Neuro 15: Consciousness and sleep Flashcards
Define sleep
Stereotypic or species-specific posture
Minimal movement
Reduced responsiveness to external stimuli
Reversible with stimulation – unlike coma, anaesthesia or death
What tells you about sleep
EEG, EOG and EMG (muscle tone)
How does EEG, EOG and EMG change in stage 1&2 NREM, stage 3&4 NREM and stage 5 (REM)
EEG slows in stage 1&2 but increases a lot in 3&4, and is slow in REM
EOG is much slower in NREM 1&2, but like awake in 3&4 and very high peaks in stage 5 (rapid eye movement so EOG is going to be high!)
EMG reduces 1-4 and is almost nothing in REM… stops you acting out your dream
T/F REM is only time you dream
F… also during other stages but maybe less
How long is the sleep cycle and what is it made up of
Takes 90 minutes, goes through stage 1-5…. earlier on in sleep, NREM stages take up more time in the cycle
What is like EEG like in REM sleep
More like awake compared to stage 3/4
As well as EEG/muscular change, what other phsyioligcalt changes occur in sleep
Heart rate and respiratory changes— both reduce from stage 1-4, but increase into REM sleep and fluctuate a lot in REM
What controls sleep
Reticular activating system (brainstem systems which project fibres onto cortex, hypothalamus and thalamus)
t/f RAS allows for consciousness
True… kind of…. it’s necessary for consciousness but alone is not sufficient…. it’s like a dial, but it gates the activity of the cortex
Which brain areas promote wakefullness and sleep
wakefulness: lateral hypothalamus (orexin)
sleep: ventrolateral preoptic nucleus (in anterior hypothalamus)
Interaction of hypothalamus with the RAS
Orexin based lateral hypothalamus activates the recticular activating system
but the ventrolateral preoptic nucleus inhibits it (GABA)
How does the suprachiasmatic nucleus impact on sleep
It synchronises sleep with falling light levels….
CIRCADIAN SYNCHRONISATION of sleep/wake cycle.
It interacts with the hypothalamus (both the lateral nucleus, and the ventrolateral preoptic nucleus) and the RAS and with the pineal gland to release melatonin….
Linked to retina
Effects of sleep deprivation
Psychiatric and neurological together- Sleepiness, irritability, stress, mood fluctuations, depression, impulsivity, hallucinations
Neurological- Impaired attention, memory, executive function
Risk of errors and accidents
Neurodegeneration (?)
Somatic-Glucose intolerance Reduced leptin/increased appetite Impaired immunity Increased risk of cardiovascular disease and cancer Death
t/f sleep loss affects brain activation on fMRI
T
How can is sleep regulated (i.e. what can change if you have sleep loss)
Reduced latency to sleep onset
Increase slow wave (NREM) sleep as a proportion of sleep if you missed this
Or increase REM sleep after selective REM sleep deprivation
Function of sleep
Restoration and recovery – but active individuals do not sleep more
Energy conservation – 10% drop in BMR – but lying still is just as effective
Predator avoidance – but why is sleep so complex?
Specific brain functions – memory consolidation, …
When do dreams most often occur
REM sleep (but can be both), and more easily recalled then
What area of brain active in dreaming
Limbic system>frontal lobe
More about emotion than reality
Function of dreaming
Safety valve for antisocial emotions
Disposal of unwanted memories
Memory consolidation
Outline insomnia causes
Most transient cases
physiological: sleep apnea, chronic pain
brain dysfunction: depression, fatal familial insomnia (caused by pryon protein like CJD) or night working
Outline treatment of inoomnia
sleep hygiene, hypnotics (most enhance GABAergic circuits e.g. tamazepam or zopiclone) and sleep CBT
What is narcolepsy
Falling asleep repeatedly during the day and disturbed sleep during the night
What is hypersomnia
Too sleepy in the day…
due to arousal in the night disrupting sleep wake cycle:
- sleep apnea
- anxiety
Differentiate the type of disease of narcolepsy compared to insmnia
narcolepsy is a disease of the actual sleep/wake pathways (primary), whereas insomnia the pathway is probably fine and it’s other factors affecting this pathway
What is cataplexy and when does it occur
In narcolepsy
sudden, brief loss of voluntary muscle tone, often triggered by strong emotions e.g. laughter
T/F in narcolepsy because of the disturbed sleep, REM and NREM sleep are comensated depending on which you have less of
F: there is Dysfunction of control of REM sleep
Narolepsy is caused by what
Deficiency of orexin (=hypocretin)
What can shift work lead to
physiological processes to become desynchronised
sleep disorders, fatigue and an increased risk for some conditions such as obesity, diabetes and cancer
Is sleep a consequence or cause of neurological disease
Could be either realy
Definiton of consciousness
the state of being aware of and responsive to one’s surroundings
Elements of conscioussness
Level, content, self
Classify following in terms of VIGILANCE (awake behaviour, eyes open) and AWARENESS (level/content of consciousness…. richness of experience):
Coma General anaesthetic Locked in syndrome Veg state Dementia
Coma, very low for both
General anaesthesia similar to coma but could have tiny bit more awareness
Locked in high awareness and high vigilance (just under conscios)
Veg state- high vigilance but very low awareness
Dementia/minimally conscious state= fairly normal vigilance, but reduced awareness
Why does RF project to cortex
allowing that sensory signals to reach cortical sites of conscious awareness such frontoparietal cortex
Types of neurotransmitters in the RAS
RF projects to the hypothalamus, thalamus and the cortex
Ventral tegmental Area (dopaminergic neurones)… this relates to reward pathway mesolimbic…. VTA in midbrain
pons- Locus coeruleus (noradrenergic neurones)… this relates to pain
t/f consciousness arises from a partcular part of the brain
f.. it emerges as a result of cortico-thalamic transmission
What is important for consciousness
dynamics of neuronal activity– integrated and differentiated
HIGH INTEGRATION, LOW DIFFERENTIATION= generalised seizure (all areas of the brain doing the same thing)
LOW INTEGRATION, HIGH DIFFERENTIATION= e.g. callosotomy… areas doing different things but none of this linked with each other
How can consciousness be measured
Give TMS and then meausure activity after with EEG
You can measure how well that induced TMS travels across to other brain regions.
