Instructor: Dr. Nicola Gregory (ngregory@bournemouth.ac.uk)
Room: P115 L5 / L7 2024-2025
Trigger Warning: Content includes discussions of anxiety and depression symptomology.
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
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
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
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.
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.
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.
Symptoms may include:
Tachycardia
Palpitations
Hypertension
Sleep disturbances
Nausea
Dizziness
Fatigue
Rapid breathing
Prevalence: 5% affected
Comorbidity: 60-90% with other diagnoses
Heritability: 15-20% genetic contribution
Large environmental influence (stressful events, trauma, etc.).
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.
Usually starts in teenage years, often triggered by a traumatic event.
Heritability: 25-50%
High prevalence of undiagnosed SAD, with many not seeking treatment.
Psychological: Usually CBT or psychotherapy; self-referral available.
Pharmacological:
SSRIs are commonly prescribed.
Benzodiazepines used for severe cases.
Hyperactivation of Stress Response: Common in all anxiety disorders.
Activation occurs with a non-threatening stimulus.
Amygdala: Triggers stress response.
Hippocampus: Inhibits stress response by measuring cortisol levels; chronic stress can damage glucocorticoid receptors, leading to HPA axis activation.
Attentional Biases: Individuals with anxiety disorders disproportionately attend to threatening stimuli.
In SAD, this bias is most prominent in social contexts.
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).
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.
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.
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.
Continue discussion on depression in biological psychology.
Monoamines
Serotonin
Agonist
SSRIs
SNRIs
Norepinephrine
Brain Stimulation Techniques: tDCS, rTMS, ECT
Neuroplasticity
BDNF (Brain-Derived Neurotrophic Factor)
Cognitive Function
Diagnostic criteria and prevalence of depression
Understand monoamine theory and neuroplasticity theory
Explore brain stimulation for treatment
Investigate neural structure/function differences in depression.
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.
Approximately 10% of the population is affected.
Genetic factors play a role, particularly in affective disorders.
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.
Monoamine Theory: Depression linked to underactivity of serotonin/norepinephrine systems.
Neuroplasticity Theory: Depression associated with decreased neuroplasticity.
Debate exists regarding the effectiveness of SSRIs for mild to moderate depression; more significant effects noticed in severe cases.
Antidepressants increase neuroplasticity, correlating with improved depressive symptoms; linked to BDNF.
Monoamine theory: Focuses on monoamine underactivity.
Neuroplasticity theory: Connects depression with diminished neuroplasticity.
Alternatives are considered if pharmacological methods fail.
Techniques include tDCS, rTMS, and ECT for treatment-resistant cases.
Both techniques target the prefrontal cortex; shown to improve depressive symptoms over multiple sessions.
Studies have shown grey matter reductions in crucial brain areas, such as the prefrontal cortex and amygdala.
Mood-congruent memory: Depressive mood enhances the recall of negative memories.
Summarize models and treatment options, considering the structural, functional, and cognitive impacts of depression.
Include suggested readings and additional resources for deeper insights into the topics discussed.