chapter 18 biopsychology of psychiatric disorders n.
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Chapter 18 Biopsychology of Psychiatric Disorders

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Chapter 18 Biopsychology of Psychiatric Disorders. The Brain Unhinged. Psychiatric Disorders. AKA psychological disorders Disorders of psychological function that require treatment by a mental health professional

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psychiatric disorders
Psychiatric Disorders
  • AKA psychological disorders
  • Disorders of psychological function that require 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
psychiatric disorders1
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
psychiatric disorders2
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?
anxiety disorders
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
anxiety disorders1
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
treatment of anxiety disorders
Treatment of Anxiety Disorders
  • Benzodiazepines (Librium, Valium)
    • Also used as hypnotics, anticonvulsants, muscle relaxants
    • GABAA agonists – bind to receptor and facilitate effects of GABA
    • Highly addictive
  • Serotonin agonists (Buspirone, SSRIs)
    • Reduce anxiety without sedation and other side effects
animal models of anxiety
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
neural bases of anxiety disorders
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
affective disorders
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
causal factors in affective disorders
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
antidepressant drugs
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
selective monoamine reuptake inhibitors
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
effectiveness of drug in treating affective disorders
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
monoamine theory of depression
Monoamine Theory of Depression
  • Underactivity of serotonin (5HT) and norepinephrine (NE)
    • 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
diathesis stress model
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
sleep deprivation
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?
brain damage and unipolar depression
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
tourette s syndrome
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
tourette s syndrome1
Tourette’s Syndrome
  • Usually treated with neuroleptics – although effectiveness is not well-established
  • Effectiveness of D2 blockers suggests abnormality in basal ganglia-thalamus-cortex feedback circuit
  • “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
causal factors in schizophrenia
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
antipsychotic drugs
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?
dopamine da theory of schizophrenia
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
dopamine da theory of schizophrenia1
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 D1 and D2 receptors, it and the other butyrophenones bind to D2
  • Degree that neuroleptics bind to D2 receptors is correlated with their effectiveness
problems with the d 2 theory
Problems with the D2 Theory
  • Clozapine, an atypical and effective neuroleptic, acts at D1, D4, and serotonin receptors. But – some binding to D2
  • 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
problems with the d 2 theory1
Problems with the D2 Theory
  • Positive symptoms - presence of abnormal
    • incoherence, hallucinations, delusions
  • Negative – absence of normal
    • flat affect, cognitive deficits, little speech
  • Conventional neuroleptics (D2 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