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B32 - chapter 10.doc

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Department
Psychology
Course
PSYB32H3
Professor
Konstantine Zakzanis
Semester
Summer

Description
CHAPTER 10 – MOOD DISORDERS: GENERAL CHARACTERISTICS OF MOOD DISORDERS: mood disorders: involve disabling disturbances in emotion, from the sadness of depression to the elation and irritability of mania. DEPRESSION – SIGNS AND SYMPTOMS: depression: an emotional state marked by great sadness and feelings of worthlessness and guilt Depression in children often result ins in somatic complains. In older adults, depression is often characterized by distractibility and complaints of memory loss. Symptoms of depression exhibit some cross-cultural variation, probably resulting from differences in cultural standards of acceptable behaviour. Although it is commonly believed that people from non-western cultures emphasize somatic symptoms of depression, while people from western cultures emphasize emotional symptoms, studies suggest that people from various cultures tend to emphasize somatic symptoms rather than the emotional symptoms. psychologizers: people who emphasize the psychological aspects of depression. Most depression, although recurrent, tends to dissipate with time. About one third of depressed people suffer from chronic depression. MANIA – SIGNS AND SYMPTOMS: Mania: an emotional state or mood of intense but unfounded elation accompanied by irritability and impractical grandiose plans. The person in the throes of a manic episode, which last from several days to several months, is readily recognized by his loud and incessant stream of remarks, sometimes full of puns, jokes and rhyming... FORMAL DIAGNOSTIC LISTINGS OF MOOD DISORDERS: Diagnosis of Depression: The formal diagnosis of a major depressive disorder MDD) requires the presence of five of the following symptoms for at least two weeks.  sad, depressed mood, most of the day, nearly every day  loss of interest and pleasure in usual activities  difficulties in sleeping (insomnia), or a desire to sleep a great deal of time  shift in activity level, becoming either lethargic (psychomotor retardation) or agitated  poor appetite and weight loss, or increased appetite and weight gain  loss of energy, great fatigue  negative self-concept, self-reproach and self-blame, feelings of worthlessness, and guilt  complaints of evidence of difficulty in concentrating such as slowed thinking and indecisiveness  recurrent thoughts of death or suicide what is controversial s whether a patient with five symptoms and a two-week duration is distinctly different from one who has only three symptoms for 10 days. Even with fewer than five symptoms and duration of less than two weeks, co-twins were also likely to be diagnosed with depression and patients were likely to have recurrences. Five symptoms – increased weight, decreased weight, psychomotor retardation, indecisiveness and suicidal thoughts – were not independently associated with the diagnosis. These findings have implications for the possible revision of the diagnosis criteria for MDD. MDD is one of the most prevalent of the disorders. Lifetime prevalence rates range from 5.2% to 17.1%. MDD is abut two times more common in women than in men. The gender difference does not appear in preadolescent children, but it emerges at age 14 and seems to be maintained across the lifespan. Current and lifetime prevalence rates are higher among younger than older persons. Participants with MDD who had certain coexisting personality disorders had a significantly longer time to remission of symptoms than did MDD patients without any personality disorder. kindling hypothesis: the notion that nce a depression has already been experiences, it takes relatively less stress to induce a subsequent recurrence. What is not clear is whether the apparent reduced role of life events stress in subsequent depressions is because depression has become autonomous and no longer requires stress (the autonomy hypothesis) or whether the person has become sensitized to stress (the sensitivity hypothesis) and even small amounts of stress are sufficient to induce depression. Diagnosis of Bipolar Disorder: Bipolar I Disorder: involving episodes of mania or mixed episodes that include symptoms of both mania and depression. A formal diagnosis of a manic episode requires the presence of elevated or irritable mood plus three additional symptoms. Some clinicians do not regard euphoria as a core symptom of mania and report that irritable mood and even depressive features are more common. The following symptoms must be sufficiently severe to impair social and occupational functioning: • increase in activity level at work, socially or sexually • unusual talkativeness; rapid speech • flight of ideas or subjective impression that thoughts are racing • less than the usual amount of sleep needed • inflated self-esteem, belief that one has special talents, powers and abilities • distractibility, attention easily diverted • excessive involvement in pleasurable activities that are likely to have undesirable consequences, such as reckless spending. occurs less often than MDD, occurs equally often in men and women, like MDD, tends to recur HETEROGENEITY WITHIN THE CATEGORIES: Some bipolar patients experience the full range of symptoms f both mania and depression almost everyday, termed a mixed episode. Other patients have symptoms of only mania or only depression during a clinical episode. Bipolar II disorder: patients have episodes of major depression accompanied by hypomania, a change in behaviour and mood that is less extreme than full-blown mania. Some depressed people may be diagnosed as having psychotic features if they are subject to a delusions and hallucinations, a useful distinction among people with unipolar depression. Depression with psychotic features is more severe than depression without delusions and involves more social impairment and less time between episodes. Some patients with depression may have melancholic features where people find no pleasure in any activity and are unable to feel better. Patients with melancholic features had more co-morbidity i.e. with anxiety, more frequent episodes, and more impairment, suggesting