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Semester 2 exams - Manchester Cogneuro > Brain and behaviour > Flashcards

Brain and behaviour Flashcards

1
Q

what is mental representation

A

the sense in which properties of the outside world (e.g colours/objects) are copied/simulated by cognition

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2
Q

what is neural representation

A

way in which properties of the outside world manifest themselves in the neural signal (e.g different spiking rates for stimuli)

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3
Q

In what direction does neuraxis go

A

rostral to caudal ( front to back)

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4
Q

what are the 3 planes of the brain

A

transverse, saggital, horizontal

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5
Q

what is the horizontal plane parallel to

A

the ground

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6
Q

what is the horizontal plane parallel to

A

the ground

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7
Q

what is the sagittal plane parallel to

A

the neuraxis, it is perpendicular to the ground

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8
Q

at what angle does the transverse plane intersect the neuraxis

A

right angle intersection

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9
Q

how much does the brain weigh

A

1400g , 2% of body weight

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10
Q

how much oxygen does the brain does the brain consume and how much of the blood supply does it use up

A

around 20% for both

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11
Q

what are the 3 protective layers of the brain called. What are the individual layers called

A

The layers are called Meninges. The outermost layer is the dura mater. The middle layer is the arachnoid, the last layer is the pia mater

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12
Q

Where is cerebrospinal fluid kept?

A

In the subarachnoid space (between arachnoid and pia) and in the ventricles of the brain

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13
Q

what are brain ventricles

A

hollow chambers in the brain filled with CSF

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14
Q

What generates/produces CSF

A

choroid plexus

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15
Q

What is the total volume of CSF at one time and how many times does this turnover within a day

A

125-150ml, 3-4 times a day

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16
Q

What is hydrocephalus

A

the consequence of CSF not being reabsorbed and there being too much liquid in the brain (can occur in babies)

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17
Q

what is the cerebral cortex

A

a thin wrinkled layer of tissue covering brain, consisting of two hemispheres

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18
Q

what is the neocortex

A

thin layer of cerebral cortex

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19
Q

what is special about dolphin brains

A

they have more crumpling in their cerebral cortex but they have a thinner neocortex

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20
Q

what are the two divisions of the cerebrum

A

white and grey matter

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21
Q

what is grey matter composed of

A

cell bodies of neurons

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22
Q

what is white matter composed of

A

axons and dendrites of the neurons, bundles of ‘cables’ connecting regions of the brain & spinal cord

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23
Q

what are the four divisions of the cerebral cortex

A

Frontal Lobe
Parietal Lobe
Temporal Lobe
Occipital lobe

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24
Q

what are the primary cortices of the cortex

A

primary auditory , primary motor , primary visual , primary somatosensory

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25
Q

what is the function of the primary somatosensory cortex

A

receives info from body sense; different regions receive info from different body parts

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26
Q

what is brodmanns area

A

a region of the cerebral cortex defined based on its architectonics (structure & organisation of its cells)

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27
Q

what is the limbic system

A

a set of structures involved in learning, memory and emotion

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28
Q

what are the structures of the limbic system

A

limbic cortex, hippocampus, amygdala, fornix & mammillary bodies

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29
Q

what is the basal ganglia

A

set of structures involve in processing info for motor movement

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30
Q

what are some of the major structures of the basal ganglia

A

Caudate Nucleus
Putamen
Globus Padillius

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31
Q

what is the tectum (part of mesencephalon) involved in

A

fast eye movements (vision)
and the auditory pathway

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32
Q

what does the tegmentum (part of the mesencephalon) have a role in

A

motor movement

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33
Q

what are the pons involved in

A

sleep & arousal

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34
Q

what is the cerebellum involved in

A

motor co-ordination & smooth execution of movement

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35
Q

what does the mylecephalon contain and what does this make it involved in

A

the medulla oblongata. basic life functions (breathing, swallowing etc) and sleep wake cycles

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36
Q

what roots carry sensory info to the CNS

A

dorsal (afferent)

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37
Q

what roots carry motor info away from the CNS, towards the effector

A

ventral (efferent)

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38
Q

how many pairs of afferent and efferent nerves do we have in the spinal cord

A

31

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39
Q

how many sets of cranial nerves do we have

A

12

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40
Q

which nervous system is responsible for ‘fight or flight’ functions

A

sympathetic

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41
Q

which nervous system is used for ‘rest and restore’ functions

A

parasympathetic

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42
Q

what do motor neurons do

A

control muscle contraction and gland secretion

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43
Q

what do sensory neurons do

A

detect changes in external and internal environment

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44
Q

which type of neuron is ONLY in the CNS and are involved in cognition

A

interneurons (both Sensory and motor neurons are in both PNS &CNS )

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45
Q

what is the difference between a unipolar, bipolar and multipolar neuron

A

Multipolar neuron – one axon and many dendrites attached to soma.
Bipolar Neuron – one axon and one dendrite attached to soma.
Unipolar Neuron – one axon attached to soma; axon divides, one branch receiving sensory information - other sending the information into CNS

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46
Q

what type of glial cell acts as an immune cell

A

microglia

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47
Q

what do astrocytes do

A

Provide physical support to neurons
Provide nourishment
Clean up debris and form scar tissue when neurons die

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48
Q

what do oligodendrocytes do

A

-support axons and produce the myelin sheath - insulation lipids

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49
Q

what do oligodendrocytes do

A

-support axons and produce the myelin sheath - insulation lipids

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50
Q

what is the blood brain barrier

A

semipermeable barrier between the CNS and circulatory system which helps regulate the flow of nutrient rich fluid into the brain

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51
Q

what is the area postrema and why is it bad

A
  • region of medulla where blood- brain barrier is weak - allows toxins in blood to stimulate this area which initiates vomiting, poison expelled from the body
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52
Q

in a sodium potassium pump, what goes in and out and how many go in and out

A

3 sodium in per 2 potassium out

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53
Q

in an action potential, what channels open and close in what order

A

Sodium channels open when threshold is reached
Potassium channels open in rising phase
Sodium channels close at peak
potassium channels start to close as resting potential is reached

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54
Q

what is the all or none law

A

when an action potential occurs, it happens in full

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55
Q

what is rate law

A

variations in intensity of stimulus are seen in variations in rate at which the axon fires

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56
Q

what happens in saltatory conduction

A

AP’s are conducted along myelinated axons and the AP seems to jump from one node of ranvier to the next

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57
Q

What is EPSP and what would cause it to occur

A

excitatory depolarization of the postsynaptic membrane. Likely to be caused by sodium channels opening

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58
Q

what is IPSP and what would lead to it occuring

A

inhibitory hyperpolarization of the postsynaptic membrane. Caused by opening of chloride or potassium channels

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59
Q

what is neuronal intergration

A

the process where inhibitory & excitatory postsynaptic potentials summate & control rate of firing of a neuron

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60
Q

what is psychopharmacology

A

the study of the effects of drugs on the nervous system & on behaviour

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61
Q

what is the nocebo effect

A

people feeling worse after an intervention that should have no ill effects

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62
Q

what neurotransmitter typically causes depolarisation/ an excitatory response

A

glutamate or norepinephrine

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63
Q

what neurotransmitter(s) typically cause an inhibitory response

A

GABA, glycine or opiods

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64
Q

what neurotransmitters can exhibit either an excitatory or inhibitory response

A

acetylcholine, dopamine and serotonin

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65
Q

what type of receptors does ACh bind to

A

nAChR, mAChR

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66
Q

what kind of receptors does GABA bind to

A

GABA1, GABA2

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67
Q

what kind of receptors does glutamate bind to

A

NMDA, AMPA

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68
Q

what kind of receptors does serotonin bind to

A

5-HT receptor (serotonin aka 5-HT)

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69
Q

What happens at a cholinergic synapse

A

Voltage gated calcium channels open, leads to release of ACh vesicles into synapse. ACh binds to postsynaptic receptors, leads to sodium channel opening & thus depolarisation.

