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YEAR 2 - The Nervous System > 24. Higher Cerebral Functions (HT) > Flashcards

24. Higher Cerebral Functions (HT) Flashcards

1
Q

What are the 5 main systems in the CNS and how does the limbic system fit into this?

[CONCEPTUALLY USEFUL]

A
  • The limbic system receives input from the sensory system and interconnects with the reward system and decision making system.
  • It outputs to the smooth and cardiac muscles via the hypothalamus releasing hormones and controlling the autonomic nervous system
  • Using the example of seeing a cute cat, the skeletal muscle won’t change, but the pupils will dilate due to control by the limbic system
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2
Q

What is the limbic system? What is the function?

A
  • Several functionally and anatomically interconnected brain structures
  • Functions: Emotions and memories (but also episodic memory without emotional content), as well as control of the self-preservation functions that are related to emotional stimuli (e.g. heart rate increases when scared)
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3
Q

Define an emotion and feeling.

A

Emotion:

  • Autonomic, behavioural and cognitive response triggered by a stimulus (e.g. pupil dilation, increased heart rate in fear)

Feeling:

  • Conscious perception of an emotional response
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4
Q

How many emotions do humans have?

A
  • 6 basic emotions -> Sadness, surprise, happiness, disgust, anger, fear
  • There are also complex emotions made up of two of these, such as disgust + anger = contempt
  • There are other complex emotions that cannot be made up of two of these, such as love, jealousy, pride, sympathy
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5
Q

How does the limbic system control functions necessary for self preservation and species preservation?

A
  • The hypothalamus controls autonomic and endocrine functions, especially in response to emotional stimuli.
  • Involved in motivation and reinforcing behaviours
  • Critical to particular types of memory
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6
Q

What types of emotional stimuli can the limbic system respond to?

A
  • Naturally significant stimuli (e.g. sweet taste, pain)
  • Stimuli made significant by association (i.e. conditioning)
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7
Q

Which sensory system is the limbic system closely connected to?

A

Olfactory

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8
Q

What are the components of the limbic system?

[IMPORTANT]

A
  • Amygdala
  • Hippocampus
  • Parahippocampal gyrus
  • Cingulate gyrus
  • Hypothalamus (mammillary bodies)
  • Orbitofrontal cortex
  • Basal forebrain (nucleus accumbens + parts of basal ganglia)
  • Some thalamic nuclei (anterior dorsomedial)
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9
Q

What is the limbic lobe?

A
  • An arc-shaped region of cortex on the medial surface of each cerebral hemisphere, consisting of parts of the frontal, parietal and temporal lobes
  • Broca identified it and thought that it was concerned primarily with smell
  • Papez, however, suggested that it was more concerned with emotion and that we must also consider the hypothalamus and higher cognitive function in addition to this
  • The modern view also takes into account the orbitofrontal cortex, amygdala and medio-dorsal nucleus of the thalamus
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10
Q

Label this.

A
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11
Q

What is the Papez circuit?

A

The circuit found within the limbic system.

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12
Q

Draw and describe the Papez circuit.

[IMPORTANT]

A

The circuit goes in this order:

  • Cingulate gyrus (1)
  • Parahippocampal gyrus (via the cingulum)
  • Denate gyrus + Hippocampus (2) (via the perforant path)
  • Fornix/fibria
  • Mammillary bodies (3)
  • Mammillothalamic tract
  • Anterior nucleus of dorsal thalamus

And then back to the cingulate gyrus.

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13
Q

Label this monkey brain.

A
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14
Q

What is the amygdala and where is it found?

A
  • It is a collection of nuclei in the medial part of the anterior pole of the temporal lobe.
  • It is part of the limbic system and it one of the most important parts of the brain for emotion.
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15
Q

Describe the structure and function of the different parts of the amygdala.

A

There are 3 main groups of nuclei:

  • Basolateral (green) -> Receives input from the auditory, somatosensory and nociceptive systems. Responsible for emotional response and emotional (reward) memory.
  • Centromedial -> Outputs to produce visceral responses (e.g. heart rate increases)
  • Cortical -> Part of the olfactory cortex
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16
Q

Describe how the different parts of the amygdala work together.

A

Basolateral amygdala receives combined sensory input and is responsible for emotional responses. It projects the the centromedial amygdala, which is responsible for visceral responses (e.g. increases in heart rate).

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17
Q

Summarise the inputs to the amygdala. What is each responsible for?

A

Inputs to the basolateral and central nuclei:

  • All sensory association cortex (combined sensory input) -> Both directly and via the thalamus
  • Cortical amygdala -> Part of olfactory cortex
  • Entorhinal cortex and hippocampus -> For memory, allowing the building up of an emotional memory
  • Cingulate area -> Feelings (top-down control)
  • Prefrontal area -> Reward processing (top-down control)
  • Septal area -> Reward and reinforcement
  • Mediodorsal thalamus -> Memory
  • Brainstem -> Visceral sensory

Spec: Olfactory system, sensory association cortex, hypothalamus and brainstem

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18
Q

Summarise the outputs from the amygdala. Where does each output from?