it may be more severe type of depression. Both manic and depressive episodes may be characterized as having catatonic features, such as motor immobility or excessive, purposeless activity. Both may also occur within four weeks childbirth; in this case PTSD (Postpartum). Both bipolar and unipolar disorders can be sub-diagnosed as seasonal if there is a regular relationship between an episode and a particular time of the year. The most prevalent explanation is that it is linked to a decrease in the number of daylight hours; seasonal affective disorder (SAD). A Study found that one in five people in an Inuit community were depressed. Icelanders go without light for many months in the winter, yet as a group, they have surprisingly low levels of SAD, 1.2%. Might have lower rate because they have adapted genetically to reduce sunlight and are somehow protected against SAD. CHRONIC MOOD DISORDERS: Cyclothymic disorder: the person has frequent periods of depressed mood and hypomania, which may be mixed with, may alternate with, or may be separated by periods of normal mood lasting as long as two months. during depression, they feel inadequate; during hypomania, their self-esteem is inflated. They withdraw from people, then seek them out in an uninhibited fashion. They sleep too much and then too little. The person with dysthymic disorder is chronically depressed – more than half the time for at least two years. insomnia or sleeping too much; feelings of inadequacy; ineffectiveness, and lack of energy; pessimism; an inability to concentrate and to think clearly; and a desire to avoid the company of others. Women are 2-3 times more likely than men. Many people with it have episodes of major depression, as well, a condition known as double depression. PSYCHOLOGICAL THEORIES OF MOOD DISORDERS: PSYCHOANALYTIC THEORY OF DEPRESSION: Freud; during the oral period, a child’s needs may be insufficiently or oversufficiently gratified, causing the person to become fixated in this stage. With this arrest in psychosexual maturation, the person may develop a tendency to be excessively dependent on other people for the maintenance of self-esteem. Freud hypothesized that after the loss of a loved one, the mourner first interjects, or incorporates, the lost person’ he identifies with the lost one, perhaps in a fruitless attempt to undo the loss. Because we unconsciously harbour negative feelings toward those we love, the mourner then becomes the object of his own hate and anger. The period of introjections is followed by a period of mourning work, separates himself from the person who has died or has died or disappointed him and loosens the bonds imposed by introjections. But the mourning work can go astray and develop into an ongoing process of self- abuse, self-blame and depression in overly dependent individuals. COGNITIVE THEORIES OF DEPRESSION: Beck’s Theory of Depression: depressed individuals feel as they do because their thinking is biased toward negative interpretations. The negative schemata acquired by depressed persons are activated whenever they encounter new situations that resemble in some way, perhaps only remotely, the conditions in which the schemata were learned. An ineptness schema can make depressed individuals expect to tail most of the time, a self- blame schema burdens them with responsibility for all misfortunes and a negative self-evaluation schema constantly reminds them of their worthlessness. Negative schemata, together with cognitive biases or distortions, maintain what Beck called the negative triad: negative views of the self, the world, and the future. The following describes the principal cognitive biases: • arbitrary inference: a conclusion drawn in the absence of sufficient evidence or of any evidence at all. • Selective abstraction: a conclusion drawn on the basis of only one of man elements in a situation. • Overgeneralization: an overall sweeping conclusion drawn on the basis of a single, perhaps trivial, event. • Magnification and minimization: exaggerations in evaluating performance. IN Beck’s theory, our emotional reactions are a function of how we construe our world. The interpretations of depressed individuals do not mesh well with the way most people view the world, and they become victims of their own illogical self-judgements. Depressed people endorse more negative words and fewer positive as self-descriptive. Second, they have a cognitive bias; they gave greater recall of adjectives with depressive content, especially if the adjectives were rated as self-descriptive. depressed people take longer to colour-name words that varied in their content; neutral, depression-oriented words, suggesting that these themes were more cognitively accessible for them. A deployment of attention task to show that dysphoric and clinically depressed individuals do not seem to selectively attend to negative or positive material but that non-depressed individuals have a protective bias that involves diverting their attention away from negative stimuli and focusing instead on positive stimuli. Beck and others have found that depression and certain kinds of thinking are correlated, but a specific causal relationship cannot be determined from such data; depression could cause negative thoughts, or negative thoughts could cause depression. The data do not equivocally support the idea that negative thinking causes depression. Helplessness/Hopelessness Theories: Learned Helplessness: • An individual’s passivity and sense of being unable to act and control his or her own life is acquired through unpleasant experiences and traumas that the individual tried unsuccessfully to control • Seligman’s dogs acquired a sense of helplessness when confronted with uncontrollable aversive stimulation. Attribution and Learned Helplessness: • Depressive paradox: depressed people hold themselves responsible for their failures. But if they see themselves as helpless, how can they blame themselves? • Attribution: the explanation a person has for his behaviour. • The attributional revision of the helplessness theory postulates that they way in which a person cognitively explains failure will determine its subsequent effects: o Global attributions: “I never do anything right”; increase the generality of the effects