Emotion and Anxiety Flashcards

1
Q

what are the 3 related but distinct dimensions of the emotional response

what do each mean

A

(a) subjective (i.e. verbal report about how an individual feels);
(b) behavioural (i.e. what an individual does): this could include behaviour in social situations, changes in facial expression e.g. to show rage, freezing to danger, psychomotor retardation in depression;
(c) physiological: this includes changes in heart rate and respiration (autonomic responses), and neuroendocrine responses such as adrenaline or corticosteroids secreted from the adrenals.

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2
Q

Why do humans find it hard to describe their emotional feelings (2)

A

intrinsically difficult

linguistic constraints

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3
Q

how do behavioural indices of emotion between humans and animals

A

measured precisely in animals, but in humans they consist mainly of self-report or observations of symptoms by human observers, often clinicians

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4
Q

what is a reinforcer

A

a stimulus that if it occurs, terminates or is omitted because of a response of the animal, the probability of that response occurring in the future is altered. Reinforcers increase a type of response

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5
Q

what is a positive reinforcer

A

stimulus that increases a response

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6
Q

what is a negative reinforcer

A

involves removal of a negative condition to strengthen behaviour
eg starting to cycle to work and finding that the negative condition (traffic) has been avoided

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7
Q

what is punishment

A

given after the behaviour is exhibited and reduces responding as a consequence.

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8
Q

what are the major physiological repsosnes to emotion that are usually measured (5)

A

heart rate,
blood pressure, galvanic skin resistance (GSR),
muscle tension
arousal measured as desynchronisation of the EEG

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9
Q

What is GSR

A

galvanic skin resistance

a measure of the skin’s electrical conductance (often called SCR), as affected by sweating

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10
Q

What are the physiological reactions to a spider in a patient with arachnophobia

what can we infer about these responses then

A

increases in heart rate,
skin conductance, vasomotor activity
decreased respiration

in response even to a picture of a spider

these autonomic changes are correlates of anxiety, but it is still not entirely clear whether a similar or different pattern of bodily responses accompanies other emotional feelings e.g. of joy or anger

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11
Q

What did James hypothesise about emotion

A

the bodily changes follow directly the perception of the exciting fact, and that our feeling of the same changes as they occur IS the emotion

thus we don’t run bc we are afraid, we area afraid because we run

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12
Q

What did Lange propose at the same time as James

A

emotion could be experienced as organic symptoms (thus essentially introducing the notion of psychosomatic illness)

thus the idea that emotional experience derives from bodily experience is generally called the James-Lange theory

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13
Q

What did Cannon argue about emotion

A

argued strongly against the view that bodily feelings
contributed to emotional experience, mainly on the grounds that the viscera are relatively
insensitive structures and that visceral changes mediated by autonomic activity are too slow to be a
source of emotional feelings, which can arise very rapidly

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14
Q

Give an experiment that supported Cannon’s argument against the James-Lange theory

(don’t describe the whole thing)

A

artificial induction of the visceral changes typical of strong emotions, e.g. by injecting adrenaline to produce tachycardia, did not actually produce emotional experiences. (Schachter and Singer, 1962)

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15
Q

What did Hohmann find that supported the james-Lange theory

A

subjective feelings of anger and fear were diminished in subjects with spinal cord transection
and that the effect was greater the higher the level of the lesion.

subjects could act
as if they were angry in appropriate situations, but this “anger” subjectively lacked emotional colouring and intensity.

Therefore, although certain aspects of emotion (eg the thoughts or cognitions associated with specific emotions) apparently remained intact when the viscera were disconnected from the CNS, emotional experience was greatly reduced.

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16
Q

What were the 4 main groups in the Schachter and Singer study of 1962

A
  1. Epinephrine Ignorant: subjects were told (while being injected) that the injection was mild and harmless with no side effects. Therefore, the subject had no externally provided explanation of his/her bodily state.
  2. Epinephrine Misinformed: subjects were told to expect totally inaccurate side effects e.g. numbness of feet, itching.
  3. Epinephrine Informed: subjects were told to expect hand tremor, palpitations and flushing.
  4. Placebo: subjects received injections of saline and were told the same as group 1.
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17
Q

How were the 4 groups divided in the S and S emotion experiment

A

into two experimental conditions (or contexts) designed to elicit Euphoria or Anger.

