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Year 2 - BRS > 4.4 - Mood disorders > Flashcards

4.4 - Mood disorders Flashcards

1
Q

What is the lifetime (and 12-month) prevalence of bipolar-I and bipolar-II?

A
  • bipolar I - 1.0% (0.6%)
  • bipolar II - 1.1% (0.8%)
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2
Q

What is the lifetime rate of major depressive disorder (MDD)?

A

Lifetime rate of MDD is 10-20%, with studies across countries showing evidence that it is increasing with an earlier age of onset

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3
Q

What is the gender distribution for bipolar I, II and MDD?

A
  • bipolar-I is F=M
  • bipolar-II and MDD is F>M (in a 2:1 ratio for MDD)
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4
Q

What % of disability-adjusted life years (DALYs) do mental and substance abuse disorders take up?

A
  • 7% of DALYs worldwide
  • within mental and substance abuse disorders, MDD accounts for 40% and bipolar for 7% of DALYs
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5
Q

What are the two used disease classification systems?

A
  • DSM-V (US manual)
  • ICD (WHO manual)
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6
Q

What is the DSM (US manual)?

A

The American Psychiatric Association’s ‘Diagnostic and Statistical Manual of Mental Disorders’ - latest is DSM-V from 2013

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7
Q

What is the WHO manual (ICD)?

A

International Classification of Diseases (ICD) - latest is ICD-10 from 1994, ICD-11 currently being implemented

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8
Q

Until 1980, what was the Kraepelinian definition of manic depressive illness (MDI)?

A
  • any recurrent mood episodes of any kind (depressive or manic) constituted the diagnosis of MDI
  • thus MDI meant bipolar illness plus unipolar depressive illness
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9
Q

What are mood disorders?

A
  • where the fundamental disturbance is a change in affect/mood to depression (with/without associated anxiety) or to elation
  • the mood change is usually accompanied by a change in the overall level of activity
  • most of the other symptoms are either secondary to / easily understood in the context of the change in mood and activity
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10
Q

What is the onset of mood disorders like?

A

Most of these disorders tend to be recurrent and the onset of individual episodes can often be related to stressful events or situations

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11
Q

What are the DSM-V criteria for depressive episodes? (8)

A

Occurrence of 2 weeks or more of depressed mood AND the presence of 4/8 out of the following:

  • sleep alterations (insomnia / hypersomnia)
  • appetite alterations (increased / decreased)
  • diminished interest or anhedonia
  • decreased concentration
  • low energy
  • guilt
  • psychomotor changes (agitation or retardation)
  • suicidal thoughts
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12
Q

When is the longitudinal diagnosis of major depressive disorder formed?

A

If no manic or hypomanic episodes in the past are identified, then the diagnosis of a current major depressive episode leads to a longitudinal diagnosis of MDD

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13
Q

What are the three subtypes of MDD according to DSM-V?

A
  • atypical features (which represent mainly increased sleep and appetite, along with heightened mood reactivity)
  • melancholic features (defined by no mood reactivity, along with marked psychomotor retardation and anhedonia)
  • psychotic features (the presence of delusions/hallucinations)
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14
Q

What are the three core symptoms of depression?

A
  • low mood
  • anergia
  • anhedonia
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15
Q

What are the three biological symptoms/attributes affected in depression?

A
  • sleep
  • libido
  • appetite
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16
Q

What are the three psychological symptoms/attributes affected in depression?

A
  • the world
  • oneself
  • the future
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17
Q

What thoughts, behaviours, feelings and physiological symptoms are present in the typical cycle of low mood?

A
  • thoughts - “what’s the point”
  • behaviours - lie in bed all day, ruminate
  • feelings - low, flat, irritable
  • physiological symptoms - exhaustion
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18
Q

What thoughts, behaviours, feelings and physiological symptoms are present in the typical cycle of high mood?

A
  • thoughts - “I’m the best” “I can do all these things”
  • behaviours - impulsive, increased activity
  • feelings - elation, excitement
  • physiological symptoms - increased energy, race sensitisation
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19
Q

What are the DSM-V criteria for manic episodes?

