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.

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