[IMPORTANT]

A
  • Amygdalofugal tract
    • To the hypothalamus
    • From the baslolateral and central nuclei
  • Stria terminalis
    • To the hypothalamus, thalamus nucleus accumbens (in forebrain) and septal nuclei of the forebrain
    • From the medial nuclei
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19
Q

What is shown here?

A
  • Orange arrow -> Amygdalofugal pathway
  • Green arrow -> Stria terminalis
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20
Q

Describe the path of the stria terminalis.

A

It goes from the amygdala to the septal area, thalamus and hypothalamus, which it does in a looping fashion around the diencephalon.

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21
Q

How does the the amygdala cause autonomic and endocrine components of emotional responses?

A

It outputs to the hypothalamus, which controls these functions.

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22
Q

Give some clinical and experimental evidence for the role of the amygdala.

[EXTRA]

A
  • Klüver and Bucy (1939) described a syndrome in monkeys following bilateral lobectomy of the anterior temporal lobe.
  • The animals showed visual agnosia, excessive oral tendency, visual attentiveness, placidity and lack of fear/anger, hypersexuality and eating changes
  • In humans, a similar condition is observed (Klüver-Bucy syndrome), which can occur as a result of Alzheimer’s, trauma, heat stroke and other conditions
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23
Q

Summarise in detail the functions of the amygdala.

A
  • Processing social indicators of emotion -> Especially facial expressions and vocal expressions of fear
  • Emotional conditioning -> Learning to associate certain stimuli with fear
  • Consolidation of emotional memories -> Memories with stronger emotions (e.g. someone crying) are remembered more strongly
  • Inducing the actual feeling of fear?
  • Olfactory processing
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24
Q

Describe how emotional conditioning can occur in the amygdala.

A

Via Pavlovian conditioning:

  • Painful stimulus (e.g. electric shock) is transmitted to the somatosensory thalamus and then somatosensory cortex
  • These then pass it to the lateral nuclei of the amygdala
  • Similarly, the harmless stimuli is also transmitted to the lateral nuclei of the amygdala (e.g. a sound transmitted via the auditory cortex)
  • The lateral nuclei of the amygdala process these and pass the information to the central nuclei, which control the hypothalamus’ control of responseses
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25
Q

How do lesions of the amygdala affect processing of social indicators of fear?

A

The patient may struggle to recognise and understand facial and vocal expressions of fear.

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26
Q

Give some experimental evidence for the amygdala being involved in feelings of fear.

[EXTRA]

A

(Feinstein, 2011):

  • Studied patient SM, who had Urbach-Wiethe disease with bilateral amygdala damage
  • IQ, memory, language and perception were unimpaired
  • But the patient had impaired fear conditioning, recognition of facial expressions, and fear-related social experiments
  • This was tested by exposing the patient to various animals (e.g. spiders) and scary films, none of which produced indications of fear
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27
Q

Describe how the limbic system is involved in olfaction.

A
  • Cortical amygdala is part of the primary olfactory cortex -> It distinguishes the intensity of odours
  • The primary olfactory cortex outputs to multiple areas:
    • Secondary olfactory cortex (orbitofrontal cortex) via the thalamus -> This distinguishes pleasant and unpleasant smells
    • Ventrolateral amygdala
    • Hypothalamus
    • Entorhinal cortex
    • Septum
    • Nucleus accumbens
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28
Q

Describe the structure of the hippocampal formation and hippocampus itself.

A

Hippocampal formation:

  • Hippocampus
  • Dentate gyrus
  • Subiculum
  • Entorhinal cortex (in parahippocampal gyrus)

Hippocampus:

  • Made of Cornu Ammonis (Ammon’s horn), which has parts CA1-4
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29
Q

Which sensory system can elicit particularly strong memories and why?

A
  • Olfactory system, because it is connected strongly to the entorhinal cortex that is part of the hippocampal formation.
  • This means that smells can bring about very vivid memories.
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30
Q

What is this?

A

Hippocampus

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31
Q

Draw the location of the hippocampus relative to the rest of the limbic system.

A

The hippocampus lies in the medial part of the temporal lobe “tucked into” the inferior horn of the lateral ventricle.

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32
Q

What is the function of the hippocampus?

A

Memory

(In particular, episodic memory, which refers to the ability to recount past events)

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33
Q

Summarise the inputs and outputs of the hippocampus.

[EXTRA?]

A

Note that the top input and output on these lists are part of the Papez circuit, which you do need to know.

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34
Q

Draw the circuitry of the hippocampus.

[EXTRA?]

A
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35
Q

What process underlies the formation of memories by the hippocampus?

A

Long-term potentiation (LTP)

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36
Q

What are the two types of LTP?

A

When two neurons synapse onto just one neuron:

  • If one synapse is active when the other is not -> Only the first synapse is strengthened
  • If first synapse is active strongly while the second synapse is active weakly -> Both synapses are strengthened

The second type may explain why we build strong associations between smells and memories.

