bipolar and depressive disorders Flashcards
bipolar and depressive disorders
Diagnosis of the bipolar and depressive disorders involves considering a client’s current status and history in terms of three mood episodes: A manic episode is characterized by an abnormally and persistently elevated, expansive, or irritable mood and increased activity or energy for at least one week. It includes three or more characteristic symptoms (e.g., inflated self-esteem or grandiosity, decreased need for sleep, flight of ideas) and marked impairment in functioning, a need for hospitalization to avoid harm to self or others, and/or the presence of psychotic features. A hypomanic episode is characterized by an abnormally and persistently elevated, expansive, or irritable mood; increased activity or energy; and three or more symptoms of mania for at least four consecutive days. Symptoms are not severe enough to cause marked impairment in functioning or a need for hospitalization and do not include psychotic features. A major depressive episode is characterized by five or more characteristic symptoms with at least one symptom being depressed mood or loss of interest or pleasure in most or all activities. Symptoms last for at least two weeks and cause significant distress and/or impaired functioning.
Bipolar Disorders:
The bipolar disorders include bipolar I disorder, bipolar II disorder, and cyclothymic disorder. The diagnosis of bipolar I disorder requires at least one manic episode that may or may not have been preceded or followed by one or more major depressive or hypomanic episodes. The diagnosis of bipolar II disorder requires at least one hypomanic episode and at least one major depressive episode. The diagnosis of cyclothymic disorder requires numerous periods of hypomanic symptoms that do not meet the criteria for a hypomanic episode and numerous periods of depressive symptoms that do not meet the criteria for a major depressive episode. The minimum duration of symptoms for cyclothymic disorder is two years for adults or one year for children and adolescents.
- Etiology of Bipolar Disorder:
Bipolar disorder has been linked to heredity, neurotransmitter and brain abnormalities, and circadian rhythm irregularities: In terms of heredity, twin, family, and adoption studies have confirmed that bipolar disorder has a strong genetic component. For example, twin studies report concordance rates of .67 to 1.0 for monozygotic twins and about .20 for dizygotic twins (Dubovsky, Davies, & Dubovsky, 2003). Neurotransmitters that have been linked to bipolar disorder include norepinephrine, serotonin, dopamine, and glutamate (Ayano, 2016), and structural and functional abnormalities have been found in several areas of the brain including the prefrontal cortex, amygdala, hippocampus, and basal ganglia (Miklowitz & Johnson, 2014). Circadian rhythm irregularities linked to bipolar disorder include abnormalities in the sleep-wake cycle, the secretion of hormones, appetite, and core body temperature (Nusslock & Frank, 2012).
- Treatment of Bipolar Disorder:
Treatment often includes a combination of psychosocial interventions and pharmacotherapy. Evidence-based psychosocial interventions include family focused therapy, psychoeducation, interpersonal and social rhythm therapy, and cognitive-behavior therapy. With regard to pharmacotherapy, lithium is usually most effective for “classic bipolar disorder” which is characterized by separation of manic/hypomanic and depressive episodes by long periods of recovery, a low likelihood of mixed mood states and rapid cycling, and an onset between 15 and 19 years of age. In contrast, anticonvulsant and second generation antipsychotic drugs are most effective for “atypical bipolar disorder,” which is characterized by mixed mood states, rapid cycling, a lack of full recovery between episodes, and an onset between 10 and 15 years of age (Aiken, 2018). (Note that this distinction between classic and bipolar disorder is not a DSM-5 categorization and that DSM-5 provides the specifier “with atypical features” for bipolar disorders that involve mood reactivity and at least two of the following: significant weight gain or increase in appetite, hypersomnia, leaden paralysis, interpersonal rejection sensitivity.)
Depressive Disorders
The depressive disorders include major depressive disorder, persistent depressive disorder, and disruptive mood dysregulation disorder. The diagnosis of major depressive disorder requires five or more symptoms of a major depressive episode for at least two weeks with at least one symptom being depressed mood or loss of interest or pleasure in most or all activities. The diagnosis of persistent depressive disorder requires a depressed mood with two or more characteristic symptoms (e.g., poor appetite or overeating, insomnia or hypersomnia, feelings of hopelessness) for at least two years in adults or one year in children and adolescents. The diagnosis of disruptive mood dysregulation disorder requires the presence for at least 12 months of (a) severe and recurrent temper outbursts that are verbal and/or behavioral, are grossly out of proportion to the situation or provocation, and occur three or more times each week; and (b) a persistently irritable or angry mood that is observable to others most of the day and nearly every day between outbursts.