AChE(enzyme) breaks down ACh and its reuptaken

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70
Q

what kind of receptor is a nicotinic receptor , what is it stimulated by and what is it blocked by

A

ionotropic, stimulated by nicotine, blocked by curare

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71
Q

what kind of receptor is a muscarinic receptor, what is it stimulated by and what is it blocked by

A

metabotropic, muscarine, blocked by atropine

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72
Q

what is botulinium toxin

A

ACh antagonists, prevents release

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73
Q

what is black widow spider venom

A

ACh agonist, triggers release, causes convulsions

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74
Q

Which neurotransmitters are monoamines

A

dopamine, norepinephrine, epinephrine, serotonin

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75
Q

what is a tolerance

A

A state in which organism no longer responds to a drug * A higher dose is required to achieve the same effect

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76
Q

what is dependence

A

a state in which an organism functions normally only in the presence of a drug

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77
Q

what neurotransmitter is involved in addiction and regulating control of attention

A

dopamine

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78
Q

what is the nigrostriatal system and can be caused by its degeneration

A

it starts in the substania nigra and ends in the basal ganlia, it plays a role in the control of movement. Parkinson’s is caused by the degeneration of this system

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79
Q

what does cocaine do to the brain

A

inhibits dopamine uptake from the synapse, causing an increased activation fo the reward system

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80
Q

how does serotonin move around the brain

A

via the raphe nuclei

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81
Q

what are the effects of ecstasy on serotonin

A

blocks the reuptake of serotonin, bringing more of it to the synapse

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82
Q

what does ecstasy cause

A

neurotoxcity which causes nerve terminal degeneration & possibly memory impairment

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83
Q

what are the most common neurotransmitters in the CNS

A

GABA, glutamate, glycine

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84
Q

what is the most important excitatory neurotransmitter in the brain

A

glutamate

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85
Q

what is the most important inhibitory neurotransmitter in the brain

A

GABA

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86
Q

What are some physical changes stress brings to the body

A

changes in breathing
exacerbate existing mental health conditions
changes in eating
diarrhoea/constipation

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87
Q

what are some of the results of chronic stress

A

hypertension/ heart attack
headache and migraines

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88
Q

In the everson-rose study in 2014, they did a multi-ethnic study of atherscelorsis and measured stress as burden in 5 domains. What did they find

A

chronic stress at baselines was predicted an increased likelihood of stroke over the follow up period (even after accounting for extraneous variables)

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89
Q

who coined the fight or flight term

A

walter cannon

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90
Q

what is a cause of acute physical stress

A

injury

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91
Q

what is a cause of acute psychological stress

A

a deadline

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92
Q

what is a cause of acute social stress

A

humiliation

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93
Q

what is a cause of chronic physical stress

A

hunger/cancer

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94
Q

what is a cause of chronic psychological stress

A

chronic work pressure

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95
Q

what is a cause of chronic social stress

A

chronic isolation

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96
Q

what structures are involved in the HPA axis

A

hypothalamus, anterior pituitary gland & adrenal cortex

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97
Q

what neurotransmitters/hormones are involved in the HPA axis

A

Cortisol, ACTH (adrenocorticotropic hormone) and CRH (corticotropin releasing hormone)

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98
Q

what does the adrenal gland release

A

cortisol & epinephrine

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99
Q

what does too much cortisol cause

A

cushings syndrome

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100
Q

what does too little cortisol cause

A

addisons disease

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101
Q

what were the 3 stages stressors lead to in Seyle’s animal experiments

A

Alarm, resistance, exhaustion

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102
Q

In Berns experiment in which participants experienced 100% of a voltage at the start of the experiment, what were the resulting choices of the participants.

A

Extreme dreaders chose to experience more voltage immediately (e.g 90% in 3 seconds) than less voltage for a longer time (e.g 60% for 27 seconds)

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103
Q

what can dwarfism be caused by

A

stress

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104
Q

what hormone can directly suppress the activity of the immune system

A

cortisol

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105
Q

kiecolt-glaser experiment featuring 13 caregivers and 13 controls.

What was the observed affect of stress on the caregivers

A

wounds take longer to heal in caregivers

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106
Q

what did glaser find out in their study featuring 40 1st year med students during exam season

A

their immune responses weakened and they had increased risk of epstein barr virus

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107
Q

What are some psychological modifiers of stress

(name at least 3)

A
  • Outlets of frustration
  • sense of predictability
  • perception of life improving
  • sense of control
  • social support
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108
Q

what is stress reactivity

A

the way in which we respond to stress

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109
Q

when is the lowest amount of noradrenaline released

A

during sleep

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110
Q

when is the highest amount of noradrenaline released

A

during stress

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111
Q

An observed cohort of people have increased risk of heart disease and type 2 diabetes at age 50 due to what kind of stress

A

Prenatal stress

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112
Q

What is metabolic imprinting and what effect does it have

A

the foetus learning food is ‘scarce’ so it becomes good at storing consumed food and retaining salt.

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113
Q

Kajante et al 2002 study on men with recorded birthweights and size.

what was the relationship found between birthweight and basal cortisol levels during adulthood

A

the lower the birthweight, the higher the basal cortisol levels in adulthood

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114
Q

what effects are seen in rats when the mothers underwent prenatal stress

A
  • evidence of greater anxiety- freezing in bright lights, difficulties learning,
    *amygdala shows greater glucocorticoid receptors
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115
Q

what was seen in rats with postnatal stress (maternal seperation)

A

showed increased glucocorticoid response to stress (more fearful)
lower adult height

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116
Q

study regarding a romanian orphanage

what were the differences in cortisol levels between the canadian kids, the kids adopted early and the kids left in the orphanage for over 8 months

A

The kids left in the orphanage showed significantly higher cortisol levels. The other 2 groups had similar cortisol levels

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117
Q

Vuilleumier fMRI study on distinguishing houses and faces.

When faces were fearful, what affect did this have on judging houses

A

it took longer for the P’s to process them

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118
Q

Vuilleumier fMRI study on distinguishing houses and faces.

What brain areas had more activation when viewing faces

A

Fusiform gyrus has increased activity when responding to faces
Amygdala was more active when incidentally viewing fearful faces

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119
Q

what area of the brain is seen to conduct bottom-up signalling to indicate threats in the environment

A

amygdala

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120
Q

what regions of the brain are responsible for top down regulation to prevent the triggering of constant stress responses

A

medial prefrontal cortex & anterior cingulate cortex

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121
Q

Outline some types of substance use disorders.

A

Reinforcement
Craving and relapse
Different types of substances (opiates, stimulants, nicotine, alcohol, and cannabis)
Hereditary elements

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122
Q

What is substance abuse?

A

Is a pattern of drug use in which people rely on a drug chronically and excessively and not for therapeutic reasons.

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123
Q

What is addiction or dependence?

A

Refers to being physically dependent on a drug in addition to abusing it.

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124
Q

What is the risk of cocaine abuse disorder?

A

Psychotic behaviour, brain damage, death.

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125
Q

What is the risk of designer drug abuse disorder?

A

Untested, potentially contaminated

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126
Q

What is the risk of intravenous drug abuse disorders?

