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Psychology & Neuroscience of Psychosis > Pharmacological interventions > Flashcards

Pharmacological interventions Flashcards

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1
Q

What characterises the psychopathology of psychosis?

A

Pathology of

  • perception
  • thinking
  • beliefs
  • selfhood

Patient experiences a fundamental transformation

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2
Q

What is the most common symptom of acute psychosis?

A

Loss/lack of insight

  • patient doesn’t realise the falseness of their new reality
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3
Q

Which organic dysfunctions can be the direct cause of psychosis?

A
  • Endocrine disorders
  • Metabolic disorders
  • Autoimmune conditions
  • Psychoactive drugs
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4
Q

What characterises the negative symptoms of psychosis and schizophrenia?

A
  • Loss of function
  • Loss of drive, motivation, ambition, emotion, interests, romantic relationships, intellectual life
  • Negative symptoms carry more prognostic and diagnostic weight than positive symptoms
  • Poorer long-term outcomes
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5
Q

Which psychoactive substances can cause an acute psychotic episode after single use?

A
  • Strong synthetic cannabinoids
  • K2
  • LSD
  • Ketamine
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6
Q

Which psychoactive substances can cause an acute psychotic episode after repeated use?

A
  • Methamphetamine

- Crack cocaine

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7
Q

What is the Indian snakeroot plant Rauwolfia serpentina?

A
  • First effective treatment of psychosis
  • Contains reserpine
  • Used in Indian and Chinese medicine
  • Trials conducted in 1950s showed reserpine was effective in treating schizophrenia
    (depletes nerve varicosities of monoamine NTs, including dopamine)
  • By the end of 1950s, consensus decided that reserpine was less effective in schizophrenia
  • > its use diminished
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8
Q

When did genuine effective pharmacological treatments for psychosis emerge?

A

Early 1950s-1970s

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9
Q

What were the consequences of the emerging pharmacological treatments for psychosis in the mid-20th century?

A
  • Symptomatic improvement (not just sedation) for mania, thought disorder, delusions and hallucinations
  • Maintenance treatment could prevent a relapse back into psychosis
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10
Q

When were the benefits of lithium and chlorpromazine confirmed in randomised controlled trials?

A

1954

  • Lithium for mania
  • Chlorpromazine for schizophrenia
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11
Q

What was the consequence of the introduction of antipsychotic drugs?

A
  • Massive reduction in the number of hospital beds occupied by mental ill patients
  • Social change
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12
Q

What is the priority in the acute stage of psychosis?

A

Symptom relief

  • antipsychotics are highly effective
  • symptoms of agitation, hallucinations, delusions can be addressed safely and efficiently
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13
Q

What is the priority in the maintenance stage of psychosis?

A

Avoid relapse

  • high proportion of patients go on to experience further episodes of psychosis
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14
Q

What is the main predictor of relapse?

A

Non-adherence to medication

  • patients who discontinue medication have fivefold higher chance of relapse
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15
Q

What are common predictors of relapse?

A
  • Presence of substance abuse
  • Critical comments
  • Poor premorbid adjustment
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16
Q

What is associated to each relapse?

A

Progressive social and functional decline

  • psychopathology becomes less responsive to treatment
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17
Q

What are the rates of relapse in the first year of recovery in those on medication and those off medication?

A
  • 77% relapse in those off medication

- 3% relapse in those on medication

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18
Q

What does the meta-analysis of Leucht and colleagues (2012) on antipsychotic drugs vs placebo for relapse prevention show?

A
  • Drug superior to placebo
  • Being off and on treatment made no difference to wether patient found employment, probably because other factors determine employment type
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19
Q

What is CBT for psychosis recommended for?

A
  • Recommended as treatment for psychosis by the National institute of clinical guidelines (UK)
  • Benefits for symptoms
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20
Q

To which drugs does mania respond to?

A
  • Lithium (first anti-manic agent)
  • Valproate
  • Carbamazepine
  • Antipsychotics
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21
Q

Why did psychiatrists at Maudsley Hospital (London) consider that the first lithium trial by Baastrup and Mogens (1967) was not a “proper trial”?

A
  • Open-label study

- No blinding or randomisation

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22
Q

What did RCTs in 1970 demonstrate about lithium?

A

Lithium was effective in protecting against relapse

23
Q

What is the recommendation of the British Association for Psychopharmacology regarding lithium?

A

Lithium recommended as first-line treatment for maintenance therapy on bipolar I

24
Q

What does maintenance pharmacotherapy consist of?

A

Reducing relapse

  • with antipsychotics and mood stabilisers
  • follow up of patients one or more years
25
Q

What did the study of Whistler and colleagues (2011) on the continuation of quetiapine vs switching to placebo or lithium for maintenance treatment of bipolar I disorder show?

A
  • In placebo group: 20% avoided relapse

- In quetiapine group and lithium group: 60% avoided relapse

26
Q

What does the study of Suppes and colleagues (2009) on the combination of quetiapine with lithium or divalproex as maintenance treatment for Bipolar I disorder show?

A

Combination treatments outperform mono-therapy in avoiding relapse

  • Monotherapy (lithium or divalproex): 60% chance of avoiding relapse (manic or depressive)
  • Combination (quetiapine + lithium or divalproex):
    90% chance of avoiding manic relapse
    80% chance of avoiding depressive relapse
27
Q

What was the first antipsychotic introduced in the 1950s?

