Lecture 4 - Bipolar Disorders Flashcards
Bipolar mood disorders
- inc manic and hypomanic & depressive episodes
- normal states can occur between episodes for bipolar and unipolar mood disorder
criteria for manic episodes
A. period of abnormally elevated mood and inc goal-directed activity or energy (lasts > 1 week)
B. 3 or more of the following
1. inflated self esteem
2. more talkative
3. distractability
4. excessive involvement in activities with high potential for painful consequences
5. decreased need for sleep
6. flight of ideas/thoughts racing
7. inc goal directed/psychomotor activity
C. mood disturbances causes impaired functioning, necessitates hospitalisation, or psychotic features
- can’t be explained by substance abuse
criteria for hypomanic episode
- period of abnormally and elevated inc activity etc. lasts > 4 days present most every day.
- slightly toned down variation of mania
A. 3 or more of following
1. inflated self-esteem
2. more talkative
3. distractability
4. excessive involvement in activities with high potential for painful consequences
5. dec need for sleep
6. flight of ideas/thoughts racing
7. inc goal directed/psychomotor activity
C. mood disturbance causes change in functioning
D. mood disturbance & functional change noticeable
E. not severe enough to need hospitalisation - cant be explained by substance use
Bipolar I disorder: DSM5
- criteria met for at least 1 manic episode (A to D)
- presentation not better explained by schizophrenia-spectrum disorder
- specifiers are same for MDD
- do not have to meet criteria for MDD to be diagnosed with bipolar I - must have mania but no depressive episode
Bipolar II disorder
A. criteria have been met for at least one hypomanic episode episode and at least one major depressive episode
B. never been a manic episode
C. presentation not better explained by schizophrenia-spectrum disorder
D. symptoms of depression/unpredictability caused by mood alteration causes clinical distress / impairment in functioning
- the specifiers same as MDD
diagnostic differences between Bipolar I and Bipolar II
- in Bipolar I: full mania, depressive symptoms which may or may not meet threshold for depressive episode
- in Bipolar II: person experiences hypomania but below threshold for mania, depressive symptoms meet criteria
cyclothymic disorder
- clinical mood changes less severe than bipolar
- numerous periods of depressive then hypomanic symptoms > 2 yrs
- no period of mood stability lasting longer than 2 months
- never met criteria for a full manic, hypomanic or depressive episode
- rapid cycling = significant impairments
- cyclical mood changes more severe than normal but less severe than mood swings in bipolar
differences in depressive symptoms between MDD and Bipolar
Bipolar: more severe and frequent, more role impairment, shorter, also psychotic features
MDD: high anxiety, insomnia, physical symptoms
prevalence of bipolar disorders
- male 0.8% BP1 0.9% BP2
- female 1.1% BP1 1.3% BP2
- africa: 0.1-1.83%
- europe: 0.6 - 6.2%
- worldwide 1% BP1 1.5% BP2
- does not vary with ethnicity consistently
- around 40% with MDD experiencce hypomanic symptoms
- not treated = episodes of mania 3-6m
- episodes of depression usually longer 6-12m
- age of onset has 3 peaks: approx 17, 26, 42
prodromal symptoms (Faedda et al. 2015)
- mood lability
- subclinical depression/hypomania
- major depression
- other specified bipolar & related disorders
- neurocognitive impairments
clinical course of bipolar
- syndromal recovery rates 77% at 6m and 84% 1 year
- recurrence was 26% within 6m 41% by 1 year and 60% by 4 years
- younger at first ep = risk of recurrence higher
the brain in bipolar disorder
- default mode network: brain activity when restfully awake inc contemplation, remembering, planning etc.