A

Risk of contracting infectious diseases, overdose and death, harm caused to individual’s life

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127
Q

What is the risk of alcohol abuse disorder?

A

Cirrhosis of the liver, increased risk of heart disease and stroke, korakoff’s syndrome.

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128
Q

What is the risk of smoking?

A

Increased risk of many cancers, heart disease, stroke etc.

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129
Q

What is the importance of positive reinforcement in regards to substance abuse?

A

Positive reinforcement:
- The addition of a reinforcing stimulus following a behaviour that makes it more likely that the behaviour will occur again in the future.

Taking substances that give a positive effect, this will reinforce the behaviour of taking the drug.

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130
Q

Outline the relationship of timing and reinforcing stimuli in drug abuse.

A

Reinforcing stimuli have a greater effect if it occurs immediately after the behaviour.

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131
Q

What are some neural mechanisms of positive reinforcement in drug abuse?

A

Drugs trigger the release of dopamine in the nucleus accumbens (NAC)
Process of addiction begins in the mesolimbic dopaminergic system.
Produce long term changes in other brain regions - starting with the ventral tegmental area (VTA)

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132
Q

What is the nucleus accumbens (NAC) associated with?

A

It triggers the release of dopamine as a neural mechanism of positive reinforcement.

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133
Q

Where does the process of addiction start?

A

In the mesolimbic dopaminergic system.

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134
Q

Where do long term changes in the brain start in relation to positive reinforcement (in drug use)?

A

Starting with the ventral tegmental area (VTA).

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135
Q

Saal et al. (2003) did a study administering an addictive drug on mice, what did they find in relation to drug abuse?

A

there was increased strength of the excitatory synapses on dopaminergic neurons in the Ventral tegemental Area after a single administration

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136
Q

Outline the dopamine pathways in the mind.

A

Involves (from centre of brain to front):
- Striatum
- Substantia nigra
- VTA
- Nucleus accumbens
- Frontal cortex

137
Q

What are the functions of the dopamine pathways?

A

Rewards (motivation)
Pleasure, euphoria
Motor function (fine-tuning)
Compulsion
Perseveration

138
Q

Outline the functions of the serotonin pathways.

A

Mood
Memory
Memory processing
Sleep
Cognition

139
Q

When do synaptic changes that are responsible for the compulsive behaviours that characterise addiction occur?

A

Only after continued use.

140
Q

Which area of the brain plays a critical role in instrumental conditioning?

A

Basal Ganglia

141
Q

What is the basal ganglia?

A

A cluster of subcortical nuclei deep to cerebral hemispheres

142
Q

Outline the parts of the basal ganglia.

A

Caudate nucleus
Globus Pallidus
Putamen
Nucleus Accumbens
Amygdaloid complex
Tegmentum
Red nucleus
Substantia Nigra

143
Q

What is negative reinforcement?

A

The removal of something unpleasant.

144
Q

What is tolerance?

A

Decreased sensitivity from continued use.

145
Q

What are withdrawal symptoms?

A

Generally the opposite of the drug itself - the body may have started to compensate for the disturbed homeostatic mechanisms.

146
Q

Outline how negative reinforcement potentially maintains addiction.

A

Withdrawal symptoms are unpleasant, taking the drug removes them, producing negative reinforcement.

147
Q

Outline what can cause craving and relapse.

A

the combo of a long period of abstinence long-lasting brain changes.
Drug-related stimuli can elicit classically conditioned responses in substances abusers, both physiologically and subjectively - leads to craving

both lead to relapse.

148
Q

What did Franken (2003) suggest about craving and relapse?

A

That they are due to ‘attentional bias’ - cued by the cognitive processes and increases in dopamine in response to drug stimuli.

149
Q

What did Franken’s (2003) review indicate about drug-related stimuli?

A

Indicated that there were increases in the nucleus accumbens in response to drug-related stimuli.

150
Q

Volkow et al. (2006) used imaging and presented participants with cocaine cues, what did he find as a result of this experiment.

A

dopamine increased in relation to cocaine-cues in the dorsal striatum but not the ventral striatum (where the nucleus accumbens is located).

151
Q

What does opiate stimulation cause and what are the areas of the brain associated?

A

Analgesia (pain relief)
- periaqueductal grey matter
Hypothermia (lowering of body temp)
- Preoptic area
Sedation (Relaxation/sleep)
- Mesencephalic reticular formation
Reinforcement (behavioural reinforcement)
- Ventral tegmental area and nucleus accumbens

152
Q

What did Wise et al. (1995) find in his studies into rats?

A

Increases of 150-300% in levels of dopamine in rats’ NAC while the rat pressed a lever that delivered heroin.
Rats will also press a lever to inject opiates into the NAC or the ventral tegmental area.

153
Q

What actions does cocaine have in the nervous system?

A

Deactivates dopamine transporter proteins, blocking the reuptake of dopamine.

154
Q

What actions does amphetamine have in the nervous system?

A

Inhibits the reuptake of dopamine but directly stimulates the release to dopamine from terminal buttons.

155
Q

Outline the findings by McGregor & Roberts in relation to dopaminergic terminals and drug usage (1993).

A

Blocking dopamine receptors or destroying dopaminergic terminals in the NAC causes cocaine and amphetamines to lose much of their reinforcing effect.

156
Q

What is the relationship between the insula and smoking addiction?

A

Damage to the insula disrupts smoking addiction.

157
Q

Naqvi et al. (2007) did a study featuring 19 smokers with insula damage following brain injury and 50 smokers without insula damage following brain injury, what did they find?

A
  • No difference in whether or not they had quit when they participated in the study
  • However, those who had insular damage were significantly more likely to have a disruption of smoking addiction
158
Q

Nicotine is associated with the release of dopamine in which area? What does it do?

A

The NAC
reinforces the behaviour

159
Q

What are the some potential effects of alcohol?

A

Mild euphoria
Anxiolytic (reduces the discomfort of anxiety)
Disinhibition
Alcohol myopia (tendency for people to respond near and immediate cues while ignoring more remote cues and potential consequences).

160
Q

What is the general neural mechanism of alcohol?

A

Increases the activity in the dopaminergic neurons of the mesolimbic system.

161
Q

What are the two major sites of action of alcohol?

A

Indirect antagonist at NMDA receptors (glutamate)
Indirect agonist at GABAA receptors (inhibitory)

162
Q

What is the relationship between NMDA receptors and negative effects due to alcohol?

A

Increased sensitivity of NMDA receptors, after suppressive effect of alcohol is removed, can trigger seizures and convulsions.

163
Q

What is the other reinforcing effect of alcohol that is not the dopaminergic system?

A

Endogenous opioids.

164
Q

Why is the level of opioid receptors associated with alcohol?

A

The level of opioid receptors increases with abstinence and is thought to be related to cravings for alcohol.

165
Q

Outline Korsakoff syndrome.

A

Often seen in malnourished alcoholics
Caused by a lack of vitamin B1 in the brain and exacerbated by the toxic effects of alcohol.
Damage to the areas of the thalamus and the mammillary bodies - structures important for encoding new memories.

166
Q

What is the principal psychoactive component of cannabis?

A

Tetrahydrocannabinol (THC)

167
Q

What are the receptors that mediate the psychotropic effects of THC? What does blocking these do?

A

Cannabinoid Type 1 (CB1) receptors
Blocking these receptors abolishes the high produced by smoking cannabis.

168
Q

What can blocking CB1 receptors play a role in other drug interactions?

A

Blocking CB1 receptors in mice can abolish the reinforcing effect of cannabis, morphine, and heroin and reduce the reinforcing effects of alcohol.

