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  • 1. Chapter 15 Behavioral Neuroscience of Psychiatric Disorders The Brain Unhinged
  • 2. Psychiatric Disorders
    • AKA psychological disorders
    • Disorders of psychological function that warrant treatment by a mental health professional
    • Neuropsychological disorders - a product of dysfunctional brains – but so are psychiatric disorders
    • Historically:
      • Neuropsychological disorders – brain problem
      • Psychiatric – mind problem
  • 3. Psychiatric Disorders
    • More influenced by experiential factors
    • Tend to be the product of more subtle forms of brain pathology
      • Underlying dysfunction may yet to be identified, but are suggested by the effectiveness of treatments
    • Tend to be less well understood
  • 4. Psychiatric Disorders
    • What are the advantages and disadvantages of societal acceptance of psychological disorders as diseases with a biological basis?
    • Are there some conditions for which this acceptance already exists?
  • 5. Schizophrenia
    • “ splitting of psychic functions”
      • Refers to the breakdown of integration of emotion, thought, and action
    • Affects 1% of the population
    • A diverse disorder – multiple types exist with varied profiles
    • Some symptoms: delusions, hallucinations, odd behavior, incoherent thought, inappropriate affect
      • Only 1 needed for 8 months for diagnosis
  • 6. Causal Factors in Schizophrenia
    • Clear genetic basis
      • Inherit an increased risk for the disorder
    • Multiple causes
      • Several different chromosomes implicated
      • Associated with various early insults – infections, autoimmune reactions, toxins, traumatic injury, stress
    • Appears that interference with the normal development of susceptible individuals may lead to development of the disorder
  • 7. Antipsychotic Drugs
    • Much of our understanding of schizophrenia is a consequence of the drugs that are able to treat it
    • Chlorpromazine – calms many agitated schizophrenics and activates many emotionally blunt
    • Reserpine – also found to be effective
    • Both drugs are not effective for 2-3 weeks and Parkinson-like motor effects are seen
      • Suggesting a role for what neurotransmitter?
  • 8. Dopamine (DA) Theory of Schizophrenia
    • 1960 – link between DA and Parkinson’s Disease established
    • Side effects of antipsychotic drugs suggests role for dopamine: Drugs work by decreasing DA levels, disorder is a consequence of DA overactivity
      • Reserpine depletes brain of DA and other monoamines by making vesicles leaky
      • Amphetamine and cocaine are DA agonists and produce psychosis
      • Chlorpromazine antagonizes DA activity by binding and blocking DA receptors
  • 9. Dopamine (DA) Theory of Schizophrenia
    • In general, the higher affinity a drug has for DA receptors, the more effective it is in treating schizophrenia
    • Haloperidol – an exception
      • While most antipsychotics bind to D 1 and D 2 receptors, it and the other butyrophenones bind to D 2
    • Degree that neuroleptics bind to D 2 receptors is correlated with their effectiveness
  • 10.  
  • 11.  
  • 12. Problems with the D 2 Theory
    • Clozapine, an atypical and effective neuroleptic, acts at D 1 , D 4 , and serotonin receptors. But – some binding to D 2
    • Neuroleptics act quickly at the synapse, but don’t alleviate symptoms for weeks.
      • Indicates some slow-acting change must occur.
    • Schizophrenia associated with brain damage.
