Exam 1 Flashcards
1
Q
What is the common sense definition of consciousness?
Start of Lecture 1
A
Consciousness is what goes away when one falls into dreamless sleep; interpreting/understanding consciousness from a perspective of loss or absentness
The utility in this definition is that it informs us that consciousness is everything
2
Q
What is the behavioral definition of consciousness?
A
Consciousness is associated with the availability of a rich behavioral repertoire
The utility in this definition is that behavior is tangible - it can be studied and observed
3
Q
Are animals conscious (sophisticated birds and bees)?
A
Most answer yes according to the behavioral definition of consciousness, for they possess a behavioral repertoire
Birds can be taught categories, even arbitrary catgeories…thus, some say we should grant consciousness to invertebrates
4
Q
What is the functional definition of consciousness?
A
Consciousness is the ability to perform certain cognitive functions
“Proper scientific theories of consciousness are those that specify which functions are necessary for consciousness to arise”
By this definition, those who are conscious must be able to perform two different types of information-processing computations:
1. The selection of information for global broadcasting
2. The self-monitoring of those computations
5
Q
What is the Turing test?
A
Test to decipher between machine and human
Now, machines can pass the Turing test…new concern: will machiens develop faster than the mechanisms to determine whether they are human?
6
Q
What is the neurological definition of consciousness?
A
Established on the basis of levels of consciousness. That is, there are different states of consciousness that are associated with behavioral/cognitive conditions
Glasgow coma scale can be used for this purpose
7
Q
What is the Glasgow coma scale?
A
The Glasgow Coma Scale (GCS) is a neurological scale designed to assess a person’s level of consciousness after a brain injury; can be used to examine neurological differences at different levels of consciousness (e.g., wakefulness, locked-in syndrome, dreamless sleep, etc.)
8
Q
What is prosopagnosia?
A
Inability to recognize faces; people with prosopagnosia also can’t imagine faces and do not dream of faces
9
Q
What is the neurophysiological definition of consciousness?
A
Definition of consciousness that relies on the implication and identification of NCCs
10
Q
What are neural correlates of consciousness (NCC)?
A
“The minimal neuronal mechanisms jointly sufficient for any one conscious perception”
For every conscious percept, there will be an NCC. Inducing the NCC will induce the perception; inactivating the NCC will eliminate it.
11
Q
What are content-specific NCCs?
A
physical mechanisms whose activity determines a particular phenomenal distinction within an experience
12
Q
What is a full NCC?
A
physical substrate supporting conscious experiences in their entirety, irrespective of their specific contents; union of all content-specific NCCs
13
Q
What are background conditions?
A
factors that enable consciousness without contributing directly to its content (appropriate glucose, O2 and neuromodulatory milieu, afferent inputs for adequate cortical excitability), sensory input, and motor output chains
14
Q
What is the philosophical definition of consciousness?
A
Consciousness is a subjective experience - “what it is to be”
That is, “to be conscious is to have experiences;” experiences meaning “to be” from the inside, like awareness
This is the primary definition we stick with for the purpose of this class and beyond
15
Q
How is an experience a cause-effect structure?
A
There is a one-to-one correspondence between the properties of experiences and those of cause-effect structures
In the context of consciousness, an experience is considered a cause-effect structure because it reflects the way our brains process information and generate subjective experiences. This concept can be understood through several key points:
Cause-Effect Mechanisms: Our brains interpret sensory inputs (causes) and produce experiences (effects). This process involves complex neural activities where specific stimuli lead to particular responses or experiences.
Predictive Coding: The brain uses past experiences to predict future events, creating a cause-effect model of the world. Experiences are not just passive reactions to stimuli but are actively constructed by the brain’s predictions and the actual sensory inputs.
Consciousness as Integration: Consciousness integrates information from various sources (causes) to produce a coherent experience (effect). This integration allows for a structured perception of the world, where experiences are linked to specific causes (e.g., seeing lightning and anticipating thunder).
Temporal Dimension: Experiences have a temporal structure where past events influence the perception of current events, and expectations shape the interpretation of sensory information. This temporal aspect underlines the cause-effect nature of experiences, as the sequence of events and the brain’s responses create a continuous flow of consciousness.
Subjective Quality: The subjective quality of experiences, or qualia, reflects the internal cause-effect processes that give rise to the unique way we perceive the world. This includes how emotions, thoughts, and sensations are intertwined and influence each other, forming complex cause-effect relationships that constitute our conscious experience.
16
Q
Is consciousness self-reflection?
A
No, to be conscious is to have an experience.
Consciousness can be dissociated from behavior, executive functions, language, episodic memory, working memory, and attention.
17
Q
Is consciousness of the environment?
A
No, to be conscious is to have an experience.
Consciousness can be dissociated from behavior, executive functions, language, episodic memory, working memory, and attention.
18
Q
Is consciousness just of objects?
A
No, to be conscious is to have an experience.
Consciousness can be dissociated from behavior, executive functions, language, episodic memory, working memory, and attention.
19
Q
Explain how consciousness can be dissociated from behavior and functions
A
To be conscious is to have an experience.
Therefore, consciousness can be dissociated from behavior, executive functions, language, episodic memory, working memory, and attention.
20
Q
Is consciousness just responsiveness?
A
No, to be conscious is to have an experience.
Consciousness can be dissociated from behavior, executive functions, language, episodic memory, working memory, and attention.
Imagine playing tennis in the vegetative state. This might indicate responsiveness, but does it indicate consciousness?
21
Q
How are neurons quantitatively distributed throughout the brain?
A
Cerebral cortex: 16 billion neurons, 100 trillion synapses
Basal ganglia: 0.4 billion neurons
Cerebellum: 70 billion neurons
Spinal cord: 1 billion neurons
Brainstem: < 1 billion neurons
22
Q
What is the “hard” problem of consciousness?
End of Lecture 1
A
“…imagine that there is a machine, whose structure makes it think, sense, have perceptions;
we could conceive it enlarged, keeping the same proportions, so that we could enter into it, as into a mill.
…when inspecting its interior, we will find only parts that push one another, and never anything which we could explain a perception.”
23
Q
How do we determine full NCC?
Start of Lecture 2
A
contrast conscious vs. unconscious states
24
Q
How do we determine content-specific NCC?
A
contrast conscious states where a specific conscious content is present vs. absent (e.g., via tasks)
25
What is problematic with regard to the diagnoses of minimally conscious states and vegetative states?
40% misdiagnosis rate
26
Does responsiveness = consciousness?
No, this is an important distinction when reviewing the NCC
You can be unresponsive but still conscious (e.g., dream states, paralysis, etc.)
