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Aneesha Flashcards BRS 2 > Mood disorders > Flashcards

Mood disorders Flashcards

1
Q

Define mood disorders

A

The fundamental disturbance is a change in affect or mood to depression (with or without anxiety) or elation
Mood change is usually accompanied by a change in overall level of activity

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2
Q

What is the onset and course of mood disorders like?

A

Most of these disorders tend to be recurrent and onset of each episode is often related to stressful events/ situations

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3
Q

What is the prevalence of MDD and bipolar?

A

MDD: 10-20%, but there’s evidence it’s increasing with earlier age of onset
Bipolar I: 1%
Bipolar II: 2%

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4
Q

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

A

Bipolar I- F=M
Bipolar II and MDD- F>M, 2:1 for MDD

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5
Q

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

A

7%
Of this, MDD accounts for 40% and bipolar for 7%

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6
Q

Diagram of typical cycle of low mood (unipolar and bipolar depression)

A
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7
Q

What are the DSM-5 criteria for depressive episodes?

A

Occurrence of 2 or more weeks of depressed mood with at least 4/8 of the following:
Lack of pleasure/ anhedonia
Low energy
Sleep changes (insomnia, hypersomnia)
Appetite changes (Increased, decreased)
Poor concentration
Psychomotor changes (agitation, retardation)
Guilt
Suicidal thoughts

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8
Q

What are the three core symptoms of depressive episodes?

A

Anhedonia, anergia, low mood

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9
Q

What are the 3 biological symptoms/attributes affected in depressive episodes?

A

Sleep, appetite, libido

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10
Q

What are the 3 psychological symptoms/attributes affected in a depressive episode?

A

Oneself
The world
The future

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11
Q

When is a longitudinal diagnosis of MDD formed?

A

If no manic/ hypomanic episodes were identified in the past, diagnosis of a current major depressive episode leads to diagnosis of MDD

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12
Q

What are the 3 symptom subtypes in DSM-5 for MDD?

A

Atypical features (which represent mainly increase in sleep and appetite, along with heightened mood reactivity)
Melancholic features (no mood reactivity, anhedonia, marked psychomotor retardation)
Psychotic features (presence of delusions/ hallucinations)

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13
Q

Diagram of typical cycle of high mood

A
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14
Q

What are the symptomatic criteria for manic/ hypomanic episodes?

A

Elated or irritable mood and at least 3/7 of the following:
Decreased need for sleep or increased energy
Distractability
Grandiosity or inflated self esteem
Flight of ideas or racing thoughts
Increased talkativeness or pressure of thoughts
Increased goal directed activities or psychomotor agitation
Impulsive behaviour (sexual impulsivity, spending spree)

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15
Q

What pattern of symptoms leads to a DSM-5 diagnosis of type I bipolar disorder?

A

If these symptoms are present for minimum 1 week with notable functional impairment, a manic episode is diagnosed, leading to diagnosis of bipolar I

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16
Q

What pattern of symptoms leads to a diagnosis of a hypomanic episode?

A

If these symptoms are present for minimum 4 days without notable functional impairment, a hypomanic episode is diagnosed

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17
Q

What episodes are necessary for a DSM-5 diagnosis of type II bipolar disorder to be made?

A

only hypomanic episodes and at least 1 major depressive episode (no manic episodes)

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18
Q

What’s diagnosed if manic symptoms occur for less than 4 days or specific thresholds not met for manic or hypomanic episodes?

A

Unspecified bipolar disorder

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19
Q

When can’t hypomania be diagnosed?

A
  • If psychotic features are present since they involve notable impairment by definition
  • If patient is hospitalised- it’s a manic episode not hypomanic
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20
Q

Is bipolar disorder still diagnosed if manic/hypomanic episodes are caused by antidepressants?

A

Yes according to DSM-5 (important change from DSM-4)

21
Q

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

A
  • MDD can be without sad mood and mania can be without euphoric mood
  • Mood is variable and most consistent clinical features for diagnosis are psychomotor changes
22
Q

What is cyclothymia?

A

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

23
Q

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

A

Most commonly depressive episode (85% of the time)
Manic episode 10% of the time
Mixed episode 5% of the time

90-100% of patients with manic episode will have more episodes

24
Q

How prevalent is anxiety in bipolar patients and what does its presence do to prognosis/ outcome?

A

Highly prevalent- 30-70% of bipolar patients
Worsens prognosis and outcomes

25
Q

How common is it for MDD patients to seek help?

A

Low

26
Q

a)For which reasons are bipolar and unipolar disorders seen as different in 70s?
b)What new evidence is there?

A

a)- Bipolar illness has earlier age of onset (19 vs 20)
- Bipolar depressive episodes are shorter (≤3 months vs 1-12 months in unipolar)
- Bipolar episodes are more frequent than in unipolar
- Genetic specificity- manic episodes were found in families of people with manic episodes but not in families of those with unipolar depression
- Different treatments used- antidepressants for unipolar depression vs neuroleptics and lithium for bipolar

b)- MDD is commonly diagnosed in children, way below mean onset of late 20s
- Brief depressive episodes occurring multiple times a year are diagnosed in MDD patients commonly whereas this would be rare if MDD was different illness from bipolar disorder
- Genetic studies found high rates of depressive episodes without mania in bipolar patients and frequent occurrence of bipolar illness in relatives of those with unipolar depression
- Treatment now overlaps considerably- neuroleptics and lithium is effective for both mania and depression both in bipolar and unipolar

27
Q

How does heritability differ in bi and unipolar?