Specifiers provided in DSM-5 for major depressive disorder include with peripartum onset and with seasonal pattern: The specifier with peripartum onset applies when the onset of symptoms is during pregnancy or within four weeks after delivery. Up to 80% of women experience “baby blues” after the birth of their children and, according to DSM-5, about 3 to 6% have symptoms that are sufficiently severe to meet the criteria for a major depressive episode during pregnancy or the weeks or months following delivery. [Note that other sources report higher rates of major depressive disorder with peripartum onset, usually within the 10 to 20% range (e.g., English et al., 2018).] The specifier with seasonal pattern applies when there’s a temporal relationship between mood episodes and time of year, which is usually winter. This disorder is also known as seasonal affective disorder (SAD), and its symptoms include hypersomnia, overeating, weight gain, and a craving for carbohydrates. It’s been linked to a lower-than-normal level of serotonin and a higher-than-normal level of melatonin, which is a hormone that plays an essential role in the sleep-wake cycle. SAD is often responsive to phototherapy which involves exposure to bright light that suppresses the production of melatonin.
During childhood, the rates of depression are similar for boys and girls; however, the rate for females increases in early adolescence while the rate for males remains fairly stable. Explanations for this gender difference incorporate the impact of biological and psychological factors. For example, there’s evidence that the increase of hormonal levels at puberty sensitizes females but desensitizes males to the stress of negative life events (Allen, Barrett, Sheeber, & Davis, 2006). The higher rate for females persists into adulthood, with female adolescents and adults having a rate that is 1.5 to 3 times higher than the rate for male adolescents and adults.
The yearly National Survey on Drug Use and Health (NSDUH), a nationally representative survey of U.S. adolescents and adults, provides information on the rates of one or more major depressive episodes in the past 12 months (Twenge, Cooper, Joiner, Duffy, & Binau, 2019). From 2009 to 2017, the highest rates of depression (with three exceptions) were for respondents ages 12 to 17 followed by, in order, respondents ages 18 to 25, 26 to 49, and 50+. The exceptions were in 2009, 2010, and 2017: In 2009, respondents ages 12 to 17 and 18 to 25 had a similar rate; in 2010, respondents ages 18 to 25 had a slightly higher rate than those ages 12 to 17; and, in 2017, respondents ages 12 to 17 and 18 to 25 again had similar rates. NSDUH data also indicate that rates of depression increased substantially between 2009 and 2017 for the two younger age groups but remained relatively stable for the two older age groups.
. Etiology of Major Depressive Disorder:
Major depressive disorder has been linked to heredity; neurotransmitter, hormone, and brain abnormalities; and cognitive and behavioral factors. With regard to heredity, twin, family, and adoption studies have confirmed a genetic component. For example, twin studies have found that the concordance rate for unipolar depression is about .50 for monozygotic twins and .20 for dizygotic twins (Dubovsky, Davies, & Dubovsky, 2003). Studies looking at neurotransmitters have found that depression is related to low levels of serotonin, dopamine, and norepinephrine. Depression has also been associated with abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis, which plays an important role in the body’s reaction to stress: Exposure to chronic stress (especially early in life) has been found to lead to persistent hyperactivity of the HPA axis and hypersecretion of cortisol, the primary stress hormone, which are associated with an increased risk for depression (Nandam et al., 2020). In addition, neuroimaging studies have linked depression to structural and functional abnormalities in the prefrontal cortex, cingulate cortex, hippocampus, caudate nucleus, putamen, amygdala, thalamus, and several other areas of the brain (e.g., Pandya, Altinay, Malone, & Anand, 2012). With regard to the prefrontal cortex, the studies have found that depression is associated with abnormally high levels of activity in the ventromedial prefrontal cortex (vmPFC) and abnormally low levels of activity in the dorsolateral prefrontal cortex (dlPFC) and that remission of depressive symptoms in response to psychotherapy or an antidepressant is associated with the opposite pattern – i.e., to decreased activity in the vmPFC and increased activity in the dlPFC (Koenigs & Grafman, 2009).