27
Describe lesion studies as a type of neuroscientific evidence for NCCs
Lesion studies are causal - strong evidence for a given structure being necessary or not; plasticity may lead to functional reorganization in chronic cases
28
Describe stimulation studies as a type of neuroscientific evidence for NCCs
Stimulation studies are perturbational - immediate effects provide strong evidence for a given structure being causally involved; non-specific effects may be related to network recruitment
29
Describe recording and neuroimaging studies as a type of neuroscientific evidence for NCCs
Recording and neuroimaging studies are correlational - can help study a large number of different conditions, but correlation versus causality may be more difficult to assert - ideally requires meta-analysis to quantify consistency of results across many different conditions
30
Are the cerebellum or hippocampus required for consciousness (i.e., are they NCCs)?
Strong evidence that neither the cerebellum nor hippocampus are required to be conscious
31
Is the cortico-thalamic system important for consciousness (i.e., is it an NCC)?
Strong evidence that cortico-thalamic system is important for consciousness
32
Are the posterior brain regions important for consciousness (i.e., are they NCCs)?
Strong evidence that posterior brain regions are important for consciousness
33
Are feedback connections important for consciousness (i.e., are they an NCC)?
Strong evidence that feedback connections are important for consciousness
34
Which brain regions have strong evidence for their role, or lack thereof, in consciousness (i.e., what are the most likely NCCs)?
Some of the evidence for the NCC is pretty strong:
- Neither the cerebellum nor hippocampus is required to be conscious
- Cortico-thalamic system is important for consciousness
- Posterior brain regions are important for consciousness
- Feedback connections are important for consciousness
35
What brain regions remain the objects of debate regarding their role in consciousness as NCCs?
Some cases remain the objects of debate regarding role in consciousness:
- Role of the striatum is debated with regard to consciousness
- Role of the thalamus is debated with regard to consciousness
- Role of the claustrum is debated with regard to consciousness
- Role of primary versus higher-level cortical regions is debated with regard to consciousness
- Role of prefrontal cortex is debated with regard to consciousness
- Role of different cell types or cortical layers are debated with regard to consciousness
36
What is the result of widespread lesions of the corticothalamic system with regard to consciousness?
Widespread lesions of corticothalamic system cause irreversible coma; this is evidence for the corticothalamic role in consciousness (strong potential to be NCC)
37
Is spinal cord activity an NCC?
No, the spinal cord plays no role in consciousness (e.g., quadraplegic)
38
What is the result of ablation, agenesis, or degeneration of the cerebellum with regard to consciousness?
Complete ablation, agenesis, or degeneration of the cerebellum hardly affects consciousness (aligns with strong evidence that cerebellum is not an NCC)
This is bizarre because the cerebellum has 4x more neurons than the cerebral cortex
39
Why is it surprising that the cerebellum has little effect on consciousness?
Cerebellum has 4x more neurons than the cerebral cortex
40
What is the result of hippocampal lesions with regard to consciousness?
Bilateral hippocampal lesions do not cause unconsciousness, but may cause decrease in visual imagery and decrease in visual contents of consciousness during mind wandering (aligns with strong evidence that hippocampus is not an NCC)
41
What is the result of basal ganglia lesions/degeneration with regard to consciousness?
Bilateral basal ganglia lesions/degeneration do not cause unconsciousness; seen in a child who was bedridden and had no verbal skills as a result of basal ganglia degradation yet maintained consciousness (basal ganglia and striatum role in consciousness still object of debate)
42
What is the result of akinetic mutism (dysfunction of fronto-striatal circuits AKA basal ganglia and medial frontal cortex) with regard to consciousness?
Patients with akinetic mutism (dysfunction of fronto-striatal circuits, specifically basal ganglia and medial frontal cortex) display decreased responsiveness but typically remember everything after episode ends (i.e., fronto-striatal circuits, including basal ganglia, play no role in consciousness, but true role is still object of debate)
43
What neurotransmitter is the best indicator of consciousness?
Acetylcholine (ACh) is the best neurotransmitter indicator if consciousness as it is elevated during both wake and REM sleep (aka dream state).
The problem with labeling ACh as the "neurotransmitter of consciousness) is that dreaming doesn't always occur during REM, meaning their are unconscious periods of REM (double dissociations between arousal and consciousness).
44
What is the effect of claustrum stimulation with regard to consciousness?
Claustrum stimulation was reported to cause unconsciousness.
However, bilateral claustrum lesions/degeneration do not cause unconsciousness.
Therefore, role of claustrum in consciousness (as NCC) is up for debate.
45
What is the result of claustrum lesions/degeneration with regard to consciousness?
Bilateral claustrum lesions/degeneration do not cause unconsciousness.
However, claustrum stimulation was reported to cause unconsciousness.
Therefore, role of claustrum in consciousness (as NCC) is up for debate.
46
What evidence exists regarding the thalamus and thalamic systems with regard to consciousness (i.e., is the thalamus an NCC)?
Coma and vegetative state can be observed after bilateral thalamic lesions, BUT these lesions usually also involve neighboring white matter tracts connecting to the brainstem arousal centers.
Moreover, pure thalamic lesions do not cause coma.
Also, loss of consciousness during anesthesia coincides with cortical slowing while thalamus is still awake.
Furthermore, during REM/paradoxical sleep (PS), there is preserved cortical arousal while thalamus is asleep. That is thalamus off does not equal loss of consciousness. If you lesion the thalamus, you can remain conscious.
Therefore, role of thalamus with regard to consciousness (as NCC) is up for debate. Based on this information, general consensus is that thalamus is not an NCC.
47
What evidence exists regarding the primary sensory cortices with regard to consciousness (i.e., are the primary sensory cortices an NCC)?
Primary sensory cortices activity is preserved during loss of consciousness in deep sleep and anesthesia (seen in a rat model), serving as evidence that primary sensory cortices may not play a role in consciousness.
Moreover, higher-level sensory areas can also be activated unconsciously, such as those for emotional stimuli.
However, high decodability for conscious contents is found in V1 and V2 in some working memory studies.
Therefore, role of primary sensory cortices with regard to consciousness is up for debate.
48
What is the dual-stream model, and how is it involved in consciousness?
There are syndromic dissociations in lesion cases, leading many to develop the idea of independent streams for perception and action.
"Where" stream is the dorsal stream.
"What" stream is the ventral stream.
However, "simple" lesion cases can actually have more widespread network consequences, such as focal macroscopic lesions, which can lead to subtle, more widespread cortical thinning. Moreover, somatosensory feedback may guide actions in patients with visual form.
Also, dorsal stream can activate for "what," and unconscious activation of ventral stream can be observed.
Therefore, ventral stream activity is not sufficient for consciousness.
49
How are fronto-parietal regions impacted by unconsciousness?
There is a common decrease in fronto-parietal metabolism in coma, vegetative states, anesthesia, and sleep.