A

Chlorpromazine (discovered in France)

28
Q

What characterises chlorpromazine?

A
  • Proven efficacy
  • Wide safe
  • Produce dramatic reduction in hallucinations, delusions, agitation
29
Q

How were antipsychotics discovered?

A

Discovered by design:

  • Paul Janssen observed that many cyclists developed acute psychosis after use of amphetamines to combat fatigue
  • > he developed haloperidol (blocks amphetamine)
30
Q

What characterises haloperidol?

A
  • Blocks amphetamine
  • Highly effective for schizophrenic psychoses
  • In small doses: powerful treatment against hallucinations, delusions and agitation
31
Q

How is conditioned avoidance?

A

Process of inhibition learning in animals, notably with chlorpromazine and haloperidol

32
Q

How was conditioned avoidance used for antipsychotics?

A

Test to establish whether a new candidate molecule showed antipsychotic signature

  • e.g. with chlorpromazine, animal is indifferent to environmental cue which predicts danger
  • > ability to disrupt conditioned avoidance was a marker of a drug with antipsychotic activity in man
33
Q

Where are dopamine neurons found?

A

In substantia nigra (specific brainstem nuclei)

34
Q

How were Scandinavian researchers able to map out the dopamine pathways in the brain?

A

Using fluorescence methods

-> massive arborisation within the ‘higher centres’

35
Q

What makes dopamine a slow neuromodulator?

A
  • Evokes a diffuse, slow biochemical change in millions of target neurons
  • Optimised for modulating higher networks
36
Q

What is the function of dopamine?

A
  • Modulates the fast synapse
  • Can adjust the strength of connections
  • > a teaching signal
  • Critical role in learning and memory (e.g. conditioned avoidance)
37
Q

What are varicosities?

A

Highly branching pattern of dopamine neurons

38
Q

What are the three modes of firing of dopamine neurons that Wolfram Schulz identified?

A
  • Spiking every second
  • Burst firing mode
  • Switching off
39
Q

In which cases does dopamine fire in spiking every second?

A
  • Awake brain
  • Tonic concentration in target areas
  • Tonic concentration for weed-rehearsed thoughts and motor patterns
40
Q

When does dopamine enter a burst firing mode?

A
  • Happens when animal encounters new stimulus which carries a reward
  • For learning: adjusts the strength of point-to-point connections in the striatum
41
Q

When does the dopamine firing mode switches off?

A
  • When anticipated and predictable reward fails to materialise
42
Q

What happens when dopamine does not fire (firing mode switched off)?

A
  • New patterns of thought and behaviour, abandoning primitive and earlier ones
  • Refining of existing network: main form of learning in the striatum
43
Q

What are the functions of the striatum?

A
  • Critical for learning new habits of thought and movement
  • Striatal network when there’s integration of new habits of thought and movement
  • > new connections
44
Q

What is common to all antipsychotic drugs?

A

They all block dopamine D2 receptors

45
Q

What differentiates antipsychotic drugs?

A

Their propensity to act at additional receptors (other than D2)

46
Q

How to select antipsychotic drugs?

A
  • For psychotic episode: emphasis on prompt relief of symptoms
  • For maintenance: emphasis on avoiding side-effects
  • > patients stick with treatment and lower risk of relapse
47
Q

Are their drug “rankings”?

A
  • For treatment resistant patients: clozapine is superior to other drugs
  • Otherwise, there’s little difference between drugs in terms of efficacy
48
Q

What is the effect of clozapine on treatment resistant patients?

A
  • After 6 weeks: 30% get better

- After 6 months: 60-70% get better

49
Q

How does clozapine work?

A
  • Weak binding to D2 receptors

- Evidence that its unique effects come from activity at acetylcholine receptor in striatum

50
Q

What are the strengths of the antipsychotic drug clozapine?

A
  • Anti-suicidal effect
  • Reduces aggression and violence
  • No motor side effects (e.g. parkinsonism)
51
Q

What are the weaknesses of the antipsychotic drug clozapine?

A
  • Weekly and monthly blood tests are needed

- In 1% of patients it can cause potentially dangerous decrease in white blood cells (necessary to fight infections)

52
Q

What is required when using clozapine for severely disable schizophrenic patients?

A

Combination treatment:

  • provide alongside clozapine a package of rehabilitative support
  • psychosocial rehabilitation to recover quality of life
  • especially for patients disabled by negative symptoms and poverty
53
Q

What is the benefice of long-acting depot antipsychotic injection?

A

Relapse rates are considerably lower

  • Chances of relapse over the year following first psychotic episode is 7% with long-acting injectable risperidone
    vs 50% risk of relapse with oral risperidone
  • Remains in the system for many weeks: sufficient time to carefully monitor and plan for patients who discontinue or mise a dose
  • > gold standard treatment for avoiding relapse in psychotic disorders
54
Q

What is the current issue with the treatment option of long-acting intramuscular risperidone?

A

Only 50% of patients taking oral risperidone are informed about the long-acting depot injection alternative

Psychology & Neuroscience of Psychosis (16 decks)

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