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Flashcards in week 8- sleep Deck (40)
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1
Q

Behavioural definition of Sleep

A
  • Eyes Shut (humans)
  • Certain Postures
  • Inactivity
  • Reduced muscle tone
  • Reduced responsiveness
2
Q

Measures of Sleep

A

-Summated brain wave activity (EEG)
-Active eyes open wakefulness: beta activity (13-30 Hz) is present in the EEG record (desynchrony: low amplitude, high frequency waveforms)
-Eyes closed wakefulness: alpha activity (8-12 Hz) appears in the EEG record
With sleep EEG synchrony develops: (high amplitude, low frequency waveforms)
Eye movements (EOG)
Muscle tone (EMG)

3
Q

stage 1 non rem sleep

A

slow rolling eyes

K complex more than 75- lasts more than a half a second

4
Q

stage 2 non rem sleep

A

Spindle- 12-14 hz- half to2 seconds

k complex

5
Q

stage 3 non rem sleep

A

More and more k complexes= delta waves 3-2 hertz

30 5 of epoch delta waves

6
Q

stage 4 non rem sleep

A

50% delta waves

7
Q

Non REM sleep

A

-Theta and delta activity, and K Complexes and Sleep Spindles are present in the EEG record
-Stages 1 and 2 (N1, N2)
-Stages 3 and 4: delta activity (synchronized)
-Termed slow-wave sleep (SWS or N3)
-Light, even respiration and regular Heart Rate
Muscle control is present (toss and turn)
-Cognitive Activity (thought like, rational)
Difficult to rouse from SWS

8
Q

REM sleep

A
  • EMG activity extremely low
  • Presense of saw tooth waves-
  • Presence of theta activity (desynchronized EEG pattern)
  • Enhanced and variable respiration and blood pressure
  • Rapid eye movements (REM)
  • Pontine-Geniculate-Occipital (PGO) waves
  • Loss of muscle tone (paralysis)
  • Vivid, emotional dreams
  • Signs of sexual arousal
  • Assess impotence - functional vs organic
9
Q

Mental Activity in Sleep

A
  • Mental activity continues during sleep
  • Dreams occur during SWS and REM sleep
  • REM sleep is accompanied by high levels of blood flow in the visual association cortex but low levels in the inferior frontal cortex
  • REM eye movements resemble those made when a person scans a visual image
  • Nightmares can occur during stage 4 of SWS
10
Q

Ontogenetic Development of Sleep

A

50% when we are born- active sleep

Rapidly reduces then stays constant

11
Q

Structure of Sleep in the Elderly

A

Same 9- minute cycling but waking up or lighter sleep

12
Q

Possible Functions of Sleep

A
Protection
Energy Conservation
Restoration
Brain
Body
13
Q

Sleep Deprivation Studies

A
  • Human sleep deprivation studies indicate that sleep deprivation can impair cognitive function
  • Perceptual distortions and hallucinations as well as impaired ability to concentrate have been reported during sleep deprivation
  • But sleep deprivation does not result in a physiological stress response nor does it interfere with normal bodily function
  • Animal studies indicate drastic health consequences of sleep deprivation
  • Rats that are forced to walk on rotating platform lose sleep
  • Sleep deprived rats exhibited increased eating and activity and eventually became ill and died
14
Q

Biological Rhythms

A

-Many of our behaviors display rhythmic variation
SWS/REM cycles last about 90 minutes
-Daily rest-activity cycle is about 90 minutes
Circadian rhythms (“about a day”)
-One cycle lasts about 24 hours (e.g. sleep-waking cycle)
-Light is an external cue that can set the circadian rhythm
-Monthly rhythms
-Menstrual cycle
-Seasonal rhythms
-Aggression, sexual activity in male deer

15
Q

Adaptive Advantage of Biological Rhythms

A
  • Biological rhythms ensure that physiological and behavioural processes occur at times they will be of the greatest benefit.
  • In the case of humans, that sleep occurs during the dark phase when the lack of night vision would be disadvantages.
16
Q

Suprachiasmatic Nucleus

A

-The suprachiasmatic nucleus (SCN) contains a biological clock that governs some circadian rhythms
SCN receives input from
melanopsin containing ganglion cells in the retina, a pathway that may account for the ability of light to reset the biological clock (zeitgeber function)
the intergeniculate leaflet of the lateral geniculate thalamic nucleus
This pathway may mediate the ability of other environmental stimuli to reset circadian rhythms (e.g. animals own activity)
SCN lesions disrupt circadian rhythms
SCN cells don’t require direct neural connections to control circadian rhythms, but may do using chemical signals

17
Q

SCN Clock Cells

A

SCN cells exhibit circadian rhythms in activity
SCN glucose metabolism (2-DG method) is higher during the day than during the night
Each SCN cell appears to have its own clock (separate daily peaks in activity)
Yet SCN clock cells act in a synchronized fashion (a chemical rather than a neural effect)

18
Q

nature of clock cells

A

Hypothesis was that clock cells produced a protein that upon reaching a critical level, inhibited its own production
Fruit fly: two genes per and tim control the production of two proteins: PER and TIM, eventually high levels of these proteins turn off the per and tim genes, resulting in declining levels of PER and TIM proteins, which in turn activates the two genes

19
Q

Seasonal Rhythms

A

-SCN plays a role in governing seasonal rhythms
-Testosterone secretion in male hamsters shows an annual rhythm with increased secretion as length of day increases
-This annual rhythm is abolished by SCN lesions.
Pineal gland interacts with the SCN to control seasonal rhythms
-The SCN projects to the Paraventricular Nucleus (PVN), which connects with the pineal gland which secretes melatonin
-During long nights, the pineal gland secretes high amounts of melatonin
-Lesions of the SCN, or the PVN, or the neural connection between the SCN and PVN disrupt seasonal rhythms controlled by day length

