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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Chapter 18 biopsychology of psychiatric disorders

Chapter 18Biopsychology of Psychiatric Disorders

The Brain Unhinged

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