A

Euphoric or irritable mood with at least 3/7 manic criteria:

  • decreased need for sleep with increased energy
  • distractibility
  • grandiosity or inflated self-esteem
  • flight of ideas or racing thoughts
  • increased talkativeness or pressured speech
  • increased goal-directed activities or psychomotor agitation
  • impulsive behaviour (e.g. sexual impulsivity or spending sprees)
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20
Q

When is type I bipolar disorder/manic episode diagnosed?

A

If the symptoms of a manic episode are present for minimum 1 week with notable functional impairment, a manic episode is diagnosed, leading to a DSM-V diagnosis of type I bipolar disorder

Can occur with or without previous depressive episode

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21
Q

When is a hypomanic episode diagnosed?

A

If the symptoms of a manic episode are present for minimum 4 days but without notable functional impairment, a hypomanic episode is diagnosed

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22
Q

When is type II bipolar disorder diagnosed?

A

If not a single manic episode has ever occurred, but only hypomanic episodes are present, along with at least one major depressive episode –> type II bipolar disorder

Requires previous depressive episode (unlike type I)

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23
Q

When is unspecified bipolar disorder diagnosed?

A

If manic symptoms occur for less than 4 days, or if other specific thresholds are not met for manic/hypomanic episodes

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24
Q

When can hypomania NOT be diagnosed?

A

If psychotic features are present, then hypomania cannot be diagnosed (since such features involve notable impairment by definition)

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25
Q

If a patient is hospitalised, what kind of manic episode is diagnosed?

A

If a patient is hospitalised, irrespective of duration of manic symptoms, a manic episode is diagnosed

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26
Q

What if manic/hypomanic episodes are caused by antidepressants?

A

Diagnosis of bipolar disorder still made in DSM-V (important change from DSM-IV)

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27
Q

Why can it be challenged whether bipolar disorders are mood disorders?

A
  • MDD can be without sad mood
  • mania can be without euphoric mood
  • mood is variable and most consistent clinical features for diagnosis are psychomotor changes
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28
Q

What is the graph of illness course of bipolar I and bipolar II like?

A
  • bipolar I - cycle of large mania peak followed by large depression peak
  • bipolar II - cycle of small mania peak followed by large depression peak
  • cyclothymia - cycle of small mania peak followed by small depression peak
29
Q

What is cyclothymia?

A

Rare mood disorder that causes emotional ups and downs that aren’t as severe as bipolar I or II

30
Q

What is rapid cycling bipolar disorder?

A

More than 4 cycles per year

31
Q

What % of patients relapse within a year of recovery from a mood episode?

A

50-60%

32
Q

What are patients like ‘between episodes’ in bipolar disorder?

A

Patients largely autonomous between episodes

33
Q

What type of episode is usually first with bipolar-I patients?

A
  • majority of first episodes are depressive (85%)
  • 10% are manic episodes
  • 3-5% are mixed episodes
  • 90-100% of patients will develop more episodes after their first manic episode
34
Q

What symptom types are present in patients with bipolar disorder?

A
  • symptoms 47% of the time
  • majority is depressive periods (33% out of 47%)
  • manic/hypomanic symptoms
  • cycling/mixed symptoms
35
Q

How prevalent is anxiety in bipolar patients?

A
  • 30-70% of bipolar patients
  • DSM-V: “anxious distress specifier”
  • worse prognosis and outcomes
36
Q

How common is it for MDD patients to seek help?

A
  • 60-70% with MDD visited a health professional in last 6mth but only 15-20% for mental health reason
  • only 21% of those with a 12-month diagnosis of pure MDD received any antidepressant treatment within the same period
37
Q

For which reasons were bipolar and unipolar disorders seen as different in 1970s? (5)

A
  • bipolar illness had early age of onset (mean age 19y vs late-20s for unipolar depression)
  • shorter depressive episodes (on avg <3mth in bipolar vs 6-12mth in unipolar)
  • recurrent course (more frequent episodes in bipolar than unipolar, with rapid cycling in 25% of bipolar but <1% of unipolar)
  • genetic specificity (manic episodes found in families of those with manic episodes but not in families of those with unipolar depression)
  • differential treatment (antidepressants for unipolar depression vs neuroleptics/antipsychotics and lithium for mania)
38
Q