169
Q

What is rimonabant and what does it do?

A

A drug that blocks CB1 receptors which can decrease the reinforcing effects of nicotine.

170
Q

Kendler et al (2003) investigated the specificity of genetic & environmental risk factors for use & dependence of 6 classes of illicit substances. What did they find?

A

Found that environment plays a stronger role in drug use but genetics play a stronger role in determining whether the person becomes addicted.

171
Q

What is the estimated % of vulnerability to addiction can be attributed to genetic factors?

A

40-60%
Includes both variability in metabolism of the drug and variability in the sensitivity to the reinforcing effects.

172
Q

What is the most common treatment for opiate addiction?

A

Methadone which is an orally administered replacement drug.

173
Q

What is buprenorphine?

A

Blocks the effect of opiates and produces only a weak opiate effect.

174
Q

What are three therapies for drug abuse?

A

Immunotherapy
Deep brain stimulation (DBS)
Transcranial magnetic stimulation (TMS)

175
Q

What is meant by neurodiversity?

A

A biological truism that refers to the limitless variability of human nervous systems on the planet, in which no two can ever be exactly alike.

176
Q

Outline the medical model of disability.

A

Focuses on impairment first - impairment being the problem.
Focuses on fixes or services for their ‘problems’
Over focuses on what the person cannot do instead of what they can do.

177
Q

Outline the social model of disability.

A

Seeks to remove barriers to allow disabled people to participate in society.
Differentiates between between impairment and disability.
Do not ‘have’ a disability but it is experienced.

178
Q

What does ‘difference not deficit’ refer to?

A

Neurodiversity, there are variabilities in mind, not better and worse.

179
Q

What percent of the UK population are on the autism spectrum?

A

1% (140,000 school age children)

180
Q

Outline what characterises autism spectrum disorder to the DSM-5.

A

Persistent difficulties in social communication and interaction.
Restricted, repetitive patterns of behaviour, interests, or activities.
- Sensory hyper or hypo-sensitivities.

181
Q

Outline what characterises autism spectrum disorder to the social model of disability.

A

Differences in social communication and interaction.
Specific patterns of behaviour, passionate interests, or focused activities.
- Sensory hyper or hypo-sensitivites.

182
Q

What is the rate of concordance of autism between MZ and DZ twins.

A

MZ: 60%
DZ: 5%
Shows that there are genetics involved.

183
Q

Outline what a mega-analysis of brain differences between autistic (1,571) people and non-autistic (1,651) people found.

A

Smaller subcortical volumes of the pallidum, putamen, amygdala and nucleus accumbens.
Increased cortical thickness in the frontal cortex and decreased thickness in the temporal cortex.

184
Q

Name 3 co-occurring diagnoses that are common in people with autism across their lifespan.

A

ADHD (28%)
Anxiety (20%)
Depression (11%)

185
Q

What is the ratio of autistic males to females?

A

3:1

186
Q

What are some potential reasons why less females are autistic?

A

Female specific protective factors:
- oestrogens, paternal X
Male specific risk:
- fetal testosterone, Y chromosome.

187
Q

What does De Novo mean?

A

Not present in the parent (e.g. genes CNVs)

188
Q

What is a genetic reason that might explain that less females are autistic?

A

There is an excess in CNVs (copy number variants) in females.

189
Q

What reason could women not be diagnosed for autism because of?

A

Female autism phenotype - women might be better at hiding it, and autism can look very different on a girl than it does on a boy.
E.g., differences in typical interests, girls better at hiding social deficits ‘camouflaging’ - pressure to fit in.

190
Q

What is meant by camouflaging in autism?

A

It is trying to fit in via a few techniques:
- Assimilation
- Compensation
- Masking
Etc
Due to the pressures of typical social communication.

191
Q

What is meant by masking in reference to camouflaging?

A

Strategies used to hide autistic characteristics or portray a non-autistic persona.

192
Q

What is meant by compensation in reference to camouflaging?

A

Strategies used to actively compensate for difficulties in social situations.

193
Q

What is meant by assimilation in reference to camouflaging?

A

Strategies that reflect trying to fit in with others in social situations.

194
Q

What are the gender differences between the three main subtypes of camouflaging?

A

Masking: no gender differences found.
Compensation: higher in females.
Assimilation: higher in females.

195
Q

Outline the relationship between autism stigma and camouflaging behaviours.

A

Higher perceived autism stigma was associated with higher levels of self reported camouflaging behaviours.

196
Q

What are two things that a marker of a disorder should show to be seen as an adequate and reliable marker?

A

Sensitivity: be found in all members of a group.
Specificity: be exclusive to all members of that group.

197
Q

How is the behavioural profile associated with autism characterised against societal norms?

A

Use of standardised tests.
Narrow sample use:
- Undergraduate populations
- Populations without any mental health difficulties or other conditions.
- WEIRD populations (Western, Educated, Industrialized, Rich and Democratic)
Normative lens.

198
Q

What have neuroimaging studies shown about the differences between autistic and non-autistic people?

A

They have indicated neural differences during emotion processing tasks, including differences in activity of the amygdala and posterior fusiform gyrus.

199
Q

Briefly outline the study into facial expression recognition and autism.

A

METHODS:
- 255-488 participant, autistic, non-autistic and/or mild intellectual disability.
- All participants completed 2-3 behavioural facial emotion expression tasks and a fearful face-matching task in the fMRI scanner.
RESULTS:
- No significant differences between autistic and non-autistic ps in amygdala or fusiform gyrus activation.
- Autistic people who performed worse on the emotion recognition tasks, also activated the right amygdala and the fusiform face area less than autistic people who performed well on the emotion recognition tasks.

200
Q

What is alexithymia?

A

An impaired ability to be aware of, explicitly identify, and describe ones feelings.

201
Q

Outline the prevalence of alexithymia in autistic and non-autistic people.

A

Autistic people: 49.93%
Non-autistic people: 4.89%

Autistic people are more likely to experience higher levels of alexithymia compared to non-autistic people.

202
Q

What is cognitive empathy?

A

Recognising and understanding that another person is thinking or feeling something different to what you are thinking or feeling.

203
Q

What is the theory of mind?

A

The ability to attribute independent mental states to oneself and others to explain their behaviour.

204
Q

What is the Sally-Anne test?

A

A test to diagnose autism.

  1. Sally and Anne are introduced. Sally has a basket, and Anne has a box.
  2. Sally has a marble, she places her marble in her basket.
  3. Sally goes out for a walk and Anne remains behind.
  4. Anne removes Sally’s marble from the basket and places it in her own box.
  5. Sally returns some time later, and she wants to play with her marble. Where will she look, in her basket or in the box, for her marble?

A high % of autistic children will say in the box as they don’t perceive the fact that Sally doesn’t know its been moved.
Theory of mind taken into account.

205
Q

What is the double empathy problem and what disorder is it refering to?

A

Autism.
Problems arise as a combination of both parties (autistic and non-autistic) not understanding each other.

206
Q

Outline the study into peer-to-peer transfer of information.

A

Aims to see how the passing of information is impacted by the type of person involved.

METHOD:
- Diffusion chain technique (Chinese whispers)
- 72 adult participants: 3 groups per chain with 8 people each, 24 people per chain condition.
- 30 point story of a bear with no logical structure.
RESULTS:
- Autistic people share information with other autistic people as well as non-autistic people do with other non-autistic people.
- However, when there are mixed groups of autistic people and non-autistic people, much less information is shared.
- People in the mixed groups experienced lower rapport with the person they were sharing the story with.

