Psychopathology Lecture Slides 2024 PDF

Psychopathology Lecture 30h Marta Porębiak, Ph.D. Office hours: by appointment Module organization Lecture - 30h, Dr Marta Porębiak, [email protected] Workshop - prac?cal workshop, 24h, Dr Marta Porębiak, [email protected] Dr Anna Braniecka, [email protected] Lecture attendance rules Class attendance on workshops is obligatory: Absence of a maximum of 20% of hours devoted to small forms in a given module is allowed. Should a student be absent more than the accepted maximum, they should immediately report to the tutor. If a student is absent for more than 50% of hours devoted to small forms in a given module, the student fails the module. For online classes, during small forms, a working camera is required. Lecture attendance rules Students should come to the class on time. If you are absent from class, it is your responsibility to get notes, handouts, etc., from another student. We are all expected to show a common courtesy and turn off our cell phones when we arrive (or, ideally, just prior to arriving) at class. You may use a laptop if it helps you to take notes however Facebook is not intended for use during classes. Any non-class related computer activity will serve as a distraction and it will undermine your experience. Lecture organisation Before: ?me for studying assigned readings Lecture listening (& notes taking, preparing ques?ons) Q&A ?me: Feel free to ask your ques/ons any/me during the lecture! AUer: ?me for studying addi?onal materials Main textbooks Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-V), Washington, DC: American Psychiatric Publishing. For workshops: Kring, A.M., & Johnson, S.L. (2017). Abnormal Psychology (13th Ed.). Hoboken, NJ: John Wiley & Sons. Textbooks Available online free of charge: Barlow, D.H., & Durand, V.M. (2012). Abnormal Psychology: An Integrative Approach (6th Ed.), Belmont, CA: Wadsworth Cengage Learning. Or order for yourself the newest version: Barlow, D.H., & Durand, V.M. (2019). Abnormal Psychology: An Integrative Approach (8th Ed.), Belmont, CA: Wadsworth Cengage Learning. Readings Assigned for each topic (check syllabus or ﬁrst lecture slides for topic and literature order). Follow the readings order upon the order of the topics discussed during lectures. Readings Assigned for each topic (check syllabus or first lecture slides for topic and literature order). Follow the readings order upon the order of the topics discussed during lectures. Lecture topics MENTAL HEALTH: NORMS AND PSYCHOPATHOLOGY Defining and understanding the historical and integrative approach to mental health and abnormal psychology. Genetic, neuroscience, behavior, cognition and emotional dimension of psychopathology. Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 1 & 2, pp. 1-66. ASSESSING AND INVESTIGATING MENTAL DISORDERS Differences between assessment and diagnosing. Use of diagnostic manuals in psychopathology (ICD-10 and DSM – V classifications). Contemporary research methods in psychopathology. Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 3&4, pp. 68-120. Lecture topics ANXIETY DISORDERS Phobias, social anxiety, panic disorder, agoraphobia, generalized anxiety disorder Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 5, pp. 122-154. OCD Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 5, pp. 163-179. Lecture topics MOOD DISORDERS Depressive and bipolar related disorders Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integra=ve Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 7, pp. 212-267. SCHIZOPHRENIA SPECTRUM AND OTHER PSYCHOTIC DISORDERS Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integra=ve Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 13, pp. 477-509 Lecture topics PERSONALITY DISORDERS Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 12, pp. 440-475. DISORDERS RELATED TO STRESS AND TRAUMA Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 5, pp. 155-162. Lecture topics SOMATOFORM AND DISSOCIATIVE DISORDERS Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 6, pp. 180-211. FEEDING AND EATING DISORDERS Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 8, pp. 269-295. SUBSTANCE RELATED AND ADDICTIVE DISORDERS Barlow, D.H., & Durand, V.M. (2015). Abnormal Psychology: An Integrative Approach (7th Ed.), Belmont, CA: Wadsworth Cengage Learning. Chapter 11, pp. 396-439. Few words about learning psychopathology Second year syndrome/medical student syndrome dimensional approach to psychopathology family history wide prevalence of mental disorders. “If thou gaze long into an abyss, the abyss will also gaze into thee” F. Nietzsche History of insanity The history of psychopathology What does it mean to be abnormal? Insane? Why is somebody abnormal? Is there anyway we can help? What are the rights of people who are seen as abnormal? Abnormality definition Time and culture bond What is accepted? What is beyond the norms? E.g. hearing voices Psychosis v. prophet v. possessed by demons? 20% of the US population suffers from at least 1 disorder within 12 months 6% from addiction - surgeon general report (Satcher, 1999). What helps in understanding abnormality 2 levels of analysis: biological psychological/environmental Role of science and prac?ce Role of developmental changes in diagnosing and understanding psychopathology EB treatments for speciﬁc disorders. History of approaches to abnormality: prehistoric period ANIMISM Idea that everything has a soul Psychopathology was understood as a possession by spirits that control the behaviour. Ancestors, animals, gods, etc. Trephines in Palaeolithic skulls reveal a way of getting the evil spirit out of the skull. History of approaches to abnormality: Ancient Greece and Rome period Roots of biological/physical explanation Around 400 BC Hippocrates separated religion and superstition Explained mental abnormality as a disease caused by external factors Kind of brain disorder caused by 4 essential bodily fluids (humors) imbalance: blood, yellow bile, black bile, and phlegm. Treatment: Biological/medical (binding, phlebotomising – blood draining) Psychological (music, cheerful conversation, bath, massage). E.g. histeria: caused by wondering womb leading to crying, dysphoria, histerical limbparesis, pain, dizziness. Treatment: applying oils and ointments in places where the womb went to searching for food or water like an animal. History of approaches to abnormality: Middle Ages Animism & Satanism Year 500-1350 in Europe: ancient ideas abandoned Insanity seen as a devil’s work Ideas of possession by evil demons and superstitions are back. Dark Ages: wars, disasters, poverty, epidemic diseases Mass madness cases: tarantism, lycanthropy A lot of anxiety and distress à need for explanations Disease as war between evil and good Insane = possessed, evil people. Treatment: exorcisms, prayers, drinking holy water. History of approaches to abnormality: Renaissance Years 1500-1600 Care of the insane was better Placed in families (Geel in Belgium – a prototype of home-based care) Twist back to biological explanations: “stone of madness/folly” – physical explanation and treatment methods Later – a step back... H. Bosch, ca. 1494 History of approaches to abnormality: Early modern period – 17th up to 18th century ANIMALISM insane are like animals, unpredictable, dangerous, not controlling oneself, they don’t feel and don’t deserve any special conditions The devil possession still viable – Salem witch trials (1691-1692) Second part of the XVI century: overcrowded cities and tendency to remove insane from families Asylums for insane and homeless In Bethlehem in London (founded 1247), bad history of public tours in 18th century „On holidays numerous persons of both sexes, but belonging generally to the lower classes, visit this hospital and amuse themselves watching these unfortunate wretches, who often give them cause for laughter. ” – about the 1725 tour (Sausurre, 1902). Deprieved from covering from cold and ither needs urecognized and unmet (Foucault, 1965). History of approaches to abnormality: Early modern period – 18th- - beginning of XIXcentury MORAL APPROACH Phillippe Pinel (1745-1826), Paris Founder of modern psychiatry, “traitement moral” The one who unbounded mentally ill people Every person deserves dignity and care Approach executed in Paris, in Bicetre (male) and Salpetriere (female) hospitals. Between 1848-1893 Jean-Martin Charcot practiced there. England: similar approach introduced by William Tuke (1732-1822), but more religion based Community based care facilities, e.g. York Retreat. Dorothea Dix (1802-1887) in the US fought for new legislative on mental care – 32 hospitals used moral therapy. History of approaches to abnormality: end of XIXth century and beginning of XXth century (Victorian era) Second part of the XIX century – the moral therapy found to be ineffective. Finally 2 perspectives: - Somatogenic (biological, physical) - Emil Kraepelin (1856-1926); psychopathology classification system; longitudinal analysis; psychopathology sources in the brain malfunctions. - Psychogenic – new approach to psychopathology and the use of different treatments: Frantz Mesmer (1734-1815) – mesmerism, “the animal magnetism”, causes and treatment on spiritual not psychological level but it inspired further hypnosis practices. Jean-Martin Charcot (1825-1893)– used hypnosis to treat paralysis and convusions in hysteria patients, pioneer of neurology Josef Breuer (1842-1925) & Sigmund Freud (1856-1939) – hypnosis, beginnings of psychoanalysis. Current approach to psychopathology and treatment Treatment is based on psychotherapy and pharmacotherapy. Integration of psychogenic and biological approach. All started from Freud’s