Moreover, anticorrelations between fronto-parietal networks and the default network vanish with unconsciousness.
50
What is the relationship between fronto-parietal regions and the default mode network, and how does this relate to consciousness?
There are anticorrelations between lateral fronto-parietal regions and the default mode network.
However, anticorrelations between frontoparietal networks vanish with unconsciousness.
51
What sensory networks best differentiate minimally conscious states from vegetative states?
Lower-level sensory networks best differentiate minimally conscious states from vegetative state patients at the single-subject level.
FDG uptake in peristriate visual cortex (BA 18) had the highest indiviudal regional classification rate across the pooled cohort, with an AUC of 0.90.
52
What is the result of prefrontal cortex resections/lesions with regard to consciousness?
Large prefrontal cortex resections/lesions do not lead to unconsciousness, supporting the idea that much of the anterior prefrontal cortex plays no role in consciousness (controversial NCC).
Another study conducted complete prefrontal cortex resections in monkeys and found that there was also no loss of consciousness.
53
What is the result of posterior traumatic brain injury with regard to consciousness?
There is the potential for a persistent vegetative state after posterior traumatic brain injury, aligning with idea that posterior brain regions are important for consciousness.
Damage to the corpus callosum or dorsolateral upper brainstem is a strong predictor for permanent loss of consciousness.
Moreover, restricted diffusion in posterior brain predicts outcome after anoxic brain injury (possible reason behind this LOC).
54
What is the result of prefrontal and posterior cortex lesions with regard to consciousness?
Large prefrontal lesions do not cause unconsciousness.
Large posterior brain lesions predict permanent coma/vegetative state, aligning with idea that posterior brain regions are important for consciousness (likely NCC).
55
How is feedback connectivity affected by loss of consciousness?
There is decreased feedback connectivity during loss of consciousness induced by anesthesia and in vegetative states, aligning with the idea that feedback connections are important for consciousness (likely NCC).
Specifically, frontal to parietal connectivity impacted during LOC.
In particular, blockade of cortical feedback to apical dendrites of cortical neurons may be responsible for loss of consciousness during anesthesia.
56
How does feedback connectivity differ based on perception of somatosensory stimuli?
There is increased feedback connectivity for perceived compared to unperceived somatosensory stimuli.
Moreover, stimulus perception is suppressed when disrupting feedback connectivity by backward masking.
This may provide some insight with regard to the fact that feedback connectivity is important for consciousness.
57
Describe the connectivity of layer 5b cells
Large, thick-tufted pyramidal cells of layer 5b project mainly to subcortical structures and are likely involved in cortico-subcortical loops
58
Describe the connectivity of layers 2/3 and 5a/6 (IT) cells
End of Lecture 2
Thin-tufted pyramidal cells of layers 2/3 and 5a/6 (IT) have cortico-cortical connections and are more heavily interconnected.
These layers may be important for consciousness, as they receive information from the higher order cortex.
Thin-tufted pyramidal cells of layers 2/3 are the most heavily interconnected and show the most specific responses.
59
What is the importance of activating (arousal) systems?
Activating (arousal systems are important to initiate and/or maintain wakefulness. They promote EEG desynchronization and behavioral arousal.
60
How does sleep relate to disconnection?
Sleep is a state of partial sensory disconnection
61
Describe EEG and intracellular characteristics of wake state, SWS (NREM), and REM
At an EEG level, SWS (NREM) has large, slow waves, and intracellular recordings show periods of "silence" where the membrane is hyperpolarized.
In REM, intracellular recordings show a significantly heightened number of action potentials relative to wake and SWS.
The EEG of REM is notably similar to that in a wakeful state, even experts have a hard time differentiating between awake EEG trace and REM EEG trace.
62
How many activating systems are there?
There are many (>15) activating systems. About half have been characterized only in the last few years, using genetic (optogenetic/chemogenetic tools).
63
What are the activating systems of the brainstem?
The activating systems of the brainstem are:
1. Glutamate (RF)
2. Noradrenaline (LC)
3. Acetylcholine (LTD + PPT)
4. Serotonin (DR)
5. Dopamine (VTA, vPAG)
64
What are the activating systems of the hypothalamus?
The activating systems of the hypothalamus are:
1. Histamine (TMN)
2. Orexin/hypocretin (LH)
3. Glutamate/GABA (SuM)
4. GABA (LH 1, 2)
65
What are the activating systems of the basal forebrain?
1. Glutamate
2. Acetylcholine
3. GABA
66
What are the two major types of activating/arousal systems?
The two major types of arousal systems are:
1. Noradrenaline, orexin, H, serotonin
2. Acetylcholine (ACh), dopamine
The ACh, DA arousal system is much more active during sleep than the other system. It mediates dreaming during sleep and has nothing to do with disconnection.
The NA, Ore, H, 5-HT system mediates disconnection, meaning its silence is necessary for sleep/disconnection.
67
How has optogenetic/chemogenetic stimulation been so useful with regard to activating/arousal systems?
Optogenetic + chemogenetic stimulation has allowed us to establish distinct pieces of the ARAS compared to the old view, which was more or less a jumbled mess with little to no specificity.
68
How was the ascending reticular activating system (ARAS) discovered?
In a cat brain during anesthesia, EEG showed SWS traces. Then, an electrical stimulation was given. This electrical stimulation desynchronized the EEG, lending to the discovery of the ARAS system.
69
Describe the effects of the EEG desynchronization of the ascending reticular activating system (ARAS)
In a cat brain during anesthesia, EEG showed SWS traces. Then, an electrical stimulation was given. This electrical stimulation desynchronized the EEG, lending to the discovery of the ARAS system.
With regard to the ARAS system EEG desynchronization:
- Effect can be unilateral if electrical stimulation is weak
- Effect persistent after full atropinization (cholinergic antagonist)
- Effect is not due to antidromic stimulation of the pyramidal tract
- Effect is not due to orthodromic stimulation of the specific sensory pathways
- Effects can be mimicked by stimulation of the intrathalamic nuclei, but persists after their lesion (some parts of the thalamus are important for ARAS effects)
70
What is the reticular formation?
The reticular formation forms the core of the brainstem and most reticular neurons are Golgi type I neurons
71
How can the ARAS system be divided?
We can divide the ARAS systems on the basis of their projections, some dorsal (thalamic) and some ventral (hypothalamic-BF)
72
What is the role of noradrenaline (NA) and dopamine (DA) with regard to arousal systems?
Noradrenaline (NA) and dopamine (DA) play a role in the response to novelty, reward
73
What is the role of noradrenaline (NA) with regard to arousal systems?
Noradrenaline (NA) plays a role in high muscle tone
74
What is the role of serotonin (5-HT) with regard to arousal systems?