What new evidence is there for bipolar vs unipolar not being so separate? (5)

A
  • MDD commonly diagnosed in children, far below mean onset of late-20s
  • brief depressive episodes that occur multiple times yearly are diagnosed in patients with MDD commonly (but would be rare if MDD was different to bipolar)
  • genetic studies have found high rates of depressive episodes without mania in those with bipolar, and also frequent occurrence of bipolar in relatives of those with unipolar depression
  • treatment now overlaps considerably, with neuroleptic agents proven effective for unipolar and bipolar depression too
  • lithium has been well known to be effective not only for mania, but also for both unipolar and bipolar depression
39
Q

How does heritability and insight differ in bipolar vs unipolar?

A
  • bipolar has high heritability, unipolar (MDD) has around half heritability of bipolar
  • insight is preserved in depression and impaired in mania - 50% of patients with severe mania and most with hypomania deny their symptoms
  • insight has U-shaped curve in relation to severity (most impaired in hypomania and severe mania but more present in moderate states of mania)
40
Q

What mood disorder diagnosis can be easily missed and be wrongly diagnosed as what?

A
  • bipolar might be missed in patient due to lack of insight about mania/hypomania
  • patient may end up with MDD diagnosis despite a history of manic episodes
  • collateral Hx useful
41
Q

Why is diagnosing a bipolar patient with MDD dangerous?

A
  • might pick wrong treatment e.g. antidepressants (appear ineffective in treating acute bipolar depression)
  • can also cause acute manic/hypomanic episodes
  • have been shown to worsen long-term course of bipolar illness in some esp those with rapid cycling course –> more mood episodes including depressive states over time
42
Q

What are attention biases in depression?

A
  • depression is characterised by biases in maintaining/shifting attention = difficulties for depressed people to disengage from negative material
  • depressed people have a prolonged maintenance of attention over negative images (e.g. people frowning) and decreased attention for positive images
  • this is also seen in remitted depressed adults and those at high risk of developing depression
43
Q

What are memory biases in depression?

A
  • preferential recall of negative compared to positive material (one of most robust findings in depression literature)
  • bias toward negative material or away from positive material
  • memory biases also present in individuals at risk (high in neuroticism) and in recovered individuals
44
Q

What are the facial expression recognition/perceptual biases in depression?

A
  • increased recognition of negative faces and/or decreased recognition of happy faces
  • emotion recognition deficits in MDD
  • reduced recognition of all basic emotions except sadness
  • some seen in healthy individuals at risk (high neuroticism)
45
Q

What is the depressed brain’s response to simply seeing emotional face expressions?

A

Enhanced amygdala response to negative faces (even in absence of awareness)

46
Q

What is the role of the amygdala?

A
  • medial temporal lobe region that is involved in perception and encoding of stimuli relevant to current or chronic affective goals, ranging from rewards/punishments to facial expressions of emotion to pleasant images
  • amygdala generally sensitive to detecting and triggering responses to arousing stimuli, but is biased towards detecting cues signalling potential threats (like expressions of fear)
47
Q

What does an acute single dose of different antidepressants do to facial expression processing?

A
  • noradrenergic antidepressants (reboxetine, duloxetine) - better recognition of happy faces
  • serotonergic antidepressants - mirtazapine (decreased recognition of fearful faces); SSRI citalopram (mixed results - sometimes found to increase fear recognition)
48
Q

What is the neurofunctional effect of an acute single dose of SSRI?

A

Both increased and reduced amygdala response to SSRIs

49
Q

What does 7 day treatment of antidepressants do to facial expression processing?

A
  • noradrenergic and serotonergic antidepressants - reduced recognition of anger and fear
  • neurofunctional - reduced amygdala and mPFC response to fear
50
Q

What is the clinical response to escitalopram (gold standard SSRI) to brain after 6 weeks of treatment?