development of psychoanalysis as a treatment method (initially for neuroses) Unconsciousness primate Defence mechanisms Symptoms as results of impulses and desires that have been repressed, supressed, denied, perverted, etc... Treatment: therapeutic conversation (analysis), relationship with analyst, making the unconscious conscious. Current approach to psychopathology and treatment Psychotherapy more needed and more common after IIWW Psychoanalysis as the main therapy approach till ‘30-’40, later: Behavioural (behaviour) Cognitive (cognitive processes) Humanistic-existential (values and choices) Psycho-social approach (society and environment role) + pharmacotherapy (biological approach) Current approach to psychopathology and treatment Use of medication in psychiatry since 1950’ antidepressant, antipsychotic (neuroleptics), antianxiety drugs; less hospitalization needed; longer reemission periods; psychiatry based on outpatient care; yet the problem of homeless ill patients occurs. Abnormality – what does it mean today? Suffering Maladaptiveness Irrationality Unpredictability and loss of control Rareness and unconventionality Observer discomfort Violation of standards (Seligman, Walker, &Rosenhan, 2001) Continuum of mental health Minimum Maximum| level level Mental disorder Mental disorder Health e.g. mood level in depression and bipolar disorder Continuum of mental health Minimum Maximum| level level Mental disorder Mental disorder Health e.g. mood level in depression depression and bipolar disorder Etiology of mental disorders Endogenous factors Predispositions within CNS Somatogenic factors originating in the body Ongoing somatic diseases leading to change sin the CNS Psychogenic factors originating in the soul (Greek and Roman perspective) Currently attributed to disrupted psycho-social development Endogenous causes Genetics: family studies, MZ and DZ twin studies, adoptive studies, DNA markers research. e.g. In bipolar disorder: 80%, chromosome X, but also chromosome 4, 10, 11, 12, 13, 18, 21 % 22 (incl. genes responsible for neurotransmitting serotonine and amino acids). In schizophrenia: 50%, genes in chromosomes 1, 5, 6, 8, 13, 18, & 22. In alcohol addiction : regions of chromosomes 1, 4, & 7. Chromosome 4 incl. gene coding the activity of alcohol dehydrogenase. Biochemical etiology and Neuroscience Disordered neural activity of the brain Neurotransmitters (e.g. dopamine, serotonine, GABA and other amino acids, noradrenaline, epinephrine). Specific brain regions (frontal, prefrontal and temporal cortex, limbic system, thalamus, pituitary gland etc...). e.g. stress and trauma disorders, depression, anxiety and psychotic disorders. Hypothalamic-Pituitary-Adrenal (HPA) axis Illustration after https://www.unh.edu/pacs/stress-and-your-body Somatogenic factors Processes originating from the body affecting functioning of the CNS: pathologies of the brain (organic brain disorders), somatic diseases, use of psychoactive substances. e.g. panic attack induced by drugs, psychosis in brain tumor, depression in pancreatic cancer, consciousness disorder due to epilepsy, neurodegenerative disorders due to chronic alcohol abuse, mood disorders due to thyroid disorders. Psychogenic factors Psycho-social factors Trauma and developmental disrup/ons e.g. smaller hippocampal and anterior cingulate volumes, increased amygdala ac/vity and decreased ac/vity of prefrontal anterior cingulate cortex in trauma survivors suﬀering from PTSD (Bremner, 2006). Social learning and condi/oning e.g. anxiety disorders, OCD. Processing by the CNS informa/on about the self and others may inﬂuence the CNS back! e.g. psychotherapy shapes the brain back! e.g. decrease of the limbic structures hyperactivity in depressed patients after psychodynamic treatment (Wiswede et al., 2014). Epidemiology of mental disorders Psychopathology Systemic Challenges Different criteria and diagnostic systems changing in time DSM –V and ICD-10 (11th from 2022). Under recognition of specific disorders and their under treatment E.g. 50% of psychiatry patients in Poland – diagnosed with psychosis v. only up to 10% of patients in the US – where this is coming from? Kessler et al. (2005) Lifetime prevalence estimates for mental disorders: (DSM-IV based) anxiety disorders, 28.8%; mood disorders, 20.8%; impulse-control disorders, 24.8%; substance use disorders, 14.6%; any disorder, 46.4%. Psychological Assessment of Psychopathology Evalua?on of mental func?ons and psychological health Unspeciﬁc methods (used also by psychiatrists, nurses, social workers etc.) Talk (to establish contact) Clinical Interview (to gather informa/on, may include interviewing family members, issue of objec/vity) Unstructured – non systemaIc approach, based on clinicians knowledge and experience, ﬂexible but also lowered reliability and validity (Meehl, 1996). Structured – use standardized protocols and sets of quesIons, easy to compare and replicate results. Evaluation of mental functions and psychological health Unspecific methods (used also by psychiatrists, nurses, social workers etc.) Observation (based on specific factors chosen upon prior hypotheses, best for gathering non-verbal data) Behavioral assessment – record of behaviors and thoughts of research or treatment (Bellack & Hersen, 1998), can be also done by patients themselves. Psychophysiological assessment – based on correlates of e.g. anxiety (cortisol levels), brain activity (EEG), heart rate, body temperature, skin conductance; used widely in a treatment method based on biofeedback (Allen and Shriver, 1998).. Neuroimaging – assessment of the brain regions activity in different conditions, e.g. CT, MRI, fMRI, PET scans. Fig.1. Decreases in prefrontal activity seen after psychodynamic therapy (in: Brody et al., 2001). Specific methods for psychological assessment Goal: to better understand patient’s problems and their mechanisms Standardized, normalized, objective, reliable and valid! Intelligence tests Different dimensions of intelligence, using tasks to complete, IQ based, usually time limited (e.g. Wechsler Intelligence Scale – WAIS-IV, Stanford-Binet test, Raven test) Neuropsychological assessment Measuring different abilities linked with brain functions, e.g. memory, reasoning, planning, motor speed (e.g. Bender Visual-Motor Gestalt test) Specific methods for psychological assessment Goal: to better understand patient’s problems and their mechanisms Standardized, normalized, objec?ve, reliable and valid! Psychological inventories Personality assessment ques/onnaires (e.g. Minnesota Mul/phasic Personality Inventory 2 – MMPI-2) Mood inventories (Beck Depression Inventory – BDI) Specific methods for psychological assessment Goal: to better understand patient’s problems and their mechanisms Standardized, normalized, objective, reliable and valid! Projective tests Ambiguous stimuli encouraging imaginary processes and free associations (e.g. Rorschach, Thematic Apperception Test - TAT, tests based on drawing). Projective tests – examples and controversies RORSCHACH (1921) TAT (1930’) inkblots pictures Assessment and diagnosis Assessment - evaluating the relevant factors in a client’s life to identify themes for further exploration in the treatment process. Diagnosis (sometimes a part of the assessment process) - identifying a specific mental disorder based on a pattern of symptoms that leads to a specific diagnosis. Both assessment and diagnosis can be understood as providing direction for the treatment process. Diagnosis – identification and giving a name to the mental state of the person Easy and shorthand Clue for the choice of treatment communication between options clinicians Both psychological and Talking about syndromes covers all pharmacological therapies symptoms Basis for scientific investigation in Diagnostic categories reflect also abnormal psychology etiology of the syndrome Creating inclusion criteria, defining Knowing diagnosis we have study groups etc. knowledge about possible cause Enables treatment payments and insurance reimbursements Systemic and health care value. Time as a factor in psychopathology diagnosis Chronic v. acute Is there an episodic pattern? Some mental disorders are characterized by their episodic dynamics (e.g. bipolar disorder) Factors that may bias diagnosis Context: hospital setting v. general population diagnostic processes. Expectation: clinicians expecting abnormalities are more likely to diagnose psychopathology and underestimate other explanations (e.g. prof. Szelenberger’s case of a patient with auditory hallucinations). Source credibility: influence from more experienced clinicians. E.g. Temerlin’s (1970) study on diagnosing upon recorded interview called by authority “quite psychotic” v. “quite healthy”. Culture: culture-bond syndromes, including Caribbean Ataque de nervios (mix of dissociative, anxiety, mood and somatoform disorder), Malaysian Koro (acute anxiety that the penis will recede into the body and cause death) (APA, 1994). Approaches to diagnosing abnormalities Categorical – symptoms that occur together create a category (e.g. hallucinations and delusions à psychosis) Old versions of DSM classifications - DSM-IV ICD-10. Dimensional – instead of detecting symptoms, we describe person’s functioning on specific dimensions, we get profile (e.g. patient is high on depression, low on impulsivity average on persistence) New DSM-V classification attempts to join categorical and dimensional approach (describes categories but also severity of the disorders). Classifications of diseases and diagnostic measures ICD by WHO DSM by APA ICD-11 DSM – work in progress… https://www.youtube.com/watch?v=8wIB8_EX9V8&ab_channel=Demy stifyingMedicine [2,5 