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Year Three Psychology > Psychopharmacology > Flashcards

Psychopharmacology Flashcards

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1
Q

Define psychopharmacology:

A

the study of the effects of drugs on cognition, mood, and behaviour

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2
Q

Why is psychopharmacological research difficult?

A

we only know what we happen to have found out so far

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3
Q

What is psychopharmacological research useful for?

A

drugs can be used to study functions of endogenous neurotransmitter systems (NTs). investigation of drug effects can lead to the development of treatments for medical/psychological conditions such as Alzheimer’s, schizophrenia and depression.

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4
Q

What is a confound?

A

a confound is a potential alternative cause of what appears to be a drug effect

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5
Q

How would you control for the following confounds?
A-natural recovery
B-expectation of drug effect
C-expectation of side effects

A

A- a comparison with a no treatment group
B- comparison with placebo and blinding of conditions
C- comparison with an active placebo with similar noticeable side effects

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6
Q

Describe a Randomised Control Trial (RCTs):

A

this involves a control condition and a random assignment of participants to groups

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7
Q

Describe Blinding of Conditions:

A

a blind study where participants are unaware of group assignment or a double-blind where the participant and researcher are both unaware of group assignments

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8
Q

Describe Open-Label Trials:

A

these are studies without blinding, they may still have a control group

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9
Q

What heightens the risk of a trial being unblinded?

A

when the effects are detectable and so participants can begin to guess which group they are part of

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10
Q

Describe a between-subject design:

A

comparison between participants versus a control group

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11
Q

Describe a within-subject design:

A

comparison between two conditions with the same participants

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12
Q

Why is a washout period helpful?

A

this allows drugs to leave the system before the next trial in order to not carry over effects

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13
Q

What is a phenomenological method of measuring drug effects?

A

self reported changes in subjective experience and mood

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14
Q

how can the phenomenological method of measuring drug effect reduce its susceptibility to bias?

A

by using a double blind technique

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15
Q

How can you measure changes in physiological activity and why is it important?

A

via methods such as fMRI and EEG. This is important because we can investigate the effects of drugs on people

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16
Q

Which tasks can be used to measure drug effects?

A

simple and choice tasks, vigilance, memory, and problem solving tasks

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17
Q

What changes of behaviour are indicative of drug effects?

A

changes such as social cooperation, aggression, hyperactivity etc.

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18
Q

What is the aim of neurocognitive models?

A

neurocognitive models aim to explore relationships between specific neurotransmitter systems, cognitive processes and subjective experiences

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19
Q

What could a neurocognitive model centre around?

A

the model could be of a type of drug effect (e.g. stimulant, sedative, psychedelic), or it could be of a neuropsychiatric condition (e.g. ADHD, depression, schizophrenia)

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20
Q

What are examples of neurocognitive models?

A

-noradrenaline on alertness and attentional focus for ADHD
-dopamine on stimulus salience for schizophrenia
-serotonin on emotional info processing for mood disorders

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21
Q

what is the function of:
1)dendrites
2)cell body (soma)
3)axon
4)action potential
5)enzymes
6)axon hillock

A

1-receive NTs from other neurons (chemical signals)
2-includes the nucleus and controls cell activity
3-allows electrical signal (action potential) to travel to axon terminal
4-integrate multiple excitatory and inhibitory signals to determine whether an action potential is generated
5-control synthesis of neurotransmitters stored on vesicles and released from axon terminal
6-action potentials are triggered here is there is sufficient depolarisation

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22
Q

What indicates sufficient depolarisation?

A

+ relative to -

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23
Q

what is the difference between excitatory and inhibitory?

A

excitatory increases the likelihood of a receiving neuron producing an action potential, and inhibitory decreases the likelihood

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24
Q

What are three steps of endogenous processes?

A

1- synthesis by enzymes and packaged in vesicles
2-release and bind with postsynaptic receptors
3- deactivated via presynaptic reuptake or broken down by enzymes

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25
Q

How do NTs influence ion channels?

A

NTs influence by opening and closing ion channels allowing electrically charged ions to move in or out of the post synaptic cell making it more or less likely to fire

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26
Q

What effects do some NTs have that are not direct?

A

modulating the effect of other NTs on ion channels or leading to synaptic changes.

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27
Q

What does the effect of NTs depend on?

A

receptor types

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28
Q

What happens in NT deactivation?