Behavioral and cognitive explanations include Lewinsohn’s social reinforcement theory, Seligman’s learned helplessness model, and Beck’s cognitive theory: Lewinsohn’s (1974) social reinforcement theory describes depression as the result of a low rate of response-contingent reinforcement for social behaviors due to a lack of reinforcement in the environment and/or poor social skills. This results in social isolation, low self-esteem, pessimism, and other characteristics of depression that, in turn, further decrease the likelihood of positive reinforcement in the future. Seligman’s (1974) original version of the learned helplessness model links depression to repeated exposure to uncontrollable negative life events that results in a sense of helplessness, and a reformulated version stresses the role of a negative cognitive style that involves attributing negative life events to stable, internal, and global factors. The most recent revision of the model (referred to as hopelessness theory) describes a sense of hopelessness as the proximal and sufficient cause of depression which, in turn, is the result of exposure to negative events and a negative cognitive style (Abramson, Metalsky, & Alloy, 1989). Beck’s (1974) cognitive theory attributes depression to a negative cognitive triad that consists of negative thoughts about oneself, the world, and the future.
- Age and Cultural Factors: There’s evidence that risk factors for major depressive disorder are somewhat age-related. For example, for younger adults, the risk has been linked to genetics, stressful life events, and limitations in problem-solving and other cognitive abilities. In contrast, for older adults, chronic medical illness has been consistently identified as one of the strongest risk factors, especially when the illness decreases physical functioning and contributes to social isolation (Blazer & Hybels, 2005; Caine, Lyness, & King, 1993; Lyness & Caine, 2000).
There’s also evidence that the experience and expression of major depressive disorder are related to age and cultural background. With regard to age, older adults are less likely than younger adults to refer to affective symptoms and more likely to refer to somatic symptoms, cognitive changes, and a loss of interest in usual activities (e.g., Fiske, Wetherell, & Gatz, 2009). With regard to cultural background, members of some Latino, Mediterranean, Middle Eastern, Asian, and other non-Western cultures report a larger number of somatic symptoms than members of Western cultures who report a larger number of psychological symptoms. For example, Ryder and his colleagues (2008) compared Chinese and Euro-Canadian outpatients and found that the Chinese patients were more likely to emphasize somatic symptoms (e.g., appetite and sleep disturbances, headaches, heart palpitations), while Euro-Canadian patients were more likely to emphasize psychological symptoms (e.g., depressed mood, loneliness, hopelessness).
- Comorbidity: Major depressive disorder has been linked to a number of comorbid disorders. For example, a survey of U.S. adults (Hasin et al., 2018) found that, among respondents with major depressive disorder, the largest percentage reported having a comorbid substance use disorder during their lifetimes followed by, in order, an anxiety disorder and a personality disorder. The survey also indicated that alcohol use disorder was the most common substance use disorder, generalized anxiety disorder was the most common anxiety disorder, and borderline personality disorder was the most common personality disorder. Major depressive disorder is also the most common psychiatric disorder associated with coronary heart disease (CHD), with the relationship being bidirectional: CHD can cause depression and depression is an independent risk factor for CHD (Bankier, Januzzi, & Littman, 2004; Khawaja, Westermeyer, Gajwani, & Feinstein, 2009). Finally, depression has been linked to several sleep abnormalities including prolonged sleep latency (a longer time to fall asleep), reduced REM latency (a shortened time from sleep onset to REM sleep), reduced slow-wave (stages 3 and 4) sleep, and increased REM density (more rapid eye movements per unit of time) (Nutt, Wilson, & Paterson, 2008).
