mood disorders Flashcards

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1
Q

mood disorders

A

disabling disturbances in emotion — from extreme sadness to extreme elation and irritability of mania.

Temporal patterning important in determining diagnoses &
treatment

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2
Q

physical symptoms of depression

A
  • fatigue and low energy
  • physical aches and pains. (psychosomatic symptoms; doctors may initially think its a medical disorder)
  • hard to fall asleep and wake up frequently; Others sleep throughout the day.
  • food tastes bland or that their appetite is gone, or increase in appetite.
  • Sexual interest disappears.
  • limbs feel heavy.
  • Thoughts and movements slow (psychomotor retardation; but others cannot sit still — they pace, fidget and wring their hands (psychomotor agitation).
  • lack on initiative
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3
Q

MDD DSM criteria

unipolar disorders

A

At least 5 symptoms (which MUST includE (1) depressed mood and (2) loss of pleasure)

 weight loss or change in appetite
Sleeping too much or too little
Psychomotor retardation or agitation
Fatigue or loss of energy
Feelings of worthlessness or excessive/inappropriate guilt
Difficulty concentrating, thinking or making decisions
Recurrent thoughts of death or suicide (or attempt/plan)
Symptoms are present for at least 2 weeks and represent a change from
previous functioning

• Symptoms are present nearly every day, most of the day, for at least two weeks. Symptoms are distinct and more severe than a normative response to significant loss.

  • have to take other disorders into account
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4
Q

MDD is…

A

an episodic disorder symptoms present for a period of time and then clear. (an untreated episode may stretch on for five months or even longer) subclinical depression for years..

but has to last at least 2 weeks
risk of episode increases after every episode
Controversial criteria re: number of symptoms
• But impairment appears higher with greater number of symptoms

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5
Q

Persistent Mood disorder DSM (dysthymia)

A
  • having a depressed mood for most of the day more than half of the time for two years (or one year for children and adolescents).

experience at least 2 of the following symptoms during that time:

  • poor appetite or overeating
  • sleeping too much or too little
  • low energy
  • poor self-esteem
  • trouble concentrating or making decisions
  • feelings of hopelessness.
  • symptoms do not clear for more than two months at a time and bipolar disorders are not present.
  • central feature: chronicity of symptoms, which has been shown to be a stronger predictor of poor outcome than the number of symptoms.
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6
Q

gender differences in depression

A

Women are twice as likely to experience major depression and persistent depressive disorder
THIS IS PRONOUNCED IN COUNTRIES AND CULTURAL GROUPS WITH TRADITIONAL GENDER ROLES

HORMONAL FACTORS
- hormonal factors that could explain the vulnerability of women, findings have been mixed tho
o Exposure to childhood and chronic stressors, as well as the effects of female hormones, could change the reactivity of the HPA axis, a biological system guiding reactions to stress.

SOCIAL FACTORS
o Twice as many girls are exposed to childhood sexual abuse.
o During adulthood, women are more like exposed to chronic stressors (poverty and caretaker responsibilities)
o Acceptance of traditional social roles intensify self-critical attitudes about appearance.
o worry more body image,
o the need for approval and closeness in women, may intensify reactions to interpersonal stressors
o Social roles promote emotion-focused coping among women, which may then extend the duration of sad moods after major stressors.
o women tend to spend more time ruminating about sad moods or wondering about why unhappy events have occurred.
o Men tend to spend more time using distracting or action-focused coping

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7
Q

disruptive mood dysregulation disorder

A

Severe recurrent temper outbursts in response to common stressors

o Temper outbursts are inconsistent with developmental level
o Temper outbursts tend to occur at least 3 times per week
o Persistent negative mood between temper outbursts most days, & the negative mood is observable to others
o Symptoms present for at least 12 months, do not clear for more than 3 months at a time
o Temper outbursts or negative mood present in at least 2 settings
o Age 6 +
o Onset before age 10
o In past year, no distinct period lasting >1 day where elevated mood & at least 3 other manic symptoms present

oppositional defiant disorder, ADHD and bipolar confused with this one

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8
Q

Seasonal affective disorder

A

experience depression during two consecutive winters and that the symptoms clear during the summer.