A

NT detaches from receptor and is transported back (reuptake), or broken down by enzymes

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29
Q

What is the difference between agonist and antagonists?

A

agonists mimic or enhance the effect of a NT whereas antagonists block or reduce the effect of NT

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30
Q

How do psychoactive drugs work and how can they influence NTs?

A

they interact with NT systems and can influence NT synthesis, storage, release, deactivation, and receptor interactions

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31
Q

Name two major neurotransmitters and how they work together:

A

GABA= main inhibitory NT released by 40% neurons
Glutamate- main excitatory NT released by 50% neurons
they work in opposition to maintain balance between inhabitation and excitation

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32
Q

What are examples of GABA agonists and what effects do they have?

A

Benzodiazepines, barbiturates, and alcohol.
They can reduce anxiety (specifically anxiolytic), reduce arousals (sedatives), and can promote sleep

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33
Q

What are BZDs commonly prescribed for?

A

anxiety and used as a pre anaesthetic for surgery

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34
Q

What are Barbiturates typically used for?

A

general anaesthetic, induce comas and treat epilepsy

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35
Q

What are two GABA antagonists?

A

stimulants: flumazenil and picrotoxin

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36
Q

What is an antidote for a BZD overdose?

A

flumazenil, blocks BZD site on receptors

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37
Q

What is a purpose of flumazenil besides treating overdoses?

A

it can reverse sedation after surgery

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38
Q

What is an antidote for a Barbiturate overdose?

A

picrotoxin

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39
Q

what could be used to induce a seizure ?

A

picrotoxin

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40
Q

What is ibotenic acid and how can it be dangerous?

A

a glutamate agonist. can kill nerve cells through over excitation

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41
Q

What is ketamine and how can it be used?

A

a glutamate antagonist, blocks excitatory effect of glutamate. can be used as a sedative and anaesthetic

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42
Q

Describe NMDA:

A

a receptor sub type. NDMA receptors are important in initiating long term synaptic changes necessary for learning. NMDA is also implicated in drug addiction, schizophrenia, and epilepsy

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43
Q

What is ARAS?

A

Ascending Reticular Activating System. Regulates general levels of cortical arousal, alertness, and consciousness.

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44
Q

What is ARAS the source of?

A

major excitatory neurotransmitters Noradrenaline (NA) and Acetylcholine (ACh)

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45
Q

How does ARAS communicate with other brain regions?

A

The axons of ARAS project from brain stem to higher cortical regions via thalamus

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46
Q

What was suggested by Eysenck (1967) regarding ARAS and extraversion?

A

suggested a link between ARAS and extraversion. extraverts have low resting ARAS activities and so seek out more stimulation, while introverts have high resting activity and so they avoid overstimulation

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47
Q

What is the difference in distribution between Glutamate and Gava, and Noradrenaline and Acetylcholine?

A

cells that produce glutamate and Gava can be found all over the brain and cortex. NA and ACh are not widely distributed and so are in specific regions

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48
Q

Describe the nature of the Anterior system and the Posterior system:

A

Anterior system= frontal. top down system (cognitive input first), voluntary, controlled, task and goal driven, associated with executive functioning
Posterior system= parietal. bottom up system (sensory input first), involuntary, automatic, stimulus driven attention, orienting reflex

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49
Q

Explain what is meant by Alertness, Attention, and Arousal:

A

Alertness= generalised readiness to process stimuli and respond. measured by subjective feelings or simple psychomotor tasks
Attention= enhanced processing of specific/selected stimuli. measured by behavioural performance
Arousal= physiological activation in autonomic nervous system or central nervous system

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50
Q

How is alertness measured through simple detection/reaction time tasks?

A

Mean reaction time depends on average alertness during the task or temporary increase in alertness following warning cues

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51
Q

How is alertness measured through vigilance (continuous performance) tasks?

A

person is told to respond only to pre specified target stimulus/sequence. The targets are rare and the presentation is rapid. Also involves the Anterior system. Measures average reaction time to targets, errors of omission (missed targets), and errors of commission (false alarms)

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52
Q

Why are vigilance tasks harder than simple detection tasks?

A

vigilance tasks require sustained attention and so are more cognitively demanding.

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53
Q

What are stimulants and what are some examples?

A

drugs that increase alertness and arousal; caffeine nicotine, amphetamines, methylphenidate aka Ritalin

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54
Q

What do stimulants do to noradrenaline and acetylcholine?

