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Questions and Answers
What is the relationship between chronic stress and hippocampal neurogenesis?
What is the relationship between chronic stress and hippocampal neurogenesis?
Which brain regions are highlighted as being involved in the regulation of negative emotions and reward experience?
Which brain regions are highlighted as being involved in the regulation of negative emotions and reward experience?
What role does neurogenesis in the hippocampus play in antidepressant effects?
What role does neurogenesis in the hippocampus play in antidepressant effects?
Which statement best describes the process of neurogenesis in the hippocampus?
Which statement best describes the process of neurogenesis in the hippocampus?
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What is the primary mechanism through which antidepressant treatments are thought to work?
What is the primary mechanism through which antidepressant treatments are thought to work?
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What is the average age of onset for bipolar disorder?
What is the average age of onset for bipolar disorder?
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Which of the following symptoms is NOT commonly associated with unipolar depression?
Which of the following symptoms is NOT commonly associated with unipolar depression?
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How does cyclothymia differ from bipolar disorder?
How does cyclothymia differ from bipolar disorder?
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Which statement is true regarding the diathesis-stress model?
Which statement is true regarding the diathesis-stress model?
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What approximate percentage of the U.S. population is affected by bipolar disorder annually?
What approximate percentage of the U.S. population is affected by bipolar disorder annually?
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In terms of gender, how does the prevalence of unipolar depression compare to bipolar disorder?
In terms of gender, how does the prevalence of unipolar depression compare to bipolar disorder?
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Which of the following symptoms is specifically a sign of mania?
Which of the following symptoms is specifically a sign of mania?
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What is the observed trend in hippocampal volume among patients with PTSD compared to control subjects?
What is the observed trend in hippocampal volume among patients with PTSD compared to control subjects?
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Which brain region shows increased activity in response to threat among PTSD patients?
Which brain region shows increased activity in response to threat among PTSD patients?
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How does the activity of the prefrontal cortex in PTSD patients compare to that of healthy individuals?
How does the activity of the prefrontal cortex in PTSD patients compare to that of healthy individuals?
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What effect does PTSD have on the amygdala when responding to neutral faces?
What effect does PTSD have on the amygdala when responding to neutral faces?
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What does the data suggest about the emotional regulation capabilities of PTSD patients?
What does the data suggest about the emotional regulation capabilities of PTSD patients?
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In PTSD patients, which region's hyperactivity is primarily associated with threat perception?
In PTSD patients, which region's hyperactivity is primarily associated with threat perception?
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What is the relationship between the prefrontal cortex and the amygdala in the context of PTSD?
What is the relationship between the prefrontal cortex and the amygdala in the context of PTSD?
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What does the data indicate about the overall hippocampal volume in patients suffering from PTSD?
What does the data indicate about the overall hippocampal volume in patients suffering from PTSD?
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How quickly does the amygdala activate in response to threat stimuli in PTSD patients?
How quickly does the amygdala activate in response to threat stimuli in PTSD patients?
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What can be inferred about the emotional response of traumatized controls as compared to PTSD patients?
What can be inferred about the emotional response of traumatized controls as compared to PTSD patients?
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Which symptom is NOT associated with Post-Traumatic Stress Disorder (PTSD)?
Which symptom is NOT associated with Post-Traumatic Stress Disorder (PTSD)?
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What role does childhood adversity play in the development of PTSD?
What role does childhood adversity play in the development of PTSD?
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According to the Diathesis Stress Model, what factor significantly contributes to an individual's vulnerability to PTSD?
According to the Diathesis Stress Model, what factor significantly contributes to an individual's vulnerability to PTSD?
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Which of the following statements about resilience in relation to PTSD is accurate?
Which of the following statements about resilience in relation to PTSD is accurate?
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What is a potential outcome of excessive traumatic events combined with a lack of coping resources?
What is a potential outcome of excessive traumatic events combined with a lack of coping resources?
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What is typically the most common reaction to traumatic events among the general population?
What is typically the most common reaction to traumatic events among the general population?
