Psych Mood Disorders Flashcards
what are mood changes often accompanied by?
overall change in the overall level of activity
- other symptoms are secondary to change in mood and activity
are mood disorders recurrent?
yes
- onset of individual episodes can be related to stressful events or situations
lifetime prevalence of what % for bipolar I?
0.6% (est 1%)
lifetime prevalence of what % for bipolar II?
0.8% (est 1.0%)
is rate of MDD inc/dec?
inc
- earlier age of onset too
Gender distribution of bipolar-I
F=M
Gender distribution of bipolar-II and MDD?
F>M
2 : 1
mental and substance abuse disorders accounted for what % of all DALYs worldwide?
7%
within mental and substance abuse disorders, MDD accounted for what % of all DALYs worldwide?
40%
within mental and substance abuse disorders, bipolar accounted for what % of all DALYs worldwide?
7%
thoughts in uni and bipolar depression
what’s the point
behaviours in uni and bipolar depression
lie in bed all day and ruminate
physiological symptoms in uni and bipolar depression
exhaustion
feelings in uni and bipolar depression
low, flat, irritable
DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th Edition) criteria for depression episode?
occurence of 2 weeks or more of depressed mood and the presence of 4/8 of the DSM-5 symptoms.
DSM-5 symptoms (8)
- sleep alterations
- appetite alterations/ weight alterations
- diminished interest (anhedonia)
- decreased concentration
- low energy (anergia)
- guilt/ feeling worthless
- Psychomotor changes
- suicidal thoughts or acts
what types of episodes mustn’t occur for MDD diagnosis?
manic or hypomanic episodes
subtypes for symptoms in DSM-5 for MDD
- atypical features (inc sleep, appetite and heightened mood reactivity)
- melancholic features
- Psychotic features (e.g. delusions/hallucinations)
manic episodes in accordance with DSM-5?
euphoric or irritable mood with 3/7 (at least) of the manic criteria
- If symptoms present for 1+ weeks with notable functional impairment, a manic episode is diagnosed: leads to DSM-5 diagnosis of type I bipolar disorder
- If symptoms present for 4+ days without functional impairment: hypomanic episode is diagnosed
- If no previous manic episode has occurred but only hypomanic episodes present with at least 1 major depressive episode: DSM-5 diagnosis of type II biploar disorder
DSM-5 manic criteria (7)
- decreased need for sleep and increased energy
- distractibility
- Grandiosity and inflated self-esteem
- flight of ideas/racing thoughts
- increased talkativeness/pressured speech
- increased goal-directed activities or psychomotor agitation
- impulsive behaviour e.g. sexual and spending sprees
what happens in diagnosis of mania/bipolar if not a single manic episode has occured, only hypomanic episodes + at least 1 major depressive episode?
DSM-5 diagnosis of type II bipolar disorder
what DMS05 diagnosis if manic symptoms < 4 days, or thresholds for manic/hypomanic episodes aren’t met?
- unspecified bipolar disorder
what cannot be diagnosed using DSM-5 if psychotic features are present?
hypomania (psychotic features involves notable impairment by definition)
what is diagnosed using DSM-5 if hospitalisation occurs, irrespective of durations of manic symptoms?
manic episode
what is diagnosed using DSM-5 if manic/hypomanic episodes are caused by antidepressants?
bipolar disorder
most consistent clinical feature of bipolar disorders
- psychomotor changes
what is the first episode type in bipolar I?
depressive
what % of the time will people with bipolar disorder be symptom free?
just over 50%
what % of the time will people with bipolar disorder have symptoms?
47%
is anxiety prevalent amongst people with bipolar disorder?
yes // 30-70% of bipolar patients
- worse prognosis and outcomes if you have MDD and anxiety
1980 dichotomy
- bipolar vs unipolar depression age of onset
19 vs late 20s
1980 dichotomy
- bipolar vs unipolar depressive episodes length
3m or less in bipolar, vs 6-12m in unipolar
1980 dichotomy
- bipolar vs unipolar recurrence
more frequent course cycles in bipolar than unipolar
1980 dichotomy
- genetic specifity
manic episodes found in relatives of a persons with manic episodes, but not in the families of those with unipolar depression
1980 dichotomy
- bipolar vs unipolar differential treatment
bipolar = neuroleptics and lithium unipolar = antidepressants
evidence that bi and unipolar depressions not separate
- MDD commonly diagnosed in children, below age of late 20’s
- MDD can occur in multiple short episodes in a year
- 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
- treatments overlap (neuroleptics agents effective for mania and depression in uni and bipolar depressions). Li effective not just for mania, but also for depression in bipolar and unipolar types
heritability of bipolar (twin studies)
- very heritable
- depression has only half the heritability of bipolar
is insight preserved in depression?
