States of Consciousness Flashcards
Describe the story of Ken Parks
Ken Parks, 1987: After seeing ‘Saturday Night Live’ he fell asleep on the couch, arose, got in his car, drove 23 km to his in-laws’ home, killed his mother in law, nearly killed his father in law. Then drove to the police and gave himself in: acquitted due to not being ‘conscious’
What are the three guises of consciousness?
A state
A ‘device’
A sensation
When is the an increase in accidents seen and why may this be?
Peak in traffic, domestic and work accidents around 16:00 (could be due to a state of absent mindedness.)
Who made the first EEG recordings from human subjects?
Hans Berger (1928)
What are one of the first things Hans noted about these EEG recordings?
Berger already noted different rhythms (from low to high frequency: delta, theta, alpha, beta, gamma), that are associated with different states of consciousness / sleep / alertness
How is EEG selective? Be specific
The signals are coming from synchronous synaptic currents on the apical dendrites of cortical pyramidal neurons (mainly layers 2, 3). Action potentials, or activity from other neurons types, or from deep structures and nuclei is not visible in the EEG.
What is meant by the term polysomnography?
Simultaneous recording of EEG (brain), EMG (muscle tone) and EOG (eye movements)
How do polysomnography recordings differ when awake vs asleep? (3)
Awake- Low amplitude, High frequency EEG
Saccadic eye movements
Muscle tone
Asleep- High amplitude, low frequency EEG
No saccadic eye movements
Low muscle tone (low EMG), paralysis
Check nots for waves
How are polysomnography recordings for REM sleep?
Low amplitude, high frequency, EEG
Saccadic eye movements
Low muscle tone (low EMG), paralysis
Describe normal sleep patterns
Successive sleep stages in cycles of about ninety minutes. Deep stages in early part of the night. REM sleep towards the end. Goes from stages awake-4-1-4-1-3-1-2-1-2-1-awake in chart (see docs)
Name 4 sleep disorders
Sleep paralysis
Sleep violence
Narcolepsy
Sleep walking
Describe the polysomnography recordings of sleep paralysis
muscle tone stays flat because of muscle paralysis, yet person awake; EEG and EOG like awake
Describe sleep violence
REM sleep without muscle paralysis: violent movements, acting out dreams
What happens with narcolepsy?
sudden REM onset (see docs for brain waves)
What stage of sleeping does sleepwalking usually occur?
Happens in the deepest stage (stage 4)- absent of dreams
What kind’ve behaviour can be exhibited during sleepwalking?
- Walking around house
- Preparing meals
- Urinating(in closet…)
- Driving
- drawing etc …
Typically ‘automated’ behaviour.
Who is sleep walking most often seen in the population?
Young children
What percentage of the population sleep walks
1% - 5% of the population
What can cause sleep walking?
Stress, worries,
sleep,
deprivation
Describe the polysomnography recordings of sleep walking
There is a sudden rise in EMG and EOG activity while the brain (EEG) stays in deep sleep mode
What part of the brain is deactivated during sleep compared to being awake?
Frontal cortex
What brain area is critical for maintaining the conscious state? What is it and what does it do?
Brain stem reticular Activating system (RAS) also (medial) Reticular formation
A set of nuclei in the brain stem, sends fibres to the cortex with modulatory neurotransmitter
How does the RAS project to the cortex? Give an example
Either directly, or via the intralaminar nuclei of the thalamus
For example, the Locus Coruleus projects fibres to the cortex releasing the activating (non-synaptic) neurotransmitter nor-epinephrine
How were the functions of the Medial Reticular Formation (MRF) studied? What were the results?
Effects of electrical stimulation of Medial Reticular Formation (MRF) in anesthetized cats.
- More high frequency EEG (gamma) relative to low frequency EEG (delta)
- Firing rates variable
- Oscillations go up, more high frequency oscillations
- Synchrony goes up
Cat ‘wakes up’
What other functions does this MRF carry out?
Thalamus gates the information from the senses to the cortex. The brainstem MRF modulates that thalamic gating: from ‘arousal’ to ‘sleep.’
How can this thalamic gating by the MRF occur?
Sensory information (eye, ear, paw) is transferred to the sensory cortex (PC) via the Thalamic ray cells (Th relay). Reticular Nucleus of the thalamus (ThR/ nRt) inhibits this transfer (decrease of sensation). MRF inhibits this inhibition, i.e causes stronger inputs from senses to cortex.