207
Q

Outline sleep and it’s importance.

A

It is a behaviour that is vital for normal functioning, health, well-being, and memory.

208
Q

Name the three main types of imaging that is used in sleep research and what each tracks.

A

Electroencephalography (EEG): Brain activity
Electromyogram (EMG): Muscle activity
Electro-oculogram (EOG): Eye movements.

209
Q

What are the two basic patterns of brain activity?

A

Alpha activity:
- Regular medium frequency waves of 8-12Hz
- Resting quietly.
Beta activity:
- Irregular, mostly low-amplitude waves of 13-30Hz
- Alert and attentive.

210
Q

Outline stage 1 sleep.

A

When we become drowsy we enter stage one.
Theta activity 3.5-7.5Hz.
Firing of the neocortex becoming more synchronised.
Transition between sleep and wakefulness
Lasts approximately 10 mins.

211
Q

Outline stage 2 sleep.

A

Irregular EEG during this stage.
Theta activity 3.5-7.5Hz
Sleep spindles.
K complexes (only found in stage 2)

212
Q

What are sleep spindles and what are they associated to?

A

Short bursts of waves of 12-14Hz that occur between 2-5 times a minute during sleep.
They are associated with higher scores on intelligence tests (more sleep spindles the higher the score).

213
Q

What are K complexes and what are they associated with?

A

Sudden sharp waveforms usually only found in stage 2.
They are associated with consolidation of memories.

214
Q

Outline stage 3&4 sleep.

A

High amplitude delta activity: slower that 3.5Hz
Distinction: stage 3 sees 30-50% delta activity, stage 4 over 50% delta activity.
Slow wave oscillations <1Hz

215
Q

Outline REM sleep.

A

Stage of sleep in which we dream (Rapid Eye Movement)
Profound loss of muscle tone - paralysis.
Cerebral blood flow and oxygen consumption are accelerated.
Mechanisms that regulate body temperature stop working.

216
Q

Outline acetylcholine as a neural basis of arousal.

A

Levels high in the hippocampus and neocortex.
Activating ACh neurons in the basal forebrain causes wakefulness.

217
Q

Outline Noradrenaline as a neural basis of arousal.

A

Activity of noradrenergic locus coeruleus neurons increases vigilance.
Moment-to-moment activity of noradrenergic LC neurons related to performance on tasks requiring vigilance.
Increase during wakefulness.

218
Q

Outline serotonin as a neural basis for arousal.

A

Serotonergic neurons are most active during waking, steadily decline during sleep to almost zero activity in REM sleep.
Involved in numerous processes.
Stimulation of the raphe nuclei (where most of the serotonergic neurons are found) causes locomotion and cortical arousal.

219
Q

Outline Histamine as a neural basis of arousal.

A

Histaminergic neurons are located in the hypothalamus.
Drugs that prevent the synthesis of histamine or block histamine receptors decrease waking and increase sleep.
Activity high during waking and low during slow-wave and REM sleep

220
Q

Outline Orexin as a neural basis of arousal.

A

Cell bodies that secrete orexin (aka hypocretin) are located in the hypothalamus.
Excitatory effect in the cerebral cortex and all other regions involved in arousal and wakefulness.
Orexinergic neurons in rats fire fastest in active waking. particularly when exploring and fire less frequently during quiet waking and sleep.

221
Q

Name the 5 neurotransmitters that play a role in arousal.

A

Acetylcholine
Noradrenaline
Serotonin
Histamine
Orexin

222
Q

What 3 factors control sleep?

A

Homeostatic
Allostatic
Circadian

223
Q

What is the primary homeostatic factor that influences sleep?

A

Presence or absence of adenosine.

224
Q

What is allostatic control mediated by?

A

Hormonal and neural responses to stressful situations.

225
Q

What is allostasis?

A

The process of maintaining homeostasis through the adaptive change of the organism’s internal environment to meet perceived and anticipated demands.

226
Q

How is inhibition of the arousal system governed in sleep?

A

Group of GABAnergic neurons in the ventrolateral preoptic area (VLPO) become active and supress activity of arousal neurons.

227
Q

Briefly outline the sleep/waking flip-flop model.

A

Regulated by orexinergic neurons.
- The flip-flop is on when the sleep-promoting neurons in the vlPOA are inhibited and the arousal neurons are active.
- The flip-flop is off when the sleep-promoting neurons in the vlPOA are activated and the arousal neurons are inhibited.

228
Q

What are factors that control the activity of orexinergic neurons?

A

Biological clock
Hunger related signals activate them
Satiety related signals inhibit them
Orexinergic neurons receiving inhibitory input from the vlPOA because of the build-up of adenosine (excitatory and causes wakefulness)

229
Q

Outline the relationship between acetylcholinergic neurons and REM sleep.

A

They fire at a high rate during sleep.

230
Q

Outline the process of neural control of REM sleep.

A

REM sleep flip-flop:
- During waking, the REM-OFF region receives excitatory input from the orexinergic neurons of the lateral hypothalamus, and this activation tips the REM flip-flop into the OFF state.
- When sleep/waking flip-flop switches into the sleep phase, slow-wave sleep begins.
- The activity of the excitatory orexinergic, noradrenergic, and serotonergic inputs to the REM-OFF region begins to decrease. As a consequence, the excitatory input to the REM-OFF region is removed.

231
Q

What is the role of orexin in the REM flip-flop model?

A

It keeps the REM flip-flop in the OFF position.

232
Q

Outline how paralysis occurs during REM sleep.

A

When the REM flip-flop tips to the ON state, motor neurons in the spinal cord become inhibited, and cannot respond to signals arising from the motor cortex in the course of a dream.

233
Q

What did Revonsuo (2000) suggest the role of dreams was?

A

Suggested that they represent threat-simulation.

234
Q

Briefly outline nightmares.

A

Typically defined as vivid and frightening dreams that awake the dreamer.
2-5% of the population experience frequent nightmares.
Aetiology is still unclear but greater experience associated with PTSD, depression, insomnia and being female.

235
Q

Voss (2014) did a study trying to induce lucid dreams, how did he do so ?

A

induced lucid dreams by applying fronto-temporal transcranial alternating current stimulation (tACS) at 25 and 40Hz.

236
Q

What frequency is lucid dreaming associated with?

A

lower gamma frequency in the fronto-temporal area of the brain.

237
Q

What is lucid dreaming?

A

It is the awareness that you are dreaming while the dream continues.

238
Q

What are the functions of low wave sleep?

A

Most researchers believe slow-wave sleep allows the brain to rest.
Slow-wave sleep deprivation affects cognitive abilities, especially sustained attention, but not physical abilities.

239
Q

What happens to cerebral metabolic rate and blood flow during slow-wave sleep and what does this suggest?

A

Falls by about 75%, this coupled with people’s unresponsiveness and confusion if wakened suggests that the cerebral cortex ‘shuts down’ during sleep.

240
Q

What is the rebound phenomenon?

A

If deprived of REM sleep, you will have more REM sleep in the next sleep period.

241
Q

When does the highest proportion of REM sleep occur?

A

During brain development.

242
Q

Why do adults have REM sleep if it seems to serve such an important function for brain development?

A

We continue to learn throughout life and both REM sleep and SWS (slow wave sleep) facilitate learning.

243
Q

Mednick, Nakayama, & Stickgold (2003) did a study in which particpants learned a non-declarative visual discrimination task. Some P’s took a 90 min nap during the day and EEG was used to see which P’s engaged in REM sleep and which did not. They then conducted the task again at 7pm that night.