yes
- impaired in mania
when is insight best preserved in mania?
moderate mania - hypomania and severe mania sees more severe impairment
What mood disorder diagnosis can easily be missed and what diagnosis is a patient in that situation misdiagnosed with?
bipolar diagnosis missed due to lack of insight about mania/hypomania. MDD diagnosis instead despite history of manic episodes. Collateral info (ask family/ friends) useful when in doubt about details in history taking. Family members report manic symptoms x2 frequently as patients themselves
Problems associated with misdiagnosis
antidepressants mostly ineffective in acute bipolar disorder and in prophylaxis.
-> can cause acute manic/hypomanic episodes
-> shows to worse the long-term course of bipolar illness, especially in those with a rapid-cycling course
-
attention biases in depression
- hard to disengage from negative material
what is seen on fMRI when someone with depressions given negative stimuli?
sustained amygdala response
Perigenual anterior cingulate cortex mediates negative attentional bias
increased activity of lateral inferior frontal cortex associated with impaired ability to divert attention from task-irrelevant negative information
memory biases in depreesion
- preferential recall of negative compared to positive material
facial expression recognition in depression
- increased recognition of negative faces,
- decreased recognition of happy faces
- -> also enhanced amygdala response to negative faces
what is the amygdala
- a medial temporal lobe region
amygdala function
- involved in the perception and encoding of stimuli relevant to current or chronic effective goals.
Stimuli range from rewards or punishments to facial expressions of emotions to aversive or pleasant images or films. - sensitive to detecting and triggering responses to arousing stimuli, exhibits a bias towards detecting cues signaling potential threat
[facial recognition]
patient who take noradrenergic antidepressants can identify what better?
happy faces
[facial recognition]
patient who take serotonergic antidepressants can identify what better (give 2 drug examples)?
Mirtazapine: decreased recognition of fearful faces
SSRI citalopram: mixed results (sometimes found to increase fear recognition)
what does the 7 day antidepressant treatment involve?
- noradrenergic and serotonergic antidepressants: reduced recognition of anger and fear
- > reduced amygdala and mPFC response to fear
What can we use as a marker of clinical response to antidepressants?
Early change in positive processing
In early stages of treatment we can see decreased response to fearful faces
what is the gold-standard SSRI?
escitalopram
- after 6 weeks treatment, associated with early change (at 1 week) in the amygdala, thalamus, ACC, and insula response to fearful faces
How is ACC activity linked to response to treatment for depression?
An elevated baseline ACC in depressed patients predicts a positive response to treatment (medication, neurostimulation and CBT)
what is the monoamine hypothesis of depression?
postulates that depressive symptoms arise from insufficient levels of monoamine neurotransmitter serotonin, norepinephrine, and/or dopamine
what can antihypertensive drug reserpine cause (relating to serotonin)
depletion of serotonin
post-mortem evidence of people who committed suicide shows what levels of 5-HT?
low in the brainstem
what does (tryptophan hydroxylase inhibitor) p-chlorophenylalanine do to MAOI and TCAs?
- blockade of serotonin synthesis
- prevents antidepressants effects of both MAOIs and TCAs
what is the best way to investigate brain pharmacology?
PET imaging
- selective but invasive, radioactive, expensive with less optimal temporal and spatial resolution
- tracer used is radioactive and binds to a specific target e.g. receptor
why don’t we use fMRI to investigate brain pharmacology?
it’s not very selective
how PET is used to monitor dopamine
- tracer targets dopamine receptors in the brain
- use to quantify how many receptors are present
(baseline scan)
what is a challenge scane?
PET scan taken after patient given pharmacological challenge (e.g. amphetamine to cause release of dopamine) ; causes release of transmitter
- dopamine will compete with radio tracer
- less of the tracer can bind to the receptors
- difference from baseline of binding represents how much dopamine is released from challenge given
problem with challenge scan?
30-40% of patients don’t respond to challenge
What is monoamine oxidase A and how is it affected by MDD?
Its an enzyme which breaks down serotonin
It is increased in MDD
What is serotonin also known as?
5-HT
What are the 3 triads of depression?
CORE SYMPTOMS:
Low mood
Anergia
Anhedonia
BIOLOGICAL SYMPTOMS:
Sleep
Libido
Appetite
PSYCHOLOGICAL SYMPTOMS:
Oneself
The world
The future
