Class 4: Schizophrenia and Psychotic Disorders (Chapter 9) PDF

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University of Toronto

Dr. Dean Carcone, C.Psych

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schizophrenia psychopathology mental health psychology

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This document is a lecture on schizophrenia and psychotic disorders. It covers the introduction to psychopathology, updates on the course material, and different aspects of schizophrenia, including symptoms and historical perspective. The document also includes quiz questions and case examples.

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Class 4: Schizophrenia and Psychotic Disorders (Chapter 9) Introduction to Psychopathology Instructor: Dr. Dean Carcone, C.Psych 1 UPDATES Differences between Chapter 9 and lecture: Book doesn’t include much detail about psychotic disorders other...

Class 4: Schizophrenia and Psychotic Disorders (Chapter 9) Introduction to Psychopathology Instructor: Dr. Dean Carcone, C.Psych 1 UPDATES Differences between Chapter 9 and lecture: Book doesn’t include much detail about psychotic disorders other than schizophrenia. We will discuss these in a bit more detail and review how to distinguish between schizophrenia and these other conditions Testability of videos Assignment 1 – Due Oct 11 at 1:00pm Quiz 1: 81% average SCHIZOPHRENIA Characterized by: Part of the spectrum of - profound disruption of basic psychological processes psychotic disorders - a distorted perception of reality Psychosis = “break from reality” - altered or blunted emotion - disturbances in thought, motivation, and behavior https://www.youtube.com/watch?v=iGH7hGkkMrU Facts about schizophrenia Prevalence 1% of the population 300 000 in Canada Onset Typically between 15–45 years of age Demographics Men and women at roughly equal risk Socio-economic Observed at all socio-economic levels 5 Quiz The most common type of hallucinations are __________. A. Tactile B. Visual C. Multi-sensory D. Auditory E. Olfactory 6 HISTORICAL PERSPECTIVE Schizophrenia is a complex mental disorder Very heterogeneous in terms of symptoms Difficult to predict prognosis of treatment, which treatments will work, biological markers for the disorder, etc. Although the term “schizophrenia” is derived from “splitting of the mind” it is not suggesting “split personality”, it suggests a splitting from reality We also need to be mindful of what treatment gains we should expect. Does successful treatment mean that symptoms disappear or that the patient is able to resume career/education, reconnect with friends and family, lead a normal life? HISTORICAL PERSPECTIVE People have been defined as “mad” for centuries Auditory hallucinations were rarely reported in cases of “madness”, “insanity”, or “lunacy” prior to 1700 Only in the 1880s did schizophrenia became more of a defined disorder (e.g., Kraepelin’s first classification system) Once defined, cases surged E.g., 2000% increase in Maritime Canada between 1847 and 1960 Factors such as industrialization, urban vs. rural living, and environmental changes may have a large role in the increase in schizophrenia prevalence rates E.g., industrial revolution of the late 1880s onwards PREVALENCE & DEMOGRAPHIC FEATURES Onset is usually marked by psychotic symptoms, typically in late adolescence or early adulthood Very rare for cases to appear after 45 Can be abrupt or gradual onset Men tend to develop it earlier, early to mid-20s (females later) Prognosis Poorer for males and those who have onset at younger age It is a chronic and relapsing disorder Even with favorable outcome, typically termed “attenuated psychosis syndrome” rather than “in remission” PREVALENCE & DEMOGRAPHIC FEATURES Occurs more frequently in lower SES groups Once people have the disorder, very much less likely to complete school or work Additional diagnoses are common, depression, suicide attempts, drug and alcohol abuse Places a heavy burden on the economy and society Billions of dollars annually Inpatient services Psychiatric case management Much more direct client care and supports are required Stigma Family members usually act as caregivers US statistics SYMPTOMS AND CHARACTERISTICS Traditionally, people generally thought there were three classes of symptoms; however, the textbook and DSM defines two classes (positive and negative only) Positive Negative Cognitive POSITIVE, NEGATIVE, AND COGNITIVE SYMPTOMS OFTEN ASSESSED Positive Delusions Grandiosity Conceptual disorganization Suspiciousness/ Persecution Hallucinations Hostility Excitement Negative Blunted affect Difficulty in abstract thinking Emotional withdrawal Lack of spontaneity and flow of Poor rapport conversation