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Which of the following factors can alter the structure and function of emotion circuits in the brain long-term?
Which of the following factors can alter the structure and function of emotion circuits in the brain long-term?
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What does the Diathesis Stress Model propose regarding PTSD?
What does the Diathesis Stress Model propose regarding PTSD?
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Which statement regarding the probability of developing PTSD is correct?
Which statement regarding the probability of developing PTSD is correct?
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Which brain region is characterized as underactive in the context of PTSD?
Which brain region is characterized as underactive in the context of PTSD?
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Which neurotransmitter is NOT mentioned in relation to the monoamine hypothesis for depression?
Which neurotransmitter is NOT mentioned in relation to the monoamine hypothesis for depression?
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What effect does reserpine have on monoamines relevant to depression?
What effect does reserpine have on monoamines relevant to depression?
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Which treatment is associated with the inhibition of monoamine oxidase in depression management?
Which treatment is associated with the inhibition of monoamine oxidase in depression management?
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In PTSD, which circuit is described as hyperactive?
In PTSD, which circuit is described as hyperactive?
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According to the monoamine hypothesis, low levels of which combination of neurotransmitters can lead to depression?
According to the monoamine hypothesis, low levels of which combination of neurotransmitters can lead to depression?
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Which of the following is NOT a characteristic of the HPA Axis in PTSD?
Which of the following is NOT a characteristic of the HPA Axis in PTSD?
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What is the primary role of monoamines in the context of depression?
What is the primary role of monoamines in the context of depression?
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What outcome is implied when monoamine levels are low according to the monoamine hypothesis?
What outcome is implied when monoamine levels are low according to the monoamine hypothesis?
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Which drug is associated with an increased risk of depression due to its effect on monoamines?
Which drug is associated with an increased risk of depression due to its effect on monoamines?
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Study Notes
Abnormal Psychology
- Defining 'normal' is crucial in medicine, and abnormal psychology examines behaviours and mental states deviating from this norm.
- Abnormal psychology analyzes these states concerning statistical averages and professional mental health standards.
- "Healthy" and "unhealthy" classifications are arbitrary. They depend on the personal distress or impairment of function.
- The Diagnostic and Statistical Manual of Mental Disorders (DSM) serves as a diagnostic guide.
- Symptoms must deviate from statistical averages, exhibit psychological dysfunction, and cause personal distress or impaired functioning. DSM-5 is now the current edition.
- Different editions of the DSM include different numbers of diagnoses, with recent editions like DSM5 having 541 diagnoses (in 2013).
Depressive & Bipolar Disorders (Affective Disorders)
-
Unipolar Depression: involves consistent depression, lacking manic episodes.
- Affects approximately 8% of the US population annually.
- Median onset is at age 32.
- Women are affected 2-3 times more frequently than men.
- Types include Major Depressive Disorder (MDD) and Dysthymia (a milder, chronic form often called "Pervasive Depressive Disorder").
- Symptoms of Unipolar Depression: Depressed mood, loss of ability to experience pleasure, restlessness/irritability/anxiety, low energy/concentration, sleep difficulties, constipation/aches/pains, thoughts of death/suicide.
-
Bipolar Disorder: characterized by cycles of depression and mania (extreme elation).
- Manic episodes duration varies from few days to several months.
- Depressive episodes generally last longer than manic episodes.
- Affects about 3% of the US population annually.
- Median onset is at age 25.
- Diagnosed in men and women roughly equally.
- Cyclotmic disorder is the less severe form.
Symptoms of Mania
- Mania's severity ranges from mild ("hypomania") to severe, marked by:
- High energy.
- Excessive good mood.
- Cognitive sharpness.
- Reduced need for sleep.
- Sense of power.
- Rapid, unorganized speech.
- Racing thoughts.
- Impatience.
- Irritability.
Stress & Depression (The Diathesis-Stress Model)
- The diathesis-stress model emphasizes two key factors underlying depression.
- 1. Vulnerability: inherent predisposition to depression.
- 2. Stressful Life Events: a trigger that leads to a higher chance of depression for those predisposed.