Serotonin (5-HT) plays a role in motor output and response to CO2
75
What is the role of acetylcholine (ACh) and GABA with regard to arousal systems?
Acetylcholine (ACh) and GABA play a role in EEG activation
76
What is the role of orexin with regard to arousal systems?
Orexin plays a role in consolidation of wake as well as feeding
77
How do the sleep and wake systems interact with one another?
Sleep and wake systems inhibit each other, a process that is primarily mediated by orexin and GABAergic cells in the preoptic area + basal forebrain.
Specifically, the inhibitory effects of GABA promote sleep, while the stimulatory effects of orexin promote wake.
78
Where do locus coeruleus neurons project?
Locus coeruleus neurons project almost everywhere in the brain. We used to think everywhere except the basal ganglia, but this is no longer accepted.
This means noradrenaline projects nearly everywhere.
79
Describe locus coeruleus (noradrenergic arousal system) neuron firing in sleep vs. wake
Locus coeruleus neurons fire during wake and are silent in NREM and REM sleep in a mouse. Moreover, these neurons start firing before EEG activation.
80
How is optogenetic stimulation or inhibition used to target locus coeruleus neurons?
Halorhodopsin (chloride pump) is sensitive to yellow light and causes inhibition of locus coeruleus cells.
Chennelrhodopsin2 (cation pump) is sensitive to blue light and causes activation of locus coeruleus cells.
81
What is the result of optogenetic stimulation of locus coeruleus neurons?
Optogenetic stimulation of locus coeruleus cells induces EEG activation and behavioral arousal.
In other words, this stimulation of noradrenergic neurons during sleep increases the probability of NREM to wake or REM to wake transitions.
See above notecard for how this stimulation works.
82
How are sleep and wake states altered in noradrenaline deficient mice?
Knockout mice lacking noradrenaline have similar lengths of wake, NREM, and REM. However, knockout mice have much lower latency to sleep than control mice, meaning they fall asleep much faster, even with amphetamine administration.
This shows the role of the locus coeruleus and the noradrenergic system in promoting wake.
83
How does the locus coeruleus relate to plasticity?
The locus coeruleus promotes the expression of plasticity-related genes during wake.
Unilateral chronic lesions of locus coeruleus do not affect the wake EEG, but decrease the induction of immediate-early genes and plasticity-related genes during wake. In other words, unilateral locus coeruleus stimulation results in decreased plasticity effects relative to bilateral.
84
Describe the effects of the locus coeruleus noradrenergic system with regard to EEG, sleep, and behavioral arousal
Activation of the locus coeruleus noradrenergic system is sufficient to induce EEG desynchronization and behavioral arousal from sleep.
Activation of the locus coeruleus noradrenergic system is not necessary, neither for behavioral arousal, nor for EEG desynchronization.
Low locus coeruleus activity may be key for sensory disconnection.
85
Are histaminergic neurons required to initiate waking?
Histaminergic neurons are wake-specific but do not anticipate EEG activation; they are not required to initiate waking.
86
How do histaminergic neurons relate to connectedness?
Histaminergic neurons may be key for connectedness. During cataplexy, or loss of muscle tone, only histamine neurons are active (relative to serotonin cells and noradrenergic cells), indicating that they allow for maintained connectedness.
87
Describe the firing of orexinergic neurons
For information about orexinergic firing see slide 38 of Lecture 4
88
What is the result of optogenetic stimulation of orexinergic neurons?
Genetic targeting of channelrhodopsin2 to orexin neurons activates orexin neurons. Activation of orexinergic neurons wakes a mouse from slow wave sleep (SWS) and REM sleep, but after several seconds.
Moreover, optogenetic activation of orexinergic neurons no longer works if locus coeruleus neurons are inhibited, showing that orexinergic neurons are dependent on locus coeruleus neurons.
89
How do orexin neurons relate to the wake state?
Orexin neurons are indispensable (absolutely necessary) for maintaining waking. No orexin = sleep. Orexin knockout in animal models leads to narcolepsy.
90
Describe the effects of the orexin system with regard to EEG, sleep, and behavioral arousal
Activation of the orexin system is sufficient to induce EEG desynchronization and behavioral arousal from sleep (but via locus coeruleus, on which it is dependent).
Activation of the orexin system is not necessary for behavioral arousal nor for EEG dysnchronization, but is key for consolidated waking.
91
What does EEG desynchronization indicate?
EEG desynchronization may indicate arousal and alertness and can often indicate a transition to active brain states (like wake).
92
How does cholinergic neuron firing differ in different sleep and wake states?
The firing of brainstem cholinergic neurons is high in wake and REM sleep but low in NREM sleep.
The firing of basal forebrain cholinergic neurons is high in wake and REM sleep but low in NREM sleep. Acetylcholine neurons start firing at the transition between NREM and REM sleep.
93
What is the result of optogenetic stimulation of cholinergic neurons?
Optogenetic stimulation of basal forebrain cholinergic neurons during NREM sleep leads to wake or REM sleep.
However, there is no change when the stimulation occurs during wake or REM sleep.
This makes sense because the firing of basal forebrain cholinergic neurons is high in wake and REM sleep but low in NREM sleep.
94
What is the result of chemogenetic stimulation of the cholinergic system?
Chemogenetic stimulation of the basal forebrain cholinergic system has no effects on wake duration nor sleep fragmentation, but it has large effects on the EEG power spectrum (decreased low frequency power).
95
Describe the effects of the cholinergic system with regard to EEG, sleep, and behavioral arousal
Activation of the cholinergic system opposes bistability and promotes the transition to "desynchronized" states like wake and REM sleep.
Activation of the cholinergic system does not promote behavioral arousal nor the maintencance of wake per se.
96
What mediates the acetylcholine EEG activating effects on neurons?
Acetylcholine (ACh) EEG activating effects on neurons are mediated by both muscarinic and nicotinic receptors.
Muscarinic effects:
-There is increased excitability/depolarization due to block of a leak potassium current.
-There is increased excitability/depolarization due to block of slow afterhyperpolarizations.
Nicotinic effects:
-Release of glutamate from thalamo-cortical axons
-Release of ACh from cholinergic neurons (e.g., from basal forebrain neurons)
- Release of noradrenaline from locus coeruleus neurons
- Inhibition of VLPO neurons (via NA)
97
What is the effect of cholinergic antagonists (anticholinergic drugs) with regard to sleep and wake?
Atropine and other cholinergic antagonists cause the appearance of slow waves in waking. Moreover, there is reported dissociation with anticholinergic drugs (partial or total dissociation between EEG and behavior?).
Anticholinergic drugs cause vivid hallucinations, similar to dream states, which cause sensorimotor hallucinatory experiences.
98
Describe the firing of dopamine cells
There is tonic and burst firing of dopamine cells in the rat VTA.