Passive/apathetic social Stereotyped thinking withdrawal Cognitive/General Somatic concern Unusual thought content Psychopathology Anxiety Disorientation Guilt feelings Poor attention Tension Lack of judgment and insight Mannerism and posturing Disturbing of volition Depression Poor impulse control Motor retardation Preoccupation Uncooperativeness Active social avoidance HALLUCINATIONS Hallucinations are misinterpretations of sensory perceptions that occur while a person is awake and conscious Can occur for any sensory modality, but auditory hallucinations are the most common Must be perceived as distinct from the person’s own thoughts (i.e., not their own internal thought dialogue) and may include instructions to perform actions that involve self-harm or danger Underlying problem may be a misattribution of sensory experience and inability to discriminate between internal and external sources of information Inability to recognize their own thought dialogue and a tendency to attribute these thoughts to external sources (for auditory hallucinations) HALLUCINATIONS Anyone has the propensity to experience a hallucination Hallucinations also occur in many medical disorders: people with visual disorders (e.g., Charles Bonnet syndrome), Sensory deprivation, Parkinson’s disease, migraines, delirium, narcolepsy, Alzheimer’s/dementia, drug use https://www.youtube.com/watch?v=syjEN3peCJw HALLUCINATIONS These describe realistic perceptions in the absence* of external sensory sensory occurring while the person is fully awake. Auditory hallucinations may be heard inside or outside the head; typical examples include: A voice keeping running commentary of behavior/thoughts Two or more voices conversing with each other Distinguishable words, not muffled Visual hallucinations may be simple (e.g., shapes/colours) or complex (e.g., people, animals) Must not be an illusion or and misperceptions of a real external stimulus Tactile hallucinations, e.g., feelings of electricity, bugs/insects Need to distinguish between symptoms with an actual origin Hallucinations in taste or smell More difficult to assess If interested, here is a great TED talk on hallucinations: https://www.youtube.com/watch?v=SgOTaXhbqPQ https://www.youtube.com/watch?v=EvN7R1oRuOI https://www.youtube.com/watch?v=A-H7iJMo4fc DELUSIONS Delusions are implausible beliefs that persist despite reliable contradictory evidence Reflect a disorder of thought content Could include a complex belief system or just a single belief relating to one aspect of daily life May develop in people who make interpretations too quickly and jump to conclusions based on minimal evidence May also be a bias in reasoning so that negative events are always perceived as coming from environment or from other people Type Content Examples DELUSIONS Persecutory A belief that the individual is being conspired “Strangers on the street are (aka Paranoid) against, deceived, or persecuted (sabotage, undercover agents following ridicule, deception) me” Referential A belief that events, objects, or other “Each song that a DJ selects for individuals have personally relevant a radio playlist represents a meanings. Advertisement may be a signal to special truth about my life” eat a certain breakfast. Somatic Perception of a change or disturbance in “My body is inhabited by personal appearance or bodily function. extraterrestrial beings that give me headaches” “Inner organs are now dust” Religious Unusual religious experiences or beliefs. Not “Satan is leaving messages for uncommon to describe self as living out a me in television programs and biblical prophecy. emails” Grandiose Possession of special or divine powers, “I have the power to change the abilities, or knowledge course of history” DELUSIONS Examples of SCID screening questions: Has it ever seemed like people were talking about you or taking special notice of you? What about receiving special messages from the TV, radio, or newspaper, or from the way things were arranged around you? What about anyone going out of their way to give you a hard time or trying to hurt you? Have you ever felt that you were especially important in some way or that you had special powers that other people could not do? Have you ever felt that something was very wrong with you physically, even though your doctor said nothing was wrong… like you had cancer or some other terrible disease? Have you ever been convinced that something was very wrong with the way a part or parts of your body looked? https://www.youtube.com/watch?v=8EyQgD51OPg MOTOR & GROSSLY DISORGANIZED BEHAVIOR Disruptions in motor function: Catatonia: significant reduction in motor responsiveness Can include Waxy flexibility: allowing others to move their body and