Psych - Mood disorders Flashcards
What is the fundamental disturbance in mood disorders according to ICD-10?
change in affect/mood to depression (with or without associated anxiety) or to elation
What is the mood change in mood disorders often accompanied by, according to ICD-10?
accompanied change in overall level of activity
How do other symptoms usually fit into mood disorders according to ICD-10?
most other symptoms are either secondary to, or easily understood in the context of, the change in mood and activity
What is the frequency like in mood disorders according to the ICD-10?
most mood disorders are RECURRENT
What can trigger individual episodes in mood disorders according to ICD-10?
often triggered by stressful events or situations
What resources or criteria are used to classify mood disorders?
→ DSM : diagnostic + statistical manual of mental disorders, US manual, latest is DSM-5
→ ICD : international classification of diseases (ICD), WHO manual, latest is ICD-10
What is the lifetime prevalence of bipolar-I?
1%
What is the lifetime prevalence of bipolar-II?
1.1%
What are the lifetime rates of major depressive disorder?
10-20%
What is the gender distribution for bipolar-I?
F : M = 1 : 1
What is the gender distribution for bipolar-II?
F : M = 2 : 1
What have studies across the country noted about the rates of MDD and the age of onset over time?
increasing rate of MDD with an earlier age of onset
What is the DSM-5 criteria for a depressive episode within mood disorders?
occurrence of 2 weeks or more of depressed mood + presence of 4 of these: → sleep alterations → appetite alterations → diminished interest or anhedonia → low energy → guilt → psychomotor changes (e.g. agitation or retardation) → suicidal thoughts
What is the diagnosis for someone with no manic or hypomanic episodes in the past, but still current major depressive episodes?
longitudinal diagnosis of Major Depressive Disorder (MDD)
What are the features listed in the DSM-5 for MDD?
→ 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).
What triad of biological symptoms could depression affect?
→ libido
→ sleep
→ appetite
What triad of psychological symptoms could depression affect?
→ oneself
→ the future
→ the world
What triad of core symptoms could depression present with?
→ low mood
→ anergia
→ anhedonia
What is the criteria for mania according to the DSM-5?
euphoric or irritable mood with 3 or more of 7 of :
→ 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 (such as sexual impulsivity or spending sprees)
What is the criteria for a manic episode diagnosis according to the DSM-5?
→ mania symptoms being present for minimum 1 week
→ with notable functional impairment
What is the criteria for a hypomanic episode diagnosis according to the DSM-5?
→ mania symptoms being present for minimum 4 days
→ without notable functional impairment
What leads to a diagnosis of bipolar-I?
presence of manic episodes + depressive episodes
What leads to a diagnosis of bipolar-II?
→ no manic episodes
→ only hypomanic episodes
→ at least one major depressive episode
What leads to a diagnosis of Unspecified Bipolar Disorder?
→ manic symptoms for less than 4 days
→ other thresholds for manic or hypomanic are not met
What features distinguish mania from hypomania significantly?
impairment to functionality:
→ psychotic features present
→ hospitalisation
What percentage of people relapse within a year of recovery from mood episodes?
50-60%
How are patients between episodes?
largely autonomous
What percentage of first episodes are depressive for Bipolar-I?
85%
What percentage of first episodes are manic for Bipolar-I?
10%
What percentage of first episodes are mixed for Bipolar-I?
3-5%
What are the different long-term statuses of patients with bipolar disorder?
→ majority symptom free (53%)
→ depressive symptoms (32%)
→ manic / hypomanic symptoms (10%)
→ cycling / mixed symptoms (6%)
How many bipolar patients also have anxiety?
30% - 70%
What does the DSM-5 call anxiety affecting bipolar patients?
Anxious Distress Specifier
How does anxiety affect bipolar patients?
worse prognosis + outcomes
What percentage of people with MDD visit a health professional? How many for mental health reasons?
→ 65%-70% visit health professionals
→ 15-20% for mental health reasons
How many of those with a 12-month diagnosis of MDD get antidepressant treatment?
only 21%
What was the main difference identified between bipolar and unipolar identified by the DSM-3?
→ bipolar (presence of manic episodes)
→ unipolar (without any history of mania)
What were the other differences between bipolar and unipolar in the DSM-3 in the 1980s?
→ Bipolar = early age of onset (mean age of 19 rather than late 20s fo unipolar)
→ Shorter depressive episodes (in average 3m or less in bipolar vs in average 6-12m in unipolar).
→ Recurrent course (more frequent episodes in bipolar than unipolar illness, with rapid cycling, defined as four or more episodes yearly happening in about 25% of bipolar illness cases, but in <1% of unipolar depression cases).
→ Genetic specificity (manic episodes were found in families of persons with manic episodes, but not in families of persons with unipolar depression).
→ Differential treatment (antidepressants for unipolar depression vs neuroleptics and lithium for mania)
What is the newer evidence that shows that bipolar and unipolar may be more similar?
→ MDD is commonly diagnosed in children, far below the mean onset of the late 20s.
→ Brief depressive episodes that occur multiple times yearly are diagnosed in patients with MDD commonly, whereas such course of illness should be rare if MDD was a different illness than bipolar disorder.
→ Genetic studies have found high rates of depressive episodes, without mania, in persons with bipolar illness, and also frequent occurrence of bipolar illness in relatives of those with unipolar depression.
→ Treatment now overlaps considerably, with neuroleptic agents proven effective not only for mania, but also for depression, both in bipolar and unipolar types.
