Identifying Youth at Clinical High Risk for Psychosis

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1 Identifying Youth at Clinical High Risk for Psychosis Jean Addington PhD University of Calgary Department of Psychiatry 1 Identifying Youth at Clinical High Risk for Psychosis Part 1: What do we know about risk for and the prodrome for psychosis 2 WHAT IS PSYCHOSIS? The word psychosis is used to describe conditions which affect the mind, where there has been some loss of contact with reality. When someone becomes ill in this way it is called a psychotic episode. 3 1

2 TYPES OF PSYCHOSIS Drug induced psychosis Organic psychosis Brief psychotic episode Schizophreniform disorder Schizophrenia Delusional disorder Bipolar disorder Schizoaffective disorder Psychotic depression 4 Symptoms of schizophrenia and other psychotic disorders POSITIVE SOCIAL DEFICITS hallucinations delusions COGNITIVE thought disorder PROBLEMS bizarre behavior NEGATIVE flat or blunted affect OTHER alogia depression anhedonia anxiety low energy somatic concerns Withdrawal 5 Genetic Risk General population 1% 2 nd degree relative 2-6% 1 st degree relative 6-13% Identical twin 48% 6 2

3 Clinical Course of Schizophrenia Premorbid Prodromal Progressive Residual Behavioral Functioning Onset of Psychosis Psychotic Symptoms B Early Intervention Is Key Premorbid Prodromal Progressive Residual Behavioral Adaptation?? First Episode Treatment Psychotic Symptoms B Early Interest in the Sz Prodrome The psychiatrist sees too many end states and deals professionally with too few of the pre-psychotic [states] With this in mind, it would seem as if we should lay great stress on the prompt investigation of failing adjustment, rather than, as is so often the case, wait and see what happens I feel certain that many incipient cases might be arrested before the efficient contact with reality is completely suspended, and a long stay in institutions made necessary. Sullivan, H.S., The onset of schizophrenia. Am. J. Psychiatry, 6, pp

4 Terminology Genetic high risk Prodromal Clinical high risk 10 Prodromal Syndromes Identified by a structured interview Attenuated positive symptom syndrome Unusual thought content, delusional ideas Suspiciousness/persecutory ideas Grandiose ideas Perceptual abnormalities, hallucinations Disorganized communication Genetic risk + deterioration syndrome Miller et al., 2003; Yung et al

5 Identifying Clinical High Risk Distressed Functioning poorly Have significant disability Help-seeking Willing to accept professional help Different from subgroup who report isolated psychotic symptoms in apparent absence of distress, disability or progressive change and who do not desire assistance 13 Variable Transition Rates Study N Rate Follow-up PACE (Aus) % 12-mo PRIME (Yale) 13 54% 12-mo PRIME (NA) 60 35% 12-mo RAP (NY) 34 27% 6-mo EDIE (UK) 23 22% 12-mo CARE (SD) 50 15% 12-mo Toronto 50 20% 12-mo 14 Survival Distribution Function in NAPLS Consortium % Non-Converted to Psychosis UHR Cases (N=291) Genetic HR Cases (N=43) Controls HSC & NPC (N=250) 0-mo 6-mo 12-mo 18-mo 24-mo 30-mo Follow-Up Epoch Cannon et al., 2008, Archives Gen. Psychiat. 15 5

6 From research what do we know about the Clinical High Risk Group? 16 Recruitment Difficulties CHR Conversion FE 0 Presentation in 1 year at the Toronto PRIME & FE Clinics 17 Symptomatic High level of depression and anxiety Many present with a range of comorbid diagnoses 18 6

7 Social Functioning Clinical High Risk subjects consistently demonstrate deficits equivalent to those seen in FE subjects in current social functioning premorbid social functioning social cognition facial affect recognition social judgments Addington et al Brit J Psych; Addington et al. in press Schiz Res 19 Cognitive Deficits Cognitive performance profiles intermediate to normal control and FE psychosis cohorts across domains of attention, memory and executive ability Preliminary but inconsistent results with respect to lower deficits in those who progress to psychosis (verbal memory and vigilance) Evidence of olfactory identification deficits that were specific to the CHR group that developed schizophrenia 20 Stress Hormones Association between stress and psychosis onset might be mediated by the effect of stress-induced cortisol secretion on neurotransmitter systems (dopaminergic and glutamatergic) Cortisol secretion is higher in prodromal cases who convert 21 7