  • common in northern than in southern climates;
  • show greater changes in melatonin in the winter
  • show a change in their retinal sensitivity to light (genetic)
  • Some people, though, seem to respond to those physical changes (of the winter) self-critically
  • excessive sleep & and increased appetite in winter

can apply to BD
– Biplolar disorders = depressed in winter, manic in summer

treatment

  • antidepressant medications and CBT
  • light therapy has been shown to help relieve depression
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9
Q

Catatonic depression

A

Stuporous state or catalepsy » End state reaction to imminent doom?

  • echolalia (fitting on spectrum with schizophrenia)
  • psychomotor disturbances
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10
Q

Melancholic depression

A

Melancholic: » Full criteria met for MDD »

BUT More severe somatic symptoms e.g. loss of libido, anhedonia, guilt
* its the complete loss of pleasure whereas is MDD its a reduced loss not a complete loss

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11
Q

Atypical depression

A

Depressive episodes and dysthymia

  • Oversleep, overeat, can still find pleasure
  • More common in women, early onset
  • More: symptoms, severe, suicide, comorbidity
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12
Q

Postpartum depression

A

Postpartum:

Onset within first 4 weeks of childbirth
* 13% post-childbirth, hormonal?

NOT “baby blues” – 80% for few days, normal stress response (but it only goes for a couple of nights as people with PP depression it doesn’t go away

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13
Q

comorbidity among depression

A
  • MDD and persistent depressive disorder are often associated, or comorbid, with other psychological disorders.
  • About 60 percent for anxiety disorder at some point
  • Other common comorbid conditions include substance-related disorders, sexual dysfunctions and personality disorders.
  • MDD - world’s leading causes of disability
  • MDD is also related to a high risk of other health problems, including death from medical
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14
Q

Rapid cycling:

A

– Move quickly in & out of depressive or manic episodes
– >3 manic or depressive episodes
– ↑ suicide attempts and episodes of depression
– 20-40% of people with bipolar (60-90% female more common)
– ↑ in frequency over time
– Can transform to ‘rapid switching pattern’ without breaks

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15
Q

mood disorders aetiology

genetics

A
  • Probability of having a mood disorder 2-3 x greater if relative (sibling, mother or aunty) has a mood disorder
  • studies of MZ (identical) and DZ (fraternal) twins heritability estimates around 37% (quite high)
  • Bipolar disorder is among the most heritable of disorders. (but can be for any mood disorder)
    » Severity, recurrence, age at onset predict rate
  • Bipolar→ any mood disorder up to 90%

IDENTIFYING GENES
>160 loci (genes located) linked – few well studied or replicated
» Serotonin transporter gene
» DRD4.2 gene
» Likely a set of genes that confers vulnerability

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16
Q

neurotransmitters in mood disorders

A
  • norepinephrine, dopamine and serotonin.
  • Past –> mood disorders would be related to having too much or too little of a neurotransmitter,
  • More recent –> mood disorders might involve changes in receptors that respond to the presence of neurotransmitters in the synaptic cleft (focused on dopamine and serotonin.
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17
Q

serotonin

A

Serotonin thought to regulate emotional reaction
» ↓ serotonin dysregulates others neurotransmitters (the imbalance is what creates problems)
» balance rather than absolute levels?
» dysfunction = altered sensitivity of postsynaptic
receptors?

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18
Q

Amygdala

A
  • elevated activity of the amygdala among people with MDD.
  • when shown negative words or pictures of sad or angry faces, people with current MDD have a more intense and sustained reaction in the amygdala than do people with no MDD
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19
Q

Striatum

A
  • people with depression- diminished activation of the striatum during exposure to emotional stimuli, particularly when they are receiving positive feedback that they have earned a reward
  • A specific region of the striatum (called the nucleus accumbens) is a central component of the reward system in the brain and plays a key role in motivation to pursue rewards
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20
Q

The neuroendocrine system: cortisol dysregulation

A
  • amygdala is overly reactive among people with MDD and the amygdala sends signals that activate the HPA axis
  • people with Cushing’s syndrome: which causes oversecretion of cortisol, frequently experience depressive symptoms.
  • Even among people who are depressed but do not have Cushing’s syndrome, cortisol levels are often poorly regulated — that is, the system does not seem to respond well to biological signals to decrease cortisol levels.
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21
Q

Social factors in depression:

A
  • Childhood adversity, such as early parental death, physical abuse or sexual abuse, increases the risk that later, in their adolescence or adulthood, the person will develop depression and that the depressive symptoms will be chronic
  • there is much evidence that stress can cause depression.
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22
Q

diatheses

A

some people must be more vulnerable to stress than others.
- Diatheses could be biological, social or psychological.

lack of social support
o People who are depressed tend to have sparse social networks and to regard those networks as providing little support
o Low social support may lessen a person’s ability to handle stressful life events.