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37
Q

What do lesions of the hippocampus cause?

[IMPORTANT]

A

Associative learning & episodic memory impairment.

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38
Q

Compare the roles of the left and right hippocampus.

[EXTRA?]

A
  • Left hippocampal lesions impair verbal/logical recall
  • Right hippocampal lesions impair visuo-spatial memory
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39
Q

Describe the functional organisation and cell types of the hippocampus.

[EXTRA?]

A

Posterior hippocampus -> Memory and spatial navigation:

  • Place cells support a cognitive map of known location (like taxi drivers remembering a map) and also allow episodic memory
  • Time cells fire at successive moments in temporally structured events

Anterior hippocampus -> Anxiety-related behaviours:

  • CA1 neurons connect to the amygdala

Note that this mapping is matched in the entorhinal cortex that connects to the hippocampus.

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40
Q

What is the main output tract of the hippocampus?

A

Fornix

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41
Q

How is the fornix clinically relevant?

[EXTRA?]

A

It carries cholinergic fibres to the hippocampus, which are affected in Alzheimer’s disease and kickstart the whole process.

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42
Q

Summarise the inputs and outputs of the mammillary bodies.

[EXTRA?]

A

Inputs:

  • From hippocampus via fornix (Papez circuit)

Outputs:

  • To anterior nucleus of thalamus, via mammillothalamic tract (thence to cingulate gyrus) (Papez circuit)
  • To midbrain tegmental motor structures (pedunculopontine nucleus)
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43
Q

Which part of the limbic system is responsible for reward? How?

A

Nucleus accumbens:

  • It receives input from other limbic areas, including the amygdala and hippocampus
  • Importantly it also receives dopaminergic input from the ventral tegmental area (this is the indicator of reward)
  • Onward signalling from the nucleus accumbens does not directly determine outcomes, but it can influence decision-making centres
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44
Q

Where is the orbitofrontal cortex?

A

It is part of the prefrontal cortex.

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45
Q

What is the function of the orbitofrontal cortex?

[IMPORTANT]

A
  • Behavioural inhibition
  • Inhibitory self-control
  • Emotional regulation

The latest opinion is that the orbitofrontal cortex does not only suppress unwanted behaviours and desires, but also encodes a ‘value’ of certain tasks, taking into account various factors such as difficulty, so that it can provide an updated value for these tasks. Thus, it underlies good and bad choices.

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46
Q

Summarise the inputs and outputs of the orbito-frontal cortex.

[EXTRA?]

A
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47
Q

What are the functions of individual neurons in the orbitofrontal cortex?

A

Different neurons have different functions:

  • Guide behaviours (I will do X to achieve Y)
  • Signal the hedonic experience of reward
  • Place a subjective value on a given reward
  • Detect error
  • One trial learning
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48
Q

How are some orbitofrontal neurons involved in detecting error?

[IMPORTANT]

A
  • There needs to be a comparison of the predicted reward obtained from an action with the actual reward obtained
  • OFC neurons provide VTA neurons with a prediction of the reward of potential choices, and DA neurons in turn project back to OFC with error signals to update them
  • This drives learning
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49
Q

Describe an experiment that demonstrates the orbitofrontal cortex assigning a ‘value’ to a reward.

[EXTRA]

A
  • Monkeys were shown different cards that indicated either a high-risk, medium-risk or low-risk situation
  • In the high-risk situation, the monkeys could receive either much more or much less juice than in the low-risk situation
  • The researchers found two populations of neurons in the OFC:
    • Economic risk neurons -> The rate of firing changes depending on the risk of the situation. If the outcome of the situation is known with certainty, there is no difference in firing, regardless of the reward size.
    • Value neurons -> The rate of firing changes depending on the reward size, if it is known. If it is not known with certainty (as in the experiment), then there is no change in firing depending on the risk.
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50
Q

What is one trial learning?

[EXTRA?]

A
  • When a single experience is associated with an outcome, without repeated exposure to strengthen this.
  • An example is taste aversion, where even just one bad encounter with food can put you off for life
  • The orbitofrontal cortex is responsible for this
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51
Q

Compare the functions of the medial and lateral orbitofrontal cortex.

[EXTRA?]

A

Lateral OFC:

  • Evaluates various decisions independently of each other
  • Determines an instantaneous, subjective value (e.g. eating this chocolate cake would be great!)
  • It integrates information from amygdala, hypothalamus, insular cortex (taste, disgust), DA neurons in midbrain (can heighten value attributed to a signal), sensory info from thalamus in order to do this

Medial OFC:

  • Compares these individual options in order to make a choice
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52
Q

What are the consequences of orbitofrontal cortex lesions?

[IMPORTANT]

A
  • Perseveration [IMPORTANT] -> This is a deficit in reversal of learning
    • Inability to change goals and activities
    • Inability to change problem-solving strategy, etc.
  • Loss of significance of stimuli (e.g. pain)
  • Behavioural changes, especially in disregarding laws
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53
Q

Summarise the main types and subtypes of memory/learning.