A

they mimic or enhance the effects of noradrenaline and acetylcholine. they are noradrenergic or cholinergic agonists.

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55
Q

What are sedatives and what are some examples?

A

they are drugs that reduce alertness and arousal. These include GABA agonists, noradrenergic beta blockers, and cholinergic antagonists

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56
Q

Where is the main source of Noradrenaline and how does it move around the brain?

A

The Locus Coeruleus (LC, blue spot) in the brain stem are the main source of NA. They project to higher brain areas including via the thalamus

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57
Q

What are the effect of drugs that increase NA-ergic activity?

A

psychostimulants increase alertness whereas anxiogenic have anxiety producing effects

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58
Q

Describe Amphetamines?

A

Amphetamines are synthetic drugs produced from ephedrine and pseudoephedrine. they increase the release and block the reuptake of noradrenaline and dopamine

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59
Q

What are the acute effects of Amphetamines?

A

they have subjective effects. can include feelings of energy and alertness, however increase anxiety as a high dose

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60
Q

What are the effects of Amphetamines on task performance?

A

Low doses improve performance in psychomotor and vigilance tasks. High doses impair task performance and increase distractibility

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61
Q

Explain Yerkes-Dodson Law regarding arousal (1908):

A

Inverted U relationship between arousal and task performance. Under arousal and over arousal can both impair performance. increasing arousal with a psychostimulant can improve performance if the arousal is low, or impair the performance if the arousal is high. This may be due to arousal narrowing attentional focus which can be too narrow for optimal performance on complex tasks.

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62
Q

What are the effects of drugs that reduce NA ergic activity?

A

sedative affects reducing alertness and anxiolytic (anxiety reducing) effects.

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63
Q

Describe Noradrenergic beta blockers:

A

e.g. propranolol which is mainly used clinically for effects on blood pressure and heart). They are B receptor Antagonists.

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64
Q

What neurons release acetylcholine?

A

cholinergic neurons

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65
Q

How is acetylcholine sent throughout the brain?

A

Cholinergic nuclei in upper brain stem project to thalamus and regulate arousal and sleep/wake cycle.

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66
Q

What does acetylcholine activate:

A

systems associated with alertness, attention, learning, and memory

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67
Q

What are cholinergic inhibitors used for?

A

they are used in Alzheimer’s treatment (ACh) because the cells in the basal forebrain are lost in the disease. inhibitors increase ACh availability

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68
Q

What do cholinergic receptor agonists do and what is an example?

A

e.g. nicotine. Mimic the effects of ACh at their receptors increasing subjective alertness

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69
Q

What do cholinergic antagonists do?

A

they block the effects of ACh at receptors therefore reducing subjective awareness

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70
Q

In what way are cholinergic antagonists similar to Alzheimer’s?

A

they cause general cognitive impairment (delirium) which is similar to Alzheimer’s symptoms.

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71
Q

What is Scopolamine?

A

Scopolamine is a cholinergic antagonist found in various toxic plants e.g. deadly nightshade family

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72
Q

Explain Wesnes et al. (1988) study with scopolamine:

A

Wesnes gave scopolamine or a placebo and measured the task performance on various cognitive tasks. people on scopolamine felt less alert (in self rating), missed more targets in vigilance tasks, responded more slowly in vigilance tasks, and had poorer memory performance in word recall.

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73
Q

What amount of population does ADHD effect?

A

estimated to effect about 5% of population. More frequently detected in males than females, but this doesn’t mean it is definitely more common in males.

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74
Q

When are ADHD symptoms more prevalent?

A

characteristics are first present in childhood and in 50% of cases persists into adulthood

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75
Q

What are the main ADHD symptoms?

A

inattention, hyperactivity, impulsivity, forgetfulness, distractibility

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76
Q

How can ADHD be treated with drugs?

A

often treated with psychostimulant drugs such as Adderall (amphetamine), and Ritalin (methylphenidate). they increase levels of noradrenaline and therefore dopamine in the brain

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77
Q

What are newer drug treatments for ADHD?

A

newer drug treatments more selectively target noradrenaline levels (e.g. atomoxetine, a noradrenaline reuptake inhibitor) as opposed to also effecting dopamine

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78
Q

Describe Zeiner et al. (1999) study on response to methylphenidate in boys with ADHD:

A

36 boys aged 7 to 11 following a double blind placebo controlled procedure with a within subjects design. Three weeks of daily treatment, one week washout period. Assessments were carried out in the final week of each treatment.

