Chapter 6 Depressive and Bipolar Disorders Depressive and Bipolar Disorders
Depressive and Bipolar Disorders
Definitions
Depression: A low, sad state characterized by significant levels of sadness, lack of energy, low self-worth, guilt, or related symptoms.
Mania: An episode marked by euphoria or frenzied activity, where individuals may have an exaggerated belief in their unlimited potential.
Depressive disorders: A group of disorders marked by unipolar depression, which refers to depression without a history of mania.
Bipolar disorder: A disorder characterized by alternating or intermixed periods of mania and depression.
Unipolar Depression: The Depressive Disorders (Part 1)
Prevalence:
8% of U.S. adults suffer from severe unipolar depression in any given year.
5% suffer from mild forms of unipolar depression.
20% of all adults experience unipolar depression at some point in their lives.
Average age of onset is 19 years.
Higher rates observed among chronically ill elderly individuals.
Unipolar Depression: The Depressive Disorders (Part 2)
Symptoms:
Emotional symptoms: Feelings of misery, emptiness, humiliation, and experiencing little pleasure.
Motivational symptoms: Lack of drive, initiative, and spontaneity.
Behavioral symptoms: Reduced activity and productivity.
Cognitive symptoms: Negative self-perception, self-blame, pessimism.
Physical symptoms: Physical aches including headaches, dizziness, or general pain.
Between 6% and 15% of individuals with severe depression die by suicide.
Unipolar Depression: The Depressive Disorders (Part 3)
Types according to DSM-5:
Major depressive disorder
Persistent depressive disorder
Premenstrual dysphoric disorder
Major Depressive Episode (Part 4)
Definition: A period lasting at least 2 weeks during which a person displays an increase in depressed mood or a decrease in enjoyment across most activities for the majority of the day.
Associated symptoms: Requires at least 3 or 4 of the following:
Significant weight or appetite change.
Daily insomnia or hypersomnia.
Daily agitation or reduced motor activity.
Daily fatigue or lethargy.
Daily feelings of worthlessness or excessive guilt.
Daily reduction in cognitive abilities, such as concentration.
Focus on death, suicidal thoughts, plans, or attempts.
Causes significant distress or impairment.
Major Depressive Disorder (Part 5)
Criteria:
Presence of a major depressive episode.
No history of mania or hypomania.
Persistent Depressive Disorder:
Symptoms consistent with major or mild depression for at least 2 years.
Symptoms not absent for more than 2 months during that period.
No history of mania or hypomania.
Causes significant distress or impairment.
Comparing Depressive and Bipolar Disorders
Prevalence and demographics:
Major depressive disorder:
1-year prevalence: 8.0%
Female-to-male ratio: 2:1
Typical age at onset: 18−29 years
Higher prevalence among first-degree relatives
Percentage receiving treatment: 50%
Persistent depressive disorder:
1.5−5.0%
Female-to-male ratio: between 3:2 and 2:1
Typical age at onset: 10−25 years
Higher prevalence among first-degree relatives
Percentage receiving treatment: 62%
Bipolar I disorder:
1.6%
Female-to-male ratio: 1:1
Typical age at onset: 15−44 years
Elevated rates among first-degree relatives
Percentage receiving treatment: 49%
Bipolar II disorder:
1.0%
Female-to-male ratio: 1:1
Typical age at onset: 15−44 years
Elevated rates among first-degree relatives
Percentage receiving treatment: 49%
Cyclothymic disorder:
0.4%
Female-to-male ratio: 1:1
Typical age at onset: 15−25 years
Elevated rates among first-degree relatives
Percentage receiving treatment: Unknown
PsychWatch: Sadness at the Happiest of Times
Postpartum (peripartum) depression:
Symptoms: Extreme sadness, despair, tearfulness, insomnia, anxiety, intrusive thoughts, compulsions, panic attacks, inability to cope, suicidal thoughts.
Causes: Triggered by hormonal changes of childbirth, genetic predisposition, psychological and social changes.
Treatment options: Self-help groups, antidepressant medications, cognitive-behavioral therapy, interpersonal psychotherapy, or combinations thereof.
Treatment is effective for most women seeking help.
The Biological Model of Unipolar Depression (Part 1)
Biological view:
Studies of genetic factors, biochemical factors, brain circuits, and immune system indicate that unipolar depression has biological causes.
Genetic factors:
Family pedigree studies, twin studies, and gene studies provide insights into hereditary patterns in depression.
Molecular biology advances allow better understanding of the biological underpinnings.
The Biological Model of Unipolar Depression (Part 2)
Biochemical factors:
Low activity of neurotransmitters serotonin and norepinephrine associated with depression.