Family problems
oexpressed emotion (EE) — defined as a family member’s critical or hostile comments towards or emotional overinvolvement with the person with depression.
o High EE strongly predicts relapse in depression.

Interpersonal style
o an excessive need for reassurance has been found to predict depression.
o depressive symptoms seem to elicit negative reactions from others
-

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23
Q

personality aetiology

A

Neuroticism

  • neuroticism tendency to experience frequent and intense negative affect, predicts the onset of depression
  • neuroticism is also associated with anxiety

Longitudinal studies → predicts onset of depression
Trait most associated with depression
» Support in twin studies
Positive affect as a predictor = less clear
» Low extraversion doesn’t always precede
depression

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24
Q

Rumination theory

A

emphasises the tendency to dwell on negative moods and thoughts.

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25
Q

Beck’s theory aetiology cognitive

A
  • negative triad: negative views of the self, their world and the future
  • acquired negative schemas through experiences
  • negative schema is activated whenever the person encounters situations similar to those –> cause cognitive biases, or tendencies to process information in certain negative ways

Rumination theory

  • Susan Nolen-Hoeksema (1991) suggested that a way of thinking called rumination may increase the risk of depression.
  • tendency to repetitively dwell on sad experiences and thoughts, or to chew on material again and again.
  • women tend to ruminate more than men do, perhaps because of sociocultural norms about emotion and emotion expression.
  • evolutionarily adaptive to focus on negative events in order to solve problems

Depression in bipolar disorder

  • The triggers of depressive episodes in bipolar disorder appear to be similar to the triggers of major depressive episodes  negative life events appear to be important in precipitating depressive episodes in bipolar disorder.
  • Similarly, neuroticism, negative cognitive styles expressed emotion and lack of social support predict depressive symptoms in bipolar disorder.

Predictors of mania

  • reward sensitivity
  • sleep deprivation.

Reward sensitivity
- disturbance in the reward system of the brain
- people with bipolar disorder describe themselves as highly responsive to rewards on a self-report measure
- specifically, life events that involve attaining goals, such as gaining acceptance to university or getting married  trigger for B1 (for those who are biologically vulnerable)
Sleep deprivation
- Experimental studies indicate that sleep deprivation can precede the onset of manic episodes. I

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26
Q

Beck’s theory aetiology cognitive

A
  • negative triad: negative views of the self, their world and the future
  • acquired negative schemas through experiences
  • negative schema is activated whenever the person encounters situations similar to those –> cause cognitive biases, or tendencies to process information in certain negative ways
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27
Q

Rumination theory

A
  • Susan Nolen-Hoeksema (1991); rumination may increase the risk of depression.
  • tendency to repetitively dwell on sad experiences and thoughts, or to chew on material again and again.
  • women tend to ruminate more than men do, perhaps because of sociocultural norms about emotion and emotion expression.
  • evolutionarily adaptive to focus on negative events in order to solve problems
28
Q

Depression in bipolar disorder

A
  • The triggers of depressive episodes in bipolar disorder appear to be similar to the triggers of major depressive episodes = negative life events appear to be important in precipitating depressive episodes in bipolar disorder.
  • Similarly, neuroticism, negative cognitive styles expressed emotion and lack of social support predict depressive symptoms in bipolar disorder.
29
Q

predictors of mania

A

Predictors of mania

  • reward sensitivity
  • sleep deprivation.
30
Q

reward sensitivity in BD

A
  • disturbance in the reward system of the brain
  • people with bipolar disorder describe themselves as highly responsive to rewards on a self-report measure
  • specifically, life events that involve attaining goals, such as gaining acceptance to university or getting married  trigger for B1 (for those who are biologically vulnerable)
31
Q

sleep deprivation

A
  • Experimental studies indicate that sleep deprivation can precede the onset of manic episodes. I
32
Q

interpersonal psychotherapy

A
  • depression is closely tied to interpersonal problems
  • examine major interpersonal problems (role transitions, interpersonal conflicts, bereavement and interpersonal isolation)
  • helping the person identify his or her feelings about these issues, make important decisions and effect changes to resolve problems related to these issues.
33
Q

interpersonal psychotherapy

A
  • depression is closely tied to interpersonal problems
  • examine major interpersonal problems (role transitions, interpersonal conflicts, bereavement and interpersonal isolation)
  • helping the person identify and explore feelings and encourage expression
  • improving communication
  • make important decisions and effect changes to resolve problems related to these issues.
    – Discussing IP problems
    – Finding more effective modes of behaviour
    – Brief ~ 16 sessions
    – Generally helpful in MDD & dysthymia
34
Q