limbs and then maintain that position Grossly disorganized behavior: Difficulty with goal-directed behavior (e.g., finding your way to class; cooking/preparing a meal) Unpredictable movements Problems dressing or hygiene Inappropriate sexual behavior QUIZ Priya, a 34-year-old woman, has been exhibiting some unusual behavior recently. She has become increasingly preoccupied with seemingly random occurrences in her daily life. For example, she firmly believes that the way people arrange their furniture or the license plate numbers she sees on the road are direct messages meant specifically for her. Sarah is convinced that these messages hold a profound and personal significance, and she spends hours each day analyzing them for hidden meanings. She is adamant that these messages are a part of a grand conspiracy meant to communicate with her alone. What type of delusion is Sarah most likely experiencing? A) persecutory B) somatic C) religious D) grandiose E) referential 24 NEGATIVE SYMPTOMS Represents deficits and losses in normal functioning Avolition, refers to the inability to initiate and persevere in activities (apathy, often manifesting in a lack of personal hygine) Affective flattening, referring to a lack of emotional expressiveness, failing to convey any feeling in their face, tone, body language Anhedonia, denotes lack of pleasure or rewarding experiences Usually associated with deficits in academic and occupational functioning as well as adjusting to the community DISORGANIZED SPEECH & THOUGHT DISORDER Characterized by a number of presentations: Unusual-sounding, nonsensical speech Loosening of associations: loss of logical connections between ideas Tangential thinking: moving from one topic to another quickly https://www.youtube.com /watch?v=T9U5UcgOfzo More easily observable and can serve as an objective index of disturbance than symptoms like hallucinations and delusions Markers of Schizophrenia Cognitive Deficits 71-75% Slowness writing symbols paired with numbers (processing speed) 63-80% Impaired ability to filter out redundant information (sensory gating) 62-75% Impaired learning and recall of words and stories (verbal memory) 50-71% Impaired ability to attend to one message and ignore another (dichotic listening) 53-64% Reduced ability to generate words rapidly (phonemic word fluency) 52-62% Slow and inaccurate detection of specified letters (ability to sustain attention) 27 THE PROGRESSION OF SCHIZOPHRENIA AND FUNCTIONAL DECLINE 28 Know DSM-5 DIAGNOSTIC CRITERIA FOR SCHIZOPHRENIA This (A) Two or more of the following, each present for a significant portion of time during a 1-month period (or less if treated). At least one symptom must be #1-3 (1) Delusions (2) Hallucinations (3) Disorganized speech (frequent derailment, incoherence) (4) Grossly disorganized or catatonic behavior (5) Negative symptoms (diminished emotional expression, avolition) (B) For a significant portion of the time since onset of disturbance, level of functioning in one or more areas (work, interpersonal, self-care) is below level achieved prior to onset. (C) Continuous signs of the disturbance persist for at least 6 months. This 6-month period must include at least 1 month of symptoms (or less if treated) as defined in criterion A (active-phase symptoms) and may include periods of prodromal or residual symptoms. During these prodromal or residual periods, the signs may be manifested by only negative symptoms or by two or more symptoms listed in A with an attenuated form (e.g., odd beliefs, unusual perceptual experiences) (D) Rule out schizoaffective disorder, MDD, BP with psychotic features because either no depression/manic episodes have occurred concurrently or were not present for most of the total duration of A symptoms. (E) Not attributable to substance, medication, medical condition. (F) If autism or communication disorder present, diagnosis can be given if only delusions or hallucinations present, for at least 1 month or less if treated. CASE EXAMPLE Gregory Baker 20-year-old man Brought to the ER by campus security “I am the Joker – I am looking for Batman” BREAK TIME ACTIVITY “Realistic Schizophrenia Simulation” – headphones, please! https://www.youtube.com/watch?v=63lHuGMbscU OTHER PSYCHOTIC DISORDERS Delusional Disorder One or more delusions with a duration of 1 month or more Diagnosis of SCZ never been met Brief Psychotic Disorder Presence of one (or more): delusions, hallucinations, disorganized speech, grossly disorganized/catatonic behavior At least one symptom from the first three categories The duration is 1 day to 1 month (then it may become…) Schizophreniform Disorder Two (or more) of the following symptoms for at least one month: delusions, hallucinations, disorganized