- Treatment of Major Depressive Disorder: The treatment of major depressive disorder ordinarily consists of a psychosocial intervention and/or pharmacotherapy. APA’s (2019) Clinical Practice Guideline for the Treatment of Depression Across Three Age Cohorts provides treatment recommendations for children and adolescents, adults, and older adults (ages 60 and over): (a) For children, the guideline states that there is insufficient evidence to recommend any particular psychosocial or pharmacological treatment. (b) For adolescents, it recommends cognitive-behavioral therapy (CBT) or interpersonal psychotherapy for adolescents (IPT-A) as a psychosocial intervention and fluoxetine as a first-line medication. However, it notes there is insufficient evidence to recommend either of these treatments (psychotherapy or fluoxetine) over the other. (c) For adults, the guideline recommends that clinicians offer patients either psychotherapy or a second-generation antidepressant (an SSRI or SNRI). The psychotherapies it recommends are CBT, mindfulness-based cognitive therapy (MBCT), interpersonal therapy (IPT), behavioral therapy, psychodynamic therapy, and supportive therapy. Although it does not recommend one therapy over the others, it recommends CBT or IPT plus a second-generation antidepressant as a combined treatment. (d) For older adults, the guideline recommends that clinicians offer patients either group cognitive-behavioral therapy (group-CBT) or the combination of IPT and a second-generation antidepressant. If neither of these treatments is acceptable to the patient or is unavailable, the guideline provides a conditional recommendation for individual CBT alone or in combination with usual care, pharmacotherapy, IPT alone or in combination with pharmacotherapy, or group problem-solving therapy. It also states that there is insufficient evidence for recommending self-guided bibliotherapy or life review therapy for older adults.
Several other interventions have some research support as effective treatments for depression: (a) The use of St. John’s wort is supported by studies showing that it has similar therapeutic effects as SSRIs have for mild and moderate depression as well as lower dropout rates and fewer side effects (e.g., Cui & Zheng, 2016; Ng, Venkatanarayanan, & Ho, 2017). However, St. John’s wort has not been shown to be effective for severe depression, and it interacts with certain other drugs. For example, taking St. John’s wort with an SSRI or other medication that increases serotonin levels can cause serotonin syndrome, and taking it with alprazolam (Xanax), bupropion (Wellbutrin), or certain statin or immunosuppressive drugs can reduce the effectiveness of those drugs. (b) Ketamine has been used as an anesthetic since the 1960s and has also been found to be effective as a fast-acting treatment for treatment-resistant depression (TRD) and suicidal ideation (e.g., Kryst et al., 2020). It exerts its therapeutic effects by increasing glutamate levels and is prescribed as a nasal spray (esketamine) that is used in conjunction with an oral antidepressant. Because of its potential for severe side effects, esketamine is self-administered under the supervision of a healthcare provider in a healthcare setting. (c) Electroconvulsive therapy (ECT) has been shown to have a high success rate when used to treat severe depression but is ordinarily used only when other treatments have not been effective or when the severity of symptoms requires a quick treatment response (e.g., when the individual is at high risk for suicide). A disadvantage of ECT is that it causes both anterograde amnesia (an inability to form new memories after ECT) and retrograde amnesia (an inability to recall events that occurred before ECT): Anterograde amnesia usually resolves within a few weeks after the last ECT session. Retrograde amnesia affects recently acquired memories more than remote memories. It begins to resolve within weeks to several months after the last ECT session, with older memories returning before more recent ones. However, many patients experience persistent gaps in memory for events that occurred pre-ECT. Retrograde amnesia is more severe for bilateral placement of electrodes than for right unilateral placement and for a larger number of treatment sessions and less time between sessions (Weiner & Husain, 2015). (d) There is evidence that similar outcomes are obtained whether psychotherapy for depression is delivered via telepsychology or face-to-face (e.g., Osenbach, O’Brien, Mishkind, & Smolenski, 2013).
Suicide in the United States
Suicide rates in the United States increased from 2000 to 2018 but then decreased slightly from 2018 to 2020. Rates have been consistently higher for males than for females, with rates from 2000 to 2020 being 3 to 4 times higher for males. Overall, the suicide rates were highest in 2020 for individuals ages 75 and older and for American Indians/Alaska Natives followed by, in order, Whites, Hispanics, Blacks, and Asians/Pacific Islanders. However, when gender and age are both considered, the highest rate for males in 2020 was for those 75 years of age and older, but the highest rate for females was for those 45 to 64 years of age. With regard to race/ethnicity and age, in 2020, the highest rates for American Indians/Alaska Natives, Hispanics, and Blacks were for those ages 25 to 34, while the highest rate for Whites was for those ages 45 to 54 and the highest rate for Asians/Pacific Islanders was for those ages 85 and older (Centers for Disease Control and Prevention, 2022; Garnett, Curtin, & Stone, 2022; Suicide Prevention Resource Center, n.d.).
