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Mood Disorders Mood Disorders. Aims  By the end of the session you will be able to do the following:  Recognize symptoms that contribute to the diagnosis.

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Presentation on theme: "Mood Disorders Mood Disorders. Aims  By the end of the session you will be able to do the following:  Recognize symptoms that contribute to the diagnosis."— Presentation transcript:

1 Mood Disorders Mood Disorders

2 Aims  By the end of the session you will be able to do the following:  Recognize symptoms that contribute to the diagnosis of unipolar and bipolar depression.  Compare and contrast contemporary perspectives in their explanations of unipolar and bipolar depression.  Describe and compare different treatment approaches used to treat unipolar and bipolar depression.  Critically be aware of the shortcomings of assessment, diagnosis and treatment and their implications socially, ethically and legally.

3 Depression types Depression Types Unipolar Depression Bipolar Depression

4 Unipolar Depression

5 Major depressive episode 1. Presence of at least five of the following symptoms during the same two week period:  depression mood for most of the day, nearly everyday,  markedly diminished interest or pleasure in almost all activities, most of the day, nearly every day,  insomnia or hypersomina nearly everyday, psychomotor agitation or retardation nearly everyday,  fatigue or loss of energy nearly everyday,  feelings of worthlessness or excessive guilt nearly everyday, reduced ability to think or concentrate, or indecisiveness, nearly everyday,  recurrent thoughts of death or suicide, a suicide attempt, or a specific plan for committing suicide.  Significant distress or impairment. Major Depressive Disorder 1. The presence of a major depressive episode 2. No history of a manic or hypomanic episode. DSM-IV-TR

6 Epidemiology  7% adults suffer from severe unipolar depression, 5% mild form, in any given year (Kessler et al, 2005).  17% will experience an episode of severe unipolar depression at some point in their life (Kessler et al 2005).  Women are twice as likely to experience severe episodes (26% women compared to 12% of men experience have an episode as some point in their life) (Weissman et al, 1991).  Half people with unipolar depression recover within six weeks and 90% recover within a year, some without treatment (Kessler, 2002).  Most of them will have at least one other episode of depression later in their lives (Boland & Keller, 2002).

7 Symptoms EmotionalMotivationalBehaviouralCognitivePhysical Sad. Lack of drive, spontaneity, initiative. Less active, productive. Negative view of themselves. Headache, indigestion, dizzy spells, pain. Anger, anxiety, agitation. Force to go to work, talk to friends. Move slowly Inadequate, undesirable, inferior, evil Depression misdiagnosed as other medical problems. Miserable, empty, humiliated. Uninterested in life Speak slowly Expect the worst, hopelessness, helplessness. Disturbances in sleep, appetite, Little pressure out of anything. Wish to kill themselves Confused, distracted, not solve simple problems.

8 1. Biological Model Evidence from genetic and biochemical studies suggests that Unipolar depression has biological causes.

9 1a. Genetic Factors  Family pedigree studies: Person with unipolar depression will have 20% of relatives with depression, compared with 10% relatives (non-depressed).  Twin Studies:  (Study 200 twins) identical twins 46% higher, fraternal twins 20% (McGuffin et al 1996).  Molecular Biology: Abnormality of 5-HTT gene (which transports serotonin in the brain). (Hecimovic & Gilliam, 2006).

10 1b. Biochemical Factors  Low activity of norepinephrine and serotonin (neurotransmitters).  Medication for high blood pressure (lowered activity of the 2 neurotransmitters). (Ayd, 1956).  Antidepressant drugs found by accident (increase activity).  More complicated, not as simple as one NT alone causes depression (Thase et al 2002).  Adrenal glands. Abnormal levels of cortisol (stress hormone) (Neumesiter et al 2005).  Melatonin “Dracula hormone” released in the dark (SAD produced more melatonin during winter) Neto & Aranjo, 2004).  Within neurons. Chemicals that carry messages which lead to deficiencies of proteins & other chemicals which impair the health of neurons (Julien, 2005).

11 1c.Biological Treatments ECT  Electroconvulsive therapy discovered by Ugo Cerletti  Electric current 65 to 140 volts sent through the brain causing a brain seizure that lasts from 25 seconds to a few minutes.  6 to 12 treatments, spaced over 2 to 4 week patients feel less depressed (Andreasen & Black, 2006).  Memory regained after a few months but some will have permanent amnesia (Fink, 2001).  Declined since the 1950’s because of effective anti- depressant drugs.