In the first condition, subjects interacted with an actor (or “stooge”) who behaved euphorically.

In the second condition, the actor behaved angrily (there was no ‘Epinephrine Misinformed’ group for this condition).

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18
Q

What was Schachter and Singer’s hypothesis

A

subjects in the misinformed group would be most affected by the external manipulations of the context of their emotional state, because they had a less adequate explanation of their bodily changes. This would then show that the same symptoms of peripheral arousal (in the 3 groups) could produce different emotions, depending on the external environmental context (evaluated cognitively)

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19
Q

What were the 2 mains measures used by Schachter and Singer

A
  1. Self-report ratings (e.g. How good or happy would you say you feel at present? 0 - I don’t feel at all happy to 4- I feel extremely happy).
  2. Behavioural observations, through a one-way mirror - e.g. scores of initiating activity or agreeing/disagreeing with the actor.

pulse rate was also measured before and after the Adr injection to check it produced normal effects

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20
Q

Why is the Singer and Schachter experiment important (2)

A

(i) providing support for the James-Lange position that peripheral arousal provides a substrate for emotion
(ii) Showing the importance of cognitive factors (especially the attribution or labelling of bodily states) in interpreting this generally non-specific peripheral arousal as specific emotions

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21
Q

Which theories does the schachter and singer experiment bring together

A

theories of emotion based on peripheral arousal and those based on the neural mediation of emotional feelings and behaviour.

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22
Q

Is hunger an emotional state

A

not really

merely an internal sensation

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23
Q

What is required for hunger to be considered an emotion

A

must trigger cognitive appraisal of the situation that then elicits an emotional state.

For example, ‘anxiety’ may be elicited if the prospect of getting food in the near future is unlikely because you are living in the wilderness and finding food is becoming increasingly difficult

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24
Q

How do benzodiazepines and beta blockers affect anxiety

A

While benzodiazepines are successfully used to treat different types of anxiety, ß-adrenergic receptor blockers (e.g. propranolol) are also effective for
treating ‘somatic’ rather than ‘psychic’ forms of anxiety

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25
Q

What experiments did Tyrer perform to assess use of propranolol vs Diazepam

What were the results of the experiments (2)

A

used the Hamilton Anxiety Scale (for subjective ratings) and physiological measures, such as pulse and respiratory rate, to compare the effects of placebo, diazepam and propranolol on groups of ‘somatic’ and ‘psychic’ clinically anxious subjects

(i) Diazepam was effective for treating both psychic and somatic anxiety whereas the ß-blocker propranolol was effective only for treating somatic anxiety.
(ii) Under propranolol, ‘psychic’ anxiety patients showed a greatly reduced pulse rate but reported no subjective reduction in their anxiety

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26
Q

What elements of anxiety do bezxodiazepines affect

A

the psychic, rather than the somatic, in alleviating anxiety.

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27
Q

What did Broca identify about the emotional parts of the brain

A

identified a rim of old cortex on the medial wall of the hemisphere and called it the grande lobe limbique or ‘smell brain’ as it received information from the olfactory system.

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28
Q

What did Papez introduce for emotion in the brain

A

(Papez’s circuit) subserving emotion based not only on ideas from Broca but also observations about the consequences of brain damage in medial cortex in humans with research on the role of the hypothalamus in the control of emotional reactions in animals

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29
Q

How did Papez’s theory explain subjective emotion

A

explained the subjective experience of emotion in terms of the flow of information through a circle of anatomical connections from the
hypothalamus to the medial cortex, via the anterior thalamus and back to the hypothalamus by way of the hippocampus. cingulate cortex also involved

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30
Q

why was the cingulate cortex involved in Papez’s theory of emotion

Why was the hippocampus involved

A

when damaged, there was resulting apathy, depression and loss of emotional spontaneity,

the hippocampus was included because brain damage resulting from rabies, which included pathology in the hippocampus, resulted in emotional
disturbance

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31
Q

Who identified the limbic system

what does it involve

A

Maclean

all the structures in the original Papez circuit along with the amygdala, septum and prefrontal cortex.