min] Previously used: DSM-IV-TR DSM-Diagnostic and Statistical Manual for Mental Disorders Developed by American Psychiatric Association in 1994 (DSM-IV) Applied in psychiatry in m any countries (e.g. US) Sometimes despite ICD-10 Updated since 1952 Only for mental disorders Each disorder has its number Included strictly categorical model of disorders, multi-axis approach: clinical, personality disorders, acute medical conditions, psychosocial factors and global assessment functioning DSM-IV: strictly categorical model requiring a clinician to determine that a disorder was present or absent. No additional measures of disorders included. Creation of DSM-V (APA, 2013, p.11) Harmonization with ICD-11 the groups tasked with revising the DSM and ICD systems shared the overarching goal of harmonizing the two classifications as much as possible, for the following reasons: The existence of two major classifications of mental disorders hinders the collection and use of national health statistics, the design of clinical trials aimed at developing new treatments, and the consideration of global applicability of the results by international regulatory agencies. Complicates attempts to replicate scientific results across national boundaries. Even when the intention was to identify identical patient populations, DSM-IV and ICD-10 diagnoses did not always agree. DSM V, 2013 Developed in 2013 by APA after 14 years of work! An integration of a dimensional approach to diagnosis and classification with the current categorical approach (from DSM-IV). Allows a clinician more latitude to assess the severity of a condition and does not imply a concrete threshold between “normality” and a disorder! More continuum-based assessment. Includes measures indicating degree of acuteness to several combined diagnoses. Focus of attention on the acuteness of symptoms helps clinicians gather more information and thus more insight in creating a treatment plan - better assessment and better intervention planning. DSM V (APA, 2013) For example, autism spectrum disorder (ASD) combines four different categorical disorders conceptualizes them as occurring along a single spectrum focused on dysfunctional social communication and restricted, repetitive behaviours or interests. Under DSM-IV, patients with such symptoms could be diagnosed with: autistic disorder, Asperger’s disorder, childhood disintegrative disorder, or the catch-all diagnosis of pervasive developmental disorder not otherwise specified. In DSM-V t these separate disorders are actually related conditions along a single continuum of behavior à ASD with different severity level (mild, moderate, severe etc.). DSM V (APA, 2013) Patients often do not fit precisely into one category – spectrum based DSM-5 reduces that problem! Spectrum models are also preferred for hypothesis development and testing. DSM-5 reduces the number of patients who would have been diagnosed under DSM-IV’s categorical approach as having a “not otherwise specified” diagnosis. DSM-5 spectrum measures are compatible with categorical definitions. DSM - V combines the best of both categorical and dimensional approaches to provide better guidance to clinicians and, as a consequence better treatment to patients. DSM-V df of mental disorder A mental disorder is a syndrome characterized by clinically significant disturbance in an individual’s cognition, emotion regulation, or behavior that reflects a dysfunction in the psychological, biological, or developmental processes underlying mental functioning. DSM-V Emerging Measures and Models Cross-Cutting Symptom Measures - example set of questions DSM-5 Self-Rated Level 1 Cross-Cutting Symptom Measure—Adult Parent/Guardian-Rated DSM-5 Level 1 Cross-Cutting Symptom Measure—Child Age 6–17 Clinician-Rated Dimensions of Psychosis Symptom Severity World Health Organization Disability Assessment Schedule 2.0 (WHODAS 2.0) Measure: DSM-5 Self-Rated Level 1 Cross-Cutting Symptom Measure—Adult Rights granted: This measure can be reproduced without permission by researchers and by clinicians for use with their patients. Rights holder: American Psychiatric Association 23 questions 13 psychiatric domains I.depression, II.anger, III.mania, IV.anxiety, V.somatic symptoms, VI.suicidal ideation, VII.psychosis, VIII.sleep problems, IX.memory, X.repetitive thoughts and behaviors, XI.dissociation, XII.personality functioning, XIII.substance use. Each item inquires about how much (or how often) the individual has been bothered by the specific symptom during the past 2 weeks. Scoring and Interpretation Each item on the measure is rated on a 5-point scale. The clinician indicates a score in the “Highest Domain Score” column. Cuttings points: A rating of mild (i.e., 2) or greater on any item within a domain (except for substance use, suicidal ideation, and psychosis) may serve as a guide for additional inquiry and follow up to determine if a more detailed assessment for that domain is necessary. For substance use, suicidal ideation, and psychosis, a rating of slight (i.e., 1) or greater on any item within the domain may serve as a guide for additional inquiry and follow-up to determine if a more detailed assessment is needed (e.g. with the DSM-5 Level 2 Cross-Cutting Symptom Measures). Research Methods in Psychopathology Clinical case history Scientific experiment Animal models Single subject experiments Experiments of nature Comparative studies Correlational studies Epidemiological studies Clinical case Advantages Disadvantages Simplest Data based on past evidence – Documentation of rare cases selectivity of memory and memory distortions One case history – a source of hypotheses Lack of repeatability (single case) Initial stage of analysis and Difficult (or impossible) to building more complex study generalize – no inclusion criteria designs Insufficient to tell about E.g. treating tobacco dependence causality. disorder with sertraline Scientific experimentation Advantages Disadvantages Allows studying causality and aetiology Not that close to natural environment They are repeatable Animal models don’t fit exactly human Uses experimental and control group – biology and inner life researcher manipulates with the variable Random v. non-random assignment E.g. effect of sleep deprivation on mood Experimenter bias (e.g. self-fulfilling level; control: no sleep deprivation; experimental: 48h sleep deprivation. Pre prophecy) and post mood measure. Subject biases (e.g. placebo and nocebo Use of a double-blind design. effects) Double-bind design creates ethical concerns of still not receiving the treatment. Demand characteristics of the study E.g. providing information of measuring memory loss due to sleep deprivation... Experiments of nature Advantages Disadvantages Studying subjects in natural We cannot isolate the impact of environment other speciﬁc factors No manipulation is performed Rare and not repeatable General event (factor) is well Retrospecive bias. identified Studying impact of the events like natural disasters (Hurricane Dorian in Bahamas, 2019) Can be retrospective but also prospective and longitudinal Comparative studies Advantages Disadvantages Step in understanding causality No final conclusions about Compare 2 or more groups causality We don’t manipulate with variables Just conclusion about relationship between independent and dependent Using dependent and independent variable. (grouping) variables E.g. how people suffering from depression differ in sleep patterns comparing with people suffering from anxiety disorders and healthy population? Correlational studies Advantages Disadvantages Measuring rela?onship between Even strong correlation doesn’t 2 variables allow us to assume causality No manipula?on But it may suggest causation Natural environment when variables are separated in Posi/ve or nega/ve correla/on time Lack of correla/on Longitudinal studies Using correla?on coeﬃcients Epidemiological studies Advantages Rates of disorders occurrence Comorbidity Lifetime prevalence – proportion of people from general population who have ever experienced the disorder. ANXIETY DISORDERS Psychoanalytic term: neuroses Psychosis Neurosis Mental state of a confusion in A term covering a spectrum of reality, critical thinking and disorders, not just anxiety emotional functioning. disorders Serious mental condition Main characteristic: maladaptive DSM V: Schizophrenia Spectrum ways of coping with anxiety and Other Psychotic Disorders DSM V: Anxiety Disorders, Obsessive-Compulsive and Related Disorder, Trauma- and Stressor- Related Disorders, Dissociative Disorder, Somatic Symptom and Related Disorders DSM V (APA, 2013)- Anxiety Disorders SeparaIon Anxiety Disorder SelecIve MuIsm Speciﬁc Phobia Social Anxiety Disorder Panic Disorder Panic Aiack Speciﬁer (comorbid with another disorder, e.g. PTSD) Agoraphobia Generalized Anxiety Disorder Substance/MedicaIon-Induced Anxiety Disorder Anxiety Disorder Due to Another Medical CondiIon Other Speciﬁed Anxiety Disorder Unspeciﬁed Anxiety Disorder Anxiety disorders All 8 disorders are characterized by experiencing anxiety Main symptom! Common reaction to all of people Becomes a disorder if it prevents normal functioning. The Fear Response – when we sense danger (Seligman, Walker, & Rosenhan, 2001) 1. Cognitive level: recognition of immediate threat (dark shape à shark!) 