What were the results of this experiment and what do they indicate?

A

RESULTS:
- Discrimination was improved under the combination of SWS and REM, the other two conditions there was a decrease in performance.

244
Q

Tucker et al. (2006) did a study in which particiapants were trained on a declarative & non-declarative task. SOme participants had a one hour nap but only engaged in slow wave sleep (woken before REM sleep).

What were the results of this study and what do they suggest

A

RESULTS:
- Those who had SWS had ~20% more improvement that those who stayed awake.
- Shows that SWS consolidates declarative memories.

245
Q

What type of memory do REM sleep and Slow-wave sleep facilitate?

A

REM: nondeclarative
SWS: declarative.

246
Q

Outline some of the DSM-5 criteria for insomnia.

A
  • Difficulty getting to sleep, staying asleep, or having non-restorative sleep.
  • Together with associated impairment of daytime functioning.
  • Defined in relation to a person’s particular need for sleep.
247
Q

How much of the population does chronic insomnia effect?

A

Approximately 9% of the population.

248
Q

What are 5 causes of insomnia?

A

Age:
- more common in older people
Environmental factors:
- Electronic devices, noise, light - detrimental
Physiology:
- Heightened activity in the reticular activating system.
Circadian rhythms:
- Jet lag, shift work patterns.
Medical conditions and medications:
- Heart and respiratory conditions

249
Q

How is insomnia treated?

A

Typically treated with drugs but can potentially be treated with mindfulness and CBT

250
Q

What is sleep apnea?

A

form of insomnia caused by the inability to sleep and breathe at the same time.

leads to a build up of carbon dioxide in the blood which stimulates chemoreceptors.

leads to a disruption of sleep affecting daytime functioning.

251
Q

What is narcolepsy?

A

A sleep disorder characterised by the overwhelming urge to sleep.

252
Q

What is cataplexy?

A

Muscular paralysis of REM sleep while awake.
(sleep paralysis)
- Varying degree of muscle weakness.
- Can become completely paralysed while conscious.
- Generally occurs when the person feels strong emotions or by sudden physical effort.

253
Q

What are hypnagogic hallunications?

A

Dreaming while awake and paralysed - can be very realistic and terrifying.

254
Q

What causes narcolepsy?

A

There is a hereditary element.
Orexinergic neurons are attacked by the immune system, influencing the sleep wake flip-flop.

255
Q

What are some treatments of narcolepsy?

A

Most common current treatments are modafanil and sodium oxybate (stimulants).
Sleep attacks can be diminished with stimulants (ritalin)
REM sleep phenomenon (cataplexy, sleep paralysis and hypagogic hallucinations) traditionally treated with antidepressant drugs.

256
Q

What is somnambulism?

A

Sleep walking.
- More common in children
- Genetic component
- Disorder of arousal

257
Q

What is pavor nocturnis?

A

Night terrors.
- Hereditary element.
- Characterised by screams, trembling, rapid pulse, and usually no memory of what caused the terror.
occurs during SWS.

258
Q

What is nocturnal enuresis?

A

Bedwetting.
- Hereditary element.
- About 10% of 7 year olds have this
occurs during SWS

259
Q

nili et al study on people with snake phobia

The experiment had two conditions, one featuring a live snake and one featuring a toy bear (control). The participants then had the choice of whether or not they would move the snake/bear closer to them. This was all detected with an MRI scanner.what were the results of this experiment

A

When choosing, if people let the snake come closer, there was an increase in activity

When fearful people chose to advance the snake, amygdala activity was reduced

260
Q

What is fatal familial insomnia?

A

It is a neurodegenerative disorder in which there is damage to the thalamus.
- Initially presents with insomnia and very vivid dreams when the person finally manages to sleep.
- As the disease progresses it affects the autonomic nervous system and coordination.
- Disappearance of slow-wave sleep and only brief periods of REM sleep.
Ultimately leads to inability to voluntarily move or speak - leads to death.

261
Q

Briefly outline the 6 sleep disorders.

A

Insomnia – definition, causes, treatment
Sleep apnea – carbon dioxide build-up
Narcolepsy – symptoms, causes and treatment
REM sleep behaviour disorder – acting out dreams
Slow-wave sleep problems – sleep walking, night terrors, bedwetting
Fatal familial insomnia - prion disease, initially presents as insomnia, disappearance of slow-wave sleep

262
Q

Vuilleumier et al 2001 fMRI study on brain activation w/ faces & houses

The participants were presented with faces (neutral or fearful) and/or houses.

What brain region activity was linked to each and what overall was seen from the experiment

A

P’s slower at judging houses if faces happened to be fearful

Fusiform gyrus has increased activity when responding to faces

Amygdala was more active when incidentally viewing fearful faces

The parahippocampal gyrus has increased activity when responding to houses

263
Q

Etkin & wager meta analysis of fMRI studies of patients with PTSD, social anxiety disorder & specific phobia

What did the patients with these conditions
show?

A

Increased activation in amygdala (phobia/social anxiety) [the same sort of regions activate when we feel anxiety or fear]

Decreased activity in medial prefrontal cortex (PTSD)

264
Q

Metabolic imprinting

A

The foetus develops a thrifty metabolism and is better at storing food, due to the mother being placed through physiological stress

265
Q

Emotion regulation uses a balance of bottom up and top down signalling ,how?

A

Bottom up-signalling from amygdala indicates threats in the enviro

‘Top-down’ regulation from medial prefrontal cortex prevents this from triggering constant stress-responses

266
Q

Lower birthweight is correlated with

A

Higher basal cortisol levels

267
Q

What general effects does stress have on memory

A

Info encoded during stressful events is generally well remembered

Particularly if info is relevant to stressor (i.e learn to avoid house, after attack by dog)

Normally adaptive but dysregulation could result in psychological trauma (e.g PTSD)

268
Q

What is the effect of stress on memory at the encoding level.

A

Stressful films led to better memory for pictures

during stress, lower activity in hippocampus at encoding = better memory for those pictures

Poor separation of event info from relevant stimuli may overwhelm hippocampal activity

269
Q

What is the effect of stress on memory at the consolidation level?

What is an example of this being seen.

A

Stress enhances consolidation of emotional pictures (but not for neutral pictures)

Cold pressor test in which P’s had hand plunged in cold water before being asked to remember things

270
Q

What is the effect of stress on memory at the retrieval level?

What is an example of this being seen.

A

Memory retrieval during stress is impaired

Trier test - P’s have a 5 min unexpected talk followed by a 5 min arithmetic they need to remember

271
Q

What are some features of the hippocampus in relation to its involvement in memory

A

High density of glucocorticoid receptors

Stress in rats is shown to affect hippocampal neurons

272
Q

Lazarus says that people deal with stress depending on our cognitive appraisal of the situation at hand.

What classes of appraisal are there and what do they mean

A

Primary appraisal - how relevant is situation to needs
Secondary appraisal - what resources/options are available (can i blame someone else?)

273
Q

Lewin gives different types of conflict when it comes to appraising stressful situations.

What are they and what is an example of each

A

Approach-approach conflict (least stressful)
- Should i go to dinner w/ friends , or cinema w/ gf

Avoidance - avoidance conflict
- Do homework or go to bed w/o dinner

Approach avoidance conflict
-Should i propose?