12 1c. Biological Treatments Anti- depressant drugs Sub-types MAO INHIBITORS Slow down Monoamine Oxidase MAO break down norepinephrine TRICYCLICS Three-ring molecule structure 60-65% helped significantly (Khun, 1958) Block reuptake process, increasing neurotransmitter activity. SECOND -GENERATION ANTI- DEPRESSANTS Selective serotonin reuptake Increase serotonin uptake specifically. * Most in demand

13 2. Psychological Models of Unipolar depression  Psychodynamic  Behavioural  Cognitive***********

14 2a. Psychodynamic Explanations  Freud (1917) & Abraham (1916, 1911)  Emphasis on dependence and loss.  Grief and depression commonalities  Sadness, anger for the loved ones towards themselves.  In the face of loss the following groups are more likely to become clinically depressed:  Parents who failed to meet their needs during the oral stage  Parents gratified needs excessively  Devote their life to others, greater sense of loss.  Become depressed without loss  Symbolic or imagined loss- equate other events to the loss of a loved one  Object relations theorist: peoples relationships leave them feeling unsafe and insecure (Allen et al., 2004)  Support early life experiences and depression  Depressed scale administered to 1,250 medical patients, patients whose fathers died during their childhood scored higher on depression (Barnes & Prosen, 1985)  Parental bonding instrument: chid rearing style as affectionless control- low care and high protection (Shah & Waller, 2000)

15 Psychodynamic Treatments  Associate freely during therapy- suggest interpretations of the individual's associations, dreams and displays of resistance and transference, help review past events and feelings (Busch et al., 2004)  “early recall of loss may have spiralled into current depression”  Long term- only occasionally helpful.

16 2b. Behavioural Explanations  Depression results from significant changes in the numbers of rewards and punishments people receive in their lives.  Lewinsohn: positive rewards dwindle, leading to fewer constructive behaviors.  Depressed individuals experience fewer social rewards than nondepressed- environment and dark and flat mood promote this reduction (Joiner, 2002).  Treatments  Variety of strategies to increase positive behaviors (Lewinsohn et al., 1990).  Tasks pleasurable: set up weekly diary to incorporate these.  Ignore client’s depressive behaviors whilst rewarding constructive statements and behavior (i.e., going to work)  Teach effective social skills (Segrin, 2000)  Combination need to be applied for effectiveness: track record of pleasurable compared to diary of pleasant activities: effectiveness the same (Jacobson et al., 1996).

17 2c. Cognitive Explanations Two explanations Learned Helplessnes s Negative Thinking

18 Learned Helplessness  Feelings of helplessness are at the centre of depression Seligman (1975).  Learned Helplessness Theory of Depression Seligman 1960’s.  (1). No longer have control over the reinforcements in their life  (2). They themselves are responsible for this helpless state.

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20  Humans exposed to uncontrollable negative events, they later score higher than other subjects on a depressive mood survey (Miller & Seligman, 1975).  Attribution-helplessness theory (Mezulis et al 2004; Abramson et al 2002).  Attribute lack of control to internal, global and stable causes “I am useless and everything and I always will be”- more likely to have depression.  Depressed people filled out the Attribution Style Questionnaire both before and after therapy.  Before therapy: internal/global/stable pattern of attribution.  End of therapy (& 1 year later): depression improved and attribution style less likely to be internal, global and stable (Seligman et al 1988).  Analysis  Relies on animal studies (Henn & Vollmayr, 2005)  Can animals make attributions, even implicitly?

21 Negative Thinking  Beck (2002, 1967)  Maladaptive attitudes, cognitive triad, errors in thinking, automatic thoughts combine to produce a clinical disorder.  Children- “my general worth is tied to the tasks I perform” maladaptive  Attitudes: own experiences, family relationships, judgements from other people, inaccurate  Cognitive Triad: repeatedly interpret  1. their experience  2. themselves  3. their future in negative ways

22  Errors in thinking:  Arbitrary inferences: negative conclusions based on limited evidence.  Minimize positive experiences and magnify negative experiences.  Automatic thoughts  They are inadequate and situation is hopeless.  “Everyone hates me” “I'm worthless”  Support  Depressed people hold maladaptive attitudes, the more held the more depressed they are (Evans et al., 2005).  Cognitive triad- depressed recall more negative events than positive ones, select pessimistic statements, rate their behaviour in labs as poor (Ridout et al., 2003).  Errors in logic: female subjects asked to read and interpret paragraphs about women in difficult situations. Depressed subjects made more errors in logic (arbitrary inferences), in their interpretation than non-depressed women (Hammen & Krantz, 1976).