20
Q

PRIMARY SLEEP DISORDERS: Dyssomia

A
Primary Insomnia
Primary Hypersomnia
Narcolepsy
Breathing-related sleep disorder
Circadian rhythm sleep disorder
21
Q

PRIMARY SLEEP DISORDERS: Parasomnia

A

Nightmare disorder
Bruxism
Sleep terrors
Sleepwalking

22
Q

SLEEP DISORDERS RELATED TO ANOTHER MENTAL DISORDER

A

Insomnia related to another mental disorder

Hypersomnia related to another mental disorder

23
Q

Sleep disorder due to a general medical condition

A

Insomnia type
Hypersomnia type
Parasomnia type
Mixed type

24
Q

Substance induced sleep disorder

A
Alcohol
Cocaine
Amphetamine
Caffeine
Sedative, hypnotic, anxiolytic
25
Q

4 features of Narcolepsy

A

EXCESSIVE DAYTIME SLEEPINESS
CATAPLEXY
HYPNAGOGIC HALLUCINATIONS
SLEEP PARALYSIS

26
Q

prevalence of narcolepsy

A

Prevalence - 0.02-0.05%
Israel - 0.002%
Japan - 0.18%

27
Q

nacolepsy symptoms

A

Symptoms represent REM sleep components intruding into wake
cataplexy - REM sleep atonia
sleep paralysis - REM sleep atonia
hallucinations - intrusion of dreams
REM appears at sleep onset (and in MSLT)
(Day time sleepiness- cant resist the urge- sleep attacks – feel good afterwards
Catalexy- loss of skeletal tone in response to strong emotion- happinss normally- had drop- wek at knees- or severe complete loss of muscle tone
Hallucntions?
Paralysis- woken up but unable to move)

28
Q

Orexin

A

Orexin is involved in controlling sleep-wake and NREM-REM sleep transitions.
Orexin signalling is altered in Narcolepsy
Narcolepsy often develops in the teens/20’s following an illness/occasionally vaccination indicating an auto-immune component.

29
Q

Narcolepsy diagnosis

A

abnormal immune function ~ HLA subtyping
PSG (short SOL, short REM latency, increased wake)
MSLT (rapid sleep onset, REM onset)
(Chromosome 6
15-30% people have gene mutation
HLA gene mutation
Associated with autoimmune disorder
But not all people with narcolepsy have it
Not fully understood yet
Rem sleep very short
Increased wakefulness in sleep compared to normal)

30
Q

Sleep Apnea

A

APNEA = cessation of airflow
HYPOPNEA = reduction in airflow
Central sleep apnea = absence of ventilatory effort
Obstructive sleep apnea (OSA) = ventilatory effort + closure of upper airway
Prevalence is ~10-20%. Higher in males and older individuals
(Excessively sleeping during the day, no problem going to sleep
Reduce in airflow
2 forms: central sleep apnoea: body doesn’t even try to breath
Obstructive- trying to breath but closed up
Men with heart failure)

31
Q

Obstructive Sleep Apnea (OSA)

A
-SYMPTOMS
chronic loud snoring
gasping and choking episodes during sleep
excessive daytime sleepiness
cognitive difficulties
- SIGNS
obesity, especially around the neck
systemic hypertension
nasopharyngeal narrowing
32
Q

Consequences of OSA

A
Repeated arousals
Disruption of normal sleep architecture
cardiac consequences
depression / irritability
excessive sleepiness
sexual dysfunction
learning / memory difficulties
33
Q

Sleep Apnea (OSA) - Treatment

A
-BEHAVIOURAL
weight loss (including exercise)
avoidance of alcohol/sedatives before bedtime
avoidance of supine sleeping position
 -NASAL  CPAP
non-invasive
short term efficacy
Patient compliance variable (mostly quite poor)
34
Q

Sleep Apnea (OSA) – Treatment 2

A
ORAL / DENTAL DEVICES
useful in mild cases     
OXYGEN
SURGERY
invasive
not uniformly effective + risk
(Oral- only successful in 50% and need to invest 6 months 
Sugery- 50% successful and very painful )
35
Q

Parasomnias

A
Unpleasant/undesirable behaviours or experiential phenomena that occur during the sleep period.
NREM parasomnias (arousal disorders) spectrum:
36
Q

types parasominas

A
-Bruxism/
confusional arousals
-Sleep Talking
-Sleep Walking/
Sex/
Eating
-Sleep Terrors
37
Q

General Features of Arousal Disorders

A
  • Occur in association with an arousal from SWS
  • Mental confusion and disorientation
  • Relative non reactivity to external stimuli
  • Poor response to efforts to provoke behavioural wakefulness
  • Retrograde amnesia for the event
  • Only fragmentary or no recall of dream mentation
38
Q

General Features of Arousal Disorders continued

A

-Common in childhood
-Triggers: fever, sleep deprivation, alcohol, other sleep disorders.
-Sleep Walking
-Calm or agitated
-Prevalence: children 1%-17%, adults 4%.
-Sleep Terrors
-Screaming, Panic, Fear, motor activity (injury)
Inconsolable

39
Q

Treatment of Arousal Disorders

A

-Children:
Considered a natural feature of sleep.
In most instances they should not be treated as the events will cease with development.
-Adults:
Reassurance and avoidance of triggers adequate in many cases.
Tricyclic antidepressants and benzo’s can be effective.

40
Q

Delayed Sleep Phase Syndrome

A
  • Seen in children of all ages, but is a prominent feature of adolescence.
  • Difficulty of falling asleep at expected bedtimes.
  • Late (but consistent) time of sleep onset.
  • Difficult to awaken at desired time.
  • Normal sleep on delayed schedule