A
  • Declarative (explicit) -> Conscious memory of facts and events
    • Semantic -> Factual information (e.g. location of Eiffel tower)
    • Episodic -> Personal experiences (e.g. what you had for breakfast)
  • Non-declarative (implicit) -> Modes of learning that are non-conscious
    • Skills -> Learning skills and habits (e.g. how to ride a bike)
    • Category -> Assigning objects/skills in the world into classes for the purpose of generalization, discrimination, and inference (e.g. movie genres)
    • Priming -> Where identification of a stimulus is improved by an earlier encounter of that or other stimuli (e.g. being able to complete a partially completed letter once you recognise what it is)
    • Associative -> Learning to associate one stimulus with another stimulus (i.e. conditioning).
    • Non-associative -> When repeated exposure to a stimulus leads to a change in how intensely it is perceived (e.g. repeatedly hearing a sound in the background may cause you to tune it out).
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54
Q

Compare whether semantic or episodic (both declarative) memories are stored in the long term.

A
  • Semantic memories (i.e. facts) are likely to be stored in long-term memory
  • Episodic memories (i.e. experiences) are unlikely to be stored in long-term memory, as the name suggests
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55
Q

What are the two main types of non-associative (non-declarative) learning?

A
  • Habituation -> A decrease in response to a benign stimulus when the stimulus is presented repeatedly. A dog will be aroused when a strange tone is played. If the tone is played over and over, the dog will eventually no longer be aroused by the tone
  • Sensitization -> An enhanced response to many different stimuli after experiencing an intense or noxious one. For example, an animal responds more vigorously to a tone of lesser intensity once a painfully loud tone has been played.
56
Q

What are the two types of associative learning (conditioning)?

A
  • Classical conditioning (Pavlovian) -> When an conditioned stimulus is associated with an unconditioned stimulus
  • Operant conditioning -> When a certain behaviour is associated with a reward or outcome
57
Q

Is memory distributed or localized?

A
  • Memory is both distributed and localized.
  • Memory is distributed in that many parts of the nervous system participate in the representation of a single event.
  • Memory is localized in that a single event involves a limited number of brain systems.
58
Q

Summarise the main memory systems in the brain.

[EXTRA?]

A
59
Q

Describe the case of H.M. and what this teaches us about memory.

[EXTRA]

A
  • Patient H.M. suffered from epilepsy and had his hippocampus and parahippocampal regions removed as a possible treatment
  • The result of this was that he developed severe anterograde amnesia, meaning that he was unable to form new memories
  • He also had graded retrograde amnesia, meaning that his long-term past memory was more affected most regarding memories just before the operation -> He was able to recall childhood memories but struggled with memories of the years before the operation
  • This demonstrated the importance of the hippocampus in forming long-term memories
60
Q

What are the causes and symptoms of Korsakoff syndrome?

[IMPORTANT]

A
  • It is a syndrome characterised by severe memory loss and confabulation
  • It is caused by thiamine (vit. B1) deficiency, which is often seen in alcoholics
  • The mammillary bodies in the Papez circuit seem to be particularly affected
  • It is reversible
61
Q

What are the brain regions involved in declarative memory?

A
62
Q

Describe an experiment that can be used to study declarative memory in animals.

[EXTRA]

A
  • The Morris water maze involves a hidden platform that mice swim around to find
  • Within a couple of trials, the mice learn the location of the platform and immediately swim to it
  • The effect of various interventions on this memory can thus be studied
63
Q

What physiological process largely underlies memory?

A

Long-term potentiation (LTP)

64
Q

Give some experimental evidence for the existence of LTP.

A
  • When the pre-synaptic cell in the hippocampus is stimulated, it leads to increased magnitude of EPSPs
  • However, this increase in EPSP is maintained for a long time, which is known as LTP
65
Q

How does long-term potentiation in the hippocampus lead to memory formation?

[EXTRA?]

A
  • There are arrays of synapses in the hippocampus
  • Various synapses within these arrays are strengthened by LTP during memory formation
  • This leads to the formation of an engram that underlies memory formation
66
Q

Give some clinical evidence for the importance of LTP in memory formation.

[EXTRA]

A

One of the first changes seen in Alzheimer’s disease is loss of synapses, which underlies some of the early memory loss.

67
Q

What are some alternative models for memory formation?

A
  • Cellular engram (rather than synaptic engram)
  • Changes in cell excitability (anti-accommodation/ES potentiation) -> Disproved by the fact that things like anaesthetics do not alter memory
  • Reverberating circuits
  • Inhibition
68
Q

What is consciousness?

A

“Consciousness consists of inner, qualitative, subjective states and processes of sentience or awareness. Consciousness, so defined, begins when we wake in the morning from a dreamless sleep and continues until we fall asleep again, die, go into a coma, or otherwise become ‘unconscious’. It includes all the enormous variety of the awareness that we think of as being characteristic of our waking life.” John Searle

69
Q

What are the two components of consciousness?