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32
Q

What did Maclean hypothesise about the limbic system’s evolution

A

evolved to mediate visceral functions and affective behaviours including feeding, defense, fighting and reproduction

emphasised the role of hippocampus in emotional experience

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33
Q

Why was the amygdala involved in the limbic system

A

removal of the temporal lobe gave a range of symptoms termeed ‘psychic blindness’ including tameness, lack of emotional responsiveness, excessive examination of objects often with mouthing and eating of previously rejected items such as meat as well as hypersexual behaviour

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34
Q

What is another name for psychic blindness

what are the symptoms

A

‘Kluver-Bucy’ syndrome

tameness, lack of emotional responsiveness, excessive examination of objects often with mouthing and eating of previously rejected items such as meat as well as hypersexual behaviour

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35
Q

what structures would a system that mediates emotionality involve

A

both cortical & subcortical elements. Some of these areas, if not all, will be intimately connected to the hypothalamus

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36
Q

What are the principal components of the emotion system (5)

Which is now thought to be less important

A
hypothalamus, 
amygdala, 
orbitofrontal cortex, 
ventral striatum, 
cingulate cortex 

BUT NOT so much hippocampus (hippocampus important for memory)

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37
Q

why may we still think the hippocampus is involved in emotional processing

A

recent studies do implicate anterior hippocampus (or ventral hippocampus in rodents) in emotional processing

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38
Q

are all emotional brain structures used for all emotions

A

There is ongoing debate whether there is a common set of brain structures important for all emotional behaviour or whether different emotions use a different set of brain structures by virtue of the fact that different emotions evolved for different reasons.

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39
Q

What is important for emotions about the connections of the amygdala

A

e connections of the central amygdala to the brain stem and hypothalamus are well placed to initiate fearful and aggressive responses (emotional expression).

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40
Q

What are US and CS in conditioning

A

US - unconditioned stimulus

CS - conditioned stimulus

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41
Q

How can conditioned fear stimuli be blocked

A

by lesions of the central nucleus of the amygdala.

42
Q

What is the importance of the amygdala in facial expression recognition

A

e important for the recognition of fearful faces.

Lesions of the amygdala impair fear recognition.

fMRI studies have shown that the amygdala is activated when presented with emotional faces

43
Q

What are neuroses now called

what are they

A

anxiety disorders

a category of disorders in which the healthy response to, and the anticipation of, fear, becomes dysfunctional.

44
Q

What does the healthy response to fear include (3)

How does this compare to anxiety disorders

A

subjective changes (feelings of dread, thoughts of impending harm),

behavioural changes (‘flight or fight’)

physiological changes (e.g. increased heart rate, pupil dilation).

Patients with anxiety disorders show a similar triad of symptoms.

45
Q

What are the 4 main anxiety disorders

A

1) Phobias – an irrational fear of a specific object or situation
2) Panic Disorder – intense and overwhelming attacks of anxiety
3) Agoraphobia – a fear of crowds or public places that often gives rise to panic attacks.
4) Generalised Anxiety Disorders (GAD) – pervasive worry or anxiety lasting for months.

46
Q

Are OCD and PTSD anxiety disorders

why may they still be relevant here

A

used to be but no longer

much of the fundamental insight underlying certain symptoms will also be relevant for those disorders.

47
Q

What are the 3 key characteristics of a phobia disorder

A

1) Persistent fear of a situation or object which most people find tolerable.
2) Outside the phobic situation, the patient may acknowledge that the fear is irrational.
3) The patient changes their daily routine to avoid contact with the phobic object or situation. Over time, this avoidance (e.g. of going outside) becomes very debilitating.

48
Q

Name 3 common phobias

A

specific phobias

social phobia

agoraphobia

49
Q

What are specific phobias

A

either to animals (spiders, dogs), activities or inanimate objects (flying, dirt), illness or injury, or to blood and/or needles

50
Q

Why are blood/needle phobias important for doctors to know about in their patients

A

they show a physiological response to the phobic stimulus (heart rate/blood pressure decreases), which carries implications for treatment

51
Q

What is social phobia

A

an excessive fear of being observed (e.g. eating or speaking in public), linked to fear of humiliation or embarrassment

52
Q

How common are phobias requiring treatment

what is the gender difference

How common are debilitating phobia disorders? (eg cannot leave house)

A

6% of populations

more prevalent in women (~8%) than men (~4%)

1%

53
Q

IS there a genetic element to phobias (2 pieces of evidence)

A

First-degree relatives of phobic patients are around 3 times more likely to suffer phobias,

twin studies show a heritability of ~30% (also agorophobia 39%, panic disorder 44%)

54
Q

Do specific anxiety disorders breed true (3)

A

controversial

some evidence that first-degree relatives are most likely to have the same disorder as the proband (Fyer et al 1995),

but first-degree relatives are also at increased risk for other anxiety disorders and depression relative to healthy controls (Burmeister 2003).