of failure. o Attributions to stable factors: “I never test well” make them long term. o Attributions to internal characteristics: “I am stupid” are more likely to diminish self esteem, particularly if the personal fault is also global and persistent. • The individual prone to depression is thought to show a depressive attributional style - a tendency to attribute bad outcomes to personal, global and stable faults of character. Hopelessness Theory: • Some forms of depression (hopelessness depression) are now regarded as caused by a state of hopelessness, an expectation that desirable outcomes will not occur or that undesirable ones will occur and that the person has no responses available to change this situation. • Low self-esteem and a tendency to infer that negative life events will have severe negative consequences. • “weakest link” approach toward operationalizing vulnerability. The weakest link refers to the idea that a person is as vulnerable to depression as his or her most depressogenic inferential style (e.g the tendency to perceive negative events as having many disastrous consequences). • In adults diagnosed with a current or past major depressive episode at the outset, depressogenic weakest links predicted greater elevations in symptoms of depression following elevations in hassles. • An expectation of helplessness creates anxiety. When the expectation of helplessness becomes certain, a syndrome with elements of anxiety and depression emerges. • Finally, if the perceived probability of the future occurrence of negative events becomes certain, depressive predictive certainty, hopelessness depression develops. Issues in the Helplessness/Hopelessness Theories: • Circular statements such as hopelessness depression is cause by hopelessness. • Are the findings specific to depression? Depressive attributional style does not appear to be specific to depression but is related to anxiety and general distress as well. • Are attributions relevant? Do people actively attempt to explain their own behaviour to themselves, and do the attributions they make have subsequent effects on their behaviour? • One key assumptions of the helplessness/hopelessness theories is that the depressive attributional style is a persistent part of the makeup of depressed people. However, some research shows that the depressive attributional style disappears following a depressive episode. INTERPERSONAL THEORY OF DEPRESSION: Depressed individuals tend to have sparse social networks, also elicit negative reactions from others. Reduced social support may lessen an individual’s ability to handle negative life events, This tendency was especially evident among people high in autonomy. Depression and martial discord frequently co-occur. Constant seeking of reassurance is a critical variable in depression. Even when reassured, they are only temporarily satisfied. Their negative self-concept causes them to doubt the truth o the feedback they have received, and their constant efforts to be reassured come to irritate others. Social skills deficits may be a cause and consequence of depression. PSYCHOLOGICAL THEORIES OF BIPOLAR DISORDER: patients with bipolar depression have elevated levels of the dysfunctional attitudes described by Beck, as well as problems in autobiographical memory and the ability to generate solutions in problem-solving task. The manic phase of the disorder is seen as a defence against a debilitating psychological state. BIOLOGICAL THEORIES OF MOOD DISORDERS: THE GENETIC DATA: bipolar disorder is one of the mot heritable of disorders. Genes account for possibly 85% of variance in whether a person becomes manic. th Evidence favouring the hypothesis that bipolar disorder results from a dominant gene on the 11 chromosome. Within bipolar disorder, variation in the brain-derived neurotrophic factor (BDNF) gene appears to predict risk for developing rapid cycling. Some people seem to be genetically predisposed to the onset of MDD when confronted with a series of adverse life-events. Serotonin transporter gene-linked promoter region (5-HTTLPR), which is involved in modulating serotonin levels, is a significant predictor of first major depression onset following multiple adverse events. NEUROCHEMISTRY, NEUROIMAGING AND MOOD DISORDERS: The original theory posited that low levels of norepinephrine and dopamine lead to depression and high levels to mania. The serotonin theory suggests that serotonin, a neurotransmitter presumed to play a role in the regulation of norepinephrine, also produces depression and mania. However, the weight of the evidence does not completely support the notion that levels of neurotransmitters are critical in the mood disorders. Tricylclic drugs: i.e. imipramine, or Tofranil are group of antidepressant medications so named because their molecular structure is characterized by three fused rings. They prevent some of the reuptake of norepinephrine, serotonin and or dopamine by the presynaptic neuron after it has fired, leaving more of the neurotransmitter in the synapse so that transmission of the next nerve impulse is made easier. Monoamine oxidase (MAO) inhibitors: I.e. Tranylcypromine or Parnate are antidepressant drugs that keep the enzyme MAO from deactivating neurotransmitters, thus increasing the levels of serotonin, norepinephrine and or dopamine in the synapse. This action produces the same facilitating effect decried for tricylics, compensating for the abnormally low levels of these neurotransmitters in depressed people. Newer antidepressants, called selective serotonin reuptake inhibitors, i.e fluoxetine or Prozac, act more selectivel, specifically inhibiting the reuptake of serotonin. It now appears that the explanation of why these drugs work is not as straightforward as it seemed at first. Both tricyclics and MAO inhibitors take from seven to 14 days to relieve depression, but by that time, the neurotransmitter level has already returned to its previous state. Another approach to further evaluate the theories involved measuring metabolites of these NT, the by-products of the breakdown of serotonin, norepinephrine, and or dopamine found in urine, blood serum, and the cerebrospinal fluid. The problem with such measurements
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