→ Lithium has been well known to be effective not only for mania, but also for depression, both in bipolar and unipolar types.
When is insight preserved in depression and mania?
→ preserved in depression
→ impaired in mania
What percentage of patients with severe mania deny having symptoms (i.e. having no insight)?
50%
How does a patient’s insight change with the severity of their mania?
→ U-shaped curve with mania
→ severe mania or hypomania = impaired insight
→ moderate states of mania = intact insight
What does an acute single dose of noradrenergic antidepressants do?
better recognition of happy faces
What are some examples of noradrenergic antidepressants?
→ reboxetine
→ duloxetine
What does an acute single dose of serotonergic antidepressants do?
→ decreased recognition of fearful faces for mirtazapine
→ citalopram also causes mixed results (sometimes increases fear recognition)
What are some examples of serotonergic antidepressants?
→ citalopram
→ mirtazapine
What does 7 days of treatment for antidepressants in general result in?
reduced recognition of anger + fear
something about facial recognition modulation in ECGs
honestly have no clue what this is, please review section 2
What is the monoamine deficiency hypothesis?
suppressive symptoms arise from insufficient levels of monoamine neurotransmitters serotonin (or 5-hydroxytryptamine , 5-HT), norepinephrine, and/or dopamine
How does an antihypertensive drug prove the MD hypothesis indirectly?
antihypertensive drug, RESERPINE causes 5-HT depletion which has caused depression
How do antidepressants indirectly prove the MD hypothesis?
Clinically useful antidepressants all increase synaptic monoamine (some selectively 5-HT) concentrations.
What is the postmortem evidence for the MD hypothesis?
Post-mortem evidence of reduced 5-HT levels in brainstem of individuals who committed suicide
Which receptors and enzymes provide evidence for the MD hypothesis?
→ lower levels of -HT1A-receptors and 5-HT4-receptors
→ Monoamine oxidase increased in MDD
What else provides evidence for the MD hypothesis?
→ Blockade of serotonin synthesis by the tryptophan hydroxylase inhibitor p-chlorophenylalanine prevents the antidepressant effects of both MAOIs and TCAs
→ Tryptophan depletion (decreasing brain serotonin) triggers relapse in MDD successfully treated with SSRIs or cognitive behavioural therapy
→ Monoamine depletion correlates with decreasing mood both in at risk and MDD in remission
→ Depression-related traits; “pessimism” and “dysfunctional attitudes” in MDD, and traits “negativism” and “neuroticism” in healthy, related to 5-HT2A-receptor increase and serotonin decrease
Why can’t the MD hypothesis be proven directly?
very difficult to measure serotonin in the living brain
How are receptors and transmitters measured in the living human brain?
PET imaging
What are the differences between PET imaging and fMRI?
PET imaging is : → more Selective → more invasive → radioactive → expensive → less optimal temporal and spatial resolution
What does PET imaging involve?
→ Injection of a radioactive pharmaceutical (tracer, ligand)
→ tracer binds to a specific target (e.g. a receptor)
→ scanning picks up on tracer
How do we use PET imaging to quantify dopamine receptors?
→ inject Raclopride as the tracer or ligand
→ PET scan establishes dopamine density at baseline
→ present a challenge (e.g. Amphetamine challenge)
Why is it difficult to use PET scanning to quantify serotonin receptors?
many antagonist PET tracers haven’t been significantly sensitive to pharmacological challenges
What has worked in quantifying serotonin receptors with PET scanning?
5-HT release is measured using :
→ Agonist radioligand 11C-CIMBI-36
→ Pharma challenge Amphetamine
What is the measure of cerebral 5-HT release with depression?
→ measurable 5-HT release in healthy
→ no measurable 5-HT release in patients with depression
What is an attention bias?
Depression is characterised by biases in maintaining/shifting attention = difficulties for depressed people to disengage from negative material
What are examples of attention biases?
→ Prolonged maintenance of attention over negative pictures
→ reduced attention allocation to positive stimuli
How does fMRI work?
→ works by detecting the changes in blood oxygenation and flow that occur in response to neural activity
→ when a brain area is more active it consumes more oxygen
→ to meet this increased demand blood flow increases to the active area
How does fMRI identify attention biases?
→ sustained amygdala response to negative stimuli
→ perigenual anterior cingulate cortex of prefrontal cortex appears to mediate negative attentional biases
→ lateral inferior frontal cortex associated with the impaired ability to divert attention from task-irrelevant negative information
What is memory bias?
→ Preferential recall of negative compared to positive material
→ one of the most robust findings in the depression literature
Where is memory bias mostly present?
→ people with depression
→ individuals at risk (neuroticism)
→ recovered depressed individuals
What is perceptual bias?
increased recognition of negative faces and/or decreased recognition of happy faces
How does perceptual bias play into MDD?
→ robust strong evidence of Emotion Recognition deficits in MDD
→ reduced recognition of all basic emotions except for sadness
→ small effect size: may be confounded by medication
→ Enhanced amygdala response to negative faces
What is the function of the amygdala?
→ medial temporal lobe region
→ involved in the perception and encoding of stimuli relevant to current or chronic affective goals
→ ranging from rewards or punishments to facial expressions of emotion to aversive or pleasant images and films
→ amygdala generally is sensitive to detecting and triggering responses to arousing stimuli
→ exhibits a bias towards detecting cues signalling potential threats, like expressions of fear