It is likely that some risk factors will be disorder-specific whereas others will be general risk factors for multiple disorders

55
Q

What does Little Albert represent in the acquisition of phobic anxiety

A

model of Pavlovian conditioning

56
Q

What is the case of Little Albert

A

11 month-old baby was conditioned (by John Watson) to fear a white rat (the conditioned stimulus, CS) by pairing it with a loud noise (the striking of a gong: the unconditioned stimulus, US) over Albert’s head. On presentation of the rat for the first time, Albert reached out to touch the rat (presumably showing no fear). But after many exposure trials to rat + loud gong, the presentation of the rat alone elicited crying and hiding behaviour (the conditioned response, CR).

57
Q

What are the 2 questions that arise from the behavioural account of acquisition of phobias

A

1) If phobias are caused by pavlovian conditioning, why does the CR not extinguish when the CS occurs without the US?
2) If phobias are the result of Pavlovian conditioning, why are all stimuli not equipotent in causing phobias?

58
Q

If phobias are caused by pavlovian conditioning, why does the CR not extinguish when the CS occurs without the US?

A

Avoidance - prevents extinction

59
Q

What is avoidance

A

Even if the phobic patient encounters the phobic object (e.g. a dog or snake), the act of running away will cause them to interpret the experience as a ‘lucky escape’ (NB. this is a more cognitive than behavioural account).

Avoidance also acts as negative reinforcement, causing relief of anxiety

60
Q

What does Mowrer’s 2 factor model (1947) propose

A

phobic anxiety was acquired by pavlovian conditioning but maintained by operant (instrumental) conditioning (avoidance).

61
Q

If phobias are the result of Pavlovian conditioning, why are all stimuli not equipotent in causing phobias?

A

Biological Preparedness

vicarious conditioning

62
Q

What is Biological Preparedness

A

The lack of gun and knife phobias suggests some evolutionary bias towards objects and situations that were harmful to our ancestors

63
Q

What was Susan Mineka’s evidence for Biological Preparedness

A

laboratory-reared rhesus monkeys do not exhibit behavioural avoidance or emotional distress or fear to toy snakes, whereas wild-reared monkeys do, suggesting that early experience can produce phobic reactions

64
Q

What was Mineaka’s evidence for vicarious conditioning (2 experiments)

A

laboratory-reared adolescent monkeys did develop fearful or phobic responses if put into a situation where they could observe (on video for as little as 8 minutes) their parent’s fearful reactions to the same snake stimuli

They also undergo this vicarious fear conditioning to toy snakes more easily than to toy flowers, suggesting that snakes have some innate properties that are recognised by the fear system

65
Q

What evidence did Ohman at el (1975) provide for the biological preparedness theory

A

presented to human subjects in a conditioning group either 1 or 5 pairings of a picture CS and a shock US. The picture was of a potentially phobic stimulus (a snake) for half the subjects and a neutral stimulus (a flower) for the remainder. The CR (the SCR response) was measured in extinction (i.e. in the absence of the shock) after conditioning: i.e. the pictures of snakes or flowers were presented alone. To check that any change in the SCR in the conditioning group was due to the positive temporal correlation of CS and US; control groups received simple exposure either to shock alone (“sensitization” control) or to the picture alone (CS alone).

used measures of autonomic responses such as the SCR (sweating) as an index of fear conditioning

66
Q

What were the results of Ohman et al experiments on biological preparedness

A

(i) The Conditioned group showed a larger SCR than the control groups.
(ii) There was more conditioning to the phobic CS (snake) than to the neutral (flower) CS; thus, indicating that certain stimuli are more easily established than others as CSs for an aversive US.

67
Q

How are expectancies implicated in Pavlovian conditioning

How can this be manipulated to affect a CR

A

conditioning can sometimes be thought of as reflecting the formation of expectancies, so that when the signal or CS occurs, the subjects expect the US because of the predictive capacity of the CS.

Expectancies can be manipulated by verbally presented information and so one might expect the strength of a CR to be similarly affected.