Early studies indicated a correlation between high blood pressure medications and antidepressant effects, later leading to neurotransmitter interaction research.
Hormonal influences and the HPA (hypothalamic-pituitary-adrenal) axis are also implicated in depression mechanisms.
Seasonal affective disorder linked to variations in hormone levels related to seasonal changes.
The Biological Model of Unipolar Depression (Part 3)
Brain circuits:
Dysfunctional brain circuits can be identified through brain imaging studies.
Notable structures such as the subgenual cingulate demonstrate distinct contributions to mood regulation.
Abnormal activity level and blood flow rates in various brain locations alongside structural interconnectivity issues.
Abnormal neurotransmitter activities are also a key part of the dysfunctioning circuits.
The Biological Model of Unipolar Depression (Part 4)
Immune system:
Intense stress can lead to immune system dysregulation that aggravates depression.
Slower functioning of lymphocytes and increased production of CRP (C-reactive protein) correlate with depression.
Chronic inflammation linked to increased rates of migraines, IBS, chronic fatigue syndrome, rheumatoid arthritis, and other related conditions.
Biological Treatments for Unipolar Depression (Part 1)
Antidepressant drugs:
Emerged in the 1950s with two main classes:
Monoamine oxidase (MAO) inhibitors
Tricyclics
Recent developments include second-generation antidepressants.
Biological Treatments for Unipolar Depression (Part 2)
MAO inhibitors:
Biochemically slow down the production of MAO, improving neurotransmitter levels.
Can cause hypertensive crisis when interacting with tyramine-rich foods (e.g., aged cheese).
Approximately half of patients taking MAO inhibitors experience reduced symptoms.
Biological Treatments for Unipolar Depression (Part 3)
Tricyclics:
Act on reuptake mechanisms of neurotransmitters, primarily serotonin and norepinephrine, allowing them to remain active in the synapses longer.
Associated side effects, and relapse is possible if therapy is terminated abruptly.
Biological Treatments for Unipolar Depression (Part 4)
Second-generation antidepressants:
Include selective serotonin reuptake inhibitors (SSRIs) that selectively increase serotonin activity.
These drugs have a different structure from MAO inhibitors and tricyclics and have a lower incidence of side effects but still present some.
A failure rate over 40% has been reported.
Biological Treatments for Unipolar Depression (Part 5)
Brain stimulation methods:
Include treatments designed to stimulate specific brain regions related to mood regulation such as:
Electroconvulsive therapy (ECT)
Vagus nerve stimulation
Transcranial magnetic stimulation (TMS)
Deep brain stimulation
Biological Treatments for Unipolar Depression (Part 6)
Electroconvulsive therapy (ECT):
Involves electrical stimulation to cause brain seizures as a treatment for significant depression; typically administered in 6 to 12 sessions over 2 to 4 weeks.
Controversial due to the possible side effects and patient experiences associated with the procedure.
Biological Treatments for Unipolar Depression (Part 7)
Vagus nerve stimulation:
An implanted pulse generator sends electrical signals to the vagus nerve, stimulating brain functions.
Helps to alleviate severe depression without the negative side effects of ECT.
Biological Treatments for Unipolar Depression (Part 8)
Transcranial magnetic stimulation (TMS):
Involves an electromagnetic coil placed on the patient’s head, which sends currents into the brain, increasing neuronal activity in the prefrontal cortex and improving depressive symptoms.
Typically administered daily for 4 to 6 weeks.
Biological Treatments for Unipolar Depression (Part 9)
Deep brain stimulation:
An experimental treatment where electrodes are implanted in brain regions specifically involved in depression, providing artificial stimulation to normalize brain activity, particularly in the subgenual cingulate, leading to improvements in severe depression cases.
The Psychological Models of Unipolar Depression (Part 1)
Psychodynamic view:
According to Freud and Abraham, real or imagined losses may trigger a psychological regression to earlier developmental stages, followed by the introjection of feelings associated with the loss, leading to depression.
Object relations theorists believe that depression results from interpersonal relationships that cause individuals to feel unsafe and insecure, particularly in early life.
The Psychological Models of Unipolar Depression (Part 2)
Strengths of the psychodynamic view:
Research supports the idea that depression may trigger after significant loss and that early life experiences can predispose individuals to depression.
Limitations:
Early losses do not universally cause depression, and research findings are often inconsistent; certain elements are difficult to empirically test.
The Psychological Models of Unipolar Depression (Part 3)
Psychodynamic therapy:
Centers around unconscious grief related to loss, with therapists facilitating the exploration of these feelings through various techniques like free association and interpretation of past experiences.