23 Treatment: Cognitive Therapy  Designed to recognise and change their maladaptive behaviours.  Beck (1985, 1967) similar to Ellis’s Rational Emotive Therapy  Phase 1: Increase activities and elevate mood  Phase 2: Challenging automatic thoughts  Phase 3: Identifying negative thinking and biases  Phase 4: Changing primary attitudes  50-60% show a near total elimination of symptoms (Petrocelli, 2002).

24 Stress Link Link between stress and depression (Costantino et al 2006) Depressed people are more likely to have experienced stressful events one month before the onset of their disorder (Monoe & Hadjiyannakis, 2002).

25 Sociocultural Model  Everyone at risk (WHO, 2004); vary culture to culture (Draguns, 2006).  Gender: higher in women- special pressures and complex roles.  Rise with poverty, minorities, family size and number of health problems (Comer, 2007)  Social Support: influences depression (Kendler et al., 2005)  Separated or divorced x3 more depression (Weissman et al., 1991).  Live in isolation without intimacy seem to become more depressed during times of stress (Kendler et al., 2005)  Treatments  Interpersonal Psychotherapy and couple therapy  Klerman & Weissman IPT  4 interpersonal problem areas: interpersonal loss (explore grief and relationship with the lost person & explore feelings of anger-develop new ways of remembering the lost person), interpersonal role dispute (ways of resolving them), interpersonal role transition (develop social support and skills the new role requires) interpersonal deficits (extreme shyness, social awkwardness- teach them social skills and assertiveness) (Weissman & Markowitz, 2002).  Success rate similar to that of Cognitive Therapy.  Couple Therapy: depressed person in a dysfunctional relationship, recovery slower for those in a non-supportive relationship. If there is conflict this approach is beneficial and effective as the above therapies (Snyder & Castellani, 2006).

26 Bipolar Depression

27 DSM-IV-TR Manic Episode  A period of abnormally and persistently elevated, expansive or irritable mood, lasting at least one week.  Persistence of at least three of the following:  Inflated self-esteem or grandiosity, decreased need for sleep, more talkativeness than usual or pressure to keep talking, flight of ideas or the experience of thoughts are racing, distractibility, increase in activity or psychomotor agitation, excessive involvement in pleasurable activities that have a high potential for painful consequences.  Significant distress or impairment Bipolar i Disorder (full manic and depressive episodes)  The presence of a manic, hypomanic or major depressive episode  If currently in a hypomanic or major depressive episode, history of a manic episode. Bipolar ii Disorder (mildly manic- over a course of time)  The presence of a hypomanic or major depressive episode  If currently in a major depressive episode, history of a hypomanic episode. If currently in a hypomanic episode, history of a major depressive episode. No history of a manic episode.  Significant distress or impairment.  (APA,2000)

28 Causes: Biological  Neurotransmitters:  Norepinephrine activity higher with mania than of depressed control subjects (Post et al., 1980)  Resprine drug (reduce norepinephrine), mania subsided (Telner et al., 1986)  Ion activity: improper transport of these ions may cause neurons to fire too easily, resulting in depression (El-Mallakh, 2004)- abnormal functioning in the proteins that transport ions across a neurons membrane (Monkul et al.,2005)  Brain structure:  Brain imaging studies: abnormal brain structures (Lambert & Kinsley, 2005)  Basal ganglia and cerebellum is smaller- not clear of the role these play in bipolar depression yet (Monkul et al., 2005)

29  Genetic Factors  Inherit a biological predisposition to develop bipolar disorders.  Identical twins of person with bipolar depression have 40% likelihood of developing BD, fraternal twins, siblings have 5-10% compared to 1-2% general population (Swann, 2008).  Molecular biology:  Genes on chromosomes 1,4,6,10,11,12,13,15,18,21,22 (Hayden et al., 2008)  Genetic abnormalities combine to create BD (Payne et al., 2005)

30 Treatments  Psychotherapist- no success  Anti-depressant drugs- limited effectiveness  Lithium Therapy (Cade, 1949)  Doses: too little- no effect; too much: intoxication-slurred speech, dizziness, kidney failure, death.  Effective in treating manic episodes (Grof, 2005)  60% patients improve and experience fewer new episodes as long as they carry on taking lithium (Carney & Goodwin, 2005)  Relapse risk 28x greater when stop taking antibipolar drugs (Suppes et al., 1991).  Helps overcome depressive episodes to a lesser degree than manic episodes (El-Mallakh, 2006)  Changes synaptic activity  Adjunctive Psychotherapy  Lithium therapy alone is not effective, 30% may not respond to this therapy or relapse (Julien, 2005)  Use individual, group, family therapy as an adjunct to lithium treatment (Colom & Vieta, 2006) helps to hold a job and social functioning.

