arousal and sleep

8/2/2019 Arousal and Sleep

1/72


2/72

AROUSAL

Arousal is a physiological and psychologicalstate of being awake

It involves the activation of : 1.reticular activation system

2.autonomic nervous system

3.endocrine system


3/72

Actvation of these 3 systems

leads to 1.Increase heart rate

2.Blood pressure

3.Sensory alertness

4.Mobility

5.Readiness to respond


4/72


5/72


6/72


7/72

Arousal system

1.Originates from brain stem with connectonsextending throughout the cortex

2.Connections are based on neuro transmittersA.Acetyl choline

B.Norepinephrine

C.DopamineD.serotonin


8/72


9/72

Arouasl is imporatant in

regualting. 1.consciousness

2.Attention

3.Information processing

4.Mobility

5.Flight or fight response

6.Sexual activity


10/72

Yerkes-Dodson law

Shows the relationship between arousal and

performance


11/72
http://images.google.com/imgres?imgurl=http://www.lboro.ac.uk/departments/hu/groups/sleep/sleep.jpg&imgrefurl=http://www.lboro.ac.uk/departments/hu/groups/sleep/telegr.htm&h=514&w=634&sz=138&hl=en&start=1&tbnid=3Se511XYAjcwHM:&tbnh=111&tbnw=137&prev=/images?q=sleep&gbv=2&ndsp=18&svnum=10&hl=en&sa=N


12/72

SLEEP

Sleep is as critical to survival as eating&drinking

It has an on signal & offsinal

Sleep is not a unitary process

Circardian rhythm

Sleep deprivation results in hallucinations

Signals thought to be initiated internally Manipulation of external cues has little effect

on the sleep awake cycle
http://images.google.com/imgres?imgurl=http://www.lboro.ac.uk/departments/hu/groups/sleep/sleep.jpg&imgrefurl=http://www.lboro.ac.uk/departments/hu/groups/sleep/telegr.htm&h=514&w=634&sz=138&hl=en&start=1&tbnid=3Se511XYAjcwHM:&tbnh=111&tbnw=137&prev=/images?q=sleep&gbv=2&ndsp=18&svnum=10&hl=en&sa=N


13/72

Blood factor & sleep

Sleep served torestore neural energy

depleted by fatigue


14/72

Toxine theory & sleep

During waking hours fatigue toxinsaccumulate and when these toxins exceed agiven optimum level they trigger sleep

It is said that fatigue signal is in blood


15/72

Neural factor and sleep:

( study by Bremer in 1935) Surgically removed sensory inputs to the

brain and observed resulting EEGs recorded

from cortex

Encephale isole-cut between brain stemand spinal cord

1.all sensory input was eliminated from belowneck

2.EEG activity still revealed normal sleep wake patterns


16/72


17/72

Cerveu isole

1.Upper part of the brain stem and mid brain

level2.Optic and olfactory nerves left intact

3.Cut indeed abolish waking activity

4.Thes e indicate that sleep wake cycle dependsupon neural input from sensory systems


18/72


19/72

Cut at midbrain level reduces the amount ofsensory stimulation reaching the cortex

It detaches connection from other parts ofbrain stem


20/72

Wake center

Donald Lindsley-midbrain reticular lesion-abolished wakefulness

Moruzzi& magoun

electrical stimulation of

midbrain reticularformation wakefulness


21/72


22/72

Wake center

1.sensory input is not necessary to maintainsleep wake cycle

What is signal? Wake center

1. midbrain reticular formation

2.center turns wakefulness on3.when damaged it turns

wakefulness off


23/72

The neural mechanism of

sleep Michael Jouvet

1.passive theory-sleep is a passive

phenomenon ,like slowing a car Sleep is caused by activity in the wake center

dying out because of fatigue

Active theory-sleep is caused by sleep areaactively inhibiting wake area


24/72


25/72


26/72

Sleep circuit

In order to be a sleep circuit it should ful fill

It must produce sleep when stimulated

Must produce wakefulness when removed Hess & others found that low frequency

electrical stimulation in the medial thalamus-sleep

Subsequent studies-sleep control notconfined to the medial thalamus only


27/72

Other areas involved in

sleep 1.non specific projection nuclei of thalamus

2.preoptic area in the hypo thalamus

3.several areas in the lower brain

A. pontine reticular formation

Raphe nucleus

Stimulation in all these areas -sleep

Lesion in preoptic area - insomnia


28/72


29/72

Sleeping and EEG pattern

Sleep is not an unitary process

It has different depths and stages

Analysis is possible by distinct EEG activity


30/72


31/72


32/72


33/72


34/72


35/72

awaken brain -EEG pattern

awaken brain

1.show very fast activity 20-25 cps (beta waves)