      • Little damage to DA circuitry
      • Damage not explained by DA theory
    • Neuroleptics are only effective for some
  • 13. Problems with the D 2 Theory
    • Positive symptoms - presence of abnormal
      • incoherence, hallucinations, delusions
    • Negative – absence of normal
      • flat affect, cognitive deficits, little speech
    • Conventional neuroleptics (D 2 blockers) mainly effective at treating positive
    • Negative – might be caused by brain damage
    • May be best to think of schizophrenia as multiple disorders with multiple causes
  • 14. Affective Disorders
    • Depression – normal reaction to loss, abnormal when it persists or has no cause
    • Mania – opposite of depression
    • Bipolar affective disorder
      • Depression with periods of mania
    • Unipolar – depression only
      • Reactive – triggered by negative event
      • Endogenous – no apparent cause
  • 15. Causal Factors in Affective Disorders
    • Affective disorders are very common
      • ~6% suffer from unipolar affective disorder at some point, ~1% from bipolar
    • Genetics
      • Concordance rate higher for bipolar than unipolar
    • Stressful experiences
      • More stress reported by those seeking treatment for depression than controls
  • 16. Antidepressant Drugs
    • Monoamine oxidase inhibitors (MAOIs)
      • Prevent breakdown of monoamines
      • Must avoid foods high in tyramine – ‘cheese effect’
    • Tricyclic antidepressants
      • Block reuptake of serotonin and norepinephrine
      • Safer than MAOIs
    • Selective monoamine reuptake inhibitors
    • Lithium – mood stabilizer
      • Not a drug – treats bipolar
  • 17. Selective monoamine reuptake inhibitors
    • Selective serotonin-reuptake inhibitors (SSRIs)
      • Prozac, Paxil, Zoloft
      • No more effective than tricyclics, but side effects are few and they are effective at treating other things
    • Selective norepinephrine-reuptake inhibitors (SNRIs)
      • Also effective
  • 18. Effectiveness of Drug in Treating Affective Disorders
    • Results are comparable with MAOIs, tricyclics, and SSRIs
      • About 50% improve, compared to 25% of controls
    • Drugs help those experiencing depression, but do not prevent future episodes
  • 19. Monoamine Theory of Depression
    • Underactivity of the monoamines serotonin and norepinephrine
    • Consistent with drug effects
      • Up-regulation of receptors at autopsy of depressed individuals consistent with this
    • Problem with theory – not all respond to monoamine agonists
  • 20. How Prozac Works
  • 21. Diathesis-Stress Model
    • Inherited genetic susceptibility (diathesis) + stress = depression
    • Support is indirect
      • Depressed people tend to release more stress hormones
      • Fail dexamethasone suppression test – normal negative feedback on stress hormones not functioning
  • 22. Sleep Deprivation
    • More than 50% of depressed patients improve after one night of sleep deprivation
    • Short-lasting: depression returns when normal sleep pattern resumes
    • Not explained by any theory
    • What does this suggest?
  • 23. Brain Damage and Unipolar Depression
    • Amygdala
    • Prefrontal cortex
      • Both involved in perception and experience of emotion
    • Terminal structures of the mesotelencephalic DA system
      • Consistent with anhedonia (lack of pleasure) experienced by the depressed
  • 24. Anxiety Disorders
    • Anxiety – fear in the absence of threat
    • Anxiety disorder – when anxiety interferes with normal functioning
      • Accompanied by physiological symptoms – tachycardia, hypertension, sleep disturbances, nausea, etc.
    • Most prevalent psychiatric disorders
  • 25. Anxiety Disorders
    • Generalized – stress and anxiety in the absence of a causal stimulus
    • Phobic – similar to generalized, but triggered by a stimulus
    • Panic disorders – may occur with other disorders, but also alone
    • Obsessive-compulsive disorders (OCDs) – obsessive thoughts alleviated by compulsive actions
    • Posttraumatic stress disorder
  • 26. Treatment of Anxiety Disorders
    • Benzodiazepines (Librium, Valium)
      • Also used as hypnotics, anticonvulsants, muscle relaxants
      • GABA A agonists – bind to receptor and facilitate effects of GABA
      • Highly addictive
    • Serotonin agonists (Buspirone, SSRIs)
      • Reduce anxiety without sedation and other side effects
  • 27. Animal Models of Anxiety
    • Assess anxiolytic potential of drugs - assume that defensive behaviors are motivated by fear, and that fear and anxiety are comparable
      • Elevated-plus-maze: time in open arms indicates less anxiety
      • Defensive-burying: More time burying, more anxiety
      • Risk-assessment test: Time freezing and assessing risk indicate anxiety level
    • Validated by effectiveness of benzodiazepines – but not all anxiety treated with such drugs
  • 28.  
  • 29. Neural Bases of Anxiety Disorders
    • Drugs suggest a role for serotonin and GABA
    • Amygdala, due to its role in fear and defensive behavior, thought to be involved
      • No pathology yet identified
  • 30. Tourette’s Syndrome
    • A disorder of tics, involuntary movements or vocalizations
    • Begins in childhood
    • Major genetic component
    • Many also have signs of ADHD and/or OCD
    • No animal models, no genes identified, imaging difficult due to tics
  • 31. Tourette’s Syndrome
    • Usually treated with neuroleptics – although effectiveness is not well-established
    • Effectiveness of D 2 blockers suggests abnormality in basal ganglia-thalamus-cortex feedback circuit
  • 32. Bringing a Drug to Market
  • 33. New Drugs
    • Why does it take so long for new drugs to be brought to market?
    • Have we become a society that believes in better living through chemistry?