A
  • Wakefulness (level of consciousness) -> How awake or asleep you are
  • Awareness (content of consciousness) ->To what extent you are aware of the external surroundings and internal world.

For a patient to maintain consciousness, both of these components must be maintained. Essenitally, wakefulness describes the quantitative degree of consciousness, whereas awareness relates to the qualitative aspects of the functions mediated by the cortex, such as attention, etc.

70
Q

Draw a graph of various forms of consciousness according to the two parameters: awareness and wakefulness.

A
71
Q

Give an example of a state where there is high wakefulness but low awareness.

A

Sleepwalking, Vegetative state, Seizures

72
Q

Give an example of a state where there is low wakefulness but high awareness.

A

REM sleep has higher awareness than deep sleep, which explains why we might remember some dreams from REM sleep.

73
Q

Summarise how sleep waves change during the different stages of sleep.

A

Note how REM sleep and being awake are very similar.

74
Q

What are some hypotheses about the function of sleep?

A
  • Energy metabolism
  • Repair and detoxification
  • Homeostatic synaptic plasticity
  • Memory consolidation
75
Q

Define coma.

[IMPORTANT]

A
  • A coma is a deep state of prolonged unconsciousness in which a person cannot be awakened, fails to respond normally to painful stimuli, light, or sound, lacks a normal wake-sleep cycle and does not initiate voluntary actions.
  • Clinically, a coma can be defined as the inability consistently to follow a one-step command. It can also be defined as a score of ≤ 8 on the Glasgow Coma Scale (GCS) lasting ≥ 6 hours.
76
Q

What is a defining feature of coma?

A

Unresponsiveness

77
Q

Name some causes of coma.

A
78
Q

Clinically, how can level of consciousness (wakefulness) be assessed?

A

Using the Glasgow coma scale.

79
Q

Clinically, how can contents of consciousness (awareness) be assessed?

A

Contents of consciousness often difficult to evaluate in the clinic because level of consciousness is often reduced at the same time. For example, it is hard to assess someone’s alertness when they are asleep.

80
Q

What are some disturbances of the contents of consciousness?

A
  • Confusion -> Inability to maintain a coherent sequence of thought and actions
  • Delirium -> Agitated, hypersympathotonic, often hallucinatory
  • Illusion -> A misperception of sound, sight, or touch
  • Hallucination -> A spontaneous endogenous perception
81
Q

What are some states that are similar to coma?

A
  • Vegetative state
  • Locked-in syndrome
  • Catatonia
82
Q

What is the vegetative state and how is it different from coma?

[IMPORTANT]

A
  • It is where a patient was in a coma but is has now opened their eyes
  • There are signs of extensive damage to both cerebral hemispheres: Babinski, decerebrate or decorticate posturing, no response to visual stimuli, no corrective nystagmus in VOR
  • Autonomic nervous system function often preserved but may show hyperactivity
  • Yawning, grunting, picking with hands, random limb and head movements may occur

In other words, the vegetative state has similarly low awareness to a coma, but it has much greater wakefulness (as shown by the movements, etc.).

83
Q

What is locked-in syndrome?

[EXTRA]

A

Pseudo-coma:

  • Patients who are awake but selectively deefferented—no means of producing speech or limb, face, or pharyngeal movements
  • Results from infarction or haemorrhage of the ventral pons, which transects all corticospinal and corticobulbar pathways but leaves RAS intact
  • Vertical eye movements and blinking (Nn. III and IV) after basilar artery thrombosis often intact
84
Q

What is catatonia?

[EXTRA]

A
  • Generic term for peculiar motor activities associated with major psychosis
  • Patients appear awake with eyes open but make no voluntary or responsive movements
  • Spontaneous eye blinking
  • “Waxy flexibility”: limbs maintain their posture after passive movement
85
Q

What is the neurocentric definition of death?

A
  • In 1995, the Royal College of Physicians deemed that death was defined as the irreversible loss of brainstem function.
  • This was because, since the advent of mechanical ventilation in the 1950s, cardiorespiratory function and brain function could be uncoupled, so a neurocentric definition was required.
86
Q

Is the vegetative state the same as brain death?

A

No, a vegetative state is reversible, brain death is not.

87
Q

What are the criteria for brain death?

A
88
Q

What are some criteria for the vegetative state?

A
89
Q

What are the criteria for sleep?

A
  1. Physical quiescence
  2. Typical body posture
  3. Specific sleeping site
  4. Elevated threshold for arousal / reactivity
  5. Rapid state reversibility (this differentiates it from coma, etc.)
90
Q

What are some ways of monitoring sleep?

A
  • Actigraphy -> Measuring movement over time. Sleep is indicated by periods of immotility.
  • Standard polysomnography -> Using EEG (electroencephalogram) and sometimes other techniques to measure sleep
91
Q

How does EEG (electroencephalography) work?