CBT

A
  • depression is caused by negative schema and cognitive biases,
  • altering maladaptive thought patterns.
  • client might be asked to complete daily monitoring homework that involves recording their thoughts whenever they experience a negative mood.
  • help the person with depression to change his or her opinions about the self, others and the world.
  • cognitive restructuring (i.e., persuading the person to think less negatively).
  • medium effect size supporting CBT for depression in adults
  • Behavioural activation (BA) is a technique used in CBT in which people are encouraged to engage in pleasant activities that might bolster positive thoughts about one’s self and life.
35
Q

Mindfulness in your daily routine

A
  • teaches people to have an intentional, non-judgemental awareness of the present moment.
  • By learning to live in the here and now, individuals may be less vulnerable to rumination and negative self-talk.

Psychological treatment of bipolar disorder

  • Medication is a necessary part of treatment for bipolar disorder, but psychological treatments can supplement medication
  • help to maintain
36
Q

Psychoeducational approaches

A

help people learn about the symptoms of the disorder, the expected time course of symptoms, the biological and psychological triggers for symptoms and treatment strategies
education helps people adhere to treatment with medications

37
Q

Psychoeducational approaches

A

help people learn about the symptoms of the disorder, the expected time course of symptoms, the biological and psychological triggers for symptoms and treatment strategies
education helps people adhere to treatment with medications
>1/2 don’t take medication consistently

38
Q

Functional family therapy

A

aims to educate the family about the illness, enhance family communication and develop problem-solving skills

Expressed emotion predicts faster relapse
 Educate family about the disorder, enhance communications, develop
problem-solving skills

39
Q

Biological treatments for depressive disorders:

A

– Antidepressant medications:

  1. Selective serotonin re-uptake inhibitors
  2. Mono-amine oxidase (MAO) inhibitors
  3. Tri-cyclic antidepressants

– All equally effective, immediate relief
– MDD & dysthymia
– Up to 70% show major improvement,
– Combining psychotherapy with AD medication bolsters odds of recovery by up to 20% above either alone

40
Q

Selective serotonin re-uptake inhibitors

A

– ‘First choice’ in drug treatment
– Temporary ↑ serotonin
– Precise mechanism?
– ↑ thoughts of suicide

in first few weeks in adolescents?
– Side effects: physical agitation,
sexual dysfunction, insomnia,
gastrointestinal upset

41
Q

Mono-amine oxidase (MAO) inhibitors:

A

– Block the enzyme MAO
– MAO breaks down nor-epinephrine, dopamine & serotonin
– Increasing availability
– Potentially serious consequences:
– Consuming tyramine → hypertension
– Some everyday medications → dangerous interaction
– Typically used as last line of treatment
– More effective with ‘atypical’ features

42
Q

mood stabilisers

A
reduce manic symptoms:
– Lithium remains gold standard
– Up to 80% experience some benefit
– 70% relapse in 5 years
– Side effects = blurred vision → coma, death!
– Where not tolerated:
– Anticonvulsants (e.g. Valproate)

anticonvulsant : mood stabiliser

Antipsychotics (e.g. Olanzapine)

  • immediate calming effect
  • reduce mania and, to some extent, depression
43
Q

Electroconvulsive therapy:

A
– Most dramatic & controversial treatment for MDD
– When all else has failed!
– 70-130 volt current through brain
– How/why it works?
– Massive functional/structural changes?
– Increases serotonin levels
– Blocks stress hormones
– Neurogenesis in the hippocampus?
– Short-term memory loss
– Decline in cognitive function 6 months
44
Q

differences b/w DSM-IV and DSM5

A
  • few new disorders
  • disorders in this area sit on a continuum b/w depression, bipolar and schiz
  • disruptive mood regulation disorder
  • premenstrual disorder
  • persistent depressive disorder (known as dysthymia before)
45
Q

premenstrual Dysphoric disorder

A

In most menstrual cycles, 5+ symptoms present in final
week before menses, improving within few days of
menses onset:

Including ≥1:
– Affective lability
– Marked irritability, anger, arguments
– Depressed mood, hopelessness, self-deprecating thoughts
– Anxiety diminished interest in usual activities, difficulty concentrating

Including ≥ 1:
– Decreased interest in usual activities
– Difficulty concentrating
– Lack of energy
– Change in appetite, overeating, or food craving
– Sleeping too much or too little
– Subjective sense of being overwhelmed or out of control
– physical symptoms
46
Q

prevalence in depression

A

MDD one of most prevalent psychiatric disorders (~16%)
 Dysthymia rarer (~2.5%)

 Twice as common in women–> Reported more often
 Three times more common in low SES individuals

Prevalence varies across cultures
 1.5% in Taiwan, 19% in Beirut
 Symptoms also vary across cultures
 Nerves & headaches common in Latino cultures
 Fatigue & weakness in Asian cultures
 But may be a complex relationship:
 Distance from equator? (further away you are higher prevalence)
Role of light exposure
 Fish consumption?
 Wealth disparity & family cohesion important

47
Q

increasing prevalence of depression why?

A

In most countries prevalence of MDD increased steadily until late 20th century

 Median age of onset now late teens to early 20s
 support structures like extended family non-existent
 marital stability often absent

Symptoms appear to change over lifespan:
 children → somatic complaints
 older adults → distractibility & memory loss
 Often comorbid with other psychiatric problems:
 60% also meet criteria for anxiety disorder

 Other comorbidities:
 substance-related disorders
 sexual dysfunction
 personality disorders
 cardiovascular disease
48
Q

DSM-5 criteria for manic and hypomanic episodes

A

at least 3 of the following ( but need 4 if mood is irritable and not elevated)
o increase in goal-directed activity or psychomotor agitation
o unusual talkativeness; rapid speech
o flight of ideas or subjective impression that thoughts are racing
o decreased need for sleep
o increased self-esteem; belief that one has special talents, powers or abilities
o distractibility; attention easily diverted
o excessive involvement in activities that are likely to have painful consequences, such as reckless spending, sexual indiscretions or unwise business investments

  • symptoms are present most of the day, nearly every day.
49
Q

For a manic episode you need…

A
  • symptoms last one week, require hospitalisation or include psychosis
  • symptoms cause significant distress or functional impairment.
50
Q

For a hypomanic episode you need…

A
  • symptoms last at least 4 days
  • clear changes in functioning are observable to others, but impairment is not marked
  • no psychotic symptoms are present.
51
Q

bipolar 1 disorder criteria

A

Criteria met for at least one manic episode
– If mood is irritable rather than elevated – requires 4 , not 3 ,other symptoms
– Hypomanic and depressive episodes common (not necessary)

 Diagnostic code based on:
» type of current/most recent episode (e.g. manic, hypomanic, depressed)
» Severity (mild, moderate, severe)
» Presence of psychotic features
» In remission/not

– May or may not be experiencing current symptoms of mania
– Episodes tend to reoccur

52
Q

Bipolar II Disorder criteria

A

Criteria met for at least one hypomanic episode
AND
Criteria met for at least one major depressive episode

– Diagnostic code as for BP I
– recurring mood episodes – usually more frequent and lengthier than BPI
– Usually present with MD episode - unlikely to complain of hypomania

53
Q

Cyclothymic Disorder criteria

A

For at least 2 years (1 in children/adolescents):

– Numerous periods of hypomanic symptoms that do not meet criteria for a manic episode

– Numerous periods with depressive symptoms that do not meet criteria for a MDD

– Symptoms do not clear for >2 mths
» cause significant distress/impairment

54
Q

prevalence of bipolar

A

– Bipolar I disorder much rarer than MDD
– Bipolar I ~ 0.6%
– Bipolar II more difficult to gauge ~ 0.4 – 2%
– Cyclothymia ~4% of mood disorders
– Cultural variation may reflect differences in labelling
behaviours as manic symptoms

onset
– > half before 25, increasing frequency in children
– Equally in men & women, women more episodes of
depression

comorbidity
2/3 meet diagnostic criteria for comorbid anxiety disorder
– 1/3 report history of substance abuse

55
Q

consequences for bipolar

A

Bipolar I disorder amongst most severe forms of mental illness

– 1/3 remain unemployed 1 year after hospitalisation for mania
– Unable to work ~25% of the time

 Suicide attempts:
– Bipolar I ~1 in 4
– Bipolar II ~1 in 5

 High risk for other medical condition:
– Cardiovascular disease
– Diabetes
– Obesity
– Thyroid disease
– Often severe