speech, grossly disorganized/catatonic behavior, negative symptoms At least one must be from the first three The duration is 1 month to 6 months (then it would be SCZ) OTHER PSYCHOTIC DISORDERS Know This Schizoaffective Disorder Basically, a major mood disorder (MDD, manic) concurrent with symptoms of SCZ See https://www.youtube.com/watch?v=oIvng9WbISo A. Two or more of the following presentations, each present for a significant amount of time during a 1- month period. At least one of these must be from the first three below. Delusions Hallucinations Disorganized speech (e.g., frequent derailment or incoherence) Grossly disorganized or catatonic behavior Negative symptoms (i.e., diminished emotional expression or avolition) B. Hallucinations and delusions for two or more weeks in the absence of a major mood episode (manic or depressive) during the entire lifetime duration of the illness. C. Symptoms that meet the criteria for a major mood episode are present for the majority of the total duration of the active as well as residual portions of the illness. D. The disturbance is not the result of the effects of a substance (e.g., a drug of misuse or a medication) or another underlying medical condition. The following are specifiers based on the primary mood episode as part of the presentation. Bipolar type: includes episodes of mania and sometimes major depression. Depressive type: includes only major depressive episodes. OTHER PSYCHOTIC DISORDERS Substance/Medication-Induced Psychotic Disorder E.g., Cannabis-Induced Psychotic Disorder Schizotypal Personality Disorder is NOT a psychotic disorder but is related to them. We will cover this in a later class Other specified psychotic disorders: Persistent auditory hallucinations Delusions with significant overlapping mood symptoms Attenuated psychosis syndrome (below threshold) Psychotic Disorder – Not Otherwise Specified DIFFERENTIAL DIAGNOSIS MDD + Psychotic Features vs Schizoaffective Disorder Patients with major depression with psychotic features (MDD with PF) only experience psychotic features during their mood episodes. In contrast, schizoaffective requires at least 2 weeks in which there are only psychotic symptoms (delusions and hallucinations) without mood symptoms. Patients with MDD with PF do not meet criterion A of schizoaffective disorder. 35 DIFFERENTIAL DIAGNOSIS Bipolar Disorder vs Schizoaffective Disorder Similar to the contrasts with MDD w/ PF, patients with bipolar disorder with psychotic features only experience psychotic features (delusions and hallucinations) during a manic episode. Again, schizoaffective requires a period of at least 2 weeks in which there are only psychotic symptoms without mood symptoms. Psychotic features in bipolar disorder do not meet criterion A of schizoaffective disorder. 36 CASE EXAMPLES Adapted from DSM-5 Clinical Cases CASE EXAMPLES Adapted from DSM-5 Clinical Cases NEUROPSYCHOLOGICAL & NEUROIMAGING FACTORS Both fields generally suggest “hypofrontality” Can affect personality, self-awareness, motivation, thinking, impulsivity, social behavior Frontal lobe function could be a predictor of SCZ itself or indicator of severity But-- frontal lobe deficiency does not provide definitive support for a diagnosis of SCZ Could be a product of lower intellectual functioning overall, as patient groups are generally 50-67% lower fMRI: less than 50% have reduced blood flow or metabolism in the frontal area during tasks NEUROPSYCHOLOGICAL & NEUROIMAGING FACTORS MRI: third and lateral ventricles are enlarged, which suggests compression or loss of existing nerve tissue Reduced grey matter volumes in medial temporal lobe (MTL), superior temporal lobe, and PFC Related to cognitive/executive function deficits Again not all patients show smaller MTLs, HCs, abnormal metabolism, etc. NEUROPSYCHOLOGICAL & NEUROIMAGING VARIABLES Finally, diffusion tensor imaging (DTI) is a different kind of MRI technique that lets us see the integrity of the pathways between brain regions (white matter paths) Specific connective tissues or tracts like the corpus callosum and those that connect frontal lobe with other areas seem to be affected in SCZ SOCIAL COGNITION FACTORS Emotion recognition is a good index of social functioning Six basic emotions are said to be universality recognized Acute Phase (Daros et al., 2014; Ruocco et al., 2014) BIOLOGICAL FACTORS Genetic contribution: is high but not 100% children of two parents = 35% Compare to Huntington’s (rare genetic disorder): 50% chance with 1 parent; 100% when both have gene A lot of molecular genetics research has been conducted, but very difficult to reproduce consistently A single gene only increases the risk of developing SCZ by 1-1.5% because there are so many