Specifically, VTA dopamine cells switch to burst mode (more firing) in REM sleep.
VTA dopamine cell activity is high in wake, even higher in REM sleep, and low in NREM sleep.
VTA dopamine cell activity decreases before the wake to NREM transition, and increases before the NREM to wake, or the NREM to REM transition.
VTA dopamine cell activity is measured with fiber photometry technology.
99
What is the result of optogenetic stimulation of dopamine cells in the VTA?
Optogenetic activation of VTA dopamine cells initiates wake from both NREM and REM sleep. Stimulation (5sec, 25 Hz) almost immediately wakes up the mouse from NREM sleep, even after 4 hours of sleep deprivation. Awakening from REM sleep is less effective.
Optogenetic stimulation of some (but not all) projections of VTA dopmaine cells promotes wake. Each of the 3 effective sites (N accumbens, central amygdala, dorso-lateral striatum) alone does not match the full effect seen with stimulaton of VTA cell bodies. mPFC stimulation is totally ineffective.
100
What is the result of chemogenetic inhibiton of the dopaminergic system?
Chemogenetic inhibition of the dopaminergic system increases NREM sleep but does change the EEG. This makes sense because VTA dopamine is low in NREM but high in wake and REM.
101
Describe dopamine cells in the ventral periaqueductal grey with regard to sleep and wake
Dopamine cells in the ventral periaqueductal grey are more active during wake.
Optical fiber recordings show vPAG dopamine neurons fire more during waking, especially at wake onset; firing in wake decreases toward sleep onset and is lowest in NREM sleep.
102
What is the result of optogenetic stimulation and chemogenetic inhibition of dopamine cells in the ventral periaqueductal grey?
Optogenetic activation of vPAG dopamine neurons drives behavioral arousal even after short sleep deprivation. Their chemogenetic inhibition increases NREM sleep even with salient stimuli.
In other words, dopamine cells in the vPAG promote waking from both NREM and REM sleep.
103
Describe the effects of the dopaminergic system with regard to EEG, sleep, and behavioral arousal
Activation of the dopaminergic system promotes the transition to wake from NREM sleep and, less effectively, from REM sleep.
Effects on EEG? Dopamine main effect seems to be more on behavioral arousal (from NREM especially) than on EEG activation.
There is a strong link between the dopaminergic system and dreaming.
104
What is the relationship between dopamine and dreaming?
End of Lecture 4
There is a strong link between dopamine and dreaming:
- Decreased dreaming in Parkinson's disease
- Increased dreaming with L-Dopa therapy
- Loss of dreaming with lesions of vmPFC
- Dopamine projections to mPFC may be involved in dreaming, not in behavioral arousal
105
During what phases of anesthesia is surgery usually performed?
Start of Lecture 3
Surgery is usually performed during phases 2 and 3. Phase 2 is vegetative state, coma and phase 3 is burst suppression.
106
How does EEG frequency and amplitude change as anesthesia deepens?
As anesthesia deepens, EEG frequency decreases.
107
How does EEG frequency and amplitude change as sleep deepens?
As sleep deepens, EEG frequency decreases and amplitude increases.
108
Describe EEG during epileptic seizures
Put simply, seizures usually show large ampitude EEG. Neurons within affected brain area generate abnormally synchronized activity.
109
What are the characteristics of partial seizures, generalized seizures, and absence seizures?
Partial seizure:
- Involves particular area of cerebral cortex
- Clonic (rhythmic) limb movement if motor cortex affected
- Aura abnormal sensation) if sensory cortex affected
Generalized seizure:
- Involves entire cerebral cortex of both hemispheres
- Behavior completely disrupted for minutes
- Loss of consciousness
- Tonic (ongoing), clonic, or tonic-clonic muscle activity
Absence seizure:
- Less than 30 sec of generalized 3 Hz waves
- Loss of consciousness
- Little motor activity, e.g., twitching mouth or eyelid
110
Describe different EEG traces during coma
For info on coma EEG see slide 4 of Lecture 3
111
Describe LFPs and spikes during wakefulness and anesthesia
For info on LFPs and spikes during wakefulness and anesthesia see slides 5 and 6 of Lecture 3
112
How does spiking in superficial and deep layers differ in wakefulness, sleep, and anesthesia?
There is greater spike rate (more firing) in deep layers of the brain during sleep and wake relative to anesthesia (and relative to superficial and mid layers).
See slide 7 of Lecture 3 for specifics.
113
Decribe cortico-cortical and thalamo-cortical circuit paths
See slide 8 of Lecture 3.
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What are the subcortical contributions to consciousness?
Thalamus - ILN
Medial septal nucleus, hypothalamus, basal nucleus of meynert, NRT, brainstem, MRF
See slide 10 of Lecture 3 for more.
115
Describe cortical effective connectivity in wakefulness, sleep, and anesthesia
Cortical effective connectivity is increased in wakefulness and less in sleep, anesthesia (i.e., less conscious = less cortical effective connectivity).
Perturbed consciousness = reduced functional connectivity.
See slide 9 of Lecture 3 for more.
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What is the result of thalamic stimulation in minimally conscious states?
Thalamic stimulation can improve responsiveness in minimally conscious states. A subject in minimally conscious state for 6 years prior to deep brain stimulation had improvements in arousal, limb control, and oral feeding following thalamic stimulation.
117
What is the result of thalamic stimulation during anesthesia?
Stimulating the central thalamus roused macaques from anesthesia.
118
When is thalamic stimulation most effective at promoting arousal/consciousness?
Thalamic stimulation is most effective when centered on central lateral thalamus.
119
How does consciousness level relate to feedforward and feedback paths?
Consciousness level modulates feedforward and feedback paths.
Feedforward:
- Carry sensory information, terminates in deeper higher level areas
- From Parietal (LIP) to frontal (FEF)
- Increased information transmission along this pathway when you wake the animal up (increased consciousness = increased feedforward)
Feedback:
- Higher level areas to lower level areas
- From Frontal (FEF) higher to Parietal (LIP) lower
- Increased feedback when increased consciousness
See slide 14 of Lecture 3 for more information.
120
Describe intracolumnar signaling in wakefulness, sleep, and anesthesia
Intracolumnar signaling:
- Layer 2 to Layer 5
- Within column
- Parietal intracolumnar signaling is higher when you are conscious compared to frontal conscious intracolumnar signaling
See slide 15 of Lecture 3 for more info.
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How can dendro-somatic signaling of layer 5 cells be altered?
Cholinergic antagonist, anesthesia, glutamate antagonists (mGluR), and thalamus deactivation all decouple dendro-somatic signaling while still allowing significant response in dendrites.
Anesthesia decouples dendro-somatic signaling in layer 5 pyramidal cells. Dendrites can kinda respond, but the soma cannot.
