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Psychotic Disorders

Psychotic Disorders. Biochemistry of Schizophrenia. Early Dopamine theory: the positive symptoms of schizophrenia result from excessive activity of dopamine in brain. Support for Theory. action of neuroleptic drugs. action of amphetamines.

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Psychotic Disorders

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  1. Psychotic Disorders

  2. Biochemistry of Schizophrenia Early Dopamine theory: the positive symptoms of schizophrenia result from excessive activity of dopamine in brain Support for Theory • action of neuroleptic drugs • action of amphetamines • abundance of D2 receptors in SCZ

  3. Revised Dopamine Theory of Schizophrenia (or genetic predisposition) Davis et al (1991)

  4. Glutamate Hypothesis of Schizophrenia • SCZ symptoms may be due to faulty NMDA receptors • (first posed by Kim et al, 1980) • Evidence • action of PCP and ketamine (Adler et al, 1999) • genes that predispose to SCZ affect function of NMDA receptors • (Steffanson et al, 2002; Egan et al, 2004) • post-mortem studies show changes in NMDA receptors in SCZ • (Clinton & Meador-Woodruff, 2004) • glutamate neurons have a regulatory effect on dopamine and GABA

  5. Bottom Line: biochemical picture of schizophrenia involves dysregulation of dopamine – and maybe glutamate however, the picture is not simple

  6. Brain Abnormalities in Schizophrenia • enlarged ventricles • most consistent finding (replicated 90 times) • for 12 of 15 twins, the schizophrenic twin could be identified • by enlarged ventricles • decreased frontal and temporal lobe volumes • reduced amount of gray matter • reduced size of hippocampus and amygdala • increased activation of basal ganglia • (site of mesolimbic dopamine projections) • hypofrontality reduced activation of frontal lobes

  7. Neuropsych Findings • SCZs have impairment in working memory (Forbes et al, 2009) • and concentration Hoff et al, 1992) • SCZs (and 1st degree relatives) have impaired eye tracking • (Holzman., 1988) • 28 studies: SCZ have lower IQ than general population • SCZs have difficulties in sustained attention (Cornblatt, et al, 1989) • SCZs have difficulty with facial emotional recognition • (Dougherty et al, 1974) • SCZs have difficulty with habituation and sensory gating • (Braff et al, 1992; Quednow et al, 2008)

  8. Conclusions on Etiology • diathesis/stress model seems appropriate • diathesis is most likely a biological predisposition • genetic influence • perinatal (birth trauma) • gestational (flu or winter birth) • exposure to environmental toxins • stress = stressful life event or accumulation of events • biochemical dysregulation (dopamine plus other neurotransmitters) • may lead to both positive and negative symptoms and • may also lead to brain abnormalities (e.g. enlarged ventricles)

  9. Treatment of Schizophrenia • Overall goals of treatment: • decrease frequency and severity of episodes • maximize functioning between episodes • THERE IS NO CURE • Controlled studies suggest: • psychodynamic therapy is not helpful and may be harmful • family therapy and education important • early intervention leads to better outcome • illness self-management is important

  10. Pharmaceuticals 1. Conventional antipsychotics(neuroleptics) Phenothiazines Haloperidol (Haldol) Chlorpromazine (Thorazine) Fluphenazine (Prolixin) Side Effects: sedation anticholinergic (dry mouth, constipation, tachycardia) extrapyramidal (tremors, hypertension) weight gain tardive dyskenesia (involuntary movement disorder)

  11. Pharmaceuticals 1. Conventional antipsychotics(neuroleptics) Phenothiazines Haloperidol (Haldol) Chlorpromazine (Thorazine) Fluphenazine (Prolixin) Side Effects: sedation anticholinergic (dry mouth, constipation, tachycardia) extrapyramidal (tremors, hypertension) weight gain tardive dyskenesia (involuntary movement disorder) Depot: rather than oral, time-release meds may be injected

  12. Pharmaceuticals 1. Conventional antipsychotics(neuroleptics) Phenothiazines Haloperidol (Haldol) Chlorpromazine (Thorazine) Fluphenazine (Prolixin) Note that conventional antipsychotics address positive symptoms only (may even make negative symptoms worse) Side Effects: sedation anticholinergic (dry mouth, constipation, tachycardia) extrapyramidal (tremors, hypertension) weight gain tardive dyskenesia (involuntary movement disorder)

  13. Atypical Antipsychotics Clozapine (Clozaril) Advantages: no extrapyramidal side effects good for treatment-resistant patients Disadvantages: very expensive agranulocytosis (reduced white blood cell count) dose-related seizures Risperidone (Risperdal ) Olanzapine (Zyprexa): Advantages: more helpful with negative symptoms fewer extrapyramidal side effects Disadvantages: dizziness, orthostatic hypotension, weight gain Aripiprazole (Abilify) partial dopamine agonist, minimal side effects

  14. NMDA Receptor Drugs • Amino acids (glycine and D-serine) may enhance • glutamate neurotransmission • (Lane et al, 2008)

  15. rTMS (Transcranial Magnetic Stimulation)?

  16. Psychosocial Therapy GOALS A. Psychotherapy symptom management compliance with treatment support skills training relapse prevention B. Social relapse prevention re-assimilation into community family training (crisis planning, communication skills) EE reduction

  17. Best Combination of Treatments APA (1997) 1. Biological: Antipsychotic drugs 2. Psychological: supportive therapy, behavioral skills 3. Social: family counseling, group psychoeducation

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