A
  • EEG measures the potential differences between two points on the scalp (or on the surface of the brain).
  • EEG can be described in terms of frequency (Hz) and amplitude (microvolts) of voltage fluctuations.
92
Q

Describe the EEG during different stages of sleep.

[IMPORTANT]

A
  • Wakefulness
    • Low amplitude, fast waves
  • Stage 1 (Non-rapid eye movement)
    • Slightly larger amplitude, quite fast waves
    • Slow eye movements
  • Stage 2 (Non-rapid eye movement)
    • Larger amplitude waves
    • Includes sleep spindles (bursts of activity) and K-complexes (large waveforms) -> These are characteristic of stage 2 NREM
  • Stage 3 (Non-rapid eye movement)
    • High amplitude, slow waves (1-4Hz)
  • REM (Rapid eye movement)
    • Appears very similar to wakefulness
93
Q

What differentiates wakefulness from stage 1 NREM sleep?

A

Wakefulness in a relaxed subject with eyes closed is differentiated from sleep by the presence of alpha EEG activity in 50% or more of the epoch.

94
Q

What are sleep spindles and K-complexes? What are they a defining feature of?

A

They are characteristic of stage 2 NREM sleep.

95
Q

What are two factors that may affect the EEG pattern of sleep?

[IMPORTANT]

A
  • Age
  • Some diseases (e.g. Schizophrenia and neurodegenerative diseases)
96
Q

What is this?

A

EEG spectral analysis:

  • EEG signals at different sleep stages feature different wave frequency compositions
  • To quantatively analyse the contribution of each wave frequency, you can plot a graph of power against frequency.
97
Q

What are neural oscillations?

A
  • AKA brainwaves
  • These are rhythmic or repetitive patterns of neural activity in the CNS
98
Q

Describe the system that is responsible for generating sleep waves.

[EXTRA?]

A

Thalamocortical system:

  • Cortical neurons send excitatory projections onto reticular thalamic (RT) nucleus neurons and thalamocortical (TC) neurons
  • Thalamocortical (TC) also send excitatory projections onto the cortex and the reticular thalamic (RT) nucleus neurons
  • Reticular thalamic nucleus neurons are inhibitory (GABAergic) and send projections onto the thalamocortical (TC) neurons
99
Q

Name the main types of sleep waves and their frequency.

[EXTRA?]

A
  • Infra-slow (0.02-0.1 Hz)
  • Slow:
    • Slow oscillation (0.2-1 Hz)
    • Delta (1-4 Hz)
    • Spindle (7-15 Hz)
    • Theta (4-10 Hz)
  • Fast (20-60 Hz)
  • Ultra-fast (100-600 Hz)
100
Q

Give an example of an abnormality of the EEG in schizophrenic patients.

A

There are no sleep spindles, which explains why there is no spike on this spectrum.

101
Q

Give some experimental/clinical evidence for the parts of the brain that are involved in sleep.

[EXTRA]

A

Von Economo first noted that:

  • Lesions in the anterior part of the hypothalamus often lead to insomnia
  • Lesions in the brainstem often lead to sleepiness/coma

(Gong, 2000):

  • Expression of c-fos is an indirect marker of neuronal activity because c-fos is often expressed when neurons fire action potentials.
  • Most of the brain shows decreased activity during sleep, indicated by decreased c-fos, but there are some parts that show increased c-fos, which may indicate that they play an important role in sleep.
102
Q

Describe which parts of the brain are active during the awake state. (i.e. what parts of the brain maintain consciousness)

[IMPORTANT]

A

Brainstem reticular activating system.

Activity is predominantly at cholinergic and aminergic projections up from subcortical nuclei to areas of the cerebral cortex, which maintains its function. These include:

  • Laterodorsal/pedunculopontine tegmental nucleus
  • Locus coeruleus
  • Orexin-producing neurons in the hypothalamus
  • Basal forebrain
103
Q

Describe which parts of the brain are active during the sleep state.

A

A thalamic population of neurons (Ventrolateral/median preoptic area) predominate during sleep and act by inhibiting the ascending systems that drive the awake state (see previous flashcard).

Therefore, there is switching between populations of neurons when going to sleep and waking up, but what drives these switches is yet unknown.

104
Q

What is the reticular activating system? What parts of the brain are involved?

A
  • It is a series of nuclei and pathways in the brainstem that are involved in the maintenance of the awake state.
  • They project up to the thalamus, hypothalamus and basal forebrain regions -> These then project to the cerebral cortex to maintain wakefulness (and there are direct projections to the cortex).
105
Q

What neurotransmitters are involved in the control of sleep (in the reticular activating system, etc.)?

A
  • Acetylcholine
  • Noradrenaline
  • Histamine
  • Dopamine
  • Serotonin
  • Orexin
  • GABA

GABA, ACh and orexin are mentioned in the spec.

106
Q

What are some areas of the brain important to sleep that are mentioned in the spec?

