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Understanding Schizophrenia J. Daniel Ragland PhD Associate Professor of Psychiatry
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Clinical Features Brain disorder - impairs ability to perceive, understand and interpret the environment. 1% worldwide. Impaired function - social and motivational Behavioral syndrome - positive and negative symptoms Onset in late teens to early 20s Unremitting course with later onset & better outcome for women Genetically complex - like heart disease Genetic & environmental factors Multiple genes with variable penetrance
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Symptoms At least 4 weeks of 2 of the following Hallucinations Delusions Negative symptoms Disorganization Minimum duration of 6 months of continuous signs of illness Functional decline!
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First treatment Prodrome onset Early development Adolescence Premorbid phase Prepsychotic phase First episode Relapses 10 15 20 25 Age Residual phase Untreated illness Clinical Course Keshavan
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Heterogeneity of Schizophrenia Symptom diversity DSM subtypes; paranoid, undifferentiated, disorganized, catatonic Other typologies; type I and type II (Crow), deficit and non deficit (Carpenter) People have increasingly tried to understand symptoms rather than the disorder itself
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Epidemiology 1% of population world wide Males and females equally affected but females have later onset and better functional outcome Onset in late adolescence, early adulthood Loss of function, inability to achieve expected function 10% SSI/SSDI, 2% GNP in direct care costs and lost productivity
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Genetics Highly heritable Risk increases with relationship e.g. 10% for first degree relative or fraternal twin, 50% concordance for monozygotic twin Environmental factors certain but poorly characterized (intrauterine malnutrition, viral illnesses, perinatal insults, drug exposure)
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t Discrete (disease) Continuous (liability) 0 1 Affectation status reflects an underlying quantitative trait: liability, susceptibility, risk of developing disease. (Endo)Phenotypes
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Causes of Schizophrenia Risk gene/environment interactions Altered neurodevelopment leading to symptoms in early adolescence/young adulthood Gross structural changes in the brain Specific functional changes in the brain Alterations in local circuit architecture Alterations in dopamine neurotransmission
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Gross Pathology n=63 Age 78.3 (SD=9.7, Range 67 - 99) Brain Weight 1192 g (SD=143, Range 932 - 1520) PMI 12.6 hrs (SD=4.9, Range 932 - 1520) Diagnoses ‘Normal brain’ 45 Alzheimer’s disease 5 Lewy body variant AD 1 Parkinson’s disease 2 Cerebrovascular lesions 6 Meningioma 2 Metastatic adenocarcinoma (lung) 1 Adult polyglucosan body disease 1
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PHFtau NFTs Ab SPs Neurodegenerative Lesions Arnold et al., 1998
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Neuron Density and Size Arnold et al., 1995
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Entorhinal Cytoarchitecture Dispersion Index Effective Radius N S N S 1.4 1.0 0.6 40 20 0 Arnold et al., 1997
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Molecular Components of Structural Plasticity Axons & Terminals Dendrites & Spines LTP Synapsin-1 Synaptophysin SNAP25 VGluT-1 VGaT GAP43 NCAM Dysbindin b-Dystrobrevin Homer MAP2 NFM/H-P- Synaptopodin F-actin Drebrin EphA4 Homer pGluR pNMDAR1 N-cadherin pCamKII Rim 1
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Specific functional changes in the brain Right BA 9 Left BA 10/46 FE Schiz FE Other Psych Neg. Sx in Patients r=-.46, p<.01 Dis. Sx in Patients r=-.40, p<.05 Dis. Sx in Patients r=-.55, p<.005
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Alterations in dopamine neurotransmission The classical dopamine hypothesis (too much dopamine in schizophrenia) rested on the observation that DA releasing drugs can cause psychosis, and the discovery that antipsychotics were dopamine antagonists.
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Alterations in dopamine neurotransmission C11 Racolpride displacement reflects DA release
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Increased subcortical DA related to psychosis
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Alterations in dopamine neurotransmission Decreased prefrontal activity may lead to subcortical DA dysregulation and psychosis Decreased PFC function VTA Increased DA +
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Progressive Neuro- developmental Model Keshavan
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Management of Schizophrenia Early intervention important for improving functional outcome Medication treatments Psychosocial Treatments
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Future Directions in the Treatment of Schizophrenia More optimistic view of outcome Much stronger focus on early intervention and prevention e.g. early psychosis clinics and prodromal studies Specific treatments for cognition in schizophrenia As molecular pathways associated with neural phenotypes become understood new, non dopamine based therapies Renewed emphasis on rehabilitation, supported employment etc.
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The classical dopamine hypothesis (too much dopamine in schizophrenia) rested on the observation th
The classical dopamine hypothesis (too much dopamine in schizophrenia) rested on the observation that DA releasing drugs can cause psychosis, ...