP: 20-40 sec cyclic rhythm, periods of cerebral activation (Phase A) followed by periods of deactivation (Phase B) -> unstable sleep
NCaP: stable sleep
ERPs: time-locked changes in EEG, precise timing of cortical arousal
valence + latency: eg. N100 is a negative wave appearing 100ms after stimulus onset
Power Spectral Analysis: finer measure of EEG
by computing Fast Fourier Transforms
results combined by averaging data in different frequency bands, results presented as EEG power (absolute or relative)
elevated powers in Beta band -> increased cortical actvation
increase in slower band eg. delta -> decreased cortcial activation
Limitation: averaging multiple nights together obscures real differences
Polysomnography: sleep continuity (lately, time awake, total sleep time, quality) & sleep architecture (% of time spent in different stages)
EOG, EMG, EEG to score sleep recordings & achieve sleep staging
additional measures: airflow, respiratory effort, oxygen saturation (to detect sleep disorders eg. sleep apnea)
not practical on a daily basis but useful to evaluate subjective sleep complaint and to rule out other sleep disorders
typically 2-3 consecutive nights
first night effect: for good sleepers, worst sleep efficiency on the first night in the lab
reverse first night effect: for insomniacs, sleep might actually improve in the lab
Neuroimaging:
many methodological issues: sample sizes, sleeping in the machine
SPECT: visualization of cerebral metabolism (PET is better option, more accurate)
fMRI
-> could classify different insomnia subtypes
Subjective: sleep diary eg. self-recording of bedtime, arising time, sleep onset latency, total sleep time, sleep quality etc. -> good to capture night-to-night variability
Frequencies/Waves:
Slow waves: 0-1 Hz
Delta: 1-4 Hz
-Theta: 4-7 Hz
Alpha: 7-11 Hz
Sigma: 11-14 Hz
Beta: 14-35 hz
Gamma: 35-60 Hz
Changes in Insomniacs seen in the measures
ERPs:
N350 smaller during stage 2
greater P300 before sleep onset & shorter response latencies -> hyperaroused
larger P1, N1 & smiler P2 -> hyperarousal upon awakening in the morning
lower P50 amplitudes -> enhanced sensory processing, inhibition deficit
LORETA: less current density in cerebral regions involved in affect & cognitive performance ie. OFC, mPFC, ACC during wake
CAP: Activation phase (A) was longer in insomniacs, phase B was shorter, CAP rate was greater in insomniacs -> poor subjective sleep quality -> greater arousal in EEG
SPECT: decrease in cerebral blood flow in mPFC, occipital, parietal, deactivation in basal ganglia -> hypometabolic
PSA: more Beta & less Delta activity at sleep onset, higher relative Beta activity during wakefulness in psychophysiological insomniacs, increased Beta in REM & NREM, higher cortical arousal in Beta bands
PET: increased global cerebral glucose metabolism during NREM, smaller decrease in cerebral activity from wakefulness to NREM -> during sleep, enhanced metabolism
Polysomnography: insomniacs spend more time in stage 1, less time in SWS, they display more frequent stage shifts through the night
Spielman's behavioral model
Trait factors based on biopsychosocial model:
Bio: hyperarousal, hyperreactivity
Psycho: worry, rumination
Social: bed partner keeping incompatible sleep schedule, social pressures
Maladaptive strategie:
Excessive time in bed (leads to decreased sleep efficiency, more frequent & longer awakenings)
Staying in bed while awake (because it is at least restful) -> leads to association of bed with arousal, not with sleep
chronic insomnia when maladaptive strategies result in conditioned arousal
Evidence: insomniacs report improved sleep in novel environments
acutely, insomnia due to trait & life stress events (precipitating factors) -> it becomes sub chronic when it is reinforced by maladaptive coping strategoes
Refinement: distinction between somatic (physiological) & cognitive (psychological) arousal
Neurocognitive Perspective
chronic insomnia developed like in the behavioral model: high frequency EEG is a result of classical conditioning
insomniacs are overly aroused at somatic & cognitive level-> state of hyperarousal interferes with sleep initiation & maintenance & with daily activities
focus on one form of conditioned arousal (cortical arousal, somatic, measure of brain activity): EEG activity in Beta & Gamma ranges is elevated in insomniacs -> high frequency EEG activity around sleep onset in a primary feature of chronic insomnia
Conditioned arousal may lead to enhanced sensory & information processing, also alterations in STM & LTM formation
After insomnia has become chronic (predisposing & precipitating factors identified), neurocognitive factors (conditioned arousal ie. cortical & cognitive alterations ie. sensory processing etc.) interplay with one another
Paradoxes/ Discrepancies between PSG measures & subjective impressions regarding sleep quality & quantity
Insomniacs identify themselves as having been awake when awakened from PSG sleep: they tend to identify PSG sleep as wakefulness 73% of time
-> EXPLANATION: Sleep state misperception occurs as a result of high frequency EEG increases in information processing. The ready perception of distressing environmental stimuli blurs the phenomenological distinction between sleep & wakefulness
Insomniacs tend to overestimate sleep latency & underestimate total sleep time as compared to PSG measures: they estimate that it takes them 1-45 minutes longer to fall asleep and that they sleep 30-45 minutes less
-> EXPLANATION: These numbers roughly approximate the amount of time that there is persistent high frequency EEG activity after sleep onset. Insomniacs are correctly estimating the time required to disengage from the environment.
Insomniacs appear to derive more benefit from medication than objectively seen. Mediation has only very small effects.
-> EXPLANATION: Hypnotics diminish the ability to process information & they promote anterograde amnesia. So, the patient overestimates treatment gains relative to PSG.
Objective paradox: Hypnotics don't normalize sleep architecture nor produce "sleeplike" EEG. Hypnotics decrease stage1 & increase stage2 but don't normalize SWS or REM
-> Benzodiazepine signature: high frequency component (sigma)
EXPLANATION: The answer might reside in how one conceives of high frequency EEG activity. The Benzodiazepine signature is faster than tonic delta activity but it is also slower than Beta & Gamma frequencies that characterize wakefulness. It is possible that Benzos produce the anticipated effect of slowing EEG but it is observed in a different range.