Dendrites and soma increase activity when awake, and dendrite to soma coupling increased during wake state.
Dendrites can still receive info from other neurons to an extent when anesthetized, but the soma cannot respond during anesthesia.
Thalamus deactivation also decouples dendro-somatic signaling in layer 5 cells, nearly in the same manner as described above: soma response is worse when thalamus is deactivated, and so is dendrite response, but dendrite effects are smaller and they can still mostly response when the thalamus is deactivated.
122
How do contributions to consciousness compare between the frontal cortex and parietal cortex?
The parietal cortex contributes more to consciousness than frontal cortex, as shown by experiments that "decode" consciousness.
Specifically, the thalamus, caudate, and parietal cortex all contribute more to consciousness than the frontal cortex.
123
Describe functional connectivity as an NCC
End of Lecture 3
Functional connectivity between CL thalamus and cortex increases during consciousness.
There is also increased feedback (to superficial layers) and feedforward (to medial/frontal cortex) projections during consciousness.
124
How are arousal thresholds altered in sleep?
Arousal thresholds are increased in sleep. Slow wave sleep (SWS) has the highest arousal threshold in response to sound, shown in college students, rats, and across 3 age groups.
In general, higher slow wave activity = higher arousal threshold.
Arousal thresholds are also increased in phasic and tonic REM sleep in response to sounds, but phasic REM sleep is as deep as SWS, and tonic REM sleep is similar to N2, which is lighter NREM sleep. So, arousal threshold higher in phasic REM than tonic REM.
125
How are cortical evoked potentials altered in sleep?
The amplitude of the cortical auditory evoked potentials is higher in NREM SWS sleep than in wake or REM sleep.
Early components are mostly unaffected or slightly delayed and reduced; late components are mostly affected (increased cortical responses for auditory and visual stimuli, reduced cortical responses for painful stimuli).
126
Describe sleep/wake changes in evoked unit firing in the auditory pathways
Little sleep/wake changes in evoked unit firing in primary and higher order auditory cortex.
In the primary and higher order auditory cortex, a lot of things don't change firing when there is sound, the distribution is very balanced. The response to sound is bidirectional (up or down) in both areas with no clear depressive effect of sleep.
127
What do evoked responses reflect?
Evoked responses mainly reflect the input (synaptic activity), not the output (spiking).
128
How do auditory responses in NREM and REM sleep relate?
Auditory responses in NREM sleep are poor predictors of responses in REM sleep. 1/3 of evoked auditory units show opposite responses in NREM and REM sleep: The mechanisms of controlling the flow of auditory stimuli may differ in NREM vs. REM sleep.
129
Can increased acoustic threshold in SWS be shown at the neural level?
Increased acoustic threshold in SWS in primate primary auditory cortex is shown at the neural level. In total, there were 169 units (69 responding to weak sounds, 106 to strong sounds). Note that strong stimuli did not cause arousal.
Despite these experiments, they do not provide a neural basis for the increased arousal threshold to loud sounds in NREM/SWS, and they do not address the mechanisms for auditory disconnection in REM sleep.
130
How do auditory responses and stimulus adaptation change across NREM and REM sleep?
Auditory responses and stimulus-specific adaptation in rat primary auditory cortex are preserved across NREM and REM sleep.
131
How does sleep affect neuronal responses in the auditory cortex vs. perirhinal cortex?
Sleep differentially affects early and late neuronal responses to sounds in auditory and perirhinal (object recognition memory) cortices.
Response in perirhinal cortex biggest in wake, middle in REM, smallest in NREM.
Response to sounds in the primary and higher order auditory cortex is very similar.
See slide 23 and later of Lecture 6 for more info.
Response to sounds decreases in both NREM and REM sleep only in the higher order auditory cortex (not perirhinal).
Peak latency in early vs late responding units is much smaller in the auditory cortex than in the perirhinal cortex. Early units are unaffected even in perirhinal, late units are affected even in auditory. The decreased response in NREM sleep depends on whether the unit is early or late responding, NOT on the cortical area per se. BUT, long latency does predict decreased response in REM.
132
How does speed of acoustic stimuli differ in NREM and wake?
In NREM sleep acoustic stimuli reach the cortical input layer (L4) as well, and as fast, as in wake (no gate in the primary thalamus).
133
To what does the medial auditory thalamus respond, and what is the effect of this response?
The medial auditory thalamus responds only to arousal-promoting stimuli and triggers arousal.
134
Describe acoustic communication takeaways
There is no thalamic gate for acoustic stimuli (at least in core thalamus), so in NREM sleep acoustic stimuli reach the cortical input later as well, and as fast, as in wake.
Interareal and interlaminar communications are impaired with NREM sleep (explains higher threshold).
Some evidence for early decrease in response in midbrain (non-lemniscal pathway).
135
Describe the auditory system summary as discussed in this lecture
There is no evidence for a (core) thalamic gate.
There is evidence for a cortical "gate" after the input layer.
There are decreased sensory responses already in midbrain reticular formation.
136
Is sleeping with eyes open uncommon?
Sleeping with eyes open is not uncommon. Inability to close eyelids during sleep is called nocturnal lagophthalmos and could lead to fragmented sleep.
137
How is LGN synaptic transmission affected in NREM sleep?
Synaptic transmission (pre and post-synaptic) in cat LGN is reduced in NREM sleep. The amplitude of the postsynaptic response decreases from alert to non-alert, is lowest in SWS, increases in REM sleep, especially with PGOs.
138
How are optic tract fibers affected by non-alert states?
The excitability of the optic tract fibers is reduced in non-alert states. The amplitude of the antidromic response is also decreased in SWS.
139
How does unit activity of the LGN differ in wake and sleep?
In the cat visual thalamus (LGN), during wake most LGN neurons respond to light flashes; in sleep, the same units respond in brief clusters.
In general, there is more "responsiveness" in waking than in NREM sleep in the cat visual cortex (unit activity). Most units in the visual cortex respond in wake only or wake and NREM sleep. REM sleep was not studied.
27 units respond in waking and NREM sleep: the early response is similar, but the late response is missing in NREM sleep. Meanwhile, 15-18 units respond only in waking, and do so late.
140
Describe the visual system summary
There is some vidence for a thalamic gate in NREM sleep.
There is evidence for a cortical "gate" after the input layer in NREM sleep.
Nothing is known about the visual system during REM sleep.
141
Describe the somatosensory system summary
There is a focus on early (pre-thalamic) pathways.
There is a depressed response to tactile and proprioceptive stimuli in REM sleep, but no change in NREM sleep compared to waking.
Very little is known about the thalamocortical system.
142
How are cortical pain responses altered in sleep?
Late components of cortical responses evoked by painful stimuli in humans are reduced, but only in stage 2 sleep.
