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Chapter 9

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Department
Psychology
Course
PSY100H1
Professor
M.Fournier
Semester
Fall

Description
Chapter 9 Overview • Bipolar disorder: manic-depression; one of the two major types of mood disorders • Mania: great energy and enthusiasm for everything; ideas, talking and thinking at a great speed • Depression: energy and enthusiasm gone and slow to think, talk and move; joy drained from life • Unipolar depression: one of the major types of mood disorders; experience only depression, no mania; suicide a serious problem Symptoms of depression • Emotional symptoms: sadness, deep unrelenting pain; no emotional reactions; lose interest in everything in life (anhedonia) • Physiological symptoms: bodily functions disrupted; changes in appetite, sleep and activity levels can take many forms; early morning wakening common, where people awake at 3-4 AM and can’t go back to sleep • Behavioural symptoms: lack energy and feel chronically fatigues; walking, gestures, reactions and speech slowed down (psychomotor retardation); subset have psychomotor agitation and can’t sit sill and fidget aimlessly • Cognitive symptoms: thoughts filled with worthlessness, guilt, hopelessness and even suicide; trouble concentrating and making decisions; can experience delusions and hallucinations in some severe cases (depressing and negative in content) Diagnosis • Major depression: one DSM category of unipolar; diagnosis requires that a person experience either depressed mood or loss of interest in usual activities, plus at least four other symptoms chronically for at least two weeks; need to be severe enough to interfere with daily functioning • Dysthymic disorder: less severe form of unipolar depression but more chronic; must be experiencing depressed mood plus two other symptoms for at least two years; must never have been without symptoms for more than a two month period • Double depression: experience both major depression and dysthymic disorder; chronically dysthymic and occasionally sink into episodes of major depression; even more debilitated; less likely to respond to treatments • Co-morbidity: over ½ of people with unipolar diagnosis have another psychological disorder, commonly substance abuse, anxiety disorders and eating disorders; can prefigure or be consequence of another disorder • Subtypes: apply both to major depression and depressive stage of bipolar o With melancholic features: physiological symptoms particularly prominent o With psychotic features: experience delusions/hallucinations during major depressive episode o With catatonic features: strange behaviours collectively known as catatonia, ranging from complete lack of movement to excited agitation o With atypical features: odd assortment of symptoms like positive mood reactions to some events, significant weight gain or increase in appetite, hypersomnia, heavy or laden feelings in limbs, long-standing pattern of sensitivity to interpersonal rejection o With postpartum onset: onset of major depressive episode occurs within four weeks of delivery of a child; can occasionally develop mania postpartum and receive diagnosis of bipolar disorder with postpartum onset; 30% of women experience postpartum blues (emotional lability, frequent crying, irritability and fatigue) in the first few weeks after giving birth; will pass within two weeks of birth for most; 1 in 10 will experience postpartum seriously enough to warrant depressive diagnosis o With seasonal pattern: also called seasonal affective disorder; history of at least two years of experiencing major depressive episodes and fully recovering from them; seem to be tied to number of daylight hours; can develop mild forms of mania or have full manic episodes during summer months and are diagnosed with bipolar disorder with seasonal pattern; mood change can’t be result of psychosocial events; lifetime prevalence of 2.9% but 11% in people with depression history; important role of genetic adaptation to high latitudes Prevalence and course • Prevalence: number one source of disability in Canadian workforce; between 8- 12% lifetime prevalence in Canada; less than in US; 15-24 year olds most likely to have had major depressive episodes recently; lower rates in older people but go up in those 85+ (severe, chronic and debilitating) • Depression and the elderly: lower rates perhaps due to lower willingness to report symptoms, common occurrence in context of medical illness and likelihood of pre-existent mild cognitive impairment OR depressives likelier to die before reaching old age or can develop more adaptive coping skills and psychologically healthier outlook as they age • Gender differences: women twice as likely as men to experience both mild depressive symptoms and severe depressive disorders; found in many countries, ethnicities and age groups; differences shrink with advancing age with increasingly higher rates for men who never married • Course: long-lasting and recurrent for some; depressives spend an average of 16 weeks with significant symptoms; high risk for relapse; history of