31 On a lighter note: creativity and abnormality: The price of creativity  Useful in the arts (Ludwig, 1995)  Ancient Greeks: divine madness-inspired creative arts  Today- expectation that creative geniuses to be psychologically disturbed.  Artists and writers more likely to suffer from mood disorders (Lauronen et al., 2004)  Sources of inspiration?  Work results in becoming disturbed?  Predisposition, early life experiences?  Majority are stable and medication for those who need it enhances their creativity.

32 Frezied Masterpiece: Messiah (wrote it in less than a month during a manic episode)

33 Today: preventative measures in a hectic and pressurised world Laughter being the best medicine

34 Symptoms of Mania  Dramatic and inappropriate rises in mood.  Active and powerful emotions in search of an outlet.  Irritable and angry- others get in the way.  Want constant excitement, involvement & companionship  Do not know that they are overwhelming, domineering & excessive.  Talk and walk fast- there is not enough time  Flamboyant- clothes, money  Poor judgement, cannot see pitfalls because of being too quick, do not listen to others.  Inflated opinion of themselves  Self-esteem- approaches grandiosity.  Difficulty to be in touch with reality  Energetic- little sleep, feel and act wide awake (Gupta et al., 2004)

35 Seminar Reading   Is Electroconvulsive Therapy Ethical?   YES: Max Fink from Electroshock: Restoring the Mind (Oxford University Press, 1999)   No: Leonard R. Frank from “Shock Treatment IV: Resistance in the 1990’s,” in Robert F. Morgan, ed., Electroshock: The Case Against (Morgan Foundation, 1999).

36 Reading   Nevid, J.S., Rathus, S.A., & Greene, B. (2008). Abnormal Psychology In A Changing World. (7 th ed.). Pearson Prentice Hall: London. Chapter 8, pp   Oxman, T., Hegel, M., Hull, J., & Dietrich, A. (2008, December). Problem-solving treatment and coping styles in primary care for minor depression. Journal of Consulting and Clinical Psychology, 76(6), Retrieved January 23, 2009, doi: /a

37   Cohen, L., Gunthert, K., Butler, A., Parrish, B., Wenze, S., & Beck, J. (2008, December). Negative affective spill over from daily events predicts early response to cognitive therapy for depression. Journal of Consulting and Clinical Psychology, 76(6), Retrieved January 23, 2009, doi: /a   Constantino, M., Manber, R., DeGeorge, J., McBride, C., Ravitz, P., Zuroff, D., et al. (2008, December). Interpersonal styles of chronically depressed outpatients: Profiles and therapeutic change. Psychotherapy: Theory, Research, Practice, Training, 45(4), Retrieved January 23, 2009, doi: /a

38   Tackett, J., Quilty, L., Sellbom, M., Rector, N., & Bagby, R. (2008, November). Additional evidence for a quantitative hierarchical model of mood and anxiety disorders for DSM-V: The context of personality structure. Journal of Abnormal Psychology, 117(4), Retrieved January 23, 2009, doi: /a   Lau, J., & Eley, T. (2008, November). Attribution style as a risk marker of genetic effects for adolescent depressive symptoms. Journal of Abnormal Psychology, 117(4), Retrieved January 23, 2009, doi: /a

39   Gross, H., Shaw, D., Moilanen, K., Dishion, T., & Wilson, M. (2008, October). Reciprocal models of child behaviour and depressive symptoms in mothers and fathers in a sample of children at risk for early conduct problems. Journal of Family Psychology, 22(5), Retrieved January 23, 2009, doi: /a

40 One Hour Video   Chapter Eight Mood Disorders Depression is one of the most common psychological problems. In this program, psychologists and biologists look at the causes and treatment of both depression and bipolar disorder and show the progress that has been made in helping people return to productive and satisfying lives.  

41 End


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