2.awaken neurons are active in a randomfashion

3.The fluctuations in voltage are so out of phasethat they tend to cancel one another out andproduce desynchronized low amplitudewaves


36/72

Brain falls asleep

Pattern of activity undergoes a pronouncedtransformation

Waves become much larger and much slower Moves from 8 to 10 per second (alpha)

As person relaxes 2 or 3 cps (delta)

Then the person falls into deep sleep


37/72

Slow wave sleep -80% of sleeping hours

20%-paradoxical sleep

Paradoxical sleep-brain shows waking state

even though body remains asleep


38/72

During paradoxical sleep there is fast,desynchronized,low amplitude activity incortex and most of subcortex

Exception is hypocampus which shows aslow regular rhythm known as theta waves

The body is even more relaxed during

paradoxical sleep than during slow wavesleep,as evidenced by the reduction in muscletone


39/72

Its very harder to wake a person fromparadoxical sleep than from slow wave sleep


40/72

Dreaming & EEG.

During paradoxical sleep that dreamingoccurs(Nathaniel kleitman&collegues)

Dreaming is marked by fast low amplitudeEEG activity in the cortex

Eye balls move during dreaming

Rapid eye movement sleep_ the stage ofsleep where eyeball move as if a person werefollowing a moving object with his eyes


41/72

Most people awakened during REM sleepreport dream

This does not mean that dreaming onlyoccurs at paradoxical sleep

Dreaming also occur during slow wave sleep


42/72

Musle relaxation

It may serve as an important safety device

Apparently the limb body during paradoxicalsleep reflects an active inhibitory mechanismin the brain that may protect determinesfrom acting out their dreams


43/72

Behavioral nightmares

Jouvet damage to locus of coeruleusproduce behavioral night mares

The eyes of the cat in the middest of thisnightmare are close d and its behavior has norelationship to external events

The cat becomes extremely active

It hisses and claws as if acting out a dream

N l t l f d i l l


44/72

Neural control of paradoxical sleep

and slow wave sleep-Jouvet

Jouvet concentrated onthe neural control of sleep

He given special attentionto brain stem

His subjects were cats ascats shows both types ofsleep


45/72

Paradoxical sleep-Jouvet

During paradoxical sleep cats show uniquespike ie;patterns reffered to as PGO spikes

According to Jouvet

Paradoxical sleep is controlled by pontinereticular formation (nucleus reticularis pontiscaudalis)

Lesion abolish REM sleep

Stimulation induce REM sleep


46/72

Slow wave sleep

Slow wave sleep is controlled by the area inbrain stem raphe nucleus

Lesion - abolish slow wave sleep

Stimulation - induce slow wave sleep

Slow wave sleep depends on both raphenucleus & its interaction with the cortex

Paradoxical sleep primarily depend upon thepontine reticular formation

Raphe neucleus and reticualr formation


47/72

Raphe neucleus and reticualr formation


48/72

Cortex and slow wave sleep

Animal CNS is incomplete at birth ,show onlyparadoxical activity during sleep

Paradoxical activity in the brain stem

As cortex develops slow wave activityappears during sleep

Eg:pigs neural development including cortexis virtually complete at birth

Pigs show both paradoxical sleep and slowwave sleep at birth


49/72

Chemical codes for sleep

Raphe nucleus-serotonin(neuro transmitter)

Serotonin control slow wave activity

Elevating serotonin level will result inincreased sleep time at day time for thenormal animals

Elevated serotonin level but lesion raphenucleus serotonin compensate for lesion andrestore normal slow wave activity.