interactions BIOLOGICAL FACTORS Likely Not Tested BIOLOGICAL/PSYCHOLOGICAL FACTORS Pregnancy and birth complications: Mother’s exposure to flu/illness during pregnancy increases risk Birth-related complications can increase risk Additional factors: High-risk children appear to display withdrawn and socially reclusive behavior, antisocial/aggressive behavior, motor difficulties, and lower than average intellectual abilities Family environment: Family hostility, lack of support, critical attitudes, over- involvement High expressed emotion directed at family members with the disorder Also occurs in families of people with mood/eating disorders ETIOLOGY OF SCHIZOPHRENIA Psychoanalytic: emotional traumas, inadequate parenting Severely rejecting mother = schizophrenogenic Sociocultural: strong correlation between poverty and schizophrenia, replicated many times since the 1930s social drift: people from lower SES classes get “stuck there” reduced IQ associated with extreme poverty may prevent work/education and lead to amotivation effects of poverty: more substance use, stigma, homeless disparities between rich and poor are more visible in large urban cities (e.g., Toronto, Chicago) Diathesis-stress models are popular for schizophrenia A biological vulnerability that is inherited or acquired early in life “Switches” in the brain turned on by stress MOST FAMOUS ETIOLOGICAL MODEL: MEEHL’S MODEL “Hypokrisia” = biological diathesis that causes nerve cells to Biological diathesis be abnormally reactive to incoming sensory info (similar in (hypokrisia) autism) Can be suppressed by other genes No Cognitive Disease progression results in subtle cognitive disturbance called cognitive slippage: information is disorganized, SCZ slippage incoherent, and scrambled → increases thought disorder risk High IQ can prevent further progression Expression of cognitive slippage leads to unpleasant social No Aversive experiences, amplifying pain, weakening pleasure, making SCZ drift social relationships difficult Leads to aversive drift (negative symptoms) If person has all three dispositions, higher propensity for SCZ No (“Schizotype”) but can still be spared Schizotype SCZ SCZ more likely when exacerbating factors involved: SCZ shyness, anxiety, low energy, weak motivation, and low ability, talent, low SES MEEHL’S MODEL Aside from being just very complicated (i.e., not parsimonious), one criticism is that Meehl’s theory lacks integration of why the disorder emerges in adolescence Lack of empirical support for the three specific factors (hypokrisia, cognitive slippage, aversive drift) As we’ve seen, there are a nlot of biological/cognitive/social factors relevant to the development of symptoms, not one specific factor in each area Subtle brain injuries that affect areas that normally mature in adolescence may be important (e.g., prefrontal cortex) Stress of maturation on the weakened brain may precipitate the illness Hormonal interaction with stress may be another avenue Neuroanatomical and neurochemical theories are also more evolved than what Meehl has suggested BIOLOGICAL FACTORS THE DOPAMINE HYPOTHESIS Dopamine – catecholamine family of neurotransmitters Chlorpromazine blocks dopamine receptors (D2) 49 Abnormal concentrations of dopamine **receptors** NEUROCHEMICAL FACTORS Dopamine is central to the disorder in more than one way: 4 neurocircuits are involved: (1) Mesolimbic: involved in reward and regulation of emotional behaviors Too much dopamine signaling here (1) leads to hallucinations/delusions (2) Mesocortical: Involved in emotional and cognitive functioning, executive functions (2) Too little dopamine signalling here (hypofrontality), leads to negative and cognitive symptoms NEUROCHEMICAL FACTORS (1) Mesolimbic (2) Mesocortical (3) Nigrostriatal (4) Tuberoinfundibular Untreated SCZ High dopamine Low dopamine Normal Normal signaling signaling Effects Positive symptoms Cog/Neg. symptoms TREATMENT: MEDICATIONS Historical: insula coma, psychosurgery, frontal lobotomies, shocks Typical antipsychotics (Dopamine receptor antagonists) Chlorpromazine: reduced agitation, mania, mood disturbances, and reduced the positive symptoms of schizophrenia May actually exacerbate negative/cognitive symptoms Minority benefit, others have unpleasant side effects NEUROCHEMICAL FACTORS (3) Nigrostriatal pathway: from substantia nigra → striatum Normally allows to make coordinated movements (3) Typical antipsychotics lead to low dopamine signaling, resulting in parkinsonian symptoms (4) tuberoinfundibular pathway: Normally dopamine inhibits prolactin release in the infundibular area Typical antipsychotics lower dopamine (4) signaling, which releases the pathway and stimulates the mammary glands (in both men and