Week 6 - anxiety & depression 2024- no video
Week 6: PaWeek 6 - anxiety & depression 2024- no videort 1 – Anxiety Disorders
Instructor: Dr. Nicola Gregory (ngregory@bournemouth.ac.uk)
Room: P115 L5 / L7 2024-2025
Trigger Warning: Content includes discussions of anxiety and depression symptomology.
Lecture Information
Subject: Biological Psychology
Dates:
Lecture 1: November 13, 2024, 10:00 - 12:00
Lecture 2: November 15, 2024, 11:00 - 13:00
Location: Bournemouth University
Key Terms
Anxiety
Stress
Anxiety Disorders
Generalized Anxiety Disorder (GAD)
Social Anxiety Disorder (SAD)
Stress Response
HPA Axis (Hypothalamus, Pituitary gland, Adrenal gland)
Corticotropin-releasing hormone (CRH)
Adrenocorticotropic hormone (ACTH)
Cortisol
Sympathetic and Parasympathetic Nervous System
Hippocampus
Amygdala
Insula
Glucocorticoid receptors
SSRIs (Selective Serotonin Reuptake Inhibitors)
GABA (Gamma-Aminobutyric Acid)
Orbitofrontal Cortex
Resting-State Functional Connectivity
Learning Outcomes
Understanding the types of anxiety and their diagnostic criteria
In-depth study of Generalized Anxiety Disorder and Social Anxiety Disorder
Exploration of the stress response
Examination of key brain areas involved (e.g., amygdala, hippocampus, HPA axis)
Cognitive neuroscience related to anxiety disorders
Overview of pharmacotherapy for anxiety disorders
Anxiety Overview
Definition: Chronic fear without a specific threat
Symptoms of anxiety include tension, worry, and physical manifestations.
Can be both innate and learned; may have adaptive qualities but can hinder functioning if excessive.
Classification of Anxiety Disorders (DSM V)
Types:
Separation Anxiety Disorder
Selective Mutism
Specific Phobia
Social Anxiety Disorder
Panic Disorder
Agoraphobia
Generalized Anxiety Disorder
Note: OCD and PTSD are categorized separately in DSM V.
Generalized Anxiety Disorder (GAD)
Affects approximately 5% of the population.
Characterized by excessive worry over 6 months, difficult to control.
Accompanied by at least three of the following:
Restlessness / Edginess
Trouble concentrating
Increased fatigue
Irritability
Muscle tension
Sleep disturbances
Symptoms cause significant distress and impaired function.
Not due to substances, medical conditions, or other mental disorders.
Physiological Symptoms of GAD
Symptoms may include:
Tachycardia
Palpitations
Hypertension
Sleep disturbances
Nausea
Dizziness
Fatigue
Rapid breathing
Aetiology of GAD
Prevalence: 5% affected
Comorbidity: 60-90% with other diagnoses
Heritability: 15-20% genetic contribution
Large environmental influence (stressful events, trauma, etc.).
Social Anxiety Disorder (SAD)
Definition: Intense fear in social situations due to potential scrutiny.
Key features include:
Fear of embarrassment or humiliation
Anxiety provoked in social situations, often leading to avoidance.
Persistent fear lasting over 6 months, causing distress and functional impairment.
Must not be attributable to substances or other mental conditions.
Aetiology of SAD
Usually starts in teenage years, often triggered by a traumatic event.
Heritability: 25-50%
High prevalence of undiagnosed SAD, with many not seeking treatment.
Treatment Options for Anxiety Disorders
Psychological: Usually CBT or psychotherapy; self-referral available.
Pharmacological:
SSRIs are commonly prescribed.
Benzodiazepines used for severe cases.
Neural Mechanisms in Anxiety Disorders
Hyperactivation of Stress Response: Common in all anxiety disorders.
Activation occurs with a non-threatening stimulus.
Regulation of Stress Response
Amygdala: Triggers stress response.