The Psychological Models of Unipolar Depression (Part 4)
Strengths of psychodynamic therapy:
Successful case reports exist, particularly with modestly depressed individuals with clear histories of loss.
Limitations of psychodynamic therapy:
Often not effective for more passive and exhausted patients who may withdraw from therapy too early.
The Psychological Models of Unipolar Depression (Part 5)
Cognitive-behavioral view:
Suggests that depression is a result of problematic behaviors and dysfunctional thinking.
Behavioral dimension includes the interaction of positive life rewards and depression.
A decrease in positive reinforcement is linked to fewer favorable behaviors, leading to a downward spiral of depression.
The Psychological Models of Unipolar Depression (Part 6)
Negative thinking:
Beck posits that unipolar depression is caused by maladaptive attitudes, cognitive distortions, and automatic thoughts.
The cognitive triad includes negative views of one's self, experiences, and expectations of the future.
Seligman’s learned helplessness theory links depression to feelings of loss of control over life events attributed to internal, stable, and global factors.
The Psychological Models of Unipolar Depression (Part 7)
Learned helplessness:
Seligman suggests that feelings of no control over life’s events lead individuals to feel responsible for their helplessness.
Influential modifications to learned helplessness attribution indicate that internal attributions lead to depression, while external attributions reduce the likelihood of helplessness and subsequent depression.
MindTech: Texting: A Relationship Buster?
Texting as a prevalent communication method may negatively impact interpersonal relationships:
Avoidance of face-to-face communication can lead to conflicts.
Reduces emotional connections and may cause misunderstandings.
Associated with broader feelings of stress and unhappiness.
Psychodynamic Treatments for Unipolar Depression (Part 1)
Cognitive-behavioral therapy (CBT):
Focuses on increasing constructive and pleasurable activities to improve mood and motivation.
Involves rewarding non-depressive behaviors, reintroducing enjoyable activities, and enhancing social skills (Lewinsohn).
Psychodynamic Treatments for Unipolar Depression (Part 2)
Beck's cognitive therapy:
Involves guiding patients through four phases to recognize and alter their negative cognitive processes, including:
Increasing activities and mood elevation, challenging automatic thoughts, and changing underlying attitudes.
Psychodynamic Treatments for Unipolar Depression (Part 3)
New-wave cognitive-behavioral therapists:
Disagree with Beck's assertion that all negative thoughts must be eliminated.
Employ mindfulness techniques and other methods to help clients manage negative cognitions as they occur.
The Sociocultural Model of Unipolar Depression (Part 1)
Family-social perspective:
Declines in social rewards can contribute to depression.
Depressed individuals often showcase social deficits leading to avoidance by others, reducing their social interactions and supports.
The Sociocultural Model of Unipolar Depression (Part 2)
Interpersonal psychotherapy (IPT):
Focuses on resolving interpersonal issues contributing to depression, including:
Interpersonal loss
Role disputes and transitions
Deficits in interpersonal skills.
Studies indicate IPT can be equally as effective as cognitive therapies for treating depression.
The Sociocultural Model of Unipolar Depression (Part 3)
Multicultural perspective:
A notable link exists between gender and depression rates, with women being twice as likely to be diagnosed than men across cultures.
Women typically experience depression at a younger age, with more frequent and longer-lasting episodes that respond less favorably to treatment.
The Sociocultural Model of Unipolar Depression (Part 4)
Theories explaining gender differences in depression:
Artifact theory suggests that gender discrepancies in diagnosis may stem from biases.
Hormonal and life stress factors relate to greater stressors faced by women.
Body dissatisfaction and lack of control theories reflect pressures leading to depression in women.
The Sociocultural Model of Unipolar Depression (Part 5)
Global prevalence of depression reflects core symptoms that are recognizable around the world, though specific expressions can differ based on culture.
In non-Western countries, individuals often articulate physical symptoms, evolving to more cognitive expressions as Westernization progresses.
The Sociocultural Model of Unipolar Depression (Part 6)
Cultural variability:
Limited differences appear in depression symptoms across racial groups in the U.S., though recurrence and prevalence vary markedly among ethnic minorities.
The distribution of depression is not uniform, indicating the need for tailored approaches in understanding and treating depression.
Sociocultural Treatments for Unipolar Depression (Part 1)
Culture-sensitive therapies:
Address the unique issues faced by cultural minorities, incorporating cultural values and stressors and often integrated with standard psychotherapy techniques.
Integrating the Models
Developmental psychopathology perspective:
Unipolar depression is thought to originate from an interplay of biological, psychological, and sociocultural factors, deeply influenced by early life trauma.