women) leading to undesirable side effects (1) Mesolimbic (2) Mesocortical (3) Nigrostriatal (4) Tuberoinfundibular Untreated SCZ High dopamine Low dopamine Normal Normal signalling signalling Effects Positive Cog/Neg. symptoms symptoms Typical Normal (even) Lower Low Low Antipsychotic (D2 Antagonist) Effects Lack of Cog/Neg Parkinsonism Elevated prolactin pleasure/reward symptoms (motor movements, (undesirable side effects) (substance tardive dyskinesia) abuse potential) Atypical antipsychotics are now preferred (Dopamine and serotonin receptor antagonists) Examples: Risperidone and olanzapine Provides symptom control with fewer side effects Many do not experience full recovery for occupational, cognitive, and daily living skills, or social skills TREATMENT: PSYCHOTHERAPY More challenging given the complexity and most commonly used as an adjunct to medication CBT approach developed by Beck and colleagues: Targets: emotional disturbance, psychotic symptoms, social disabilities, and risk of relapse Techniques: psychoeducation, normalization of symptoms, belief modification, and coping strategy enhancement, reduce catastrophic misinterpretations Taught how to interpret relevant environmental events and how to response appropriately to social cues while interacting and communicating with people https://www.youtube.com/watch?v=JG0w1Ig3eyA TREATMENT: PSYCHOTHERAPY Social Skills Training Correcting the functional disabilities and social impairments Appropriate social interactions, coping with stress, household management, developing employment-related abilities Cognitive Remediation and Emotion Recognition Training Target specific thinking skills such as memory and attention by teaching compensatory strategies, exercises, group discussions, with the goal of enhancing cognitive ability Family Therapy Active involvement from family members in treating the disorder, helping the individual adjust Focus on emotional communication and miscommunications, problem-solving, and stress-related coping skills Likely Not TREATMENT: EARLY ACCESS, AWARENESS, AND PREVENTION Tested Focus on Youth Psychosis Prevention Clinic (CAMH) is dedicated to the early identification and treatment of people aged 16 to 35 who are at risk of developing psychosis. “We try to identify and treat early signs of psychosis as early as possible. The people we help are young people who become distressed by changes in their thoughts, perceptions and feelings. These changes may be difficult to describe to others and often become a source of concern for young people and their families. Mental and emotional problems are often like physical problems; the sooner they are treated, the better. In the past it was common to delay active treatment until clear signs of psychosis appeared. However, the longer an illness is left untreated, the greater the disruptions to the person’s ability to study, work, make friends and interact comfortably with others. Psychosis happens when a person loses contact with reality and cannot tell the difference between what is real and what is not. Psychosis usually appears in a person’s late teens or early twenties. About three out of every 100 people will have a psychotic episode in their lifetime. [The program involves] six months of follow-up care. This includes weekly or biweekly appointments with a psychiatrist for symptom monitoring to ensure symptoms do not progress. It may include psychosocial treatment, such as our ten-week group therapy program designed to provide skills and stress reduction techniques for coping with or reducing risk symptoms. It may also include medication prescription and monitoring. Clients will work in collaboration with the treatment team to develop a care plan that fits their needs” TREATMENT: EARLY ACCESS, AWARENESS, AND PREVENTION TREATMENT: EARLY ACCESS, AWARENESS, AND PREVENTION …. acute exposure to both natural and synthetic cannabinoids can produce a full range of transient symptoms, cognitive deficits, and psychophysiological abnormalities that bear a striking resemblance to some of the features of schizophrenia. Also clear is that, in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. Finally, exposure to cannabinoids in adolescence confers a higher risk for psychosis outcomes in later life and the risk is dose-related. However, it should be remembered that the majority of individuals who consume cannabis do not experience any kind of psychosis. Radhakrishnan, R., Wilkinson, S. T., & D’Souza, D. C. (2014). Gone to pot–a review of the association between cannabis and psychosis. Frontiers in psychiatry, 5, 54. WHAT PEOPLE WITH SCHIZOPHRENIA WANT YOU TO KNOW https://www.youtube.com/watch?v=y--hNvtcIVk

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