Happiness and mania Flashcards
Definition of happiness
‘mental or emotional state of wellbeing’
Aristotle thought it comprised ‘hedonia’ (pleasures) and ‘eudamonia’ (a life well lived)
Structures involved in happiness
Damasio 2000 - same brain areas active during all sorts of pleasures, from addictive drugs to viewing art, suggesting common happiness circuitry. Amygdala, aCC, pCC, precuneus, OFC. Similar structures to those of ‘liking’ and ‘wanting’.
Remember, medial OFC = valence, learning and memory of reward, middle OFC = subjective experience of pleasure, lateral OFC = sensitive to punishment from reward removal, behavioural change. More abstract rewards encoded anteriorly, more primary/sensory posteriorly.
Carlson et al 2016 - Medial frontal volume is correlated with expression of positive affect. Sky-diving increased self-reported euphoria, and the degree of increase was positively correlated with medial OFC volume and negatively with amygdala-hippocampal volume
Amygdala balance evidence
There is overlap between structures involved in fear and happiness (see Carlson et al 2016, medial OFC, amygdala, hippocampus), so is happiness achieved at the expense of sadness/fear? Healthy people do show positive bias…
Cunningham and Kirkland 2014 - subjective happiness correlated with amygdala activity in response to positive images, but no correlation (+ or -) with response to negative. So happy encoding does not come at the expense of sad encoding.
Precuneus evidence
aka medial parietal
Sato et al 2015 - subjective happiness correlated with precuneus grey matter volume. Combined score of positive and negative responses correlated with precuneus grey matter volume
Suggestion that it’s involved in integrating cognitive and emotional components
Precuneus activity altered in CBT for depression.
Mania - definition, symptoms
a state of abnormally elevated arousal, affect, and energy level, or a state of heightened overall activation with enhanced affective expression together with lability of affect.
Symptoms:
-Inflated self-esteem or grandiosity
• Decreased need for sleep (e.g. feels rested after 3 hours of sleep)
• More talkative than usual or pressure to keep talking
• Flights of ideas or subjective experience that thoughts are racing
• Increases in goal directed activity, or psychomotor acceleration
• Distractibility (too easily drawn to unimportant or irrelevant external stimuli)
• Excessive involvement in activities that have a high degree of adverse consequences (e.g. extravagant shopping,
symptoms more easily observed in hypomania - full mania leads to hospitalisation.
Bipolar disorders
- A single episode of mania is enough to diagnose BPD1.
- Hypomania may be indicative of BPD2.
- BPD1 has low rates of returning to work (30% after hospitalisation),
- high rates of suicide and hospitalisation (30x higher risk of suicide than general population),
- two thirds will experience major depressive episodes,
- two thirds will experience an anxiety disorder
Mania - neurological basis
Blumberg et al 2003 - decreased VPFC activity during an emotional stroop task, increased amygdala activity during a facial affect match task, in manic patients
Risk of switch from depression to mania was 2.6 times higher in patients taking antidepressants than controls
Acute tryptophan depletion can reduce mania
Lithium salts can reduce mania, mechanism unknown
Antipsychotics - DA agonists can trigger switch, increased DA transmission in manic phase
BPD - psychological basis - emotion maintenance
nomothymic/euthymic BPD patients (i.e. not currently manic) rate neutral stimuli as more pleasant, report higher subjective arousal to neutral stimuli, and self-report greater positive affect and the prospect of receiving rewards.
Farmer et al 2006 - after positive mood induction, BPD patients stay happy for longer, and show increased positive rumination.
Gruber et al 2013 - During positive mood induction, controls’ accuracy at rating negative stimuli remained constant (i.e. they got happier, but didn’t get less sensitive to negativity), whereas BPD patients reduced their responding to negative stimuli, as if their happiness from the mood induction came at the expense of negative feelings.
What is psychosis?
Can occur in BPD, schizophrenia “a loss of contact with reality, usually including false beliefs about what is taking place, or who one is (delusions) and seeing or hearing things that are not there (hallucinations)” Associated with impaired emotional processing and cognitive effects linked to DA function (antipsychotics block D2 receptors) and NMDA-mediated glutamate function
Schizophrenia - emotion processing
Patients make fewer negative facial expressions
Patients are worse at identifying negative facial expressions (and men worse than women)
BUT patients rate emotional stimuli (of any valence) as controls, and amygdala activity to emotional stimuli is as controls
Gard et al 2007 - Schizophrenics show reduced anticipatory enjoyment, so may not be able to use this to guide behaviour over time?
Gard et al 2011 - Schizophrenic patients have the same average emotional rating of pictures as controls, but emotional maintenance accuracy over time was worse.
BPD - psychological basis - risk/reward processing
Murphy et al 2001 - BPD patients are more likely to choose the less favourable of two response options in the Cambridge gambling task
Adida et al 2011 - in the Iowa gambling tasks, BPD patients (whether manic, euthymic or depressed) developed a preference for a deck early on, and maintained this preference even when it became clear it was a disadvantageous deck.
Ryu et al 2017 - BPD patients, but not controls, had increasing feedback-related negativity (the negative deflection of activity seen in ACC thought to denote a negative prediction error) during a probabilistic reward task. They also showed reduced reward bias initially. This suggests they have dysregulated reward integration and repetitive reinforcement, at the behavioural and electrophysiological level.
Schizophrenia - emotional salience
Modinos et al 2015 - Patients at high risk of psychosis or currently in first psychotic episode had stronger response than controls to neutral stimuli, and weaker response to affective (+ or -) stimuli. Decreased activation of inferior frontal gyrus/anterior insula, amygdala and dorsomedial PFC
Schizophrenia - diagnostic criteria
At least two of delusions, hallucinations, disorganised speech, disorganised behaviour/catatonia, negative symptoms. At least one must be of the first 3.
Social and occupational decline
Positive or negative symptoms for at least 6 months
Positive symptoms - hallucinations (inc auditory), delusions, delusional perception, thought interference
Negative symptoms - flat affect, avolition/apathy, catatonia, poverty of speech, social withdrawal, lack of attention
Rosenhan 1973 - 8 healthy controls were told to feign auditory hallucinations. All were admitted, most given antipsychotics. Told to behave normally once in hospital, and yet were kept in for an average of 19 days. Staff were told the experiment would be repeated, and went on to judge 41 patients as pseudo-patients. None were.
Schizophrenia - epidemiology
20 new cases per 100k per year
more men than women
often comorbid with drugs
young people, aged 15-55, as many aged 35 as 20
long delays before treatment, complex pathway to appropriate care.
Schizophrenia - social risk factors
Correlation with social deprivation (but Goldberg and morrison 1963 - social class effect disappears when categorised by father’s occupation, and Myers and Ben 1968 - decisions about hospitalisation and treatment are influenced by socioeconomic class, with no evidence that class had played a role in causing the disease.)
Some indication of social drift (but this may be confounded with social deprivation.)
Ethnicity and migration - 9.1 times higher risk in Afro-caribbean in UK.
Kirkbride et al 2006 - rates of schizophrenia doubled in London compared to Nottingham or Bristol, controlling for class and ethnicity
Delayed motor and cognitive development (measured by premorbid IQ) in children predicts schizophrenia (causal? or just early sign?) Ridler et al 2006 - in healthy people, infant motor development and adult executive function correlate with partially-overlapping anatomical changes, in premotor cortex and fronto-cerebellar connections. This correlatin does not exist in schizophrenic patients (as well as them having average later IMD and poorer ADE).