143
How do laser-induced pain potentials correlate with pain perception?
The amplitude of the laser-induced cortical potentials (radiant heat from laser) correlate with pain perception. As amplitude increases, perceived intensity increases.
However, laser-induced cortical potentials decrease with distraction or drowsiness and disappear in NREM stage 2 sleep.
144
Describe the pain pathways summary
Animal studies focus on early (pre-thalamic) pathways; these studies show depressed response to painful stimuli in REM sleep, but no change in NREM sleep compared to waking.
In human studies, there are depressed cortical responses to pain in NREM sleep.
145
How does responsivity to odors differ in wake and sleep?
There is low responsivity to odors in sleep. Behavioral autonomic and EEG responses to olfactory stimuli are present in sleep, but the percentage of overall responsivity to olfactory stimuli is low.
146
Describe the olfactory system summary
There is evidence for stronger inhibition in the olfactory bulb during NREM and REM sleep compared to wake.
There is no direct evidence for a cortical gate.
147
Describe the basic summary/takeaways for acoustic, visual, somatosensory, pain, and olfactory systems
Acoustic:
- cortical gate after the input layer, no primary thalamic gate (NREM + REM)
Visual:
- cortical gate after the input layer, thalamic gate? (NREM only)
Somatosensory:
- prethalamic gate in REM? Th-cx unknown
Pain:
- animals: depressed response pre-thalamic (REM only)
- humans: depressed cortical response (NREM)
Olfactory:
- cortical gate?
- increased inhibition in OB (NREM + REM)
148
How can cortical effective connectivity be measured during sleep?
Cortical effective connectivity can be measured using TMS + high density EEG.
149
How do EEG responses to TMS differ in wake and sleep?
EEG responses to TMS are long and complex in wake but not in NREM sleep (early in the night). There is much less "frantic" spiking in NREM than in wake following TMS.
150
Why is the classical view of slow wave sleep (SWS) wrong?
The classical view of SWS is that it is widespread (a global phenomenon), but in reality, most sleep slow waves are local.
151
Is REM sleep a global phenomenon?
During REM sleep slow waves do occur, but only in superficial layers (L1, L2/3, L4 or V1, S1, M1).
During REM sleep slow waves do not occur in secondary (high order) areas.
Regional slow waves are also present during REM sleep in humans. The EEG power in the SWA range is higher in REM sleep than in waking in primary cortical areas but not in higher order areas.
152
What is unique about slow waves during REM sleep?
Slow waves during REM sleep are associated with OFF periods.
153
What are the two types of cortical slow waves during REM sleep in humans?
End of Lecture 6
Frontal central sawtooth waves (slide 76) and medial-occipital (slide 75) are the two types of cortical slow waves during REM sleep in humans.
See slide 74 of Lecture 6 for specifics.
154
Where is epilepsy on the consciousness scale?
Start of Lecture 8
Epilepsy has high arousal, low awareness on the consciousness scale.
155
What is the clinical need for absence seizures?
While absence seizures were classically considered as benign, gold standard seizure drug treatments only have partial efficacy.
156
How does epilepsy relate to consciousness?
Loss of consciousness during seizures has many negative consequences. There is a high risk of serious injury and suddent death (in particular for generalized tonic-clonic seizures (GTC)), also known as SUDEP.
157
What are auras with regard to seizures?
Auras are a common characteristic of seizures; they reveal that some sort of consciousness alteration is present in seizures.
Auras include deja vu, depersonalization, and other psychic feelings.
These are typical of focal seizures.
There are also intellectual auras, which have been described as "dreamy states" with a defect of consciousness. This used to be thought of as overconsciousness.
158
How do seizure traits differ based on where they occur?
Seizure traits differ based on where the seizure occurs within the brain.
Initial motionless staring is less common in frontal lobe seizures but common in temporal lobe seizures.
Seizure duration is brief in frontal lobe seizures but longer in temporal lobe seizures.
Postictal confusion is less prominent or short in frontal lobe seizures but more prominent and longer in temporal lobe seizures.
159
3 methods for assessing consciousness during seizures
1. Consciousness in Seizure Scale - scoring of video-EEG movies to assess responsiveness
2. Responsiveness in Seizure Scale - prospective method asking "what is your name?" or "wave hello." Also need to prospectively assess reports on top of prospective assessments of behavioral responsiveness.
3. Seizure mentation questionnaire - "what was going through your mind during the event?"
160
Describe responsiveness during focal seizures
Normal responsiveness during simple tasks during focal aware seizures (SPS) contrasts with markedly decreased (but not absent) responsiveness to simple tasks during focal unaware seizures (CPS).
Focal aware = normal responsiveness
Focal unaware = decreased (but not absent) responsiveness
161
How do focal aware seizures affect behavior?
Focal aware seizures (SPS) are associated with behavioral impairment. Namely, SPS may impair complex driving tasks.
162
Is there impaired/altered consciousness during focal aware seizures (SPS)?
Patients' subjective reports after seizures suggest that some degree of impaired/altered consciousness is also frequent during SPS - although to a lesser extent than in focal unaware seizures (CPS)
163
What is the responsiveness profile of GTC seizures?
Unlike SPS and CPS, GTC are typically accompanied by complete unresponsiveness.
Subjective reports of conscious experience during GTC are extremely rare.
164
What is a paroxysmal depolarizing shift?
Paroxysmal depolarizing shift represents a sudden and rapid depolarization of the neuronal membrane potential, which leads to a burst of action potentials. This is followed by a period of hyperpolarization, during which the neuron is less excitable.
The PDS is significant because it is considered a hallmark of epileptic activity within the brain. During the depolarizing phase, the neuron's membrane potential becomes less negative, often due to an influx of sodium (Na+) ions, which triggers the rapid firing of action potentials. This burst of electrical activity can contribute to the synchronized neuronal firing typical of epileptic seizures.
165
What is the ictal penumbra, ictal wavefront, and ictal core?
Ictal Core: The ictal core refers to the central region of seizure activity where the neuronal discharges are most intense. This is the primary site where the seizure originates, also known as the seizure focus or epileptogenic zone. In the ictal core, neurons exhibit highly synchronized activity, which is characteristic of the seizure. The pathological processes leading to seizure generation are most pronounced in this area, and it is typically the target for surgical interventions in drug-resistant epilepsy.
Ictal Wavefront: The ictal wavefront describes the dynamic boundary between the actively seizing tissue (ictal core) and the surrounding areas that are not yet involved in the seizure activity. It is essentially the front line of the spreading seizure activity. As the seizure progresses, this wavefront moves outward from the ictal core, recruiting adjacent neuronal regions into the seizure. The speed and direction of the wavefront's propagation can vary depending on the underlying neural network and the type of seizure. The "wave" is characterized by rapid spikes (tonic, clonic firing).