2. Somatic – body reaction (heart rate increases, sweating, adrenaline) 3. Emotional – feelings of panic, dread, terror, chills 4. Behavioral – fight, flight (escape or avoid), freeze. The anxiety as a symptom Differentiated from fear (due to real or perceived specific danger, threat is immediate) Anxiety – emotional response, generalized distress due to some situation, imagined object etc. There is no real danger involved at the moment. The threat is anticipated only. The difference with fear is on the cognitive level. Anxiety as a trait or as a state? Psychology of personality e.g. using STAI In psychiatry 2 core psychiatric symptoms Anxiety Disturbed mood Both could be present in a lot of disorders (not just anxiety disorder). Is that a fear or anxiety? Separation Anxiety Disorder – no real danger Selective Mutism – no real danger Specific Phobia – reaction is out of proportion (but it needs to be critically recognized; arachnophobia in Europe v. fear of own life in Australia) Social Anxiety Disorder – no real danger Panic Disorder – no danger at the moment or out of proportion Agoraphobia – anxiety is about getting panic attack and not receiving help. Generalized Anxiety Disorder – anxiety is not severe but consistent, without any specific cause even. Substance/Medication-Induced Anxiety Disorder – no danger at all. Anxiety Disorder Due to Another Medical Condition – no immediate danger. Anxiety disorders facts A lot of them develop in childhood and progress into adulthood if not treated (DSM V) More common in females than males, 2:1 Cancer phobia more common in females STD more common in males. Anxiety disorder is diagnosed only if the symptom cannot be akributed to another cause (physiological eﬀect of substance use, another mental or somaic condiion) One of the most common disorders Life-hme prevalence of speciﬁc phobia > 11% in the US 1% of adults don’t leave home because of anxiety disorder High comorbidity with other mental disorders 81-83% comorbid with another disorder (Nahonal Comorbidity Study, 2000). Anxiety Disorders – symptoms and recognition Separation Anxiety Disorder reluctance to go away from attachment figures persistent fear or anxiety about harm coming to attachment figures nightmares and physical symptoms of distress developmentally inappropriate Selective Mutism failure to speak in social situations when expected (e.g. school) though individual can speak and speaks in other situations. Specific phobia (DSM V) Fear or anxiety about specific objects or situation Avoidance Reaction almost always immediately induced by the phobic situation or object To a degree that is persistent and out of proportion to the actual risk Types of specific phobias, e.g.: Animal (cats, spiders, dogs, snakes); natural environment (dirt, storm, height); blood-injection-injury (approx. 4% of general population); Situational (flying, bridges, elevators); and other (STD, HIV, choking, vomiting, cancer). Specific phobia Models of eiology Neuroscience Disturbances in the serotonin, dopamine and GABA func\oning in the limbic system Increases amygdala ac\vity Creates proneness to anxiety and fear Genehc MZ twins have higher probability of phobia than DZ 31% higher rate of phobia in 1-line rela\ves of people suﬀering from phobia (Flyer et al., 1990) Behavioral Classic condi\oning (e.g. cats phobia in a pa\ent who observed killing kidens when she was 4 years old à anxiety and fear associated with cats) Lidle Albert experiment (Watson, 1920): condi\oning phobia in a stable 11-month infant Rat (+hearing loud noise)à crying when confronted with rats à fear of rats, rabbits, anything that has fur (reacDon generalized). Why specific phobias are selective? There is a set of objects people easily develop phobias (e.g. animals) while others not (e.g. knives, electric outlets, guns) Evolutionary explanation – “the grain of truth” Set of objects chosen in the evolution process Promoted those who avoided them and remained safe and alive to reproduce Cats, spiders, snakes used to be a real danger in the history of a mankind Experiment done in the 1977 by Ohman and Hugdahl in the University of Uppsala, Sweden: conditioning of fear (galvanic skin response) is easier when as the stimuli were used snakes and spiders v. houses and faces in non-clinical sample Snakes & spiders: one pairing; persistent after the experiment Houses & faces: 4-5 pairings; non-persistent That’s why it’s easier to develop fear of spiders when the one sees a spider at the time of being exposed to threatening stimuli (e.g. just before car accident) Paired with trauma it becomes a phobic object. How persistent are phobias? Few repetitions without unpleasant stimulus is enough to extinct a fear conditioned in the lab (Annau & Kamin, 1961). Real-life learnt phobias are difficult to extinct, why? Avoidance and rare reality testing Less chances to learn that the object is not harmful Supporting the idea that the threat is real Overactivated amygdala and the temporal lobe (neuroscience level) Brain circuits well established and difficult to delete (LeDoux, 1996) Genetic factors don’t change over time But we can change their expression (phenotype). Social Anxiety Disorder – DSM V (APA, 2013) Social Phobia Fear or anxiety of social situations that involve the possibility of being scrutinized. Avoidance of such stuations E.g. meeting unfamiliar people, situations in which the individual may be observed eating or drinking, and situations in which the individual performs in front of others. The cognitive ideation is of being negatively evaluated by others, by being embarrassed, humiliated, or rejected, or offending others Social Anxiety Disorder – DSM V (APA, 2013) Pathological shyness syndrome. The scale of fear is excessive and unreasonable à anxiety Usually begins in adolescence (developmental explana/on) Over 13% life-/me prevalence – US data, Na/onal Comorbidity Study, (2000). More common in women than men More comorbid with poverty (but the direc/on if causality is unknown) Hinders everyday func/oning E.g. not eaIng in public places, not ﬁnishing the exam because of other people presence. Can be speciﬁc to one kind of situa/ons only. Culture sensi/ve TKS (taijin kyofusho): fear of oﬀending or embarrassing someone (Japan) Panic Disorder – DSM V (APA, 2013) Recurrent experience of panic attacks and worries about having more panic attacks or consequences of the panic attacks (e.g., avoidance of exercise or of unfamiliar locations). Panic attacks: Emotional: abrupt surges of intense fear, anxiety or intense discomfort that reach a peak within minutes, Physical: sweating, increased heart rate, dizziness all fight or flight response, Cognitive : “I’m dying”, “I have a heart attack!”, “no one will help me”. Looks like a flight or fight response but based on the cognitive error of the threat recognition Cognitive psychology perspective (Beck and Emery, 1985; Maultsby, 1990). The error comes from misinterpreting anxiety symptoms (like increased heart rate) as life- threatening symptoms, learning to recognize them as anxiety “only” prevents panic attacks (Clark, 1989) Limited-symptom panic attacks include fewer than four symptoms. Expected - triggered response to a typically feared object or situation, Unexpected – spontaneous, for no apparent reason. Panic Disorder – DSM V (APA, 2013) Marker for severity of diagnosis, course, and comorbidity across an array of disorders including, but not limited to, the anxiety disorders (e.g., substance use, depressive and psychotic disorders). A descriptive specifier for any anxiety disorder as well as other mental disorders. Panic disorder - culture bond: US 1.7% rate, Germany 2.6% rate, Italy 2.9% rate v. Taiwan 0.4% Week prevalence of a panic attack: 20% of students, 5% of the elderly (Barlow, 1988). 2-3 times more common in women Onset in the late ’20 2 etiology models: cognitive (error on cognitive level leading to hypersensitivity of the alarm system) and biological (heritable defect in the brain alarm system leading to misinterpretation) The ongoing discussion of what is the cause and what is the effect Is it possible that both changes (cognitive and neural) are caused by a third factor? Agoraphobia – DSM V (APA, 2013) “Fear of the marketplace” Fear and anxiety about two or more of the following situa?ons: using public transporta/on; being in open spaces; being in enclosed places; standing in line or being in a crowd; or being outside of the home alone in other situa/ons. CogniDve level symptoms: thoughts that escape might be diﬃcult or help might not be available in the event of developing panic-like symptoms or other incapacita/ng or embarrassing symptoms. These situa/ons are oten avoided and require the presence of a companion. Agoraphobia “Fear of the marketplace” Places where escape is difficult or embarrassing Usually (but not always) starts from a spontaneous panic attack Having a panic attack is associated with the crowded place (conditioning) and fear of not receiving help àavoidance Agoraphobia without panic attacks More focused on anxiety of incontinence, diarrhea, faintness etc. 2 more times common in women 3% life-time prevalence First symptoms in late adolescence Comorbid with panic attack disorder, depression, substance abuse and OCD Genetic factors Untreated: reemission may be spontaneous but relapses are common as well Treatment: based on removing panic attacks pharmacologically, extinction and combination of both. Generalize Anxiety Disorder(GAD) – DSM V (APA, 2013) Persistent and excessive anxiety and worry about various domains, including work and school performance, that the individual finds difficult to control. Plus physical symptoms, including restlessness or feeling keyed up or on edge; being easily fatigued; difficulty concentrating or mind going blank; irritability; muscle tension; and sleep disturbance. Anxiety is not severe but present at almost all times Not unexpected Chronic Continously present Generalize Anxiety Disorder(GAD) Pathological worrying Emotion: tensed, restless, on the edge Cognition: expecting something bad