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MD4001 Week 4 > 8. Sleep, wakefulness and EEG > Flashcards

8. Sleep, wakefulness and EEG Flashcards

1
Q

What is sleep?

A

Easily reversible state of inactivity with a lack of interaction with the environment.

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2
Q

Difference between sleep and coma?

A

coma (depressed state of neural activity)

sleep ( variation in neural activity)

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3
Q

3 states/levels of consciousness?

A

Wakefulness – animal is alert, detects objects and pays attention to them

Core consciousness –wakefulness plus emotional responses, and simple
memory.

Extended consciousness – all of the above plus self awareness, autobiographical memory, language and creativity.

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4
Q

Suggested/possbile functions of sleep?

A

Suggested functions include the processing and storage of memories, recuperation of the bodies immune system and to conserve energy.

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5
Q

During sleep the neurons of the brain are ______, but display a different type of activity from wakefulness
The sleeping brain consumes as much _______ as the wakeful brain, and sometimes more

A

During sleep the neurons of the brain are active, but display a different type of activity from wakefulness
The sleeping brain consumes as much oxygen as the wakeful brain, and sometimes more

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6
Q

What are the two main forms of externally discernable sleep?

A

1) when the eyes move rapidly from side to side (REM sleep) or
2) when they do not (non REM, slow wave or deep sleep) however there are
other determinants also.

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7
Q

Neuronal activity during different stages of wakefulness (including sleep) can be measured using an ______________

A

Neuronal activity during different stages of wakefulness (including sleep) can be measured using an

Electroencephalogram (EEG)

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8
Q

How does the EED work?

A

Post synaptic activity of individual neurons NOT picked up
Post synaptic activity of
synchronised dendritic activity
CAN be picked up.
Synchronisation is either by neuronal interconnections or by pacemaker
The more neurons that are SYNCRONISED, the BIGGER the peaks on the EEG. Lots of little wave means no syncrony but lots of activity still

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9
Q

Purpose of EEG?

A

Recordings allow the separation of REM and non-REM sleep.
Also for the subdivision of NREM sleep into its further 4 stages of sleep (each with own characteristic brain wave pattern)

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10
Q

EEG reading when awake?

A 
Eyes closed, alpha High frequency (8- 13Hz), and
low amp (50-μV)

Eyes open beta waves (14-60Hz, faster) waves of activity .

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11
Q

Stage 1 of sleep EEG reading?

A

Stage 1: Duration = 1-5min,
easily roused. Slow rolling eye movements.
Some theta waves (SLOWER frequency (4-7Hz) & HIGHER amplitude) waves

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12
Q

Stage 2 of sleep EEG readings?

A

10-15mins duration, have K complexes (short lived but high amplitude) & sleep spindles (8- 14Hz bursts, fast bursts).
No eye movement but body movement remains possible

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13
Q

Stage 3 of sleep EEG reading?

A

Stage 3: Few mins duration.
Has slower frequency
delta waves (inc amplitude) appear.
Harder to rouse. Few spindles.

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14
Q

Stage 4 of sleep EEG reading?

A

Deepest sleep, hardest to rouse. >50% EEG waves at 2Hz & high amplitude (>200μV) called delta waves. In synchrony.
Heart rate & BP lower, movement 15-30 min period

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15
Q

What is the EEG reading of REM sleep?

A

Fast beta waves and REM.

Subject easier to rouse than in stage 4. Dreaming, recalled, plus low muscle tone

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16
Q

Cycle of sleep stages?

A

From drowsy to deep sleep takes about 1 hour
Duration of REM sleep is variable.
On average there are 5 REM sleeps per night.
Minimum time between REM sleeps seems to be about 30min.

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17
Q

What is the cycle of stage in a typical nights sleep?

A

Made up of several cycles through the five stages of sleep.
Note: Stage 4 is only reached in the initial cycles thereafter the deepest sleep attained in stage 3.
Note also that time spent in REM increases.

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18
Q

Features of NREM sleep:

  • Movement/breathing?
  • Wave syncronisation?
  • Types of alpha wave subtype?
A

x
1. As the subject goes deeper into non-REM sleep, movement and breathing is depressed however movement is still possible.

  1. At stage 4 the brain shows slow waves of synchronised firing of large groups of neurones.
  2. Alpha wave subtypes:
    -visual cortex (classic type)
    -sensory motor cortex (mu type)
    -auditory (kappa type)
    Occipital is the most prominent
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19
Q

What is the reticulum formation>

A

Is a diffuse collection of at least 100 networks of neuromodulatory neurones spanning all three divisions of the brainstem
it is not homogeneous
Diverse function: posture, respiration, heart rate and sleep/arousal

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20
Q

Inputs and outputs of the reticular formation?