- Childhood adversity, and genetic predisposition are seen as central factors.
- Vulnerability + Stressful experience = potential for depression.
- Resilience, few stressful situations, and access to coping mechanisms are positive mitigating factors.
Depression & Hippocampal Atrophy
- There is a negative correlation between lifetime depression and hippocampal volume (i.e., the hippocampus is smaller).
- Individuals with a history of depression often have smaller hippocampal volumes compared to those without a history of depression.
Anxiety & Trauma-Related Disorders
- Anxiety Disorder: a persistent expression of symptoms such as tension, worry, overactive nervous system, expectancy of impending disaster, hypervigilance/arousal, irritability, and avoidance of social activities.
- A diagnosis requires the experience of several symptoms over time significantly impacting functioning.
- Fear vs. Anxiety: Fear stems from actual threats, while anxiety stems from anticipated threats.
- Classifying Anxiety Disorders: Phobias, Panic Disorder, Social Anxiety Disorder, Generalized Anxiety Disorder, Separation anxiety disorder are some examples. Anxiety is a core symptom of PTSD, but PTSD is separately categorized.
Post-Traumatic Stress Disorder (PTSD)
- PTSD results from extreme danger and stress.
- Symptoms include recurrent recollections/feelings of the traumatic event, the feeling that the traumatic event is recurring ("flashbacks"), Intense psychological distress and hypervigilance/arousal
- Not everyone exposed to trauma develops PTSD; resilience is a common reaction.
- A contributing factor for PTSD is the number of traumatic events and pre-existing anxiety disorders.
- A history of early life stressful or adverse experiences is a predictor for PTSD.
- Potential long-term neurobiology changes in emotion circuits in the brain occur after trauma.
- Smaller hippocampus and increased amygdala reactivity (to threat stimuli) are potential neurobiology features in PTSD brains
The Diathesis-Stress Model & PTSD
- Genetic predisposition and childhood adversity are important factors in developing PTSD.
- Vulnerabilities + traumatic events = higher risk for developing PTSD.
- Less exposure and readily available resources can lower the chance of developing PTSD.
Amygdala Reactivity in PTSD Patients
- PTSD patients show heightened amygdala reactivity to threat stimuli.
Dysfunctional Emotion Regulation in PTSD
- PTSD patients exhibit reduced prefrontal cortex activity and increased amygdala activity.
A Dysfunctional Emotion Regulation Circuit in PTSD
- Circuit dysfunction impacting prefrontal cortex, classical neurotransmitters (like classical NT systems), the Hypothalamic-Pituitary-Adrenal (HPA) Axis, and the Sympathetic Nervous System (SNS) activity
Treatment: Pharmacological Approaches
- Tightly linked to the monoamine neurotransmitter system.
- Reserpine, a drug used to treat high blood pressure, affects monoamine storage in vesicles.
- Iproniazid, a tuberculosis drug, shows antidepressant properties, implying an impact on monoamine breakdown.
Modern Antidepressants
- Modern options target one or more monoamines.
- Tricyclic antidepressants (TCAs) are non-selective reuptake inhibitors.
- Selective serotonin reuptake inhibitors (SSRIs) target serotonin reuptake.
- Serotonin-Norepinephrine reuptake inhibitors (SNRIs) target serotonin and norepinephrine reuptake.
- Norepinephrine-Dopamine reuptake inhibitors (NDRIs) focus on norepinephrine and dopamine reuptake.
Prozac & Serotonin Reuptake Inhibition
- Prozac is an SSRI that blocks serotonin reuptake at the synapse, leading to a longer-lasting and augmented postsynaptic effect.
A "Chemical Imbalance"?
- While monoamine-enhancing drugs can alleviate depression, an imbalance isn't definitively established.
Antidepressants: Acute vs. Chronic Treatment
- Antidepressant medications typically need weeks of chronic use for symptom reduction.
- Acute effects (within 30 minutes) target neurotransmitter reuptake, but chronic effects involve processes beyond simply increasing synapse neurotransmitter levels.