and awful but not clear what it is Behavior: trying different things to get rid of the worries but nothing helps Physical: muscle tension, increased activity in the frontal lobes (EEG) More common in poor people and less educated More common in urbanized regions Etiology: brain-based (chronic activation of the fear response circuit) v. cognitive- based (maladaptive thoughts) Treatment combines pharmacotherapy and CBT. Other anxiety disorders - DSM V (APA,2013) Substance/medication-induced anxiety disorder anxiety due to substance intoxication or withdrawal or to a medication treatment Substances include: alcohol, caffeine, cannabis, opiods, amphetamine, cocaine, sedatives, anxiolytic drugs etc. Anxiety disorder due to another medical condition symptoms are the physiological consequence of another medical condition E.g. endocrine diseases, metabolic disturbances, neurological illnesses (e.g. epilepsy) The illness is responsible for the anxiety. Obsessive Compulsive and Related Disorders OCD Used to be confused with schizophrenia Risk of disturbing almost delusional unwanted thoughts Used to be listed as anxiety disorder (DSM IV and DSM IV-R) But it is a way more severe Comorbid with deeper mental disorders than neuroses Pathological intensity of unacceptable thoughts bringing anxiety and lowered mood. Beyond developmentally appropriate periods Persistent and excessive OCD Obsessions: repetitive thoughts, images, urges, impulses, unwanted and intrusive e.g. ”Am I capable of hurting someone?” “I am sure that I locked my door?” “Have I switched off the oven?” Taken ways of dealing with tension triggered by obsessions become symptoms themselves Compulsions: rigid behavioral rituals or mental acts (e.g. counting, repeating) repeated in response to obsessions, e.g. hands washing, closing door specific number of times, avoiding stepping on the tile cracks,.... OCD facts comorbid with depression 67% of OCD patients suffer from depression some time in their life (Gibbs, 1996) 35-50% OCD patients meet depression criteria at the same time! 6-35% patients diagnosed with depression experience OCD (Fava et al., 2000) Especially in the periods before and after the depressive episode Note: after the depression it’s also the time of highest risk of suicide Comorbid with anxiety disorder – 76% 12% of schizophrenia and related disorders are also comorbid with OCD Prevalence: 1.1-1.8% of adults internationally More common in women in adulthood and more in men in childhood Strong evidence for hereditary genetic factors (MZ>DZ) But also higher rates of sub-clinical obsessions, compulsions, anxiety disorders Develops usually gradually Beginning in childhood and early adolescence in men Early adulthood in women OCD and related disorders – DSM V (APA, 2013) obsessive-compulsive disorder (OCD) body dysmorphic disorder hoarding disorder trichotillomania (hairpulling) disorder excoriation (skin-picking) disorder substance/medication-induced obsessive-compulsive and related disorder obsessive-compulsive and related disorder due to another medical condition other specified obsessive-compulsive and related disorder unspecified obsessive-compulsive and related disorder (e.g., body-focused repetitive behavior disorder, obsessional jealousy). OCD etiology Psychodynamic explanation: explains the origins CBT: explains the persistence Neuroscience: explains the brain changes. Psychodynamic explanation of OCD Obsessions – thoughts that serve the function of unconscious defences against anxiety from even more unpleasant thoughts and impulses Process of anxiety displacement and substitution with a new thought Obsessions remain because they successfully block access to the more disturbing thoughts Help dealing with anxiety Treatment: to make unconscious primary conflict conscious, so the patient doesn’t need to protect oneself with obsessions any longer. CBT explanation of OCD Starts from occasional obsessional thought like “what if I hit someone when driving a car?” Difficulties with distracting oneself from the thought In most of people these thoughts just come and go The thought becomes more present, more difficult to distract from Patient finds a ritual (compulsion) that helps to deal with the obsession “if I turn the engine off and on 4 times before driving I will not hit any person” Anxiety is temporarily relieved The ritual is being repeated so the faith in its power is sustained Other experiences are avoided Viscous circle confirming the pattern Treatment: blocking the compulsive ritual will eventually extinguish the obsessive thoughts Neuroscience explanacon of OCD Individual differences Overactive cortical-striatal-thalamic circuit Difficulties with selection and filtering information Difficulties with distracting oneself some thoughts become obsessive Difficulties with inhibiting repetitive compulsions Eventually obsessive thoughts and compulsions are directed towards specific objects/situations Treatment: pharmacotherapy to calm down the cortical-striatal-thalamic circuit. Obsessive Compulsive Disorder – DSM V (APA, 2013) Obsessions Compulsions Body dysmorphic disorder – DSM V(APA, 2013) Excessive pathological preoccupation with own looks (dysmorphofobia) Preoccupation with one or more perceived defects in physical appearance The defect is not observable or appears only slight to others, Repetitive behaviors e.g., mirror checking, excessive grooming, skin picking, or reassurance seeking Mental acts e.g., comparing one's appearance with that of other people. The appearance preoccupations are not better explained by concerns with body fat or weight in an individual with an eating disorder. Muscle dysmorphia is a form of body dysmorphic disorder that is characterized by the belief that one's body build is too small or is insufficiently muscular. Hoarding disorder – DSM V (APA,2013) Pathological collecting Persistent difficulty discarding or parting with possessions Regardless of their actual value (often there is no values) Strong need to save the items and to distress associated with discarding them. Results in the accumulation of a large number of possessions Cluttering active living areas. Differential diagnosis: schizophrenia. Trichotillomania – DSM V (APA, 2013) Not within developmental period Hair-pulling disorder Recurrent pulling out of one's hair resulting in hair loss Repeated attempts to decrease or stop hair pulling. Excoriation – DSM V (APA, 2013) Skin-picking disorder Recurrent picking of one's skin Resulting in skin lesions Repeated attempts to decrease or stop skin picking. Both excoriation and trichotillomania Not triggered by obsessions or preoccupations May be preceded or accompanied by anxiety or boredom, increasing sense of tension May lead to gratification, pleasure, or a sense of relief when the hair is pulled out or the skin is picked The level of self-awareness while engaging in these behaviors varies between people. Substance/medication-induced obsessive-compulsive and related disorder – DSM V (APA, 2013) Direct pathophysiological consequence of a medical disorder, substance intoxication or withdrawal. Other specified obsessive-compulsive and related disorder and unspecified obsessive-compulsive and related disorder – DSM V (APA, 2013) Symptoms that do not meet other OCD and related disorders criteria Include e.g. specific body-focused repetitive behavior and obsessional jealousy. OCD or obsessive-compulsive personality? Differential diagnosis Main difference: attitude towards the symptoms OCD – egodystonic – symptoms are experience as a source of problems, difficulty, high motivation for searching for help Personality disorder – egosyntonic – “that’s the way I am. I like clean hands, so I wash them 5 times but it doesn’t bother me”. The suffering level is lowered Sense of proud There is no evidence for comorbid OCD and obsessive-compulsive personality. MOOD DISORDERS Depressive and bipolar related disorders Mood disorders Shared symptom - episodes of disturbance in the mood level Increase - mania Decrease – depression Used to be classiﬁed together as mood disorders (DSM – IV) Currently separately classiﬁed as Depressive disorders (manifested by mood deple/on) Bipolar disorders (DSM V). Depressive disorders Depressive episode: period over 2 weeks of experiencing decreased mood, lost of pleasure and interest, weight loss or gain, sleeping disturbances, lack of energy, “S” thoughts. “Normal depression” v. clinical depression Symptoms severity, persistence, recurrence Increase within recent 50 years Used to have long recovery and treatment Depressive disorders “Beginning of 90s - new pharmacotherapy – SSRI (Selective Serotonin Reuptake Inhibitors) e.g. fluoxetine (Prozac), sertraline (Zoloft), Escitalopram (Lexapro) Dynamics in symptoms in 3 weeks after therapy – ends in 12 months or later No drug dependency, no overdose risk But possible mood decrease if the treatment is terminated too early In 50% of cases the placebo effect works! Depressive disorders - facts Born after 1975 – 3 x more life time incidence Increasing incidence rates among teenagers Current onset 300 mln people affected 800 000 dies due to depression related suicide every year Depressive disorders - facts US data (APA, 2017) 1 in 15 adults (6.7%) in any given year 1 in six people (16.6%) at some time in their life. Women more affected than men Endocrine hypothesis (earlier puberty, premenstrual dynamics, pregnancy, postpartum, perimenopause and menopause depression, social-economic factors). Not linked with race or socio-economic status. World-wide incidence diversity Highest: Greenland, Iran, Morocco, USA, Sweden, Australia Lowest: Colombia, Peru, Poland, Slovakia, Czech Republic Suicide (S) risk Globally from S: one person dies every 40s (135 people during our lecture meeting!) One of the major causes of death 10-24 years - the third leading cause of death 25-34 years – the second leading cause of death 35-54 years - the fourth leading cause of death. Should people be allowed to choose if they want to end their life? Dr Kevorkian’s perspective on assisted suicide as a way to prevent suicide Suicide - facts People who talk about killing themselves are more likely to kill themselves 80% of those who are successful with S talks about it prior to their actions (Shneidman, 1976) It’s not a clear decision whether to die or not – ambivalence It’s not like “once suicidal, always suicidal” The highest probability of committing S is approx. after 3 months of treatment More energy to proceed with that Suicide (S) risk Genehc factor: in the context of hereditary depression factors. Neuroscience: low serotonin level. Mental causes: Alcohol abuse 20% Schizophrenia 10% 50% depression Untreated depression disorder – 20% risk (Gotlieb & Hammen, 2002) Gender factors: women 3 hmes more apempt, men 4 hmes more succeed (Canepo & Lester, 1995) Men aNempts are more determined, rough (guns not pills). Cultural diﬀerences More common in industrialized countries (but not because of poverty) Japan as an example of high tolerance for S History of seppuku among samurai, Kamikaze during IIWW Honourable death Mt. Fuji – suicide forrest Depressive disorders: main features Experiencing emotional and motivational changes sadness, emptiness, irritable mood (dysphoria), lack of interest and motivation. Followed by cognitive and somatic changes that decrease person’s abilities to function. Depressive disorders etiology models Biological Gene/c Neuroscience Smaller hippocampus, bigger right hemisphere Increased levels of ACTH, corIsol Low level of noradrenaline, serotonin, dopamine in the CNS (that’s where SSRIs work but also ECT – electroconvulsive therapy). 40% comorbidity with Parkinson’s disease. Depressive disorders etiology models Psychological Psychoanalysis: melancholy close to bereavement, anger directed towards oneself to protect the object that was lost or caused losses/traumas Research indicates the role of significant losses before 11 years old (e.g. death of a parent) (Brown & Harris, 1978). Cognitive approach: Beck’s depressive triad, errors in thinking, but no explanation where it is coming from. Positive psychology: Seligman’s(1967) concept of learned helplessness manifesting in depressive symptoms. Protective factors in women (Brown & Harris, 1978) 50% of women who were bereaved by mother before 11 years old developed depression. What was special about the other half? Having close intimate relationship Part-time or full-time job away from home Less than 3 children at home Serious religious commitment Depressive disorders – DSM V (APA, 2013) Disruptive mood dysregulation disorder (children) Major depressive disorder (including major depressive episode), Persistent depressive disorder (dysthymia) Premenstrual dysphoric disorder Substance/medication-induced depressive disorder Depressive disorder due to another medical condition Other specified depressive disorder Unspecified depressive disorder. Disruptive mood dysregulation disorder Severe and recurrent (3 or more per week) Temper outbursts Inconsistent with developmental level Children with persistent irritability and frequent episodes of extreme behavioural dis-control added to the depressive disorders for children up to 12 years of age. Children with this symptom pattern typically develop unipolar depressive disorders or anxiety disorders, rather than bipolar disorders. Prevalence: 2-5% of children. Major depressive disorder – DSM V (APA, 2013) Pathological sadness Classic mood disorder Discrete episodes of at least 2 weeks' involving clear-cut changes in affect, cognition, Neuro-vegetative functions. with inter-episode remissions (>2 months without symptoms) Episodes are recurrent in majority of cases diagnosis can be based on a single episode episodes might be triggered by external life stressors (exogenous depression) or not (endogenous depression). Depressive episode Decreased mood (or dysphoric) or lack of interest or pleasure in almost all everyday activities Lasts at least 2 weeks 4 symptoms domains Emo6onal Cognitive (Beck’s Motivational Physical/Somatic Mood related Depressive Triad) Difficulties in Loss or increase in Anxiety related Negative self-image decision making (will appetite/weight Lost of graYﬁcaYon Negative world paralysis) Sleeping disturbance (food, sex) Negative future Difficult to go on (early morning “I am a hopeless with duties insomnia or person, the world is a High ambivalence hypersomnia) dark place, and there is Lost of gratification nothing good waiting for me in the future”. Major depressive disorder – DSM V (APA, 2013) Severity specifier and course: mild, moderate, severe, with psychotic features, with anxious distress, with catatonia, with melancholia lost of pleasure as the core feature, worst feelings in the morning, deacresed energy, anxiety, substance abuse as self-therapy attempt, high S risk; better respond to biological treatment), without melancholia (better respond to psychotherapy); in partial reemission, in full reemission, unspecified. Major depressive disorder – DSM V (APA, 2013) Prevalence 12-month US: 7% More common in females (up to 3 times more) Especially higher in young females – 3 times more common in 18-29 years old than >60 years old. Differential diagnosis: bereavement but: bereavement-related depression in people with other vulnerabilities to depressive disorders à worse prognosis Persistent Depressive Disorder – DSM V (APA, 2013) Dysthymia + some major depression features (DSM-IV) Chronic form of depressed mood Mood disturbance continues for at least 2 years in adults or 1 year in children Symptoms-free periods are shorter than 2 months Less commonly diagnosed than major depressive disorder. Premenstrual dysphoric disorder – DSM V (APA, 2013) Moved from an appendix of DSM-IV Over 20 years of additional of research Form of depressive disorder Begins sometime following ovulation and remits within a few days of menses Has a marked impact on functioning. Depressive disorders - DSM V (APA, 2013) Substance/medication-induced depressive disorder E.g. steroids, alcohol, opioids Elevated S risk in young adults. Depressive disorder due to another medical condition E.g. Parkinson’s disease, pancreatic cancer. Bipolar and related disorders Previously: mood disorders Why were they separated from mood disorders? “Maniac-depressive disorder”, ”affective psychosis” (XIXth century) Bridge between depression and schizophrenia and psychotic disorders shared family history, symptoms and genetics Shared symptoms Episodes of depression (not always) Episodes of mania (always): Mood: abnormally elevated or irritable Energy: abnormally high. What is mania? Mood symptoms Mo?va?onal symptoms Euphoric or irritable Hyperac/vity Not exactly opposite to depression Compulsive engagement Cognitive symptoms Physical symptoms Grandiose thoughts Hyposomnia (one of the ﬁrst Not recognizing consequences symptoms ﬁnally leading to Race of thoughts exhaus/on). Manic episode – DSM V (APA, 2013) Lasts at least 1 week, euphoric mood, excessively cheerful, high. Present most of the day, nearly every day or any duration in case of necessary hospitalization (severe)! Followed by (3 or more – 4 if the mood is only irritable): 1. Inflated self-esteem or grandiosity. 2. Decreased need for sleep. 3. More talkative than usual or pressure to keep talking. 4. Flight of ideas or subjective experience that thoughts are racing. 5. Distractibility. 6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation (i.e., purposeless non-goal-directed activity). 7. Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments). Causes marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features. Hypomanic episode: DSM V (APA, 2013) Mood disturbance & Increased energy and activity At least 4 consecutive days Most of the day, nearly every day 3 (or more) of the following symptoms (four if the mood is only irritable): 1. Inflated self-esteem or grandiosity. 2. Decreased need for sleep. 3. More talkative than usual or pressure to keep talking. 4. Flight of ideas or subjective experience that thoughts are racing. 5. Distractibility. 6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation (i.e., purposeless non-goal-directed activity). 7. Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments). The disturbance in mood and the change in functioning are observable by others. The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization. There are no psychotic features. Etiology of bipolar disorder Gene?cs: 10-fold increased risk among adult relaDves of individuals with bipolar I and bipolar II disorders. Major depressive disorder, bipolar I & bipolar II - more common among 1st- degree rela/ves of cyclothymic pa/ents. Schizophrenia and bipolar disorder likely share a gene/c origin (APA, 2013). As much aﬀects females as males. Etiology of bipolar disorder Neuroscience: Disturbances in the brain reward-system. Changes in brain activity during episode swings. http://bipolarsymptoms.com Different neurotransmitters were found to guide the episode switching process (dopamine, norepinephrine, serotonin, GABA [gamma- aminobutyrate], glutamate, acetylcholine). Etiology of bipolar disorder Treatment: pharmacotherapy valproic acid (Convulex, Depakine) Lithium (Eskalith, Lithobid) over 60 years of experience in BD treatment, treatment is challenging: monitoring Li levels, overdose risk (diarrhea, vomiting, tremor, mild problems walking, drowsiness, or muscular weakness), risk for kidney disease, risk of medication interactions. Bipolar and related disorders – DSM V (APA, 2013) bipolar I disorder, bipolar II disorder, cyclothymic disorder, substance/medication-induced bipolar and related disorder, bipolar and related disorder due to another medical condition, other specified bipolar and related disorder, unspecified bipolar and related disorder. Bipolar I disorder – DSM V (APA, 2013) The classic manic-depressive disorder or affective psychosis neither psychosis nor the lifetime experience of a major depressive episode is a requirement. At least 1 manic episode May be proceeded with depressive or hypomanic episodes Differential diagnosis: schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified Severity specification: mild, moderate, severe. Codes: with most recent manic, depressive, hypomanic, unspecified episode, with psychotic features or not. Reemission: periods when none of the mentioned episodes symptoms are present; full reemission, partial reemission. Bipolar I disorder – DSM V (APA, 2013) Other specifiers: With anxious distress With mixed features With rapid cycling With melancholic features With mood-congruent psychotic features With mood-incongruent psychotic features With catatonia With péripartum onset Bonsall et al. 2011 With seasonal pattern Bipolar I disorder – DSM V (APA, 2013) facts 12-month prevalence – between 0% to 0.6% (across 11 countries, highest in US) Gender difference: Lifetime male-to-female ratio - 1.1:1 (almost the same) Females - rapid cycling and mixed states, patterns of comorbidity with eating disorders, more depressive symptoms. They also have a higher lifetime risk of alcohol use disorder than are males and a much greater likelihood of alcohol use disorder than do females in the general population Mean age at onset: early adulthood, 18 years old But late onsets around 60s and 70s are also possible (!) – cross diagnossis is deeply needed (e.g. for CNS diseases) Social factors: More common in high-income countries Marital status: separated, divorced, or widowed more at risk S risk – 15 times higher than in general population 30% severe impairment in work functioning Differentiating with BPD – episodic, not constant, shared impulsivity and mood lability. Bipolar II disorder – DSM V (APA, 2013) Lifetime & Recurrent At least 1 episode of major depression + at least 1 hypomanic episode There has never been a manic episode! Used to be called the "milder" bipolar condition Time spend in depression Hypomanic episodes don’t impair that much functioning as maniac episode. Differentiate with: schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. Bipolar II disorder – DSM V (APA, 2013) Specifiers Current or most recent episode: Hypomanic Depressed Specify if: With anxious distress With mixed features With rapid cycling (5-15% of patients experience more than 4 episodes per year) With mood-congruent psychotic features With mood-incongruent psychotic features With catatonia With péripartum onset With seasonal pattern (applies only to the pattern of major depressive episodes) Specify course (no current episodes): In partial remission , In full remission Specify severity (episode ongoing): Mild, Moderate, Severe. Bipolar II disorder – facts Patients usually search for help while depressed – often confused with major depressive disorder. Common accompanying features: IMPULSIVITY Anxiety disorders: 75% Substance use disorders (symptoms self-management): 37% S risk life-time attempts in 1/3 of patients, more successful than BP-I, 6.5-fold higher risk of suicide among first-degree relatives of BP- II compared BP-I. CREATIVITY in milder cases, during hypomanic episodes (not interested in seeking help). Bipolar II disorder – facts Worldwide 12-month prevalence: 0.3% Onset in mid 20s (slightly later than BP-I and later than depressive) Earlier onset means more severe course 5-15% of patients at some point experience full manic episode and the diagnosis changes to BP – I Gender differences: slightly more After: Mondimore (2006) commonly diagnosed in women (due to depressive episodes). Cyclothymic Disorder – DSM V (APA, 2013) Chronic, fluctuating mood disturbance For at least 2 years (1 year in children and adolescents) Numerous periods of hypomanic symptoms + depressive symptoms The hypomanic symptoms are insufficient to meet full criteria for a hypomanic episode The depressive symptoms are insufficient to meet full criteria for a major depressive episode. The hypomanic and depressive periods have been present for at least half the time. Symptoms free periods were not longer than 2 months at a time. Not caused by a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism). Leading to distress or impairment in social, occupational, or other important areas of functioning. Mood swings in bipolar disorders commons.wikimedia.org Cyclothymic Disorder – facts (APA, 2013) Prevalence during life-?me: up to 1% Onset in adolescence and early adulthood Between 15 and 50% pa/ents ﬁnally develop BP-I or BP-II disorder In children mean onset age is 6.5 years old. Comorbid with substance abuse and sleep disorders. Gender diﬀerences: none. Schizophrenia spectrum and psychotic disorders Schizophrenia Complex and puzzling disorder Episodic disease with different course Group of diseases (schizophrenia spectrum or psychotic disorders) Main features – psychotic symptoms Disturbance in thought and perception à difficulties in recognizing reality. Mental disintegration of the inner world (affects the sense of self, thinking and perception, but also motor functions, speech, feelings) Disruption in exchanging information and energy between internal and external world (dysfunctional patterns of communication) Recurrence of symptoms, increase of social impairment, gradual withdrawal. Psychotic symptoms Posi?ve delusions hallucina/ons, Nega?ve Inc. ﬂa{ened aﬀect lack of mo/va/on, Cogni?ve History and stereotypes Social “knowledge” Facts “insane”, “mad” Shy Unpredictable Withdrawn Dangerous Anxious Out of control Preoccupied with own problems Split of personality Named schizophrenia by Bleuler Schizo/phreno = split/mind based on recognition of divided mental functions not split!) Once psychotic = forever ill The reemission may be longer than psychotic episodes Some patients stay without symptoms forever after a single episode Historical view on schizophrenia First classification df: 1896 dementia praecox - Emil Kraepelin (Germany) Premature deterioration based biologically. Eugene Bleuler (1857-1939) (Switzerland) – serious, chronic, recurrent but with possible recovery (also biological explanation, brain disease). Adolf Meyer (1866-1950) – outcome of impaired learning and interpersonal process, American psychiatry. Schizophrenia- facts Gender differences: In prevalence none Men: earlier onset (15-25 years old); women 25-35 years old. Neuroscience: (1) Mesolimbic dopamine pathway model (old, no direct evidence, replaced with striatum dopamine model) Based on correlation between schizophrenia symptoms with mesolimbic tumours and epilepsy episodes. Schizophrenia - facts Neuroscience: (2) Striatum dopamine model: Role of dopamine in onset - increased presynaptic dopamine function in the associative striatum, also GABA and glutamate release and inhibition in the striatum. Specifically dorsal regions of the striatum. Striatum - ”integrative hub for information processing in the brain” (McCutcheon, Abi-Dargham, & Howes, 2019) corticostriatal pathways overlap: limbic, associative, and sensorimotor pathways reports of abnormalities in virtually every neurotransmitter system all licensed pharmacological treatments of schizophrenia affect the dopamine system. McCutcheon, Abi-Dargham, & Howes (2019), Schizophrenia, Dopamine and the Striatum: From Biology to Symptoms, Trends in Neurosciences (42), 3, 205- 220. McCutcheon, Abi-Dargham, & Howes (2019), Schizophrenia, Dopamine and the Striatum: From Biology to Symptoms, Trends in Neurosciences (42), 3, 205- 220. Based on results from PET Measures of Presynaptic Dopamine in Schizophrenia Patients and Controls [in limbic, associative and sensorimotor striatum areas]. Similar for people who are at high risk of developing schizophrenia. Schizophrenia - facts GeneDc factors: 18—58% of risk among MZ twins (Seligman, Walker, & Rosenhan, 2001) However only 20% risk in ﬁrst-line relaIves GeneIc proneness to whole spectrum disorders (psychoIc and borderline level) Some genes shared with bipolar disorder Which speciﬁcally? Polygenic disorder. A microdeleDon in a region of chromosome 22 (22q11) may be responsible for small number of cases Region C4 of DNA located on chromosome 6 Psychiatric Genomics Consortium Sekar et al. (2016) Schizophrenia - facts Region C4 on chromosome 6 Sekar et al. (2016), Harvard Medical School, Nature: C4 is involved in eliminating the connections between neurons — a process called "synaptic pruning," which, in humans, happens naturally in the teen years. Study: Genome data about the C4 gene in 28,800 people with schizophrenia v. 36,000 people without, from 22 countries. The higher the levels of C4 activity, the greater a person's risk of developing schizophrenia. Hope for new drugs acting on inhibiting the process of synaptic pruning. However the exact inheritance pattern is still unknown... Adoption studies point out also to the role environmental factors (in gene expression) Schizophrenia - facts Complications in pregnancy and birth: Risk increased for children born after a flu/viral infection in pregnancy Numerous studies found increased risk of schizophrenia in people born from a pregnancy that has its 4th-6th month period during winter. Higher risk in children born to mothers who