8 Genomic Markers Existing studies support roles for candidate genes (eg Neuregulin 1, Dystrobrevin binding protein 1, DISC1) - suboptimal since they do not identify specific risk alleles Need large scale genomewide association studies to determine specific alleles associated with psychotic disorders Genetic susceptibility, endophentypes and gene environment interactions (DISC 1, COMT) 22 Genomic Markers Identify patterns of gene expression in peripheral white blood cells Test specific risk polymorphisms or other genetic variations NRG1 variant is associated with decreased activation of frontal & temporal regions, increased development of psychotic symptoms, decreased premorbid IQ (Nature Neuroscience, 2006) 23 Imaging Findings generally demonstrate changes post conversion but no differences to aid prediction Structural Reduction in grey matter and hippocampus after conversion Larger pituitary volume (due to activation of hormonal stress response) 24 8

9 Imaging Functional Activation of the parietal lobe, decreased activation of the anterior cingulate Small increases in activation with increasing task difficulty in the right lingual gyrus and bilateral temporal regions Significantly greater rate of change in the dorsolateral prefrontal cortical region 25 Clinical Trials 26 PACE Clinic, Melbourne Australia (Personal Assistance & Crisis Evaluation) Non-blind randomized trial Risperidone n=31; Supportive therapy n=28 At the end of treatment transition rates 9.7% and 36% Six months after the end of treatment transition rates 19% and 36% Those who were adherent in treatment phase less likely to relapse at follow-up McGorry et al., 2002, Arch Gen Psych 27 9

10 PRIME Trial Investigator (McGlashan, Yale) designed study with sites in Calgary, Toronto, & N Carolina Randomized double-blind parallel study of 60 prodromal comparing the efficacy of olanzapine, in preventing or delaying the onset of psychosis Medication versus placebo for 1 year, 1 year follow-up no medication 1 Year 16% of olanzapine treated patients & 35% of placebo treated patients converted to psychosis All those who converted in the treatment group did so in the 1 st month Olanzapine reduced conversion by 50% McGlashan et al., 2006 Am J Psych 28 Medication Concerns Concerns about drug side effects particularly if subjects are false positives Do not address potential environmental stressors psychosocial stress substances Clinical high risk individuals are help seeking but only 14-16% want medication (Addington & Addington, 2005) compared to 90-95% who consent to psychological treatments 29 The Early Detection and Intervention (EDIE ) (Manchester) Single blind randomized controlled trial of n=58 Psychological intervention Results at 12 months CBT 3 out of 35 converted Control 7 out of 23 converted from CBT group Morrison et al., 2004, Brit J Psych 30 10

11 Access, Detection & Psychological Treatments (ADAPT) RCT to evaluate the effectiveness of CBT compared to a supportive therapy (ST) in preventing or delaying the onset of a psychotic illness reducing the presenting concerns (depression, anxiety, functioning etc) of the clinical high risk group 31 Summary of ADAPT No change in negative symptoms No change in social functioning Improvement in anxiety, GAF, positive symptoms and depression Conversions only in ST group 32 Future Research Directions Can prediction algorithm with positive predictive power >80% be replicated/improved? Clinical risk factors, neurocognition, biomarkers Impacts risk/benefit calculus for prevention trials Which mechanisms account for psychosis onset? Neural, hormonal, and cognitive pathways Exogenous triggers (trauma, substance abuse, etc.) Are there alternatives to antipsychotic therapy? Lithium, Omega-3 fatty acids, Glycine? Cognitive and behavioral exercises to strengthen residual adaptive capacity? 33 11

12 North American Prodrome Longitudinal Study (NAPLS) NIMH program liaison: Robert Heinssen PhD Jean Addington PhD University of Calgary Kristin Cadenhead MD UCSD Tyrone Cannon PhD UCLA Barbara Cornblatt PhD Hillside Hospital Thomas McGlashan MD Yale University Diana Perkins MD University of North Carolina Larry Seidman PhD Harvard University Ming Tsuang MD Harvard University/UCSD Elaine Walker PhD Emory University Scott Woods MD Yale University Addington et al., (2007) Schiz. Bulletin 34 Aims for NAPLS Prospective Study To replicate clinical risk prediction algorithm in a new prospective sample and extend it by incorporating information on neurocognitive functioning 720 prodromal patients, 240 demographically matched controls Focus is on maximizing prediction (PPP and sensitivity) using measures easily implemented in community settings 35 Aims for NAPLS Prospective Study To investigate a model of neural dysconnectivity as the proximal mechanism underlying conversion to psychosis Gray matter density, functional connectivity/coherence 36 12

13 Aims for NAPLS Prospective Study To develop predictive biomarkers of risk for psychosis Mixture of hypothesis driven (MRI, EEG, Cortisol, candidate gene) and discovery-science (DNA, RNA, proteomics) methods Can be used to ascertain risk status of individuals before behavioral expression begins to escalate Can help identify novel targets for preventive interventions based on understanding of mechanisms underlying disease onset and course 37 Questions/Discussion 38 Thank you for your participation For information about Telemental Health education sessions: (403) Initiatives Telemental Health Current Telelearning Sessions 39 13

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