Hippocampus: Inhibits stress response by measuring cortisol levels; chronic stress can damage glucocorticoid receptors, leading to HPA axis activation.
Cognitive Mechanisms in Anxiety
Attentional Biases: Individuals with anxiety disorders disproportionately attend to threatening stimuli.
In SAD, this bias is most prominent in social contexts.
Cognitive Neuroscience in Anxiety
Research shows those with high social anxiety display increased focus on faces, reflecting attentional bias.
Amygdala activity is more pronounced in anxiety patients, indicating less regulation by the orbitofrontal cortex (OFC).
Pharmacotherapy for Anxiety Disorders
SSRIs: Increase serotonin availability and glucocorticoid receptors in the hippocampus, indirectly reducing HPA axis activation.
Benzodiazepines: Act as fast-acting anxiolytics but should be used sparingly due to addiction potential.
Summary and Conclusions
GAD and SAD are characterized by persistent fear triggered by inappropriate stress response activations.
Hyperactivity of the amygdala is critical in anxiety disorders and pharmacotherapy is important for treatment.
Recommended Reading
Essential: Chapter 22, Mental Illness, Bear et al.
Etkin & Wagner, 2007 - Meta-Analysis: Emotional Processing in PTSD, Social Anxiety, and Specific Phobia.
Hahn et al., 2011 - Resting-State Functional Connectivity in Social Anxiety Disorder.
Week 6: Part 2 – Depression
Continue discussion on depression in biological psychology.
Key Terms
Monoamines
Serotonin
Agonist
SSRIs
SNRIs
Norepinephrine
Brain Stimulation Techniques: tDCS, rTMS, ECT
Neuroplasticity
BDNF (Brain-Derived Neurotrophic Factor)
Cognitive Function
Learning Outcomes for Depression Lecture
Diagnostic criteria and prevalence of depression
Understand monoamine theory and neuroplasticity theory
Explore brain stimulation for treatment
Investigate neural structure/function differences in depression.
Depression Diagnosis (DSM V)
Criteria: 5 or more symptoms over two weeks; at least one must be:
Depressed mood or
Anhedonia (loss of pleasure)
Other symptoms: weight changes, sleep issues, fatigue, worthlessness, concentration difficulties, suicidal thoughts.
Prevalence of Depression
Approximately 10% of the population is affected.
Genetic factors play a role, particularly in affective disorders.
Treatment Options for Depression
Options vary based on severity:
Mild Depression: Low intensity psychotherapy (e.g., CBT)
Severe Depression: High intensity psychotherapy or antidepressants (e.g., SSRIs).
Brain stimulation for treatment-resistant depression.
Biological Models of Depression
Monoamine Theory: Depression linked to underactivity of serotonin/norepinephrine systems.
Neuroplasticity Theory: Depression associated with decreased neuroplasticity.
Antidepressants and Controversy
Debate exists regarding the effectiveness of SSRIs for mild to moderate depression; more significant effects noticed in severe cases.
Neuroplasticity Theory and Antidepressants
Antidepressants increase neuroplasticity, correlating with improved depressive symptoms; linked to BDNF.
Summary of Biological Models of Depression
Monoamine theory: Focuses on monoamine underactivity.
Neuroplasticity theory: Connects depression with diminished neuroplasticity.
Brain Stimulation Treatments
Alternatives are considered if pharmacological methods fail.
Techniques include tDCS, rTMS, and ECT for treatment-resistant cases.
tDCS and rTMS Overview
Both techniques target the prefrontal cortex; shown to improve depressive symptoms over multiple sessions.
Structural and Functional Differences in Depression
Studies have shown grey matter reductions in crucial brain areas, such as the prefrontal cortex and amygdala.
Cognitive Effects of Depression
Mood-congruent memory: Depressive mood enhances the recall of negative memories.
Conclusion on Depression
Summarize models and treatment options, considering the structural, functional, and cognitive impacts of depression.
References for Further Study
Include suggested readings and additional resources for deeper insights into the topics discussed.