68
Q

What evidence did Ohman gather that phobias may be affected by expectation

give the 2 phases and result

A

1) SCR acquisition (a) CS+ paired with a shock US; (b) CS- not paired with shock. The CS+ could be either (i) phobic or (ii) neutral, in different groups.
2) Extinction trials (no shock presented). But half the subjects were told that the shock would no longer occur (i.e. an instructed group), the other half were not told (i.e. a not instructed group).

key result was that instructions reduced SCR responding to the CS+ when a neutral stimulus was employed, but there was no effect when a phobic CS+ was used, i.e. the conditioned fear response persisted.

69
Q

What happens in flooding therapy?

A

the patient is exposed to the CS until their anxiety (eventually) subsides in the absence of the US (i.e. extinction)

70
Q

What happens in modelling therapy

A

the patient observes another person (e.g. a friend) experience the CS in a non-fearful manner

71
Q

What does modelling therapy assume

A

conditioning processes can occur vicariously: by watching another person behave fearfully (or non-fearfully) to a stimulus, our own fear reactions are modified

72
Q

What is the most influential phobia treatment

A

Systematic Desensitisation (Wolpe, 1950)

73
Q

What is Systematic Desensitisation

A

consists of several stages:

1) The patient is trained in a relaxation technique, e.g. deep breathing
2) The patient and therapist develop a hierarchical list of fear situations, from slightly scary to full exposure.

3) They are then exposed to the first
situation and implement relaxation to counter-condition their anxiety.

4) When they can handle the first situation with no fear reaction, they progress to the second scenario, and so on.

74
Q

What are some predisposing factors to phobias

A

may be biological or psychological in origin, and increase the risk of developing the disorder (e.g. being bitten by a dog in childhood).

Precipitating factors then bring this vulnerability to the surface, often in adulthood (as a clinician, think: “what has made this issue a problem at this specific point in the patient’s life?”)

75
Q

What is the trigger factor in the case of phobias

A

presentation of the phobic stimulus (other anxiety disorders’ triggers are harder to elucidate)

76
Q

What are the main cognitive biases perpetuating the phobia (3)

A

avoidance

hyper-vigilance (constantly checking for the phobic stimulus, which makes the patient detect more of them!)

thought suppression (trying not to think about the phobic stimulus, which makes the patient think about it even more)

77
Q

How can the cognitive biases of a phobia be demonstrated

A

d with the Spider Stroop task in which spider phobics are slower to read the colour of spider-associated words

78
Q

Where does the cognitive account of phobias actually diverge from the behavioural account?

A

fairly compatible and many therapists use a combination of cognitive-behavioural therapy (CBT) - highly effective in treating specific phobias in 1-6 sessions.

79
Q

What does the behavioural account of phobias imply

what do behaviourists use to support this

A

conditioning could occur with minimal awareness or appraisal of the situation

phobic patients often acknowledge that their fears are irrational when they are not in the phobic situation.

80
Q

What does the cognitive account of phobias imply

What did Thorpe et al show as evidence for this (2 experiments)

A

the person’s appraisal and interpretation of CS-US pairings are central to the development of phobias

when phobic patients are in the phobic situation, they do not appreciate their irrationality and express strong conviction in their beliefs that the dog will attack and injure them

conducted ‘pure’ cognitive therapy on arachnophobes, attempting to challenge and dispute their irrational beliefs about spiders, without any actual exposure (behavioural therapy) to spider stimuli.

A single therapy session improved symptoms and normalised attentional biases on the Spider Stroop.

81
Q

What provides the basis for modelling disorders in humans

what has this allowed

A

studying unconditioned and conditioned fear in animals

a more detailed investigation of underlying neural mechanisms and providing a way to develop anxiolytic drugs

82
Q

What structure does the acquisition of conditioned fear rely on

have we confirmed this

A

amygdala

confirmed repeatedly in numerous experiments in animals.
Lesions of the amygdala also prevent or impair fear conditioning in humans (e.g. in subjects with Urbach-Wiethe disease, in which the amygdala is calcified bilaterally – very rare)

83
Q

What clinical hypothesis has data on fear conditioning in animals and humans lead to

is this supported by clinical tests?

A

amygdala may be overactive in anxiety disorders.