Look at document for diagram
How else are signals from the thalamus to the sensory cortex modulated? Describe this mechanism
An additional mechanism by which the signals from the thalamus to sensory cortex are suppressed is formed by thalamo-cortical oscillations: Cortex, Thalamus and RNT form a reverberatory circuit that generates different rhythms. Slow rhythms prevent sensory inputs from periphery to reach cortex. These slow oscillations are disrupted by MRF stimulation (so that the activity goes back to high freqs, and signals can get through)
Therefore, in what three ways can the Brain stem MRF increase activation in the cortex?
- Acts on the cortex directly via activating neurotransmitters
- Disinhibits the inhibitory influence of the reticular nucleus of the thalamus
- Disrupts low frequency thalamocorticaloscillations that prevent transmission of sensory information
How was TMS used to examine the effect of sleep on the cortex?
Studied disconnection: A TMS pulse (yellow +) is given, to locally give an impulse of brain activity. EEG is measuring over the rest of the brain, to see how far this activity spreads. This is repeated at different sites. The goal was to see how far the electrical pulse would still spread while participant is asleep.
What were the results of this study that examined the effect of sleep on the cortex?
Most spread during wakefulness, much less during dreaming and even more less during deep sleep.
How can the extent to which the cortex is ‘disconnected’ during sleep be quantified?
Non-REM Sleep and anesthesia (Midazolam, Xenon, Propofol) are characterized by lower connectivity index (PCI) than the awake state.
How can the extent of connectivity in conscious and unconscious states be described in a descriptive manner?
The conscious state is characterized by intense communication between regions, while unconscious states are characterised by regions working ‘on their own’
To what extent does consciousness as a state (level) correlate with consciousness as an experience?
Normally, consciousness as a state (level) and consciousness as an experience (content) correlate with each other. But there are exceptions- REM sleep, disorders of consciousness
Describe five disorders of consciousness
Brain death- No reaction, no pupil response & reflexes, no EEG
Coma-no reactions, no sleep wake cycle, often life support needed, but reflexes work.
Vegetative state- sleep wake cycle, breathing, autonomous reaction
Minimally conscious- as in VS but sometimes regains conscious reactions and communication
Locked-in Syndrome- fully awake and conscious yet unable to respond, except with eye and eyelid movements
What is (not) observed from someone who is brain dead?
An absence of cranial reflexes
What is observed in the EEG of someone who is brain dead?
Flat EEG
What is involved in a clinical examination to assess brainstem reflexes?
- Absence of grimacing or eye opening with deep pressure on both condyles at the level of the temporomandibular joint
- Absent corneal reflex elicited by touching the edge of the cornea
- Absent light reflex
- Absent oculovestibular response toward the side of the cold stimulus provided by ice water (pen marks at the level of the pupils can be used as reference)
- Absent cough reflex elicited through the introduction of a suction catheter deep in the trachea.
How do you measure EEG from someone who may be brain dead?
EEG recorded at maximal amplification, and from electrodes that are a large distance apart is completely flat
ECG or respiration artifacts may be seen
What conditions should be excluded from this test and why?
These conditions should be excluded, as they may also cause flat EEG: Intoxications, sedative effect of drugs, neuromuscular block (e.g. muscle relaxants), hypothermia, hypoperfusion (circulatory shock) and coma caused by endocrinal or infectious (septic shock) reasons.
How do you test for brain death through an SSEP?
SSEP somatosensory evoked potential - Record response of spinal cord, brain stem and cortex to electrical stimulation of the wrist. Absence of response beyond p13/n13 is sign of brain death (but make sure noise level is not making N20 invisible).
Presence of N20 is indicating cortical response and ‘good’ prognosis.
How is a coma detected?
A scale such as the Glasgow coma scale
Burst suppression EEG
What EEG signals are typical of someone in a coma?
Burst suppression EEG: flat EEG interspersed with high voltage bursts of EEG activity
Describe How the Glasgow coma scale decides whether it is a coma?
E (eye opening) Spontaneous- 4 To speech- 3 To pain - 2 Nil - 1
M (motor response) Obeys (6) Localised (5) Withdraws (4) Abnormal flexion (3) Extensor response (2) Nil (1)
V (verbal response) Orientated (5) Confused conversation (4) Inappropriate words (3) Incomprehensible sounds (2) Nil (1)
M+E+V must equal 3-5 for a coma
What are the two usual outcomes of a coma?
