Lecture 23: Anxiety and Depression Flashcards
(23 cards)
What causes disorders?
• Biopsychosocial model – Biology – Individual psychology – Social and environmental risk factors • Diathesis-stress model: disorder may develop when an underlying vulnerability is coupled w/ a precipitating event
Biological factors
• Genetics
• Prenatal risk factors
– E.g. Malnutrition, toxin exposure, maternal illness
• Exposure to environmental toxins and malnutrition during childhood and adolescence
• Neural differences associated w/ psychological disorders
Cognitive-behavioral factors
- Cognitive behavioral approach: abnormal behavior is learned
- Revised cognitive-behavioral perspective: thoughts & beliefs are types of behavior and can be studied empirically
- The premise: thoughts can become distorted, and produce maladaptive behaviors & maladaptive emotions
Internalizing disorders
characterized by negative emotions
externalizing disorders
characterized by disinhibition
Psychological disorders: treatment
• Depends on: – Diagnosis – Type and severity of symptoms • Most disorders can be treated in more than one way: – Biological – Psychological – Often both are used for best effect!
Psychotherapy
• Goal: change patterns of thoughts, behaviors
• Estimated > 400 different approaches
• Many therapists use a variety of techniques
• “Talking therapy”
– Talking or writing about emotionally charged
events reduces blood pressure, muscle tension, and skin conduction during the disclosure and immediately thereafter
– Improves immune function via reduced stress response
Behavior therapy
Behavior is learned; hence can be unlearned
– Uses classical, operant conditioning
Cognitive therapy
Distorted thoughts -> maladaptive behaviors and emotions; treatment strategies attempt to modify thought patterns. Cognitive behavior therapy can include:
• A-B-C model (Consequences of Adversity or Activating event mediated by Beliefs)
• Cognitive restructuring
• Mindfulness-based therapy
Cognitive restructuring
- Identify thoughts/beliefs influencing the disturbing emotion
- Evaluating them for accuracy & usefulness using logic and evidence, and if warranted, modifying/replacing thoughts w/ one that are more accurate & useful
Beware of programs w/o scientific evidence
- Many available therapies have no scientific basis
* Empirical research (treatment vs. control/placebo) to show treatment is effective (e.g. randomized clinical trials)
Anxiety disorders
- Most common psychiatric disorder: lifetime prevalence ~28%
- Excessive, debilitating anxiety in absence of true danger
- Panic disorder, GAD, social anxiety, OCD
- All share some emotional, cognitive, somatic and motor symptoms, even though behavioral manifestations of these disorders are quite different
General anxiety disorder
- Excessive, difficult to control anxiety & worry not associated w/ specific object or event
- LIfetime rates under 6%; 2x more likely in women than men
- Clinically significant signs of distress & disruption of daily life
- Hypervigilance -> distractibility, fatigue, irritability, and sleep problems; as well as headaches, restlessness, light-headedness, muscle pain
Panic disorder
• Episodic attacks of acute anxiety
– Few secs to few hours
• Prevalence 3-5%; women 2x more likely than men
• Physical symptoms
– Shortness of breath, irregular heartbeat, faintness, dizziness
• Anticipatory anxiety of a panic attack
– Can -> agoraphobia
Biological causes?
• Panic attacks can be triggered by ANS activation: injections of lactic acid, breathing C02 (increased HR and respiration)
• ANS (sympathetic), central (emotional)
• Heritable (heritability ~30-60%)
– No specific gene emerging, but:
– Gene encoding BDNF: regulates neuronal
development, survival; role in LTP
– Val66Met allele of BDNF gene
• Impairs extinction of conditioned fear response
• Yields atypical activity in frontal-amygdala circuit
Neural circuits: emotion
- vmPFC
- Cingulate
- Insula
- Amygdala
- Hypothalamus
Imaging of anxiety disorder
• Increased amygdala activation
– During panic attack
– Also in GAD, social anxiety disorder when viewing angry, disgusted, fearful faces
– Activation correlates with symptom severity even in subclinical populations
• Increased insular activation
• Decreased activation in orbitofrontal, vmPFC, and anterior cingulate
Reduced frontal control?
- vmPFC suppresses amygdala activation in healthy controls but not anxiety disorder
- Reduced GABA (inhibitory) throughout cortex
- Releases amygdala from cortical control
- Amygdala –> hypothalamus
- Modulation by 5HT, NE
Anxiety disorders: cognitive components
- Tendency to perceive ambiguous/neutral situations as threatening, whereas non-anxious individuals assume they are non-threatening
- Focus excessive attention on perceived threats
- Recall threatening events more easily than non-threatening events
- Exaggerate perceived magnitude & frequency of threatening events
Situational/social components
- social learning: a person could develop a fear of flying by observing another person’s fearful reaction to the closing of cabin doors
- once learned, a fear might generalize to other enclosed spaces, resulting in claustrophobia
Treatment
• Pharmacological and cognitive-behavioral
• Anxiolytics, benzodiazepines
– GABAA receptor agonist (Cl- channel)
– Amygdala has high [ ] of GABAA Rs
– Can decrease activity in both amygdala and insula
• Influx of GABA antagonists –> panic in patients with disorder (but not controls)
5HT and Anxiety
- 5HT linked to depression & anxiety
* SSRIs (e.g. fluoxetine aka prozac) also used for treatment
Behavioral & cognitive treatments for ADs
- Evidence suggests CBT works best for most adult anxiety disorders
- Drug effects may be limited to the period during which drug was taken, whereas effects of CBT persist long after treatment
- Exposure and systematic desensitization for phobias and OCD; cognitive restructuring for panic disorder
