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Schizophrenia What Is Psychosis?

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Schizophrenia What Is Psychosis? Lecture 8 Careful Clinical Observation – chlorpromazine (Thorazine) to aripiprazole (Abilify) Psychosis and Schizophrenia What is Psychosis? • Impaired reality testing - the inability to distinguish between what is real and not real. • Presence of characteristic symptoms: – Disorders of perception (hallucinations) – Disorders of thougg(ht (delusions) – Disorganized speech (disordered associations) – Disorganized or catatonic behavior (rituals) • Note that severe episodes of mood disorders may have psychotic features as secondary symptoms and are not a primary psychotic disorder,,jpp i.e. Major Depressive Episode with pypsychosis or acute mania • Patients with personality disorders (schizotypal, schizoid, borderline and paranoid) can present with psychotic symptoms Psychotic Disorders Primary Psychiatric Disorders • Schizophrenia • Schizophreniform disorder • Schizoaffective disorder • Brief psychotic disorder • Shared ppysychotic disorder • Delusional disorder Schizophrenia • Course of Illness – Onset – Most common initial presentation during adolescence • Imaging studies show this is a period with extensive CNS remodeling – Progression – Patients fall into three general groups • A single psychotic episode followed by good mentlhtal hea lth • A lifelong pattern of remission followed by relapse • Lifelong disease with no remission Schizophrenia Symptoms • Positive syypmptoms (not normally experienced by healthy individuals) – Hallucinations – Delusions – Bizarre behavior • Negative symptoms (normally found in healthy individuals, but not present or diminished) – Social withdrawal – Apathy – Inability to experience pleasure – Loss of attention control Schizophrenia: Etiology • Genetics – Concordance for monozygotic twins about 50% v. dizygotes 10% – De novo mutations arising in paternal germ cells • Environmental factors – First and Second trimester pregnancy: Viral infections, Drug Exposure – Third trimester pregnancy: Hypertension, Diuretics • Neurological Abnormalities – Decreased size/activity of pre-frontal cortex; lateral and third ventricular enlargement; abnormal cerebral symmetry; decreased brain density; decreased volume of hippocampus, amygdala and parahippocampal gyrus – EEG shows decreased alpha waves, increased theta and delta waves, epileptiform activity. Also, saccadic eye movements (poor smooth visual pursuit • Neuro transm itter Ab norma lities: DA, 5-HT, NE , Gl u tama te Developments in Medical Treatments for Psychotic Disorders ’30s ’40s ’50s ’60s ’70s ’80s ’90s ’00 ‘05 Thioridazine Clozapine ECT Trifluoperazine Risperidone Fluphenazine Olanzapine Perphenazine Quetiapine Haloperidol Ziprasidone Loxapine Chlorpromazine Typical Atypical antipsychotics antipsychotics Aripiprazole – D2 partial agonist Drug Terminology • Antipsychotic • Major tranquilizer- a misnomer • NltiNeuroleptics - promitinent neuro lilidlogical side effects (EPS) Structure of Chlorpromazine: First Neuroleptic Antipsychotic Ethylamine Core Structure Diphenhydramine Chlorpromazine • Synthesized in 1951 by Paul Charpentier at the French pharmaceutical company Rhône‐Poulenc for use in anesthesia • Henri Laborit was French army surgeon interested in artificial hibernation for the prevention of surgical shock ‐ tested chlorpromazine because the compound had been reported to lower body temperature – Observed a tendency to go to sleep along with disinterest in what was going on • Cooling with water was used in France as a means to control agitation ‐ Chlorpromazine was ⇒ recommended to physicians in the psychiatric service at Val de Grâce military hospital in Paris Chlorpromazine – cont. • First patient to receive chlorpromazine was Jacques Lh. ‐ a 24 year old severely agitated psychotic • After 20 days on therapy physicians reported that Jacques Lh. was “ ready to resume normal life” • An additional thirty‐eight patients were given chlorpromazine by Pierre Deniker at Saint‐ Anne’s Hospital with similar outcomes • Marketed by Rhône‐Poulenc in France in 1952 under the trade name Largactil False Hypotheses Behind Chlorpromazine Clllinical Development • Phenothiazines are useful in anesthesia (they do have some slight sedative properties) • Artificial hibernation could prevent surgical shock (wrong) • The most important property of chlorpromazine was its ability to lower body temperature (irrelevant) • Patient cooling was an effective means to control agitation (wrong) 1957 Albert Lasker Award for Chlorpromazine • Henri Laborit ‐ initiated clinical studies • Pierre DikDeniker ‐ condtdducted the critica l clin ica l studies in schizophrenic patients • Heinz Lehmann ‐ disseminated the full practical significance of chlorpromazine to the medical community Henri Laborit Pierre Deniker