Not usually for a long time, usually progresses to a vegetative state or death
What usually causes persistent vegetative state?
Anoxic (deprived of oxygen) or traumatic brain injury, often following a coma
Give another name for persistent vegetative state
Unresponsiveness wakefulness syndrome
Do people in vegetative state respond to outside stimuli?
Not really, respond with basic reflexes and has random movements
What is locked in syndrome?
No movements below upper face, eyes, eyelids. Smell, vision, hearing and sensations remain present.
What causes locked in syndrome?
Trauma or occlusion of basilar artery at the level of the Pons, which leaves cranial nerves below nV and the corticospinal and bulbar tracts damaged.
Who is Jean-Dominique Bauby?
Locked in patient who wrote a book by blinking his eyes when his wife pointed to the right letter. Later wanted suicide.
What is the quality of life like in L.I.S?
Theres a happy and unhappy group, some do good with it
Describe the duration of a Coma, PVS, Minimally conscious state (MCS) and Locked in Syndrome (LIS)
Coma: Days/ weeks
PVS: Months to years
MCS: Months to years
LIS: Permanent
Describe the Sleep-wake cycle of a Coma, PVS, Minimally conscious state (MCS) and Locked in Syndrome (LIS)
Coma: None
PVS: Yes
MCS: Yes
LIS: Yes
Describe the Motor function of a Coma, PVS, Minimally conscious state (MCS) and Locked in Syndrome (LIS)
Coma: Reflexes
PVS: Reflexes, postures, withdrawal from noxious stimuli, random purposeful movement
MCS: Localises noxious stimuli, reaches for objects, hand-shape matching, scratching
LIS: Fully paralysed (quadriplegia), can (vertically) move eyes, blinking.
Describe the auditory/ visual function of a Coma, PVS, Minimally conscious state (MCS) and Locked in Syndrome (LIS)
Coma: None
PVS: Startle reflexes, orientating, fixations
MCS: Localises sound, some command following , visual pursuit
LIS: Normal vision and audition but can only respond via the eyes
Describe the verbal/manual communication of a Coma, PVS, Minimally conscious state (MCS) and Locked in Syndrome (LIS)
Coma: none
PVS: none
MCS: vocalisations, inconsistent but intelligible, gesture
LIS: Aphonic/ anarthric, i.e none or intelligible
Describe the emotion of a Coma, PVS, Minimally conscious state (MCS) and Locked in Syndrome (LIS)
Coma: None
PVS: Reflexive smiling or crying
MCS: Contingent smiling or crying
LIS: normal
Describe the consciousness of a Coma, PVS, Minimally conscious state (MCS) and Locked in Syndrome (LIS)
Coma: No
PVS: Depends on patient, only neural signs
MCS: Minimal behavioural signs of consciousness
LIS: Fully present
Further elaborate on how PVS patients can vary in terms of consciousness
When carrying out fMRI scans on patients in PVS, studies have shown that some (+/- 20%) PVS patients do not ‘fit’ the category of completely unconscious.
For example they have been shown to have stronger EEG reactions to their own name. In some studies they have been instructed for example; to think tennis for yes and navigation for know. The brain understands the instructions and ‘responds’ with the appropriate brain pattern. The brain patterns exhibited are correlated with those of healthy volunteers.
The brain can then ‘answer’ factual yes/no questions (most are answered correctly). This raises the question whether they are conscious.
As previously mentioned normally consciousness as a state and consciousness as an experience correlate with each other. Is this the case in PVS? Explain
Newer insights reach the conclusion that in PVS / UWS there is huge variability in the relation between wakefulness and conscious content. In some patients it’s the ‘classic’ relation, in others it’s like in LIS or healthy people.
How is connectivity in the brain in patients with PVS (UWS), MCS and those emerging from MCS? How was this measured?
Measuring connectivity between brain regions by combining TMS (localized impulse of activity) and EEG recording (to measure how far this activity spreads). PCI is ‘connectivity index’, indicating amount of spread. Unresponsive Wakefulness Syndrome (UWS = PVS) equals PCI of deep sleep or anesthesia. Minimally Conscious (MCS) or Emerging from MCS (EMCS) show increasingly higher PCI. Locked in (LIS) is similar to healthy awake subjects.
What conclusion can be drawn from these findings regarding the connectivity of PVS and MCS?
Connectivity in the brain correlates with clinical state of loss of consciousness (LoC)
TMS induced EEG activity spreads much further in LIS > MCS than in VS
How are these correlates between states of LoC and connectivity useful in a practical sense?