multiple episodes means higher chance of staying depressed for longer periods • Cost: productivity losses as a result of short-term disability due to depression and associated distress was $2.6 billion in 1998; once people undergo treatment for their depression, then tend to recover much more quickly and their risk for relapse is reduced; many depressives never seek care or wait too long; lingering scars and enduring problems Depression in childhood and adolescence • Prevalence: less common among children than in adults; 2.5% of children and 8.3% of adolescents can be diagnosed with MD; between 15-20% of youth will experience an episode of major depression before 20; depressive symptoms that don’t quite meet the diagnostic criteria for MD common in adolescents; highest rates in girls (25%) and American Indians (29%) • Scars of childhood depression: most likely to incur scars in childhood; long- lasting effects if self-concept is developing; interfere with learning and social relationships (kids more dependent on others); early formed negative self-view can establish long standing vulnerability for developing depression; can also increase negative thinking because it brings more negative events as stress- generation models suggest that symptoms interfere with functioning in all domains and so can increase stressors • Effects of puberty: girls’ rates of depression escalate dramatically over the course of puberty but boys’ rates do not; observable physical changes of adolescence have more do with emotional development than hormones as these affect self-esteem; body dissatisfaction closely related to low self- esteem/depression in girls; increase in depression may occur only among European-American girls Bipolar mood disorders • Symptoms of mania: elated mood often mixed with irritation and agitation; grandiose self-esteem, thoughts and impulses that can be delusional and accompanied by grandiose hallucinations; speak rapidly and forcefully; impulsive behaviours; grand plans and goals; decreased need for sleep; distractibility • Diagnosis of mania: must show an elevated, expansive or irritable mod for at least one week, plus at least three other symptoms; must impair ability to function • Bipolar I disorder: experience manic episodes meeting full criteria who eventually fall into depressive episodes; can be as severe as major depressive episodes or relatively mild and infrequent • Bipolar II disorder: experience severe episodes of depression that meet the criteria for major depression but their episodes of mania are milder and known as hypomania, which has the same symptoms of mania but is not severe enough to interfere with daily functioning and does not involve hallucinations/delusions • Cylothymic disorder: less severe but more chronic form of bipolar; alternates between episodes of hypomania and moderate depression chronically over at least a two year periods; can function reasonable well during hypomania but depression interferes with functioning • Cycles: about 90% of bipolars have multiple episodes/cycles during their lifetime; length varies (weeks or months or days); common pattern for episodes to become more frequent and closer together over time • Rapid cycling bipolar disorder: four or more cycles of mania and depression within a year • Prevalence: less common than unipolar depression; 1.7 per 100 lifetime prevalence; equal likelihood for genders and ethnic groups; developed in late adolescence or early adulthood; 50% of sufferers will experience first episode by early adulthood • Course: chronic problems in jobs and relationships; in one study, only 25% of those hospitalized recovered fully and led normal lives; best predictors of recovery compliance with medication and higher social class; symptom presence associated with deficits in social and occupational functioning and increase risk for relapse; common substance abuse impairs control and functioning • Youth: controversial whether it can be diagnosed reliably in children and young adolescents; clinicians have noted cases of juvenile onset of bipolar that tend to be atypical at initial presentation in early childhood, with common symptoms of hyperactivity but not ADHD and with the passage of time, classical cyclical episodes and mood/behavioural changes begin to emerge • Creativity and bipolar: symptoms of mania can possibly benefit highly talented/intelligence; depression seen as inspirational for artists; Lincoln, Bonaparte, Churchill, etc accomplished extraordinary feats during periods of mania and hypomania (daring strategies, energy and self-esteem); writers, artists and composers have higher than normal prevalence; more mood disorders, psychosis and suicide attempts; does mania enhance pre-existent creativity or is there a deeper link? • Hypothesis: genetic abnormalities that cause bipolar are in close proximity to the genetic abnormalities that cause great creativity; close relatives should therefore be more creative as well; creativity that is associated with a predisposition toward bipolar more easily expressed in people who do not suffer from full episodes of mania and depression but may suffer from milder mood