Evidence supports the role of a genetic predisposition, the influence of adverse childhood experiences, and the ability to overcome adversity contributes to resilience and vulnerability.
Bipolar Disorders (Part 1)
Symptoms:
Individuals with mania exhibit dramatic mood elevations as opposed to those experiencing depression, exhibiting emotional, motivational, behavioral, cognitive, and physical symptoms.
Bipolar Disorders (Part 2)
Diagnosis:
Bipolar disorders are categorized into two main types according to DSM-5:
Bipolar I disorder: Characterized by manic episodes.
Bipolar II disorder: Characterized by a history of major depressive episodes and hypomanic episodes, but no manic episodes.
Global prevalence: 1 to 2.6% of adults affected at any given time, with a 4% lifetime prevalence.
No significant gender differences though it’s more prevalent in low-income populations.
Bipolar Disorders (Part 3)
Manic episode:
Requires at least 1 week of persistent elevated mood and increased energy/activity, accompanied by at least three of the following symptoms:
Grandiosity or inflated self-esteem
Reduced sleep requirement
Rapid thought and speech pattern shifts
Distractibility
Heightened activity or psychomotor agitation
Pursuit of risky behaviors
Causes significant distress or impairment.
Bipolar Disorders (Part 4)
Classifications:
Bipolar I disorder: Presence of manic episodes with possible preceding or following major depressive episodes.
Bipolar II disorder: History of major depressive and hypomanic episodes, but no manic episodes.
Bipolar Disorders (Part 5)
Cyclothymic disorder:
Involves numerous periods of hypomanic symptoms and mild depressive symptoms lasting for 2 years or more, interspersed with periods of normal mood.
No gender differences; may develop into either Bipolar I or II.
Bipolar Disorders (Part 6)
Recurrence of mood episodes:
Within bipolar disorders, unaddressed mood episodes are frequent, with rapid cycling classified as four or more episodes within a year.
Prevalence of depressive episodes tends to be higher than manic episodes, with longer durations.
What Causes Bipolar Disorders? (Part 1)
Understanding the etiology of bipolar disorders has evolved over time, moving from minimal explanations to significant insights drawn from modern biological research
Factors include neurotransmitter activity, ion transport issues, brain structure abnormalities, and genetic predispositions.
What Causes Bipolar Disorders? (Part 2)
Neurotransmitter activity:
Increased norepinephrine correlating with mania, while low levels of serotonin are also observed.
Ion transport issues:
Dysfunctional exchange of ions across neuronal membranes correlates with bipolar symptoms.
Brain structure abnormalities:
Imaging and postmortem studies indicate notable structural concerns in areas like the basal ganglia and cerebellum, though their exact impact on bipolar symptoms remains unresolved.
Genetic factors:
Evidence from family studies and molecular approaches suggests a hereditary component to bipolar disorder.
Treatments for Bipolar Disorders (Part 1)
Before 1970, treatment options for bipolar disorders were largely ineffective until the FDA approved lithium for use as a mood stabilizer.
Introduction of subsequent mood-stabilizing drugs followed the use of lithium.
Treatments for Bipolar Disorders (Part 2)
Lithium:
Very effective for managing bipolar disorders and manic episodes.
Determining dosage is complex; too low yields no therapeutic effect, while too high can cause lithium toxicity.
Approximately 49% of individuals with bipolar disorder receive adequate treatment annually.
Other mood stabilizers:
Some patients respond more favorably to alternative medications or combinations of treatments.
Treatments for Bipolar Disorders (Part 3)
Effectiveness of mood stabilizers:
Over 60% of individuals with mania show improvement with mood stabilizers.
These medications can minimize the frequency of mood episodes.
Mood stabilizers also somewhat alleviate depressive episodes but are less effective than for manic episodes.
Treatments for Bipolar Disorders (Part 4)
Mechanisms of action of mood stabilizers:
Research indicates that mood stabilizers act on neuronal synaptic activity distinctively compared to antidepressants.
They may enhance the production of neuroprotective proteins, thus mitigating bipolar symptoms.
They also seem to regulate ionic activity (sodium and potassium) across neuron membranes.
Treatments for Bipolar Disorders (Part 5)
Adjunctive psychotherapy:
Combining psychotherapy with mood stabilizers can yield better outcomes in patients.
Forms of psychotherapy include individual, group, or family therapy, and have shown to improve client behaviors, particularly in those with cyclothymic disorders.
Making Sense of All That Is Known
Summary of causal factors in:
Unipolar depression: Biological abnormalities, reduced positive reinforcement, negative thinking patterns, helplessness, life stress, and sociocultural effects.
Bipolar depression: Similar biological abnormalities with inherited elements and stress triggers.