- DMN activity inversely cor with other networks e.g. attention and memory
- patterns of hypo and hyper connectivity in DMN in bipolar disorders
- impaired activation in PFC?
key structural differences between unipolar and bipolar depression
- lower vol in ACC for unipolar
- lower volume in the hipp and amygdala for bipolar
- lower WM integrity (cortical thinning) in bipolar
key functional differences between unipolar and bipolar
- more activation in the amygdala in unipolar towards neg emotional stimuli - suppression of emotional stimuli is not happening as much in bipolar = episodes of hypo/mania and depression
- less activation in the amygdala in unipolar towards positive emotional stimuli
- failure to deactivate the default mode during cog tasks greater for bipolar
- stronger functional connectivity in bipolar for the default mode network
- stronger functional connectivity in bipolar in pfc, acc, parietal and temporal regions and thalamus
cognition and bipolar disorder
- impairments in attention, verbal learning and memory, EFs
- some exp cog decline across the course but others resume usual levels of functioning between episodes
genetics and bipolar disorder
- MZ concordance of between 40-70%
- first-degree relatives have 5-10% risk (7x higher than general pop)
- some studies suggest genes account for 80-90% variance in liability to develop bipolar I disorder
- relatives more likely to develop unipolar depression than bipolar themselves = risk transcends mood disorder diagnostic categories = trying to separate the disorders too much is problematic
- also shared genetic risks between diagnoses of bipolar sz
- risk is polygenic = multiple SNPs in pop confer inc risk individually
polygenic risk scores
- genetic variants (SNPs) affecting 100s of loci are found more frequently in groups of people with given condition = can give polygenic risk score
- an indivs risk is based on the collective influence of many genetic variants compared to someone without the variants (a control)
socioenvironmental risk factors for bipolar disorder
- very large overlap with risk factors for MDD - affects how phenotype expresses?
- some specific factors that may differentially increase risk for bipolar disorder inc:
> childhood trauma esp emotional
> childhood neglect/adversity
> childbirth
> substance misuse (opiods)
> cannabis/cocaine use
> some other medical conditions e.g. asthma, IBS
bipolar and the immune system
- fries et al. (2019) considers how epigenetics in bipolar can be squared with its high heritability
- some genetic codes that put us at risk also put us at risk of immune disorders
- findings of consistent immune-related epigenetic alterations in people with bipolar may demonstrate how immune dysfunction is transmitted across generations
- e.g. pollution, chronic stress may damage genetic makeup
- genetic expression of the phenotype may affect our immune system = some anti-inflammatories may assist with treating symptoms
diathesis stress model
- stressful life events influence the onset of episodes by activating vulnerability. one hypothesis is this is through the destabilising effects that stressful life events have on critical biological rhythms
treatments for bipolar disorder
- mood stabilisers are used for the different mood phases of bipolar. lithium for both
- mood stabilisers used for areas e.g. epilepsy & antipsychotics which can fix manic episodes/fluctuations
- never give SSRIs alone for bipolar 1 (can push them into mania if given during depressive episode)
- bipolar 2 also given mood stabilisers but may be used in different orders. may also eb given SSRIs on their own.
- treatment usually more effective in early illness than later
lithium
- helps hypomanic and depressed phases as LT treatment (mood stabiliser)
- often prevents cycling between manic and depressive episodes
- reduces norepinephrine inc serotonin and has anti-inflammatory actions
- may change levels and properties of glutamate, GABA, dopamine, inositl and neurotrophic factors
treating depressive episodes in bipolar disorder
- SSRIs should not be prescribed on own as can worsen mania
- SSRI combined with olanzapine or another antipsychotic is typically used
- balance of risk and benefit may shift for people with bipolar II who show no evidence of hypomania with low dose antidepressants
distinguishing MDD from bipolar at first presentation
- markers of bipolar include:
> earlier age onset
> hyperphagia, hypersomnia and psychosis
> higher frequency of affective episodes
> comorbid substance use disorders, anxiety, binge eating & migraines
> family history of psychopathology - when giving antidepressants need to watch carefully for
> insufficient response
> amplification of anxiety, dysphoria and mood instability - often given small course and asked to come back to spot bipolar
psychological treatment for bipolar
- weaker evidence base
- psychological treatments can reduce episodic recurrence or stabilise depressive symptoms
- commonly used: CBT (identify triggers) psychoeducation (empowers & spot triggers) family therapy (spot triggers and when someone is entering manic episode)
- combo with medication is beneficial
bipolar similarities & differences with schizophrenia-spectrum disorders
- both groups of disorders show prodromal symptoms before initial onset and relapses
- share profiles of polygenic risk
- both disorders show cog neurological and functional progression (decline) without effective treatment
- both feature some of the same symptoms