 Cyclothymia = high risk for developing episodes of mania & major depression ~ 50%

56
Q

depression diagnoses issues

A

many people who are diagnoses with depression meet the criteria very differently

DSM deals with this by creating a range of criteria to divide the disorders into a number of specifiers

57
Q

subtype with psychotic features

A

Mood congruent - hallucinations, delusions consistent with mood state

 Mood incongruent (thought breakthroughs, thought insurgents) --> serious sub-type
» schizophrenia? 5-20%

poor treatment response
» greater impairment

Mixed subtype:
» At least 3 manic symptoms present during depressive episode, or
» At least 3 depressive symptoms present during a manic episode

58
Q

dopamine and aetiology

A

increase in dopamine

↑ dopamine = hypomania
» receptors oversensitive?
 dopamine = depressive b/h
G Protein high in mania,
low in depression
59
Q

neuroimaging and research

A

a lot of research looking at
Amygdala, prefrontal cortex, hippocampus, sub-genual
anterior cingulate

  • all important in the regulation of emotion (function assess how emotionally important/salient a stimulus is

DEPRESSION
* elevated activity of amygdala (sends signals to prefrontal cortex to determine whether stimulus is a threat)

people with depression have elevated amygdala activity to images (whether this is a pre-disposed vulnerability)

lower activation in other areas (hippocampus and prefrontal cortex) the volumes of these regions are reduced

therefore increased activation of amygdala (emotion) but decreased areas in determine the issue (and plan)
Theory → react with increased emotion but decreased ability to plan

MANIA
- basal ganglia more active?
» changes to neuronal membranes?
» Kinase C abnormally high?

60
Q

amygdala activity and sleep

A
  • when individuals didnt sleep they had an increase activity in amygdala
  • when individuals slept there was good connectivity between amygdala and prefrontal cortex
  • when they did not sleep - no connectivity between these regions
  • sleep plays important role in predisposing people to sleep disturbances

Sleep loss increases negative affect and decreases positive affect.
 Longitudinal studies suggest a link between insomnia and depression.
 Meta-analysis: Two fold increased depression risk if sleep disturbed at
baseline

61
Q

neuroendocrine system and depression

A
  • Hypothalamic-pituitary-adrenocortical axis overly active
    » Triggers release of cortisol (HPA axis)
  • Known link between depression& high cortisol levels
    » e.g. Cushing’s syndrome, animal studies

Dexamethasone suppression test
assesses regulation of HPA axis
» Cortisol not suppressed in MDD – esp psychotic
features but when it ends that are able to better regulate this axis
» Normalises when depressive episode ends
» Poor regulation of HPA axis?

Reduced hippocampal volumes
» Consequence of high cortisol levels?
» Precedes/contributes to onset of depression?

62
Q

social factors in mood disorders

A

Stressful life events

» Role well established
» 42-67% report serious life event prior to
depression
» Loss, humiliation, chronic stressors particularly
likely triggers

Lack of social support

» Sparse social networks, regarded as unsupportive
» Having a confidante reduces risk from 40% to 4%

Interpersonal problems
» Expressed emotion predicts relapse
» Poor IP problem solving predicts onset
» But depression, constant reassurance-seeking
can also create IP problems?
63
Q

SSRI

A
Selective serotonin re-uptake inhibitors
– ‘First choice’ in drug treatment
– Temporary ↑ serotonin
– Precise mechanism?
– ↑ thoughts of suicide
in first few weeks in adolescents?
– Side effects: physical agitation,
sexual dysfunction, insomnia,
gastrointestinal upset
64
Q

Mono-amine oxidase (MAO) inhibitors:

A

– Block the enzyme MAO
– MAO breaks down nor-epinephrine, dopamine & serotonin
– Increasing availability of neuotransmitters
– Potentially serious consequences:
– Consuming tyramine → hypertension
– Some everyday medications → dangerous interaction
– Typically used as last line of treatment
– More effective with ‘atypical’ features

65
Q

Tricyclic antidepressants:

A
  • one of the first ones established
    – Named after chemical structure
    – Mode unclear, initial block re-uptake of norepinephrine & serotonin
    – Complex effect on pre- & post-synaptic regulation
    – Side effects: blurred vision, dry mouth, drowsiness, weigh gain
    – Consequence: ~40% discontinue
    – Lethal if taken in excessive doses