A 
Inputs:
the cerebra (collaterals from the corticospinal pathways) the visual and auditory systems
sensory spinal systems
the cerebellum
certain brainstem nuclei

Outputs:
the thalamus,
the hypothalamus some brainstem nuclei the cerebellum
the spinal cord and the cerebral cortex

21
Q

How is the RF involved in sleep?

A

There are Arousal centers in the brainstem which project fibres to a wide variety of structures in the brain including the thalamus.

22
Q

Different physical characteristics apart in REM sleep?

A

Rapid eye movements in REM
Muscle activity of the head at it’s highest
Increases in HR
Increases in neural activity
Increases in respiration (so o2 consumptions
Association with penile erection.

23
Q

How does eye movement in 1st stage NREM sleep compared to REM?

A

1st stage NREM: Slow and rolling

REM: Rapid

24
Q

REM sleep characteristics:

  • Brain activity?
  • Dreaming?
  • Body movement?
  • inhibition of?
  • Effect of metabolism on body temp?
A
  1. The brain is very active and is most likely to be dreaming (95% likelihood), but the body is effectively paralysed.
  2. One source of activity is concerned with inhibiting motor output (excepting breathing and eye movement)
  3. Body temperature drops as metabolism is inhibited
25
Q

How is the reticular formation involved in sleep?

A

The release of NE, serotonin and ACh from neurones of the RF are required for consciousness. Each with their own projection system.
These NTs project to a variety of structures in the brain including the thalamus. The thalamus is the common synaptic target for all the systems and is richly connected to cerebral cortex

Note: Lesions of these projections results in stupor or coma

26
Q

Result of thalamus lesions on EEG waves?

A

Lesioning the thalamus abolishes (most) synchronous EEG waves

27
Q

Rhythmic stimualtion of the thalamus induces stage __ sleep?

A

stage 4 sleep (high amplitude low frequency waves).

28
Q

Which 3 structures are interconnected to control wakefulness?

A

1) Reticular formation (in the midbrain of brainstem)
2) Thalamus
3) Cerebral cortex

29
Q

Effect of reticular formation excitation and inhibition on arousal?

A

EXCITATION

  1. Excitation of the reticular formation
  2. Depolarisation (excitation) signal to the thalamus
  3. Thalamus projects a non-rhythmic output to cerebral cortex
    - -> Increased arousal (alpha waves -> beta wave)

INHIBITION

  1. Inhibition of reticular formation
  2. Hyperpolarisation (less excited) signal to the thalamus
  3. Thalamus projects a more rhythmic output to cerebral cortex
  4. Slow EEG waves in cerebral cortex detected.

I.e. RF activity = arousal

30
Q

What causes synchronised cortical slow waves in NonREM sleep?
Resultant effect of sensory input?

A

Hyperpolarised thalamus and decreased activity in the arousal centers of the reticulum.
As thalamic cells hyperpolarise further, they develop slow wave rhythmicity (due to thalamic interconnections) which serves to block ascending sensory input.

This rhymicity is transmitted to the cortex and due to a strong reciprocity between these two areas, the waves becomes synchronised across the cortex.

31
Q

What is the cause of sleep spindles and K complexes? In which sleep stages are they found?

A

Sleep spindles and K complexes are caused in part by the inherent rhythmicity of thalamic neurons as they hyperpolarise due to reduced ascending reticular formation input. Seen in in Non REM stage 2 sleep.

32
Q

Control of the descending motor output of the cortex during REM sleep?

A

During REM there is a high descending motor output which is blocked by the brainstem (locus coeruleus).
Note: Exception to the eyes, middle ear and resp centres.

Mechanism: Cholinergic neuroens from reticular formation excite thalamus and provide descending inhibitory stimuli to motor pathways.

33
Q

What are the 2 pathways of arousal?
(Pathways 1, thalamic gating.
Pathway 2: direct excitation)

A

PATHWAY 1
Dependent on thalamic gating.
Midbrain reticulum projects cholinergic excitation onto the thalamus. Only strong signals pass through.
Pathway is nearly always ON. Only inactive in NREM sleep These inputs facilitate thalamo- cortical transmission when awake.