50/72

Pontine reticualr formation

and chemical codes Pontine reticular formaton (areas related with

paradoxical sleep)- contain norepinephrine

Elevating norepinephrine increased daytime paradoxical sleep

Elevating norepinephrine by lesioningpontine reticuar pormation-compensate for

pontiner eticular formation &restoresparadoxical sleep

Interaction between slow wave


51/72

Interaction between slow wave

sleep &paradoxical sleep

Both sleeps are under the control of differentneural areas and chemical processes

Paradoxical sleep depends n some minimalamount of slow wave sleep

Eg;eliminating slow wave sleep by lesioningRaphe nucleus abolish paradoxical sleep

Lesioning of pontine reticular formation doesnot have any effect upon slow wave sleep


52/72

Conclusion -Jouvet

He arrived at a hypothesis to explain theinterrelationship between the 2 types of sleep

Postulated that during slow wave sleep serotonin metabolized

Its metabolized by the Raphe nucleus

And its break down products prime thepontine reticular formation

It release norepinephrine and produceparadoxical sleep


53/72

Complicating pictures

It is not complete explanation for sleep

Acetyl choline too has pronounced effects onsleep &wake

When acetyl choline injected into preoptic area,pontine reticular formation it affected sleep andwake

Serotonin source of slow wave sleep

Depletion serotonin level disrupts sleep

But animals recovers noramal pattern of sleepthough serotonin level remain below normal


54/72

Neural mechanism that coordinate the cyclebetween sleep and wake remain as openquestion


55/72

DREAM

Human have a strong need to dream (studies)

The function of dream is still not clear

Roffwarg has theorized that paradoxical sleep hasan important adaptive function

Stimulates neural growth during formative periods

He explained why infants show more paradoxical

sleep than adults


56/72

REM rebound-sleep experiment

An individual deprived of dreaming becomesirritable and when finally allowed to sleepshows a significant increase in paradoxical

sleep as if making up for lost dreams

The compensatory dreaming followingdeprivation is known as REM rebound

Subject behaves like a deprived organism Subjects becomes irritable &confused


57/72

They have difficulty in concentration

They undergo memory lapses

And develop strong appetite for food

Then finally allowed to sleep

They dream an abnormal amount as much as60%more than normal

Then finally returns to normal NB: (subject was awakened immediately

upon slipping into paradoxical sleep)


58/72

Developmental implications of

dreaming Children spent moretime in paradoxicalsleep than adults

Children-50%

Adults-20%


59/72

Experts studied

developmental implicationsof dreaming

Howard Roffwarg and collegues

David kretch and collegues


60/72

Howard and collegues .

Dreaming is related with mental growth anddevelopment

Evidence shows that stimulation fromexternal environment influences growthduring maturation


61/72

David kretch & collegues

Rats reared in enriched sensory environmentshow larger brains than those reared in animpoverished sensory environment.

Dreaming is a form ofself stimulation.

Dreaming promote the growth of the brainduring the early formative years.


62/72

Dreaming and mental illness

The major study is ofDement

Study was on cats

Dement injected parachlorophenylalanine &depleted serotonin(which directly initiateslow wave sleep and then paradoxical sleep)

Depletion resulted in general decrease in

sleep

Paradoxical sleep spilled over intowakefullness


63/72

First PGO spikes appeared in awaken state

2nd dream like state appeared in awaken state

Cats perked their ears &struck out at objects

that werennt there They were like hallucinating

These cats(Dements cats)didnt shown

rebound effect Human schizophrenics also dont have

rebound effect


64/72

It can be abolished by administeringchlorpromazine

Chlorpromazine is the effective medicine forschizophrenia today

Even when we cant say that shizophrenia isthe result of depleted serotonin levels in brain

Hallucinating behavior spills over to wakinghours


65/72

Role of serotonin in schizophrenia remain anopen & controversial question


66/72

Sleep disorders- insomnia

20% of US population experience sleepdisorders

Insomnia-inability to sleep

Short tern insomnia-stress,drinking ,toomuch coffee etc


67/72

prevention

Improving sleep habbits

Avoiding stimulants

Avoid taking sleepin pills

More serious insomnia is associated withpsychiatric disorders(depression)


68/72

Sleep apnea

Interrupted breathing during sleep

A person suffering from sleep apnea mayawaken 100s of times during the night

Results in no slow wave sleep &less time inREM sleep

These patients are chronically tired

in the day time and often suffer fromdepression


69/72

Sometimes sleep apnea leads to suddendeath

Airway collapses during breathing &thenblocking air flow


70/72

Restless legs syndrome

Its a common problem

Familial disorder

Unpleasant crawling

Prickling

Tingling sensations in the legs andfeet

Urge to move about for relief


71/72

Narcolepsy

Characterizd by frequent REM sleep attacksduring day time

They enter REM sleep from wakefulnesswithout going through non REM sleep.


72/72

arousal and sleep

Documents