A

Decrease in amygdala, thalamus, anterior cingulate and insula response to fearful faces

51
Q

What does elevated baseline ACC activity in depressed patients on 1 week of SSRIs show?

A

Predicts positive response to treatment (i.e. decrease in depression severity following interventions)

52
Q

Where are the nuclei where serotonergic neurones project from located?

A

In the Raphe nuclei in the midbrain where they project to all over the brain

53
Q

How many different serotonin receptors are there?

A

14

54
Q

What is the monoamine deficiency hypothesis?

A

Depressive symptoms arise from insufficient levels of monoamine neurotransmitters serotonin (AKA 5-HT), noradrenaline and dopamine

55
Q

What is the indirect evidence for 5-HT hypofunction in depression? (9)

A
  • 5-HT depletion by antihypertensive drug reserpine could cause depression
  • clinically useful antidepressants all increase synaptic monoamine (some selectively 5-HT) concentrations
  • post-mortem evidence of reduced 5-HT levels in brainstem of individuals who committed suicide
  • lower levels of 5-HT1A-receptors and 5-HT4 receptors
  • monoamine oxidase A increased in MDD
  • blockade of serotonin synthesis by tryptophan hydroxylase inhibitor prevents antidepressant effects of both MAOIs and TCAs
  • tryptophan depletion (reduced serotonin) triggers relapse in MDD successfully treated with SSRIs or CBT
  • monoamine depletion correlates with decreased mood both in at risk/remission
  • depression-related traits - pessimism and dysfunctional attitudes in MDD, and negativism and neuroticism in healthy, related to increased 5-HT2A receptor (decreased serotonin)
56
Q

What is the best brain imaging technique to investigate brain pharmacology?

A

PET imaging

57
Q

How does a PET scan compare to an fMRI?

A
  • only pro - selective
  • invasive
  • radioactive
  • expensive
  • less optimal temporal and spatial resolution
58
Q

How does PET imaging work?

A
  • injection of a radioactive pharmaceutical (a ligand that is used as a tracer)
  • the tracer binds to a specific target (e.g. a receptor)
59
Q

What radioactive tracer can we use to measure dopamine levels?

A

(11C)raclopride

60
Q

How can PET imaging be used to quantify dopamine receptors?

A
  1. baseline taken - tracer binds to dopamine receptors + quantification of how many receptors present is taken
  2. amphetamine challenge is given - amphetamine upregulates dopamine in neurones
  3. so much dopamine that it competes with the tracer
  4. new scan/measurement is taken
  5. subtract both scans to see the difference in the binding of the tracer, to see how much dopamine there is
61
Q

How can we measure serotonin levels in the brain using PET?

A
  • theoretically can be done with 2x PET scans
  • past antagonist tracers have not been sufficiently sensitive to challenges
  • can now be done using 5-HT2a agonists
62
Q

What has measuring cerebral 5-HT in brains of those with and without depression shown?

A
  • measurable 5-HT release in healthy individuals
  • no measurable 5-HT release in patients with depression
  • 5-HT release capacity reduced in patients with depression
63
Q

How do basic tryptamine psychedelics work?

A
  • psychedelics have their action in the brain’s serotonin system
  • mimic serotonin function in the body = similar effects
64
Q

What are some effects of psychadelics? (8)

A
  • ‘oceanic boundlessness’
  • spiritual experiences
  • insightfulness
  • blissful state
  • noetic quality
  • deeply felt positive mood
  • transiency
  • sense of duty
65
Q

What are some pros of psychedelic use? (3)

A
  • non-addictive
  • low physiological and brain toxicity
  • good therapeutic index
66
Q

What are some cons of the safety of psychedelic use? (4)

A
  • dysphoria
  • anxiety
  • nausea
  • headache
67
Q

What is some evidence for therapeutic value of psychedelics in treating mood disorders - what do they improve? (6)

A
  • wellbeing
  • OCD
  • end-of-life distress
  • addiction
  • depression - long-lasting effect after single intervention
  • suicidality
68
Q

What are the active components in Psilocin and Ayahuasca?

A
  • Psilocin - Psilocybin
  • Ayahuasca - DMT

Year 2 - BRS (84 decks)

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