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79
Q

What were the findings of Zeiner et al. (1999) study on Ritalin in boys with ADHD?

A

found that vigilance was improved (fewer missed targets on tests), also increased performance on working memory tasks, and decreased reported hyperactivity and conduct problems

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80
Q

Why would a stimulant drug reduce hyperactivity?

A

if ADHD involves abnormally low levels of intrinsic arousal, hyperactivity might be aimed at increasing arousal to a more optimal level as a behavioural response. this could reduce the need for hyperactivity as well as improve cognitive functioning

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81
Q

What is a theory to do with ADHD and extraversion?

A

ADHD may be an extreme end of the extraversion personality dimension.

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82
Q

What are the three Dopaminergic systems?

A

Nigrostriatal
Mesocortical
Mesolimbic

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83
Q

describe the nigrostriatal pathway and its functions:

A

substantia nigra to striatum (dorsal).
Motor Control and indirectly Executive function via fronto-striatal circuity

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84
Q

describe the Mesocortcial pathway and it’s function:

A

ventral tegmental area to pre frontal cortex.
Executive function

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85
Q

Which pathways is Parkinson’s disease related to?

A

Nigrostriatal system and Mesocortical system

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86
Q

Describe the Mesolimbic pathway and it’s function:

A

Ventral tegmental area to nucleus accumbens (ventral striatum) in basal forebrain.
Reward, Motivational drive, Salience

87
Q

What do drugs with high potential for abuse do to DA-ergic activity?

A

they increase DA-ergic activity in the ventral striatum. this led to the idea that addictive drugs hijack the brain reward systems

88
Q

What are examples of drugs that rapidly increase DA levels within the synapse?

A

amphetamine and cocaine

89
Q

What are examples of drugs that indirectly increase levels in the reward systems via effects on other NT systems?

A

nicotine and alcohol

90
Q

How can classical conditioning effect the dopamine reward system?

A

via classical conditioning stimuli associated with the pleasure/reward trigger dopamine release in the reward system

91
Q

How can cues elicit cravings?

A

cues acquire motivational salience, becoming attention grabbing, and so eliciting subjective feelings of wanting

92
Q

What is motivational salience?

A

a cognitive process that drives a person’s behaviour towards or away from a particular stimulus.

93
Q

what is the process behind elicit drug craving?

A

with repeated drug use environmental cues such as people, places, and objects which are associated with drugs can trigger dopamine release which focuses attention on drug related cues and elicits drug cravings

94
Q

Dopamine is thought to play a role in motivational salience of what types of stimuli?

A

stimuli that are potential threats or that are novel, unexpected or related to current goals

95
Q

What does the word ‘schizophrenia’ mean?

A

Split mind

96
Q

What is meant by ‘positive symptoms’ of schizophrenia?

A

psychosis: the presence of abnormal experiences and behaviour such as hallucinations (perception of non present stimuli), and delusions (beliefs that don’t correspond to reality)

97
Q

What is meant by ‘negative symptoms’ of schizophrenia?

A

absence of normal experiences and behaviours such as lack of motivation, anhedonia, and social withdrawal

98
Q

Define anhedonia:

A

the inability to feel pleasure

99
Q

What dopamine activity are the positive symptoms of schizophrenia associated with?

A

linked to increased DA-ergic activity particularly in nucleus accumbens

100
Q

What dopamine activity are the negative symptoms of schizophrenia associated with?

A

linked to reduced DA-ergic activity particularly in the pre frontal cortex

101
Q

How are increased and reduced dopamine activity in different systems related to each other?

A

The causation (whether one triggers the other) is unknown however recent evidence suggests that a disruption involving glutamate receptors might precede both

102
Q

Describe L-dopa:

A

AKA Levodopa. This is a precursor molecule that is converted into dopamine in the brain. It has been used to treat Parkinson’s disease since 1960s

103
Q

What are the side effects of L-dopa?

A

this can produce schizophrenia like symptoms in patients like delusions and hallucinations

104
Q

Which drugs can increase dopamine activity in the brain?

A

L-dopa, amphetamine, and cocaine

105
Q

Explain Amphetamine psychosis:

A

it has been recognised since the 1950s. Drugs such as amphetamines and cocaine can increase dopamine levels in the synapse. This can increase positive symptoms and cause schizophrenia type symptoms in non schizophrenics.