A

Bipolar has high heritability, unipolar (MDD) has around half heritability of bipolar

28
Q

How does insight differ in bi and unipolar?

A

Insight is preserved in depression and impaired in mania- 50% of patients with severe mania and most with hypomania deny their symptoms

29
Q

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

A

Bipolar disorder may be missed in patients due to lack of information about manic/ hypomanic epsiodes
Patients may be misdiagnosed with MDD despite a history of manic/ hypomanic episodes
Collateral information is often useful especially if you start doubting details in history taking- family members are twice as likely to report manic symptoms as patient

30
Q

Why is diagnosing a bipolar patient with depression dangerous?

A

May lead to picking the wrong treatment e.g. antidepressants which have been shown to be ineffective in treating acute bipolar illness

May also cause acute manic/hypomanic episodes

Shown to worsen long term course of bipolar illness in some subjects, especially those with rapid cycling course, leading to more episodes including depressive states over time

31
Q

What biases are present in depression?

A

Attentional biases
Memory biases
Facial expression perceptual biases

32
Q

What are attention biases in depression?

A

Depression is characterised by biases in maintaining and shifting attention- therefore it is difficult for depressed people to disengage from negative material
Depressed people have a prolonged maintenance of attention over negative pictures like frowning people and decreased attention for positive pictures
This is also seen in remitted depressed adults and those at high risk of developing depression

33
Q

How does fMRI work?

A

Detects changes in blood oxygenation and flow

34
Q

What parts of the brain are involved with depression?

A

There is a sustained amygdala response to negative stimuli
The perigenual anterior cingulate cortex (ACC) appears to mediate negative attentional biases
The lateral inferior frontal cortex is associated with impaired ability to divert attention from task-irrelevant negative info

35
Q

Where in the brain is the amygdala located

A

Medial temporal lobe region

36
Q

What is the purpose of the amygdala

A

Involved in the perception and encoding of stimuli relevant to current/chronic affective goals
While amygdala is generally sensitive to detecting and triggering responses to arousing stimuli, it’s biased towards detecting potential threats e.g. fear expressions

37
Q

Describe the memory bias in depression

A
  • There’s preferential recall of negative compared to positive material- one of the most robust findings in depression literature
  • Memory biases also present in individuals at risk of developing depression (high in neuroticism in personality traits assessment which is a sign for developing depression)
38
Q

What are the facial expression perceptual biases in depression?

A
  • There is increased recognition of negative faces and/or decreased recognition of happy faces
  • There are emotion recognition deficits in MDD
  • There is reduced recognition of all basic emotions except sadness
  • Some of this also seen in healthy individuals at risk (high neuroticism)
39
Q

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

A

Enhanced amygdala response to negative faces

40
Q

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

A
  • Noradrenergic antidepressants (reboxetine, duloxetine) give better recognition of happy faces
  • Serotonergic antidepressants:
    • Mirtazapine- decreased recognition of fearful faces
    • SSRI citalopram- mixed results (sometimes found to increase fear recognition)
41
Q

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

A
  • Noradrenergic and serotonergic antidepressants give reduced recognition of anger and fear
  • Neurofunctional- reduced amygdala and mPFC response to fear
42
Q

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

A

Decrease in amygdala, thalamus, ACC and insula response to fearful faces

43
Q

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

A

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

44
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

45
Q
  • How many different serotonin receptors are there?
A

14

46
Q

What is the monoamine deficiency hypothesis?

A

Depressive symptoms arise from insufficient levels of monoamine NTs in brain like serotonin (aka 5-HT), noradrenaline and dopamine

47
Q

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

A
  • 5-HT depletion by antihypertensive drug reserpine could cause depression
  • Monoamine depletion correlates with lower mood both in at risk and MDD in remission
  • Monoamine oxidase A increased in MDD (used to break down 5-HT)
  • Post-mortem evidence of reduced 5-HT levels in brainstem of individuals who committed suicide
  • Clinically useful antidepressants all increase synaptic monoamine (some selectively 5-HT) concs
  • Blockade of serotonin synthesis by tryptophan hydroxylase inhibitor prevents antidepressant effects of both MAOIs and TCAs
  • Tryptophan depletion leads to decreased serotonin in brain and triggers relapse in MDD successfully treated with SSRIs or CBT
  • Lower levels of 5-HT1A-receptors and 5-HT4-receptors in depression patients
  • Depression related traits e.g. pessimism, dysfunctional attitudes, negativism- are all related to 5-HT2A-receptor increase (levels of which are inversely related to serotonin levels)
48
Q

a) How can we try to measure serotonin in brain (it’s hard)?

b) How can we use it to test dopamine receptors further?

c) Can we do the same for serotonin?

A

a)- PET imaging- you inject radioactive pharmaceutical and binds to a specific target in brain
- Compared to fMRI it’s more selective, but it’s invasive, radioactive, expensive and with less optimal spatial and temporal resolution
- e.g. use (11C)raclopride to target dopamine receptors in brain and see how many there are by seeing density of accumulation of tracer in brain

b)- We can do a baseline scan
- Then can do a scan after a pharmacological challenge that releases presynaptic NT e.g. amphetamine challenge that releases dopamine
- There’s so much dopamine it competes with tracer- we can subtract the 2 scans and see the difference in binding of tracer to see how much dopamine there is

c) We’ve tried- loads of tracers been tried but they haven’t been sufficiently sensitive to pharmacological challenges since they’re all antagonists

We have tried an agonist recently which is more sensitive which worked and 5-HT can be measured. Here, MDD patients show reduced 5-HT release- more depressed patients also released less serotonin

Aneesha Flashcards BRS 2 (47 decks)

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