Ictal Penumbra: The term "penumbra" is borrowed from stroke medicine, where it describes the area surrounding an infarct that is at risk but not yet irreversibly damaged. In the context of seizures, the ictal penumbra refers to the regions around the ictal core and wavefront that are affected by the seizure but are not actively seizing. Neurons in the ictal penumbra may show altered excitability and are under the influence of the biochemical and electrical changes emanating from the core and wavefront. This area is crucial because it might be possible to intervene therapeutically to prevent the spread of seizure activity.
166
Is gamma activity phase locked in ictal rhythms?
High gamma activity (80-150 Hz) is also present in ictal penumbra, but not phase locked to slower ictal rhythms.
ECOG phase-locked high gamma (PLHG) is more focal than 2-25 Hz ictal EEg rhythms.
167
What channels are necessary for absence seizures?
Thalamo-cortical T-type channels are necessary for absence seizures. Knockouts of this channel block absence seizures.
168
What is the sleep spindle hypothesis of absence seizures?
Absence seizure spike-and-waves as pathological modifications of sleep spindles? This is a potential hypothesis, but isn't credible because spike-wave discharges (SWD) and spindles dissociate across wake/sleep.
169
Describe beta and delta waves as potential NCCs during focal (temporal) seizures
During focal aware seizures (SPS), there are increased ipsilateral beta waves but not ipsilateral/bilateral delta waves.
During focal unaware seizures (CPS), there are increased ipsilateral and contralateral beta and delta waves, but ipsilateral shows greater increases.
Delta activity is present in extra-temporal cortex during temporal lobe CPS, meaning there is sleep-like cortical activity.
170
What happens to central lateral thalamic (intralaminar) neurons during seizures?
In central lateral thalamic (intralaminar) neurons there is a decrease in firing rate and switch to burst firing. See Network Inhibition Hypothesis.
171
What is the Network Inhibition Hypothesis?
The network inhibition hypothesis proposes that seizures arise due to an imbalance between excitation and inhibition in neural networks in the brain. Normally, there is a delicate balance of excitatory and inhibitory signaling between neurons that allows normal brain function. Inhibition prevents excessive excitation and runaway signaling between neurons.
In the network inhibition hypothesis, a seizure occurs when inhibitory signaling in neural networks is impaired or excitation is enhanced, tipping the balance towards excessive excitation. This leads to hyper-synchronized bursts of activity that spread through neural networks, causing a seizure.
Specifically, the hypothesis suggests that inhibitory interneurons, which release the neurotransmitter GABA to inhibit neighboring excitatory neurons, play a key role. If these interneurons are impaired and cannot properly inhibit excitatory neurons, it can lead to hypersynchrony and seizure initiation. Factors that may impair inhibitory interneurons include alterations in GABA receptors, disruptions in chloride transport, and loss of certain subtypes of inhibitory interneurons.
The network inhibition hypothesis provides a framework for understanding how seizures arise from dysfunctional neural network activity, rather than a single focal source. It has implications for potential seizure treatments aimed at restoring balance and inhibition in neural circuits. However, there are still many open questions regarding the exact mechanisms and circuit dynamics involved in ictogenesis (seizure generation) based on this hypothesis.
172
What is the Global Workspace Theory of consciousness?
The global workspace theory proposes that consciousness emerges from a widespread network of neurons in the brain. According to this theory, multiple specialized modules or processes compete to broadcast information into a global workspace. The global workspace is a centralized information sharing network that allows communication between distant brain regions. Consciousness results when information gains access to this workspace, allowing binding and widespread distribution across the brain. So conscious experience corresponds to global availability of information. Unconscious processes remain localized within specialized modules. The global workspace enables integration and unified sense of consciousness from competing sensory, memory, emotional and cognitive inputs. Through global access, some information becomes available for reasoning, reporting and action, while information that doesn't reach the global workspace remains non-conscious. This theory provides a framework for understanding how conscious and unconscious processes interact in the brain.
173
What is the Integrated Information Theory (IIT) of consciousness?
The integrated information theory, developed by neuroscientist Giulio Tononi, aims to explain how consciousness emerges from the interactions between the different parts of the brain. It states that consciousness arises from the ability of any system to integrate information, meaning the whole is more than just the sum of its parts.
According to IIT, the quantity and quality of consciousness corresponds to the amount of integrated information generated by a complex of elements. Integrated information refers to information that is generated by the causal interactions between the parts of a system, rather than just within each part independently. The more integrated information a system has, the more conscious it is.
IIT proposes that consciousness is an intrinsic, fundamental property of reality present to the maximal degree in systems with significant integrated information. It provides a mathematical framework to measure consciousness levels calculated as "phi", or Φ, the amount of integrated information in a system. IIT remains controversial but continues to spur research into understanding consciousness from an information-theoretic perspective.
174
Explain the dissociation between consciousness and responsiveness during focal seizures
Of the 36 seizures with both measures available, 26 were concordant, including 21 seizures in which patients could not respond and could not recall. In 10 of the 36 seizures, the two measures were discordant, including nine seizures in which patients could not respond but could recall, and one in which the patient could respond but could not recall.
175
What is the result of brainstem and thalamic stimulation with regard to seizures?
Brainstem + thalamic stimulation can restore responsiveness during seizures and can even wake people from sleep and anesthesia.
176
Bicucculine in tonic-clonic seizures see slide 54 of Lecture 8
177
What are the subcortical mechanisms fo bilateral tonic-clonic convulsions?
For bilateral tonic clonic convulsions, this is caused by hyperactivity in brainstem.
If you have a hyperactive thalamus and cortex, unresponsive and no convulsion.
178
How can electroconvulsive therapy be used for bilateral tonic-clonic seizures?
There is increasing broad metabolism in generalized tonic clonic bilateral seizure.
This therapy helps ameliorate this.
179
How do GTC seizures compare to CPS?
GTC seizures have more asynchronous cortical ictal patterns that complex partial seizures (focal unaware). There is also decreased slow wave activity compared to CPS, more LOC, more cortical firing, more metabolism, increased high gamma during full body tonic clonic.
180
What does the BOLD signal of absence seizures reveal?
BOLD signals tell us that there are increases in brain activity in absence seizures. Specifically, there are activity increases then drastic decreases.
181
How do focal seizures and generalized seizures compare with regard to consciousness?
Both focal seizures and generalized seizures can present with different degrees of altered consciousness:
- Loss of consciousness is deepest in GTC seizures
- Cortical EEG slowing accompanies LOC during seizures that remain focal
- In contrast, seizure generalization is accompanied by widespread increases in cortical activity
- Absence seizures show widespread increases then decreases in cortical activity, which are more pronounced when consciousness is more altered
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