A
  • Hypothalamus
  • Brainstem
  • Basal forebrain
107
Q

Draw the cholinergic systems involved in sleep control.

A
108
Q

Give some experimental evidence for the importance of the reticular activating system (in the brainstem) in maintaining wakefulness.

[EXTRA]

A

(Carter, 2010):

  • Used optogenetics to stimulate the locus coeruleus neurons.
  • This lead to immediate sleep-to-wake transitions.

(Oikonomou, 2019):

  • However, stimulation of the dorsal raphe nucleus can lead to promotion of either sleep or wakefulness depending on whether the stimulation is tonic or burst.
109
Q

Give an example of how antidepressants can affect sleep.

[EXTRA]

A

MAO inhibitors lead to the almost complete elimination of REM sleep.

110
Q

What is orexin? Where is it released and what is its role?

A
  • Orexin neurons are found in the lateral hypothalamus
  • They send axons to the entire cerebral cortex, as well as to the brainstem and basal forebrain
  • Orexin neurons are involved in wakefulness and motivated behaviours (e.g. finding food)
  • They fire predominantly during wakefulness, and particularly during motivated behaviors
111
Q

What is another name for orexin?

A

Hypocretin

112
Q

Where is orexin released from in the brain?

A

Lateral hypothalamus releases it onto the cerebral cortex, brainstem and basal forebrain.

113
Q

What triggers orexin release from the lateral hypothalamus?

A

Orexin neurons are inhibited by glucose, and activated when glucose is low -> This makes sense because food seeking behaviours occur when you are awake, so it is useful for orexin to be released then.

114
Q

On what receptors does orexin act and how can this be exploited pharmacologically?

A
  • The biological effects of orexin-A are mediated by two G-protein coupled receptors (OX1R and OX2R).
  • Selective OX2R agonists increased wakefulness and inhibited sleep in rats.
  • Selective destruction of the orexin neurons results in the symptoms of narcolepsy.
115
Q

Give some clinical relevance relating to narcolepsy.

[EXTRA]

A
  • Narcolepsy is a condition characterised by overwhelming daytime drowsiness and sudden attacks of sleep during the day.
  • The patients show abnormal cycles during sleep, although patients typically feel refreshed after awakening in the morning. However, sleepiness will rapidly evolve within hours and becomes irresistible (“sleep attacks”)
  • It has been hypothesized that patients with NC are unable to consolidate wakefulness and sleep because of abnormal sleep-wake regulation.

(Chemelli, 1991):

  • Orexin knockout mice present with a form of narcolepsy
116
Q

What is the main brain area involved in promoting sleep (rather than wakefulness)?

A

Ventrolateral preoptic area (VLPO)

117
Q

Describe a model for how sleep switching occurs.

A
  • The basic principle of the model is that brain regions involved in promoting sleep (e.g. VLPO) and wakefulness (TMN, LC, LH, vPAG) act in opposition to each other, largely through mutual inhibitory connections.
  • When you are awake, the areas responsible for wakefulness dominate.
  • When you are asleep, the areas responsible for sleep dominate.
118
Q

Where are GABAergic neurons that are involved in sleep?

A

The neurons in the ventrolateral preoptic area (VLPO) release GABA, which leads to sleep.

119
Q

How do benzodiazepines affect sleep?

A
  • They can induce sleep since they potentiate GABAergic transmission.
  • However, this sleep does not appear to be the same as normal sleep.
120
Q

Describe how REM sleep control occurs.

A
121
Q

Describe sleep-wake cycling (i.e. what determines when sleep switching occurs).

A
  • Process S (sleep) -> Builds up gradually the longer you are awake, applying sleep pressure.
  • Process C (circadian) -> Is dependent on the internal circadian clock that drives wakefulness during the day.
122
Q

Which part of the brain is involved in the circadian rhythm?

A

Suprachiasmatic nucleus

123
Q

Describe how the circadian clock works.

A
  • The master clock in the suprachiasmatic nucleus is composed of numerous clock cells.
  • The SCN receives light information by a direct retinohypothalamic tract (RHT) to entrain the clock to the 24-h day
  • The SCN coordinates the timing of oscillators in other brain areas and in peripheral organs -> All cells have their own intracellular clocks, but they average out across organs and they are under the influence of the SCN
124
Q

Via what tract does the suprachiasmatic nucleus receive light information?

A

Retinohypothalamic tract (RHT)

125
Q

What cells in the eye detect light for the circadian rhythm?

A

Certain retinal ganglion cells -> These mean that even people who are blind due to dysfunctional photoreceptors have a circadian rhythm.

126
Q

Describe how retinal ganglion cells affect the circadian rhythm in the suprachiasmatic nucleus.

A
  • The neurons release glutamate and PACAP onto the SCN neurons
  • This leads to a cascade that ends in mPer1 expression
127
Q

Experimentally, how can we study circadian rhythms in humans?