106
Q

What do antipsychotics do to dopamine activity in the brain?

A

these drugs reduce dopamine activity in the brain and can be used to treat positive symptoms of schizophrenia such as hallucinations and delusions. they are DA agonists which block DA receptors

107
Q

What was the first effective anti psychotic drug (1950s)?

A

Chlorpromazine

108
Q

Why are antipsychotics sometimes described as neuroleptics?

A

neuroleptics meaning taking hold of nerves. This is because they make movement difficult at high doses

109
Q

What are neuroleptic side effects of antipsychotics?

A

Parkinson’s like side effects. This includes problems with movement such as tremors and rigidity, and extrapyramidal symptoms linked to reduced activity in the nigrostriatal DA-ergic system

110
Q

what are extrapyramidal symptoms?

A

unwanted, involuntary movements or other symptoms that can be caused by certain medications.

111
Q

what unpleasant subjective reactions are side effects of antipsychotics?

A

feelings of restlessness, emptiness, anhedonia, and apathy

112
Q

Define apathy:

A

loss of interest

113
Q

What is neuroleptic-induced dysphoria linked to?

A

reduced DA activity in the mesolimbic DA-ergic system

114
Q

What is an issue with the side effects of antipsychotics?

A

the side effects can lead to patients stopping medication and therefore to relapse

115
Q

Explain the dopamine hypothesis of schizophrenia:

A

positive symptoms are caused by excessive levels of dopaminergic activity. Neuroleptic drugs have a blocking function which reduces positive symptoms. Drugs which increase dopamine activity such as amphetamine, cocaine, and L-dopa increase positive symptoms

116
Q

What does the Glutamate Hypothesis of schizophrenia propose?

A

changes in dopamine activity might happen because of changes in glutamate receptors

117
Q

Explain the neurocognitive explanation of the role of DA in psychosis:

A

usually salient stimuli or event is signalled by dopamine release in the nucleus accumbens (mesolimbic pathways). in psychosis this process is disrupted so increased dopamine coincides with stimuli and events with no real significance. hence psychosis involves misattribution of salience

118
Q

what is meant by the attribution of salience?

A

a cognitive process where stimuli become attention grabbing and motivationally significant

119
Q

How can aberrant salience produce psychosis?

A

there us a prodromal period which occurs before specific positive symptoms are evident, this can last from days to years. These experiences can lead to delusional beliefs as top down cognitive processes are employed to make sense of them; therefore they are meaningful to an individual and within cultural context.

120
Q

What is the prodromal period of schizophrenia characterised by?

A

aberrant salience signalling. recurring feelings that something odd but important or threatening is happening which individuals cannot explain or understand

121
Q

What are hallucinations?

A

internally generated stimuli (thoughts, mental images, inner voices) allocated inappropriate salience and processing resources

122
Q

How can psychotic symptoms be considered a normal reaction to an abnormal situation?

A

aberrant DA signalling. hallucinations and delusions are allocated inappropriate salience and processing resources

123
Q

How effective are antipsycotics?

A

antipsychotics do not directly eliminate hallucinations or delusional beliefs but they make them less salient, less distressing, and less likely to form

124
Q

How can antipsychotic treatments be aided?

A

by psychotherapy such as CBT which can help beliefs change in the absence of aberrant salience. the combination can weaken attachment to delusional beliefs

125
Q

what is the correlation between positive symptoms and antipsychotics?

A

improvement in positive symptoms in patients taking antipsychotics progresses over time

126
Q

where do the main serotonergic systems originate?

A

brainstem, Raphe Nuclei

127
Q

True or False: serotonergic axons project widely through the brain

A

True

128
Q

aside from mood, what does serotonin play a role in?

A

memory, sleep, appetite, perception, temperature regulation

129
Q

What is 5-HT?

A

Serotonin

130
Q

How is 5-HT synthesised and stored?

A

synthesised from tryptophan (dietary amino acid) and stored in vesicles

131
Q

How is serotonin removed?

A

it is removed by reuptake transporters on the synaptic neuron

132
Q

which two enzymes is 5-HT synthesised from?

A

tryptophan and 5-HTP

133
Q

What is Acute Tryptophan Depletion (ATD)?