Functional imaging studies support this: patients with spider phobia showed increased amygdala responses, compared to healthy controls, following presentation of phobic pictures, as well as presentation of other fearful and disgust-related pictures

Schienle et al, 2005

84
Q

What has been shown to be the case for the prefrontal cortex in phobic patients

A

Under-activity of the prefrontal cortex has also been identified in phobic subjects suggesting that normally the prefrontal cortex acts to down-regulate amygdala responsivity to aversive stimuli.

85
Q

What is valium

A

diazepam (a benzodiazepine)

86
Q

What are the drugs of choice to treat anxiety

A

benzodiazepines such as diazepam

87
Q

What are benzodiazepines used to treat

A

anxiety
anticonvulsants (eg in alcohol withdrawal)
hypnotics and sleep inducers

88
Q

Why are benzodiazepines considered to be safe

A

lethal dose is rare

BUT they are associated with a dependence-withdrawal syndrome (that includes insomnia, loss of appetite and anxiety) and also cognitive impairment, especially memory loss

89
Q

How effective are benzodiazepines at treating different anxiety disorders

A

mainly to treat generalised anxiety disorder, but are much less effective for treating panic disorder or phobias

90
Q

What is the Geller Seifter Conflict procedure

A

AKA conditioned suppression

a mildly thirsty or hungry rat is trained to press a lever for water or food, respectively (or may even simply have access to water to drink), but occasionally a neutral light or tone stimulus (the to-be conditioned stimulus, CS) is presented that is terminated with a mild electric footshock punishment (i.e. pavlovian pairing between stimulus and shock)

This produces ‘conflict’ when the now conditioned fear stimulus (CS) is presented alone, resulting in a suppression of behaviour until the anxiety-eliciting CS is switched off

91
Q

What are the anxiolytic effects of benzodiazepines predicted by

A

their effects on conditioned fear in animals – effects that resemble those of amygdala lesions in that they reduce conditioned fear.

eg in the Geller Seifter Conflict

92
Q

How do benzodiazepines affect conditioned suppression

A

chlordiazepoxide (Librium) or diazepam (Valium) produce an increase in the number of responses made during periods signalled by the fear CS. This release of conditioned suppression is the “anxiolytic” effect

93
Q

What is the MOA of benzodiazepines

A

in the amygdala (where there are many benzodiazepine binding sites on GABAa receptors)

94
Q

why are animals useful for anxiolytic drug development

A

The potency of a range of benzodiazepines and other drugs in releasing conditioned suppression or reducing other behavioural measures of fear in animals correlates well with their clinical potency

95
Q

Name 3 groups of drugs that can treat anxiety

A

benzodiazepines
SSRIs
5-HT1A receptor ligands (agonists i think but not sure)

96
Q

How is the serotonin system implicated in threat response

A

subjects with the less effective (short) allele of the serotonin transporter polymorphism show increased amygdala responses to fearful facial expressions, and are at increased risk of anxiety and depressive disorders, compared to subjects with the more effective (long) allele (Hariri et al 2003)

but SSRIs decrease amygdala activity to phobic stimuli

Paradox: would be predicted that carriers of the short allele, with low expression of the transporter, would be more resilient, not more vulnerable, given SSRI’s are anxiolytic

97
Q

How do SSRIs affect the amygdala

A

amygdala over-activity to phobic stimuli is reduced

98
Q

How does the efficacy of SSRIs change throughout the course

what does this suggest

A

only effective after a few weeks of treatment

suggesting that their efficacy is dependent upon specific adaptations, e.g. regionally selective down and/or up-regulation of specific 5-HT receptors

99
Q

Why does the short allele for 5-HTT produce changes beyond the role of serotonin alone

A

serotonin has an important role in developing brain circuits and thus, the short allele of the 5-HTT, which is associated with altered activity across brain circuits in adulthood, probably has its effects on the development of these circuits

100
Q

How well do phobias and anxiety disorders respond to pharmacotherapy

A

not well
benzodiazepines effectively reduce anxiety in the feared situation but do little to affect the fear reaction when the medication is withdrawn

101
Q

Which forms of anxiety tend to by treated with benzodiazepines

When would you use other drugs to treat anxiety disorders

A

chronic forms of anxiety (e.g. GAD) that are treated effectively with benzodiazepines

ß-adrenergic receptor blockers (e.g. propanolol) are used to treat somatic anxiety

SSRIs (e.g. Prozac) are increasingly widely used to treat anxiety, especially when associated with depression