PATHWAY 2:
Direct cortical excitation. 
Is inactive during REM, come firing in NREM and most active when awake. 
Note: Lesions cause extreme sleepiness and coma.
Input from:
-Lateral hypothalamus orexin 
or 
-Basal forebrain containing GABA or ACh
34
Q

Where is the centre of NREM sleep promotion?

A

Ventrolateral pre-optic nucleus (VLPO)
Output to:
1. inhibitory projections to all major direct arousal centres + is active during sleep.
2. Neurons the lateral hypothalamus orexin
3. reticular formation cell groups.

Input:
-Inhibited by projections from arousal centres (Na, GABA, 5-HT i.e. serotonin)

35
Q

What promotes REM sleep?

A

eVLPO nucleus

extended ventrolateral pre-optic nucleus

36
Q

Where are the orexingeric neurons?

A

Lateral hypothalamus

37
Q

Orexin is pivotal in the sleep/awake switch circuitry and adds stability to the mechanism. Why?

A

Orexinergic neurons are normally active during wakefulness (lateral Hypothalamus)
These neurons project to the cerebra, the arousal nuclei and the VLPO (inhibit).
By these neurons enhancing the arousal nuclei they cause indirect inhibition of the VLPO via reciprocal inhibition pathways between the arousal centres and the VLPO.

38
Q

eVLPO and VLPO promote..

A

REM and NREM sleep.

39
Q

What is the result of 1. Orexin release and 2. VLPO firing in the swtiching between arousal and sleep?

A
  1. Orexin release
    When Orexin is released it stimulates the arousal centres and so causes inhibition of the VPLO. As long as Orexin is released the balance is shifted towards wakefulness.
  2. VLPO firing
    When the VPLO begins to fire, it inhibits both the orexinergic neurons and the arousal centres.
    This……
    -Removes the inhibition of VLPO by the arousal centre and
    - Cuts off the excitation from the orexinergic neurons thus pushing the balance quickly towards sleep.
40
Q

What is the SCN?

A

Suprachiasmatic nucleus located in the hypothalamus

41
Q

What does the suprachiasmatic nucleus control?

A
  1. Circadian cycles

2. Physiological and behavioural rhythms occurring over a 24-hour period, inc sleep/wake cycle

42
Q

Why is the circadian cycle re-set? and how?

A

In humans “free running” of the SCN clock gene gives a periodicity of about 24.5 hours
This cycle is therefore re-set each day by a variety of zeitgebers (time givers in German), the most dominant of which is the light dark cycle.

(Receptors in the retina (not rods or cones) containing melanopsin react to light and synapse directly onto the SCN resetting the clock gene.)

43
Q

Name the 2 forms of permanent insomnia?

A
  1. Rare inherited neurodegenerative process affecting the thalamus and the rostral hypnogenic (sleep) centres.
  2. Stroke resulting in blockade of the basilar artery. These patients are typically suffering from locked in syndrome and have control only over ocular movement.
    If the resultant neuronal damage includes the loss of the pontine hypnogenic centre the result can include insomnia.
44
Q 
Narcolepsy:
Age affected?
Cause?
Presentation?
Why?
A

Occurs around age 20-30yrs•

Onset due to specific loss of the Orexin containing neurons in the Lateral Hypothalamus. An inherited auto immune condition linked to chromosome 6.

Presentation:

  1. Repeatedly falling asleep during the day, regardless of current activity
  2. Limb weakness during emotional episodes (mild to extreme cataplexy)
  3. Night time or morning wakening accompanied by muscular paralysis (sleep paralysis).
  4. Vivid dream recollection just prior to wakening

Why?
Narcoleptics pass directly from awake to REM sleep (no VLPO control means no NREM)
Cataplexy and sleep paralysis caused by pontine influence (locus coeruleus) on muscle tone during REM.

45
Q

What is cataplexy?

A

Limb weakness during emotional episodes

46
Q

What is REM sleep behaviour disorder?

A

Occurs during REM sleep and happens when the descending pontine reticular formation fails to properly immobilise the body. Characterised by rapid/violent movement and behaviour

Common in males

47
Q

What is somnambulance?

A

During non-REM sleep. Often the same as REM sleep behaviour disorder but there is no memory of the dreams enacted. Occurs in NREM sleep which is why there is no memory, and happens when the midbrain reticular formation fails to paralyse the body

48
Q

Symptoms of sleep deprivation?

A

Depression which can cause the subject to be concerned about trivial illness/pain
Muscle aching
Clumsiness
Absent mindedness

MD4001 Week 4 (9 decks)

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