In an awake individual, this signal will spread across brain regions (high integration) but in asleep will not (low integration)
Can also see if the different brain areas to which the signal spreads process the signal differently (i.e. high differentiateion, heterogenous) or in the same way (i.e. low differentiation)
Can quantify this to give PCI…. pertubational complexity index (PCI)
What is ‘neural correlates of consciousness’ referring to
The minimum neuronal mechanisms jointly sufficient for any one specific conscious experience.
Primarily localized to a posterior cortical hot zone that includes sensory areas (Koch et al., 2016)
i.e. where is the brain region that corresponds to a particular experience of consciousness
3 disorders of consciousness
Coma- Absent wakefulness and absent awareness,
Vegitative state- Wakefulness but absent awareness
Minimally conscious state- wakefulness with minimal awareness
T/F brainstem death is a disorder of consciousness
F… neither is locked in syndrome
Feedforword processing vs top-down recurrent processing
feed forward=subliminal or non sonscious
Top dorwn is conscious access
We can have top-down and bottom-up processes – there are non-conscious processes that bubble up to conscious access.
State the components of a coma
- can’t be awakened
- doesn’t respond norally to painful stimulu, light or sound
- Lacks normal sleep wake cycle
- Does not initiate voluntary actiond
Which area of brain might be affected in:
vegetative state
locked in syndrome
brainstem death
vegetative state=cortex/hemispheres (intact RAS)
locked in syndrome=damage e.g. to ventral pons (motor system)…. intact cortex and intact RAS
brainstem death= irremediable damage to brainstem
In which types of strokes may visual neglect occur
parietal lobe
Differentiate hemianopia from visual neglect
Both involve part of the world not being seen
with hemianopia this is a visual pathway problem
with visual neglect this is a higher up cortical deficit
often conflated as both can occur due to stroke
Different types of waves on EEG and what EEG monitors
Monitors level of arousal
BATD: from awake to sleep
Delta= in sleep. Up to 4Hz
Theta= 4-8 Hz.
Alpha=8-13Hz
Beta=13-30 Hz (normal waking consciousness)
40Hz (gamma range) associated with creation of conscious contents via THALAMO-CORTICAL FEEDBACK LOOPS
When might alpha waves occur on ECG
When drowsy or relaxed
When might theta waves occur
Stage N1 sleep
When might delta waves occur
Stage N3 sleep
When might you get sleep spindle waves on EEG
Sumarise the EEG seen during different levels of conscioussness
stage N2 sleep
B: Awake A: drowsy, relaxed T: N1 sleep Spindles: N2 sleep D: N3 sleep
REM sleep is fast and random EEG.
What are the components of the glasgow coma scale
1-4 for eyes
1-5 for verbal
1-6 for motor
Minimum GCS score and max
min is 3
max is 15
Causes of coma
Metabolic: Drug overdose hypoglycaemia diabetes "the failures" hypercalcaemia
Diffuse intracranial: head injury meningitis SAH encephalitis epilepsy hypoxic brain injury
Hemisphere lesion: cerebral infarct cerebral haemorrhage subdural extradural abscess tumour
Brain stem: brainstem infarct tumour abscess cerebellar haemorrhage cerebellar infarct
What is coma
Unrousable unresponsiveness
What is diffuse axonal injury
Damage to white matter tracts e.g. corpus callosum…. higher order cognitive problems due to poor integration…..
can follow traumatic brain injury (e.g. after extradural haematoma etc.)
Which types of stroke could cause coma
Bitemporal medial thalamic infarcts
or strokes to do with posterior ciruclation
Which types of lesions are dangerous due to basic functin
Posterior fossa lesions
Decorticate vs decerebrate posturing
Main difference is decorticate involves flexion at the elbow
Whereas decerebrate involves extension at the elbow and pronation
Decerebrate indicated involvement of the red nucleus and indicates event further down in the brainstem