The amount of connectivity found in an individual VS patient is indicative for the prognosis, i.e. recovery towards MCS or awakening
Name one of the most confusing states to place on the chart of awareness to wakefulness
Sleepwalking
What brain structure could be considered as an “off switch”? Describe the evidence for this (2)
The Claustrum
Electrical stimulation of Claustrum in a patient with implanted electrodes for epilepsy;
Stimulating AI14 resulted in immediate impairment of consciousness, in 10 out of 10 times, with arrest of reading, onset of blank staring, unresponsiveness to auditory and or visual commands, and slowing of spontaneous respirator movements. The patient to baseline as soon as the stimulation with no recollection of the events during the stimulation period.
What EEG activity was recorded from the person who had his claustrum switched off?
(measured with intracortical electrodes are various brain regions), showed very strong reduction in correlated activity (z-scores) when claustrum was stimulated and patient lost consciousness (purple vs red points in graph in doc)
What drawbacks are there to this claustrum study?
Only one patient and may be because he has epilepsy. This is similar behaviour to one symptom of epilepsy.
What is meant by Tonic Immobility?
A type of hypnosis in chickens and other birds, rabbits, sharks and reptiles
How susceptible are humans to hypnosis
There is a huge variability in hypnotic suggestion; many tests to distinguish subjects
How can one induce someone to a hypnotic trance?
There are many techniques from a slow guiding to a rapid introduction by staring, objects, lights, touch drinks etc.
What suggestions can be made under a hypnotic state?
Hallucinating objects/ colors, the troop task effect, acting under command etc
What clinical applications has there been in hypnosis? (2)
Pain relief,
quitting smoking
Name an example of a test used to discern how susceptible someone is to hypnosis
Showing two fingers in front of someone and putting them closer together, the sooner they perceive them as touching, the easier they may be hypnotised.
Are there neural differences between people with low and high susceptibility? If so, what are they?
There are some reported differences between high and low susceptible individuals, both in structural brain anatomy, and functional activity (either in resting state or general attention tasks).
But results are quite all over the place and do not really reproduce all that well…General picture that emerges: something with executive, conflict and attention areas
What is observed when observing the neural changes that occur upon induction? How does this compare to sleep?
Sort of the same story emerges when looking at the neural changes that occur upon induction:Activation in regions linked to executive control, salience, attention or resting state (default network) either go up or down.All in all it seems more like an attention / control phenomenon than ‘sleep’
Hypnosis most likely is a complex and variable phenomenon where some changes occur in the balance between several cognitive functions
How is the stroop task associated with hypnosis
(stroop task- interference when colour and name of colour contradict)
There is a loss of this stroop interference after post hypnotic suggestion (e.g you can no longer read) (in suggestible subjects)
However what is a contradiction to this finding in hypnosis and the stroop task that is found in many hypnotic effects?
Giving the suggestion without induction works just as well
What is a common finding in hypnotism as demonstrated by the magnetic hands suggestion
Loss of a sense of agency/ control over behaviour
How much does does this come into play in stage hypnosis (loss of agency)
Crawford (1992) interviewed subjects after stage hypnosis. 23% of subjects reported the hypnotist had control over their actions they could not resist
Many play along for the fun of it however;
“I would have done anything he said. But I didn’t think he’d make me do anything bad. I trusted him. Before I got hypnotized I always thought like [hypnosis] was a partial control of your mind. Now my answer would be total control.”
Experimenter: “what do you mean?”
“I felt like I could do anything when I was up on stage… if I had to kill somebody, I could have certainly done it. That’s the control right there”
This brings up a question; would it be possible for someone to commit murder while under hypnosis?
Describe two studies which sought to investigate this question.
Orne & Evans (1965) asked highly susceptible subjects to
•Put hand in box with snake
•Throw nitric acid in face of assistant 5/6 subjects did. But so did 6/6 simulators
> People never believed dangers were ‘real’
Coe et al., 1973: 26 highly susceptibles selected, asked to deliver cocaine, get money
•3/12 did when hypnotized
•6/14 did when not hypnotized
What conclusions could be drawn from these studies concerning the extent to which people can be hypnotised to do illegal or immoral stuff?
There is a real sense of loss of agency / control, But people will inhibit the suggested actions when it is not according to their moral beliefs
therefore there is a dissociation between sense of agency and actual control of behavior