[EXTRA]

A
  • Constant routine -> Involves keeping the participants under constant conditions, including constant illumination and frequent small meals.
  • Forced desynchrony -> The participants are exposed to a light-dark cycle that is much shorter (e.g. 20hr) or longer (e.g. 28hr) than the circadian pacemaker can entrain. So the person sleeps when it is dark but the circadian rhythm is off, so this protocol is good for studying processes at various points in the circadian rhythm.

Measurements include core body temperature and melatonin measurements via blood samples or saliva.

128
Q

What hormone is involved in the circadian rhythm and where is it produced?

A
  • Melatonin
  • In the pineal gland
129
Q

Describe the action of melatonin.

A
  • The suprachiasmatic nucleus (SCN) clock regulates the timing of melatonin synthesis and release from the pineal gland
  • Melatonin has chronobiotic effects and is able to synchronize and reset biological oscillations
  • Circulating levels of melatonin communicate temporal information to a number of physiological systems and can also feedback to the SCN clock
130
Q

What is a good measure of sleep need?

A
  • Slow wave activity is seen largely during the first half of the night during sleep
  • The intensity of these waves is a good indicator of how badly the body needs sleep
  • For example, if you take a nap, then the slow waves will be decreased that night
131
Q

Give some experimental evidence for what could underlie process S (sleep drive).

[EXTRA]

A

(Porkka-Heiskanen, 2000) and (Basheer, 2004):

  • These studies give evidence for adenosine as the substance underlying sleep drive
  • The hypothesis is that adenosine release increases during waking, building up gradually and leads to inhibition of neural activity in wake-promoting brain regions
132
Q

How does sleep change with age?

[EXTRA]

A

People tend to go to sleep earlier and sleep for a shorter amount of time. But it is still debated: Do older adults need less sleep, or they are unable to generate the sleep that they still need?

133
Q

Give some clinical relevance of sleep and depression.

[EXTRA]

A
  • About 3/4 of patients with depression experience insomnia symptoms
  • (Borbély and Wirz-Justice, 1982) -> One hypothesis for this is the process S deficiency hypothesis, which suggests that this is due to reduced sleep drive
134
Q

Give some clinical relevance relating to the classification of sleep disorders.

[EXTRA]

A

The ICSD-2 lists 81 major sleep disorders in 8 major categories:

  • Insomnias
  • Sleep-related breathing disorders
  • Hypersomnias of central origin
  • Circadian rhythm sleep disorders
  • Parasomnias
  • Sleep-related movement disorders
  • Isolated symptoms, apparently normal variants and unresolved issues
  • Other sleep disorders
135
Q

Is insomnia a condition of sleeplessness or wakefulness?

[EXTRA]

A
  • Insomnia is clinically defined as difficulty with sleep initiation, sleep maintenance, or overall diminished sleep quality in association with reports of poor daytime functioning (i.e., fatigue, decreased memory and concentration, daytime distress).
  • Insomnia is a manifestation of a dysregulation of autonomic and central nervous system arousal networks producing hyperarousal.
  • The insomnia disorders can be either primary or secondary.
  • Primary insomnias can have both intrinsic and extrinsic factors involved in their etiology, but they are not regarded as being secondary to another disorder.
  • Secondary forms occur when the insomnia is a symptom of a medical or psychiatric illness, another sleep disorder, or substance abuse.
136
Q

Give some clinical relevance relating to sleep-related breathing disorders.

[EXTRA]

A
  • Central apnea syndromes include those in which respiratory effort is diminished or absent in an intermittent or cyclical fashion as a result of central nervous system dysfunction.
  • Primary central sleep apnea is a disorder of unknown cause characterized by recurrent episodes of cessation of breathing during sleep without associated ventilatory effort.
  • Obstructive sleep apnea in adults is characterized by repetitive episodes of cessation of breathing (apneas) or partial upper airway obstruction (hypopneas). These events are often associated with reduced blood oxygen saturation. Snoring and sleep disruption are typical and common.
  • Sleep apnea is associated with excessive daytime sleepiness or insomnia.
  • OSA affects 1 to 6% of adults and 2% of children. Central sleep apnea affects less than 1% of people
137
Q

What are parasomnias?

[EXTRA]

A
  • The parasomnias are undesirable physical or experiential events that accompany sleep.
  • The parasomnias consist of abnormal sleep-related movements, behaviors, emotions, perceptions, dreaming, and autonomic nervous system functioning.
  • Three parasomnias have typically been associated with arousal from non-REM sleep: confusional arousals, sleepwalking and sleep terrors.
  • REM sleep behavior disorder is a parasomnia typically associated with the REM sleep stage. RBD involves abnormal or violent behaviors that occur in REM sleep and result in injury or sleep disruption. RBD can occur in narcolepsy, and many patients with Parkinson’s disease have REM sleep behavior disorder.
  • Recurrent isolated sleep paralysis can occur at sleep onset or on awakening: it is characterized by an inability to perform voluntary movements and may be accompanied by hallucinations

YEAR 2 - The Nervous System (18 decks)

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