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 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
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 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
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 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?
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“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
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 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
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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?
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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
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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
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In general, the higher affinity a drug has for DA receptors, the more effective it is in treating schizophrenia
Haloperidol – an exception
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 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 correlated with their effectiveness receptors is
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Copyright © 2007 by Allyn and Bacon

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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
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Positive symptoms - presence of abnormal
 incoherence, hallucinations, delusions
Negative – absence of normal
 flat affect, cognitive deficits, little speech
Conventional neuroleptics (D
2 effective at treating positive blockers) mainly
Negative – might be caused by brain damage
May be best to think of schizophrenia as multiple disorders with multiple causes
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Depression – normal reaction to loss, abnormal when it persists or has no cause
Mania – opposite of depression
 Bipolar affective disorder
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 Depression with periods of mania
Unipolar – depression only
 Reactive – triggered by negative event
 Endogenous – no apparent cause
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 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
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Monoamine oxidase inhibitors (MAOIs)
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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
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 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
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 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
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 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
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 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
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 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?
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 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
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 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
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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
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 Benzodiazepines (Librium, Valium)
 Also used as hypnotics, anticonvulsants, muscle relaxants
 GABA
A agonists effects of GABA
– bind to receptor and facilitate
 Highly addictive
 Serotonin agonists (Buspirone, SSRIs)
 Reduce anxiety without sedation and other side effects
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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
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 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
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 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
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 Usually treated with neuroleptics – although effectiveness is not wellestablished
 Effectiveness of D
2 blockers suggests abnormality in basal ganglia-thalamuscortex feedback circuit
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