A

an experimental procedure to reduces levels of serotonin in the brain

134
Q

Describe the procedure of Acute Tryptophan Depletion:

A

participants follow a low protein diet for 24 hours and then ingest a drink containing concentrated mixture of amino acids but not tryptophan. the body used available amino acids to synthesise required proteins which uses available tryptophan in the body and reduces serotonin synthesis

135
Q

During Acute Tryptophan Depletion, when are physiological effects maximal?

A

after 5 hours

136
Q

what is tryptophan depletion associated with in both healthy brained and unwell people?

A

increased irritability, aggression and negative mood

137
Q

What is Tryptophan supplementation associated with in both healthy brained and unwell people?

A

positive mood, reduced irritability, reduced aggression

138
Q

Does tryptophan manipulation present the same in all humans?

A

effects widely vary between individuals

139
Q

How do SSRI’s work?

A

they inhibit 5-HT reuptake from synapses so that concentration increases and more receptors are activated

140
Q

What is Buspirone ?

A

direct 5-HT receptor agonist. mainly used to reduce anxiety and sometimes depression treatment

141
Q

How many SSRI’s are currently available in the UK?

A

7

142
Q

What are the chemical names for Fluoxetine, Sertraline, Paroxetine, and Citalopram?

A

Fluoxetine = Prozac
Sertraline = Zoloft
Paroxetine= Seroxat
Citalopram = Cipramil

143
Q

What are SSRI’s used for?

A

most common treatment for major depressive illness, and also used for anxiety disorders

144
Q

What were the findings of the effects of two different SSRI’s on the Hamilton Depression Rating in patients with Major Depressive Disorder? (Stahl 2000)

A

SSRI’s saw a bigger reduction in depressive symptoms after some time

145
Q

What were the effects of SSRI’s in healthy, non depressed subjects?

A

reduced hostility and irritability, increased social affiliations and cooperative behaviours. mainly changes in subjective feelings of hostility, aggression and irritability

146
Q

Which group had increased cooperative behaviour scores in a two person problem solving task?

A

participants given the SSRI

147
Q

Why are SSRI’s used to reduce aggression in psychiatric conditions such as schizophrenia, bipolar, bpd?

A

Evidence from the Low Serotonin Hypothesis of Impulsive or Reactive Aggression

148
Q

In a study regarding acute effects of SSRI’s on moral judgment (Crocket et al 2010), How did the SSRI group perform in contrast to the placebo and atomoxetine group?

A

SSRI group had a reduced acceptability of harming one person to save many. The effect of SSRI’s were larger in the high empathy group

149
Q

What does the study regarding Acute Effects of SSRI’s on moral judgement tasks suggest?

A

suggests individual differences in empathy and harm aversion may be related to serotonin

150
Q

How can SSRI’s aid Facial Expression Processing? (Harmer and Cowen 2013)

A

enhances facial expression recognition, particularly happiness, without changing mood

151
Q

What is the effect of ATD on facial expression processing? (Harmer and Cowen 2013)

A

impairs facial expression recognition, particularly happiness

152
Q

Describe cognitive biases in memory for people with depression:

A

depressed subjects show superior memory for negative information is a range of tasks (including autobiographical recall, memory for word lists, and implicit memory)

153
Q

Describe Cognitive biases in attention for people with depression:

A

depressed subjects take longer to name colours of negative words (lonely, hostile, useless) compared to positive words (lovely, honest, useful) in emotional Stroop task

154
Q

Describe Cognitive Biases in Facial Expression Processing for people with depression:

A

depressed subjects are more likely to interpret neutral or ambiguous expressions as being negative

155
Q

What are 3 main cognitive Biases in Depression:

A

1) Memory
2) Attention
3) Facial Expression Processing

156
Q

What are negative cognitive biases related to?

A

negative cognitive biases are related to negative level beliefs about the self, world, and others

157
Q

What may contribute to the risk of developing depression or maintaining a current depressive state?

A

Negative Cognitive Biases

158
Q

How are cognitive biases involved in therapies?

A

cognitive biases are important therapeutic targets in cognitive therapies for mood disorders

159
Q

What effects occurred after taking Citalopram without any change in subjective mood?

A

self rated hostility perception and behaviour reduced. amygdala response to fearful faces reduced. recognition of fearful faces reduced.

160
Q

How did healthy participants perform in a word recall task compared to depressed participants?

A

healthy subjects showed better recall for positive words. the acute effects of antidepressants in depressed patients showed significant increase in positive word recall

161
Q

How might SSSRI’s work if they do not effect mood directly?