Heinz Lehmann Chlorpromazine in the Clinic • Prevents hallucinations and delusions • Prophylactic: limits emergence of these symptoms Hospital Beds Occupied by Patients with Psychiatric Disorders Yearly change in the number of hospitalized patients with psychiatric disorders (thousands) 16 Miracaceole of Chl opoorprom azin e? Limitations in Treatment with Chlorpromazine • No decrease in negative symptoms • Patients often unable to function in society • Require medication – disease is not cured • Drop in number of institutionalized patients – No substitute support system provided Antipsychotic First Generation “Typical Anti ps ychotic Dru gs” Classification Prototype PhPhenothiazinesenothiazines Aliphatics Chlorpromazine (Thorazine) Piperazine Fluphenazine (Prolixin) Perphenazine (Trilafon) Piperidine Thioridazine (Mellaril) Mesoridazine (Serentil) Butyrophenone Haloperidol (Haldol) Pimozide (Orap) Thioxanthine Thiothixene (Navane) Dibenzoxazepines Loxapine (Loxitane) Dihydroindolones Molindone (Moban) General Limitations of Conventional Antippysychotics* • Gaps in efficacy – Cognitive function – NtiNegative symp toms – Depressive symptoms • Profound number of side-effects with long-term health consequences – Anticholinergic (dry mouth, ocular changes, constipation, tachycardia, etc.) – Extrapyramidal (dystonia, akathisia, parkinsonian, dyskinesia,,) TD) – Sedation – Cardiovascular (arrhythmias, blood pressure changes) – Mtbli(Metabolic (we ihtight ga in, a ltere d g lucose, hliidihyperlipidemia) – Altered hormones (hyperprolactinemia, FSH, LH → sexual side effects) – Lowered seizure threshold *Considerable differences exist among specific antipsychotic compounds Tardive Dyskinesia late appearing extrapyramidal symptom • First evidenced at many weeks or years • Involuntary purposeless and repetitive movements (fly catching, lip smacking, etc.) •Higg,gh dose, long treatment times increase risk • Irreversible in 1/3 of patients; no proven therapy • Proposed mechanism is receptor super-sensitivity Parkinson’s Disease versus Tardive Dyskinesia Michael J. Fox Michael J Fox Parkinson's Disease - YouTube Tardive Dyskinesia Patient Tardive Dyskinesia Symptoms - (AIMSDVD.com) - YouTube What Constitutes an Ideal Antipsychotic Mood-stabilizing Efficacious for properties positive and Low EPS, TD negative symptoms Ideal Cognitive Affordable benefits antipsyc hoti c No adverse Weight long-term health Neutral Improved consequences function and quality of life What is the Mechanism by Which Neuroleptic Antipsychotics Act? Dopamine Theory ofSf Sc hizoph reni a Hyperdop aminer gic Hypodopaminergic pathways pathways Positive symptoms Negative symptoms Dopamine Hypothesis of Schizophrenia Mesocortical pathway Nigrostriatal pathway Hypoactivity: (part of EP system) neggypative symptoms amotivation cognitive deficits Mesolimbic pathway Hyperactivity: Tuberoinfundibular pathway positive symptoms (inhibits prolactin release) * Antipsychotic Drugs Mechanism of Action • Blockade of dopamine (D2) receptors is associated with positive symptom therapeutic efficacy. – A threshold value of 65‐70% of D2‐receptor occupancy is needed for therapeutic response. – EPS incidence rises as D2‐receptor occupancy increases above 80%. • Blockade of Serotonin (5HT 2a) receptors is associated with negative (or mood) symptom therapeutic efficacy. (Also 5HT2c?) (Farde L, et al.: Arch Gen Psychiatry 1992; 49:538‐544) • Elevation of prolactin levels show a threshold relationship to D2‐receptor occupancy. (Schlegel S, et al.: Psychopharmacology (Berl) 1996; 124:285‐287) • Blockade of other receptors is generally responsible for side‐effects. Phenothiazines are Dirty Drugs And They Need to be Dirty Drugs to Work Effectively Compppound Receptor Potencies (Ki values nM ) DOPAMINE SEROTONIN 5HT2A/D2 DOPAMINE MUSCAR ADRENERGIC HISTAMI INIC NE D2 5-HT1A 5-HT2A 5-HT2C RATIO D1 D4 M11A2A H1 Typical Agents Haloperidol 1.2 2100 57 4500 47 120 5.5 >10,000 12 1130 1700 Fluphenazine 0.8 1000 3.2 990 3.9 17 29 1100 6.5 310 14 Thiothixene 0.7 410 50 1360 72 51 410 >10,000 12 80 8 Perphenazine 0.8 420 5.6 130 7.4 37 40 1500 10 810 8.0 LiLoxapine 11 2550 444.4 13 040.4 54 818.1 120 42 150 494.9 Molindone 20 3800 >5000 10,000 >250 >10,000 >2000 >10,000 2600 1100 2130 Thioridazine 8.0 140 28 53 3.5 94 6.4 13 3.2 130 16 Chlorpromazine 3.6 2120 3.6 16 1 76 12 32 0.3 250 3.1 Improving Therapeutic Index Animal Models • AhiApomorphine idinduce d climbi ng – In vivo measure of dopamine receptor antagonism • Prepulse inhibition – Startle response is suppressed by warning tone – Schizophrenic patients show deficits in prepulse inhibition – Antipsychotic medications enhance prepulse inhibition • Elevated plus maze – Proposed as measure of anxiety – Benzodiazepines active Antipsychotic Next Generation “Atypi cal A nti psych oti c Drugs” Classification
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