274
Q

Tice & Baumeister compared the stress levels & exam results in students. The students were classed as procrastinators and non-procrastinators, what was seen in this experiment

A

Early in year (and for longest part of year)
Procrastinators = lower stress, lower marks (stress increases over year)

275
Q

What is eustress

A

people enjoying the sensation of being stressed

276
Q

When someone goes skydiving, what is the order of what is happening physiologically

A

Innervation of sympathetic branch of autonomic nervous system
Release of adrenaline/epinephrine within 15 seconds

Release of dopamine

Greatest release, just prior to event

277
Q

Why cant you tickle yourself, what would be required to do so and what does this show about stress

A

A delay into your own tickles - if more than 3/10ths of a second - high tickle rating

Can tickle self, but needs to be unpredictable

Stress is greatest in situations that are unpredictable

278
Q

During a monkey study where monkeys would receive desirable food after pulling a lever 10 times, a bell would always be the indicative sound before the food was released. When did dopamine neurons show the biggest response and what does this show.

A

not when the monkey receives food but at the sound of the bell → bell causes anticipation of knowing itll get food

Dopamine release from Anticipation of reward

279
Q

how would one go about increasing dopamine release

A

by adding a lack of control/predictability / sense of anticipatory pleasure.

Its why getting free shit randomly feels better than getting the same thing but paying for it

280
Q

What can trigger dopamine release in relation to stress.

A

Cortisol

281
Q

What are the 3 components of an emotional response

A

behavioural
autonomic
hormonal

282
Q

what is the behavioural component of a emotional response

A

Muscle movements appropriate for the situation(walking faster)

283
Q

what is the Autonomic component of a emotional response

A

facilitate behaviours by providing quick mobilisation of energy for movement (e.g increase blood flow/heart rate)

284
Q

what is the Hormonal component of a emotional response

A

reinforce autonomic response via brain mechanisms

285
Q

What is the integration of fear controlled by

A

amygdala

286
Q

What are the 3 regions of the Amygdala involved in fear processing

A

Lateral Nucleus - main input, sends some internal & external projections
Basal Nucleus - sends internal and limited external projections
Central Nucleus -main output, sends projections to various brain regions

287
Q

What does damage to the central nucleus of the amygdala do

A

Reduces of abolishes a wide range of emotional responses
Animals no longer show fear

act more tamely when handled by humans, e.g
Lower stress levels in their blood
Less likely to develop stress induced illnesses

288
Q

What are the neural mechanisms for conditioning

A

Lateral Nucleus (LA) responsible for the establishment of a conditioned emotional response
Neurons in the LA communicate with neurons in the central nucleus (CE)
CE communicates w/ the regions that are responsible for the behavioural, autonomic & hormonal components of the conditioned emotional response

289
Q

what is extinction

A

removal of association.
(extinction ≠ forgetting)

290
Q

what region of the brain is linked to extinction

A

ventromedial prefrontal cortex

Extinction training activates vmPFC neurons
Lesions to the vmPFC impair extinction

291
Q

what did vmPFC activations help predict

A

exposure therapy outcome

– Activation in the vmPFC predict exposure therapy outcomes for people with diagnosed spider phobias

292
Q

What is affective empathy?

A

Feeling what another person is feeling through recognition, being sensitive and having an appropriate affective response.

293
Q

What are parallel and reactive responses in terms of empathy?

A

Parallel responses are where the observer shows emotions.
Reactive responses are where you elicit the emotion as a response

294
Q

What is sympathy?

A

It is the awareness of someone else’s emotion - understanding their situation.

295
Q

What is cognitive empathy?

A

Recognising and understanding that another person is feeling something different to what you are feeling.

296
Q

What are the 3 theories of emotion.

A

James-lang
Cannon-bard
Schachter- Singer

297
Q

What is the james-lang theory of emotion

A

(1-2) Emotion producing situations elicit physiological responses & behaviours
(3) Feedback from the organs & muscles involved organise how we feel emotion

298
Q

Outline the double dissociation lesion study investigating the relationship between cognitive and affective empathy.

A

PARTICIPANTS:
- 8 participants with inferior frontal gyrus lesions.
- 11 participants with ventromedial prefrontal cortex lesions.
- 11 participants with lesions outside the frontal lobes.
- 34 participants without brain lesions.
METHODS:
- All participants completed the Interpersonal Reactivity Index (IRI).
FINDINGS:
- Patients with VM lesions were impaired in cognitive empathy compared to the healthy controls (HC), whereas patients with posterior lesions (PC) and patients with IFG lesions were impaired in emotional empathy compared to the HC, VM and the PC group.

299
Q

What is prosocial motivation?

A

The intention to respond compassionately to another person’s distress.
It is the altruistic component to empathy - drive to help person with their emotional state.

300
Q

What research evidence is there for the James-Lang theory of emotion. (outline the study)

A

Participants - veterans who had spinal cord injuries
Predictions - decrease in emotional feelings in patients, worse if they show lesions higher up the spinal cord
Procedure - a structured interview

Findings:
Decreased experiences of feeling anger, sexual excitement, fear & overall feelings
The more extensive the disruption, the greater the decrease in emotional feelings

301
Q

How can we measure empathy?

A

Using a self-report Empathy Components Questionnaire (ECQ).
Contains cognitive and affective components across 27 items

(extra detail:)
6 items on cognitive ability: “the skill, capacity or potential in perspective-taking and to adopt another’s point of view”
5 items on cognitive drive: ”the motivated interest or tendency in perspective- taking and to adopt another’s point of view”
5 items on affective ability: “the skill, capacity or potential in recognizing, being sensitive to and sharing others’ emotional experiences”
4 items on affective drive: “the motivated interest or tendency in recognizing, being sensitive to and sharing others’ emotional experiences”
7 items on affective reactivity*: the skills, capacity or potential in “responding and reacting to another person’s emotional experiences”

302
Q

What were the results for the Empathy Components Questionnaire?

A

Significant sex differences for all components of affective empathy, small differences between sexes evident in cognitive empathy.

(Limitation: small undergraduate student sample)

303
Q

What is the Cannon-Bard theory of emotion

A

Provided an alternative view to how we experience emotions & included the thalamus as the mediating centre in the brain
Suggested that identification of emotion occurs at same time as bodily response → reactions are independent of each other

304
Q

What is the Schacter singer theory of emotion

A

Suggests emotional experiences based on two factors
Physiological arousal
Cognitive label

One of the first theories to bring in a cognitive component

305
Q

What is the Schacter singer theory of emotion

A

Suggests emotional experiences based on two factors
Physiological arousal
Cognitive label

One of the first theories to bring in a cognitive component

306
Q

what are the 3 core features of emotion regulation

A

Activation of a goal**
Engagement of processes responsible for altering the emotion trajectory
Impact on emotion dynamics

307
Q

What is emotional contagion?

A

Describes having fast automatic responses to emotional expressions in others
- A precursor to affective empathy.

308
Q

Describe the two empathy networks in the brain.

A

Affective:
- the inferior frontal gyrus and posterior dorsal medial frontal gyrus.
Cognitive:
- the supramarginal gyrus and anterior dorsal medial frontal gyrus.

309
Q

what is the process model of emotion regulation

A

Builds upon modal model of emotion & treats each step in the emotion-generative process as a potential target for regulation

310
Q

What did Ekman and colleagues (1969) conclude from their research about emotions and culture

A

Concluded that the expression of emotions are unlearned as they are the same in cultures that have not been exposed to each other.

311
Q

How many basic emotions are there and who found this?

A

6 universal basic emotions
Darwin (1872) and Ekman and colleagues (1969)

312
Q

Outline the study comparing the expressions of congenitally and noncongenitally blind athletes in the 2004 Paralympic games with each other and those produced by sighted athletes.