A

they show changes in cognition and social behaviour. they could change brain processing emotional information by eliminating low level perceptual cognitive bias. provides bottom up mechanism changing high level dysfunctional thoughts and beliefs

162
Q

What explains the delay between physiological changes in 5-HT levels and changes in self reported mood?

A

SSRI’s do not effect mood directly

163
Q

What approach does CBT take?

A

a top down approach to teach metacognitive skills for modifying dysfunctional thoughts

164
Q

What combination is likely to make CBT more effective?

A

antidepressants and therapy combination

165
Q

in what plant can the acid for LSD can be found?

A

fungus

166
Q

what plant is psilocybin found in?

A

magic mushrooms

167
Q

what is the meaning of psychedelic ?

A

mind revealing

168
Q

define ‘hallucinogenic’

A

causing hallucinations, can cause distortions of perception

169
Q

what is the meaning of ‘psychotomimetic’?

A

mimicking psychosis. can either trigger new or increase existing psychotic effects that can persist long term

170
Q

what are examples of symptoms of ‘altered perception’ experienced after taking psychedelics ?

A

increased colour vividness, distortion of object sizes, illusions of movement, hallucinations of geometric patterns including to complex objects and people

171
Q

describe ‘subjectively pleasant’ effects of psychedelics:

A

loss of self, feelings of boundlessness, undifferentiated unity, altered sense of time and space, often in mystical or religious terms

172
Q

describe ‘subjectively unpleasant’ effects of psychedelics;

A

loss of self, anxious ego, dissolution, frightening depersonalization or derealisation, ideas of reference and paranoia, fear, panic, dangerous behaviour

173
Q

What evidence suggests that psychedelic effects involve serotonin receptors?

A

shared indole ring structure with serotonin

174
Q

do psychedelics produce similar effects as 5HT increase or decrease?

A

no, simply increasing 5HT through the brain doesn’t produce similar effects and neither does simply reducing 5HT activity

175
Q

How many subtypes of serotonin receptors do we have?

A

at least 14

176
Q

are psychedelics 5HT agonists or antagonists?

A

only for some receptor types, they could be antagonists for other

177
Q

why might the disruption of pre frontal cortex and thalamus be the basis for psychedelic experiences?

A

PFC involves high level cognition, conceptual thinking, and sense of self. Thalamus involves sensory relay system with input from sense organs and outputs to sensory cortex. disruption of these explains disrupted sense of self, alterations in perception, and synaesthesia

178
Q

define synaesthesia:

A

experiencing things through senses in an unusual way e.g. experiencing colour as a sound or taste to colour

179
Q

what effect does psilocybin have on neural activity?

A

decreases neural activity in a number of cortical and sub cortical brain areas. the intensity of subjective experience correlates significantly with observed reductions in neural activity

180
Q

imaging shows psychedelic drugs reduce neural activity in ?????? and increase functional connectivity between ??????

A

-reduce neural activity in brain areas involved in maintaining a sense of self.
increase functional connectivity between brain -areas that don’t normally communicate much

181
Q

What acute effects of a single dose of psilocybin were found (Griffiths et al, 2006)?

A

changes in perception and cognition, and highly labile mood

182
Q

Which two drugs both produced reported mystical experiences in Griffiths et al (2006) study? what does this indicate?

A

psilocybin and methylphenidate. this suggests expectancy effects in both groups

183
Q

after two months, 50% self reported increases in well being and life satisfaction, following which drug?

A

psilocybin

184
Q

Which stringent safety precautions were taken for a methylphenidate/psilocybin double blind study?

A

-screening volunteers
-clinician input before during and after to avoid potential dangerous negative drug effects

185
Q

11/36 volunteers reported strong fear after taking what drug, and what did they compare this experience to?

A

-after taking psilocybin
-two people compared this to being in a war

186
Q

How many participants experienced paranoid thinking following psilocybin (Griffiths et al., 2006)?

A

just over 16%

187
Q

what were potential limitations to Griffiths et al., (2006) psilocybin study?

A

-the volunteers were nor representative of the general population. they were highly educated, healthy and low risk, religious/spiritual people interested in drug effects and a self reflection opportunity

-blinding to the conditions may have been ineffective

188
Q

true or false: psychedelics in therapy are illegal in the UK

A

true

189
Q

for what conditions are there reports of possible positive effects of LSD and psilocybin assisted therapy?