Chronic Treatment with Antidepressants & Hippocampal Neurogenesis
- Studies support that chronic stress can harm hippocampal neurogenesis.
- Antidepressants can improve hippocampal neurogenesis.
How Do Antidepressant Drugs Really Work?
- Stressed brains often exhibit circuit-level alterations (impaired signals, for instance) that disrupt emotional regulation, and reward/pleasure processing.
- Antidepressants likely work by targeting these dysfunctional circuits and inducing neuroplasticity changes, leading to improved brain circuit functions.
Drug Treatment for Anxiety & PTSD
- Benzodiazepines are effective anxiolytics and indirectly work on GABA receptors to enhance inhibition in the amygdala, causing increased hyperpolarization.
- These drugs can cause dependence but have short-term effectiveness.
Antidepressants for Anxiety Disorders
- Benzodiazepines are effective but not ideal for long-term use.
- SSRIs and SNRIs can also effectively treat anxiety disorders.
Antidepressant Treatment & Amygdala Reactivity
- In studies using medication like Zoloft, 8 weeks of treatment decreased amygdala reactivity to threatening stimuli.
Treatment: Psychotherapy
Psychoanalysis
- Psychoanalysis assumes conflicts cause psychological disorders and treatments aim to reveal and resolve these conflicts.
- Techniques include free association to gain insights about repressed thoughts, feelings, and memories.
Talking & Free Association
- Patients detail thoughts and feelings without censorship, and analysts work towards understanding any clues.
What Do We Like About Freud?
- The ideas of unconscious processing, development, and the role of relationships are appealing and often valid.
Why Did Academic Psychology Leave Freud Behind?
- Psychodynamic theory is complex.
- Its concepts & outcomes are difficult to test and measure objectively.
- Practical application depends heavily on subjective analysis, and individual experiences during analysis vary widely.
- The approach is very time-consuming.
Cognitive-Behavioral Therapy (CBT)
- CBT posits that psychological disorders are caused/maintained by maladaptive patterns, thought patterns, and behaviours.
- CBT therapies aim to modify maladaptive thought patterns and behaviour to improve functioning.
The Vicious Cycle of Maladaptive Thinking, Affect & Behavior
- Maladaptive thoughts lead to negative emotions.
- These emotions can perpetuate more negative thoughts and lead to behaviours that exacerbate the cycle.
Belief Modification in CBT: Challenging Rumination & Worry
- Identifying and challenging maladaptive thoughts is a key aspect.
- Therapists aim to help individuals think differently about their life by focusing on the present.
CBT & the Brain
- CBT challenges thought patterns and aims to increase activity in the prefrontal cortex. This contrasts with the overactive amygdala, by changing thinking, the amygdala can become less reactive to anxieties
Long-Term Benefits of CBT vs. Medication
- CBT is associated with reduced relapse rates after treatment compared to antidepressant medication.
Mindfulness-Based Cognitive Therapy (MBCT)
- Combining mindfulness and CBT techniques.
- The focus is on noticing present experiences.
- Goal to interrupt the cycle of harmful thoughts (rumination, worry) by training attention on the present moment.
Behavior & Exposure Therapies
- Exposure therapy/and systematic desensitization to feared/anxiety-provoking things/situations is used to modify the emotional responses/reactions.
- Virtual reality is becoming an important tool in exposure therapies.
Does Psychotherapy Work?
- Psychotherapy is effective for some mental disorders.
- CBT is particularly effective due to empirically supported treatments.
- Therapists identify and target specific environmental and cognitive triggers to reduce symptoms.
Empirically-Supported Treatments
- Some commonly used treatments are shown to be effective, like CBT for anxiety and depression.
- IPT is a popular short-term form of treatment for depression.
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Description
This quiz explores the intricate relationship between chronic stress, neurogenesis in the hippocampus, and mood disorders. It covers key concepts related to neurogenesis, the effects of antidepressants, and the prevalence of mood disorders like bipolar and unipolar depression. Test your knowledge on these critical psychological topics.