A

RESULTS:
- Few differences in found across all participants.
- Both types of blind produced facial expressions associated with anger, contempt, sadness etc.
- The range and type of emotion signals displayed were comparable to those produced by sighted athletes.
CONCLUSION:
- Suggests that emotion expression is innate and does not require learning by imitation
(Blind people never see these emotional expressions, therefore they must be innate).

313
Q

Outline the study that investigates whether emotional vocalisations communicate affective states across cultures.

A

PROCEDURE:
- Participants heard an emotional story:
- Played the Himba nonverbal emotional vocalisations from European-English speakers.
- Played European English speakers nonverbal emotional vocalisations from the Himba.
RESULTS:
- Groups were able to identify ‘basic’ emotions of their own cultural group at a higher level.

314
Q

Outline the conclusion of the study that aimed to disprove that there are 6 universal basic facial emotional states.

A

Facial expressions of emotion are culture specific, refuting the the hypothesis that human emotion is universally represented by the same set of six distinct facial expression signals.

315
Q

Outline the evidence for innate emotional expressions.

A

Facial expressions:
- Cross cultural studies
- Studies with visually impaired.

316
Q

Outline the evidence against innate emotional expressions.

A

Difference in the emotional intensity between East Asians and Western cultures.
- Still show innate emotional expression, however, difference in intensity.

317
Q

Outline the results and conclusion of the study that aimed to correlate the location of lesions in 108 people with the ability to perceive emotion in the face.

A

RESULTS:
- People who were poorest at facial emotion recognition had damage to the right somatosensory cortex.
- People with somatosensory impairments also had impairments in emotion recognition.
CONCLUSION:
- When we see a facial expression of an emotion, we unconsciously imagine ourselves making that expression.

318
Q

What is the simulationist hypothesis?

A

Emotion recognition involves simulation of the emotion that we are viewing.

319
Q

Outline the study into the simulationist hypothesis.

A

PROCEDURE:
- Participants performed a expression matching task while rTMS (repetitive TMS) was targeted at the face or finger region of the rSC.
RESULTS:
- Mean accuracy scores revealed a spatially specific effect limited to the face region of the rSC. rTMS at the face area reduced accuracy to 70% compared with accuracy of 83.25% at the finger area.
- Suggests that the Somatosensory cortex is involved in internal imitation of emotion.

320
Q

Outline the meta-analysis of emotion recognition in the brain that aimed to identify brain activity and connectivity profiles and dimensional emotions.

A

CONCLUSION:
- Consistent engagement of the amygdala and its connectivity with distributed networks across discrete and dimensional emotions.
- The left-hemisphere dominance of the amygdala and anterior insula across emotions, but category-specific lateralisation of the vmPFC (was mainly right hemisphere).

321
Q

What is N170 and what does it show?

A

It is a point on an EEG that shows that people are processing emotional expression

322
Q

What are PO8 and PO7?

A

Points in EEG that correspond with Fusiform Face Area and Occipital Face Area.

323
Q

Outline the conclusion of the study comparing facial and vocal emotion recognition and processing biases in 88 4-11 year olds and 21 adults.

A

Development trajectories of emotion processing differ as a function of emotion types and stimulus modality. In addition, vocal emotion processing showed a more protracted developmental trajectory, compared to facial emotion processing.

324
Q

Outline the key information in regards to emotion recognition.

A
  • The amygdala has a prominent role in basic and complex emotion recognition.
  • There are sex differences in laterality of the temporal response to face processing in the fusiform face and occipital face areas.
  • Developmental trajectories of emotion processing differs depending on the type of emotional expression as well as the modality (visual or vocal).
325
Q

Outline the study that explores whether oxytocin administration influenced facial emotion recognition in people with antisocial personality disorder.

A

CONCLUSION:
-Improvement of the recognition of fearful and happy facial expressions by oxytocin in young adults with ASPD.
- The increased recognition of facial fear is of high importance since the correct perception of distress signals in others is thought to inhibit aggression.

326
Q

Outline the results of the study into whether the modality of stimulus representation influences the emotional response accuracy.

A

Recognition accuracy was significantly higher in the audio-visual than in the auditory or the visual modality.

327
Q

Outline the results of the study into Testosterone and Cortisol’s impact of emotional recognition accuracy.

A
  • A positive association between testosterone and recognition accuracy as well as between cortisol and reaction time.
  • The overall effect size of testosterone by cortisol interaction with recognition accuracy and reaction time was significant but small.
328
Q

Name 3 hormones that influence emotion recognition abilities.

A

Oxytocin
Cortisol
Testosterone.

329
Q

What is alexithymia?

A

It is an externally oriented cognitive style in which there is difficulty identifying and describing feelings.

330
Q

Outline the study into whether people with alexithymia have diminished emotion-related social cognitive competencies, beyond the effect of anxiety/depressive symptoms.

A

PROCEDURE:
206 participants completed four components of social cognition as well as a measure of alexithymia.
- Recognition of others’ emotions.
- Representation of others’ affective and cognitive mental states.
- Empathy.
- Regulation of one’s own feelings.
RESULTS:
- Alexithymia significantly predicted emotion recognition, empathy, and emotional regulation but not the representation of others’ affective and cognitive mental states.
CONCLUSION:
- Emotional recognition is based on ones own ability to identify emotions personally.

331
Q

What is the vmPFC, what does it include?

A

Ventromedial Prefrontal Cortex and it includes the orbitofrontal cortex and the subgenual anterior cingulate cortex.

332
Q

What is the role of the vmPFC and what does its outputs affect?

A

It plays an important role in emotional regulation and inhibition of emotional responses (extinction).
Its outputs affects a variety of behaviours and physiological responses, including emotional responses organised by the amygdala.

333
Q

What does damage to the vmPFC cause?

A

Causes serious impairments of behavioural control and decision making.
- Inhibition (Phineas Gage)
- Decision making (EVR) - unable to distinguish between serious and trivial decisions.

334
Q

Outline an example of an impersonal moral dilemma.

A

Train going down tracks to run over 5 people, there is a track with one person on.
You have a switch (making it impersonal) that can change the train to the track with one person - what do you do?

335
Q

Outline an example of a personal moral dilemma.

A

Train going down tracks to run over 5 people, there is a track with one person on.
You have to push one person off a bridge (making it personal) to die but it will save the other 5 people - what do you do?

336
Q

Outline the results of the study into moral decision making with people with vmPFC damage.

A

People with vmPFC damage were more logical/utilitarian in their decisions in personal moral dilemmas.

337
Q

What is the TPJ and what is it involved with?

A

Temporoparietal junction and it is involved in difficult moral decision making.

338
Q

Outline the study investigating the verbal responses and emotional arousal to moral dilemmas during the process of moral decision making.

A

TLDR - patients with behavioural variant frontotemporal dementia are more likely to make difficult personal moral decisions and show more positive responses when being tasked with these dilemmas

  • 10 patients with the behavioural variant frontotemporal dementia bvFTD.
  • 11 patients with Alzheimer’s (AD)
  • 9 people without dementia (HC)
    PROCEDURE:
  • Participant were presented with computerised versions of moral dilemmas that proved the necessity for harmful action of an impersonal nature (pull switch) or personal nature (push a man off a footbridge).

RESULTS:
- The bvFTD participants in were more willing to push a man in order to stop a trolly from killing five other people, than AD participants and HC.
- The bvFTD participants showed more positive emotional responses when responding to moral dilemmas, whereas the AD and HC groups expressed distress and an unwillingness to cause direct harm to another person.

Semester 2 exams - Manchester Cogneuro (6 decks)

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