swings Biological theories of mood disorders • Family history studies: first degree relatives have 2-3x higher rates of bipolar and unipolar depression; fewer than 10% and often less than 5% develop disorder themselves (risk higher but only a minority develop); relatives of people with depression do not tend to have any greater risk for bipolar than relatives with no mood disorder; bipolar has a different genetic basis from unipolar • Twin studies: concordance rate for bipolar about 60% in monozygotic twins and 13% in dizygotic twins; physiologically based symptoms have the highest genetic component whereas negative mood/tearfulness least genetically based and were likely reactions to negative life experiences; genetic basis of bipolar symptoms between 85-89% and 71% of genetic variance for mania not being shared with depression; genetics might play heavier role for women than men • Specific genetic abnormalities: vulnerability to depression may be on the serotonin transporter gene (dysfunction in regulation of serotonin affects stability of mood); likely no single location on the gene; genetic predisposition multifactorial and needs a particular configuration of disordered genes • Neurotransmitter dysregulation: facilitate transmission of impulses across synapses; monoamines (serotonin, norepinephrine and to a lesser extent dopamine) implicated; largely concentrated in limbic system o Monoamine theories: early theory that depression was caused by a reduction in amount of norepinephrine or serotonin in synapses occurring from decreased synthesis from precursors, increased degradation by enzymes or impaired release or reuptake; mania thought to be caused by excess of monoamines or dysregulation of the levels o Recent studies: focus on number/functioning of receptors for monoamines on neurons; too few or insensitive receptors for norepinephrine and serotonin in major depression; in bipolar, its likely that receptors undergo poorly timed changes in sensitivity correlated to mood changes; abnormalities are state-dependent, or present when disorder is present but disappear when it subsides; no differences in serotonin binding potential between healthy control and depressives (Meyer) • Brain abnormalities: consistent abnormalities in four areas using CT, PET, MRI; can be caused by environmental conditions; increases vulnerability to future episodes o Prefrontal cortex: reductions in metabolic activity and in the volume of gray matter on left side found in people with serious depression or bipolar; left cortex more involved in approach-related goals; successful treatment of depression with antidepressants associated with increases in metabolic activity in left cortex o Anterior cingulate: body’s response to stress, emotional expression, social behaviour, processing of difficult information; decreased activity relative to controls associated with attention, planning, coping and anhedonia; activity increases with successful treatment o Hippocampus: critical in memory and fear related learning; smaller volume in major depressives or bipolars; lower metabolic activity in major depression; chronic arousal of body’s stress response (depressives show chronically high levels of cortisol) could damage hippocampus and inhibit development of new neurons o Amygdala: directs attention to emotionally salient and significant stimuli; enlargement and increased activity here; decreases to normal with successful treatment; may bias people towards aversive or emotionally arousing information and lead to rumination on negative memories • Neuroendocrine factors: regulates important hormones and help body respond to stressors; chronic hyperactivity in HPA and inability to return to normal functioning following a stressor; excess hormones produced by heightened HPA activity have an inhibiting effect for the monoamines; one model that chronic stress can lead to poorly regulated endocrine systems, causing overreactions and changes in functioning of monoamines • Women’s hormonal cycles: women more prone to depression during PMS, postpartum and menopause; research shown that only 3% of women experience increases in depressive symptoms (most of these women have history/vulnerability of depression and anxiety); study shows there is little to distinguish postpartum depression from non-postpartum depression; estrogen and progesterone do not have consistent direct effects on mood • Premenstrual dysphoric disorder: separate diagnosis for depressions during premenstrual period; argument over whether it should be separate or just considered an exacerbation of depression/dysthymia • Early stress as cause of neurobiological vulnerability: early traumatic stress/serious chronic stress can lead to some of the neurobiological abnormalities that predispose depression; biological responses to stress (ex: response of HPA) exaggerated or blunted; reduces with supportive care and/or pharmacological intervention Psychological theories of mood disorders • Diathesis-stress model: biological vulnerabilities triggered by stressors; psychological theories have focused on depression bec
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