A

-addiction
-OCD
-depression and anxiety in patients with life threatening or terminal illness

190
Q

What is the role of psychedelics in psychedelic assisted psychotherapy?

A

psychedelics use to facilitate and intensify ongoing therapeutic processes, not replace them

191
Q

What is an afterglow period?

A

a period of time where the effectiveness of psychotherapy is enhanced. this experience challenges patient’s current world view and increases openness to alternative perspectives suggested by a therapist

192
Q

do serotonergic actions from SSRI’s and psychedelics present the same?

A

there are possibly distinct therapeutic mechanisms for SSRI’s and Psychedelics:
SSRI’s= limbic responsivity
Psychedelics= cortical entropy

193
Q

Describe cortical entropy:

A

complexity of interactions between brain areas usually segregated from each other. its increase in psychedelic drug states is hypothesised to be a mechanism for reduced rigid thinking

194
Q

What was the issue when there was no significant difference between 25 mg psilocybin and daily placebo vs 1mg psilocybin and daily escitalopram (SSRI)?

A

There was no wat to decipher if they both worked or neither worked

195
Q

What is suggested for further psychedelic assisted psychotherapy studies?

A

both recommend larger and longer trials

196
Q

with what doses of psilocybin was there a significantly greater improvement of outcome measure?

A

25mg vs 1mg

197
Q

what is ketamine?

A

ketamine is a synthetic glutamate antagonist that blocks excitatory effects of glutamate at NMDA receptors

197
Q

What are four main issues with psychedelic assisted psychotherapy studies?

A

1) to few studies, and with small sample sizes
2)obvious acute subjective effects meaning blinding is compromised
3)many studies do not assess expectancy
4)it is unclear if effects are produced from direct pharmacological mechanism independent of mystical experience, or non pharmacological psychological reaction of a mystical experience

198
Q

What is ketamine clinically used for?

A

used as a sedative or general anaesthetic

199
Q

True or False: Ketamine is a psychedelic drug

A

False

200
Q

what are recreational effects of ketamine (when used in low doses)?

A

hallucinogenic and dissociative effects

201
Q

Describe dissociative effects:

A

producing a dream like feeling of being detached from reality

202
Q

what are acute ketamine effects?

A

sometimes described as being drunk (euphoria, dizziness, nausea), disordered thought or speech, memory impairment across a wide range of tasks, perceptual distortions and dissociation (objects and surroundings seem unreal), delusional thinking often in a paranoid nature

203
Q

What mental illness is ketamine effects similar to?

A

schizophrenia- hence the glutamate hypothesis of schizophrenia

204
Q

What happened to Brief Psychiatric Rating Scale (BPRS) scores in healthy subjects during double blind placebo controlled IV ketamine infusion?

A

BPRS scores increased, which is similar in patients with schizophrenia

205
Q

What drug has produced an antidepressant effect in treatment resistant major depressive patients?

A

ketamine

206
Q

how long could antidepressant effects of ketamine be seen for?

A

a few hours after administration and long after dissociation effect has worn off. Much faster than standard anti depressants. improvement in mood after a single administration can last for days

207
Q

what is the criteria for treatment resistance depression (Feifel et al., 2017)?

A

failed response to at least four different antidepressants

208
Q

What did low dose ketamine infusion do to depressed patients? (Feifel et al., 2017)

A

mean Beck Depression Inventory (BDI) score fell from sever to baseline mild at both 1 and 24 hours post infusion

209
Q

What are different Beck Depression Inventory (BDI) scores indicative of?

A

29+ = severe
20-28 = moderate
14-19 = mild
0-13 = minimal levels of depression

210
Q

how many patients met the criteria for remission 24 hours post ketamine infusion (Feifel et al., 2017)?

A

41.5%

211
Q

after how long did BDI improvements start to revert following ketamine infusion? (Feifel et al., 2017)

A

by one week post infusion

212
Q

what safety concerns are raised by long term prescription of ketamine?

A

risk of addiction, tolerance issues, possibilities of neurological damage

213
Q

what are some issues when interpreting research following ketamine studies ? (Rasmussen 2016)

A

-few studies
-small sample sizes
-compromised blinding
-unknown mechanism for therapeutic effects
-risk of psychotic effects
-possible expectancy effects

Year Three Psychology (4 decks)

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