experienced increased distress in pregnancy (e.g. death of a spouse, military battle). Birth complications decreasing oxygen supply (or even hypoxia) Brain damage Explanation of differences between MZ twins risks (different prenatal and birth conditions – e.g. even birth weight and condition, fingerprints indicating different brain system development) More similarities in fingerprints –more risk of schizophrenia in MZ twins (Bracha et al., 1992). Greater father’s age: proven to increase risk of schizophrenia. Psychosis – psychological explanations Childhood trauma, like abuse greatly increase the risk – umbrella review results (Radua et al., 2018) – “environmental exposures during critical developmental periods impact brain, neurocognition, affect, and social cognition” Trauma acts like a viral infection on the brain – triggers specific gene expression. Psychosis as A natural reaction to the abuse A way to survive Psychodynamic and psychoanalytic approach (McWilliams, 2011) Every symptom has its function Psychosis once saved one’s life but today it impairs it There is still need to treat it or at least to cope with it. Psychosis – psychological explanacons Expressed emotion (EE) studies (Brown, 1959) former patients who had limited contact with their relatives did better Relapses after 9 months from discharge varied: 58% in high EE families 16% im low EE families High EE = high levels of criticism (disapproval), hostility (animosity), and emotional overinvolvement (intrusiveness, symbiosis) expressed by the families. Symptom criteria for psychotic disorders Delusions Hallucinations Disorganized thinking/speech Grossly disorganized or abnormal motor behavior Negative symptoms Culture-related issues must be always concerned in diagnosing. Delusions False beliefs resist all argumentation and facts sustained even in the face of evidence against them usually bizarre and out of touch with reality Common symptom in a lot of disorders (also depression) Specific for schizophrenia – delusions not congruent with present mood Delusions - kinds Delusions of Grandeur – being especially important, “Jesus Christ”. Religious delusions Delusions of Control – one’s thoughts or behaviors are being controlled by others, “receiving instructions from aliens to be quiet”, thought insertion or withdrawal by outside force. Delusions of Persecution – fear that some group, agency or individual is “out to get me”. Ideas of reference (referential) – certain people or events having special significance for the persons, “special massages on the tv” Somatic delusions – something is drastically wrong with the one’s body, “something rotting inside the body”, “something places beneath the skin”. Hallucinations Imagine a situation of waking up from a dream though you are still asleep... – experience closest to hallucinations. Perception-like false experiences Even in the absence of stimuli Not matching the reality Vivid and clear They are taken for real because they feel real PET scans show activation of the visual or auditory cortex during visual or auditory hallucinations experienced by psychotic patients (Allen et al., 2012). Hallucinations - types Auditory – most common in schizophrenia, probably originating from inner dialogue and confusion of external sounds v. internal thoughts Visual – less common in schizophrenia but more in chemically induced psychosis Olfactory – rare, unpleasant odours Tactile – being touched, common in alcohol delirium psychotic disorder Gustatory – unpleasant tastes General somatic – feelings of body being mutilated or seriously injured, e.g. bugs crawling inside the veins. Disorganized thinking/speech Formal thought disorder Manifested as disorganized speech Symptoms: Shifts from one topic to another (derailment) Little connections in thoughts (loose association) Responses to questions not exactly related or completely unrelated (tangential) Incomprehensible and resembles receptive aphasia in its linguistic disorganization (incoherence or "word salad"). Substantially impairs communication Disorganized thinking/speech Usually is affected by the sensitivity to the most dominant associations to words and less by the context, e.g. (Seligman, Walker & Rosenhan, 2001, p.422) Pool means the same as: 1. puddle 2. notebook 3. swim 4. none of the above Disorganized thinking/speech Sometimes affected by the sound of words rather than their meaning, e.g. Clang associations – by the rhythm of words, “my dear, near, seal, here”, “university,..., plausity” Neologisms – “amorition”, ”plausity”. Grossly disorganized or abnormal motor behavior Variety of manifestations - from childlike laughing aloud to unpredictable agitation Often followed by poor hygiene, wearing inappropriate clothes or excess clothing Catatonic behavior – the most bizarre of all disorganized behaviors, though less and less common due to medication; can occur in several disorders, including neurodevelopmental, psychotic, bipolar, depressive; separate condition listed in DSM V (APA, 2013). In 35% of schizophrenia patients Catatonia A marked decrease in reactivity to the environment, e.g. - resistance to instructions (negativism or opposition) - lack of movement, frozen like (stupor) -lack of communication (mutism) - allowing to be placed in uncomfortable position (waxy flexibility) But also purposeless and excessive motor activity without obvious cause (catatonic excitement) - stereotyped movements, staring, grimacing, and the echoing of speech etc. Catatonia – DSM V (APA, 2013) 3 (or more) of the following symptoms: 1. Stupor (i.e., no psychomotor activity; not actively relating to environment). 2. Catalepsy (i.e., passive induction of a posture held against gravity). 3. Waxy flexibility (i.e., slight, even resistance to positioning by examiner). 4. Mutism (i.e., no, or very little, verbal response [exclude if known aphasia]). 5. Negativism (i.e., opposition or no response to instructions or external stimuli). 6. Posturing (i.e., spontaneous and active maintenance of a posture against gravity). 7. Mannerism (i.e., odd, circumstantial caricature of normal actions). 8. Stereotypy (i.e., repetitive, abnormally frequent, non-goal-directed movements). 9. Agitation, not influenced by external stimuli. 10. Grimacing. 11. Echolalia (i.e., mimicking another’s speech). 12. Echopraxia (i.e., mimicking another’s movements). Negative symptoms A reduction in normal behavior Usually appear before positive symptoms Associated with schizophrenia less manifested in other psychotic disorders. 2 negative symptoms prominent for schizophrenia: Diminished emotional expression – blunted, flatted affect, lack of facial expression, monotonous voice, emotionally unresponsive, followed by alogia. Avolition – lack of energy and interest in activities, without engagement. Other: Alogia - diminished speech output. Anhedonia - decreased ability to experience pleasure from positive stimuli or a degradation in the recollection of pleasure previously experienced. Asociality - lack of interest in social interactions. Schizophrenia and other psychotic disorders – DSM-V (APA, 2013) Disorders organized along a gradient of psychopathology... Diagnosis should be careful and follow the guidelines (APA, 2013, p.88): Clinicians should first consider conditions that do not reach full criteria for a psychotic disorder or are limited to one domain of psychopathology. Then they should consider time-limited conditions. Finally, the diagnosis of a schizophrenia spectrum disorder requires the exclusion of another condition that may give rise to psychosis. Schizophrenia and other psychotic disorders – DSM-V (APA, 2013) Schizotypal personality disorder – noted here but fully described within personality disorders Delusional disorder (> 1 month of delusions but no other psychotic symptoms) Brief psychotic disorder (1 day 1 month) Schizophreniform disorder (16 months of schizophrenia symptoms, no functioning decline) Schizophrenia (at least 6 months and includes at least 1 month of active-phase symptoms) Schizoaffective disorder Catatonia Substance/medication induced psychotic disorder Psychotic disorder due to another medical condition Other specified and unspecified Schizotypal personality disorder - DSM-V (APA, 2013) A pervasive paWern of social and interpersonal deﬁcits incl.: reduced capacity for close rela/onships; cogni/ve or perceptual distor/ons; and eccentrici/es of behavior. Usually beginning by early adulthood but in some cases ﬁrst becoming apparent in childhood and adolescence. Abnormali?es of beliefs, thinking, and percep?on are below the threshold for the diagnosis of a psycho?c disorder. Delusional disorder – DSM V (APA, 2013) Presence of delusions At least for 1 month Criterion A for schizophrenia has never been met. Hallucinations, if present, are related to the delusional theme (consistent). Functioning is not markedly impaired, and behavior is not obviously bizarre. If manic or major depressive episodes have occurred, these have been brief relative to the duration of the delusional periods. The disturbance is not attributable to the physiological effects of a substance or another medical condition. Differential diagnosis: body dysmorphic disorder or OCD. Life-time prevalence: 0.2% Usually social and legal consequences. But less impairment than in schizophrenia. Some people meet schizophrenia criteria in some time. Gender differences: none. Delusional disorder – DSM V (APA, 2013) Specify whether (central themes): Erotomanic type - being in love Grandiose type – own greatness Jealous type – unfaithful spouse Persecutory type – being conspired against, spied, followed Somatic type – involving bodily functions Mixed type – without dominant theme Unspecified type – e.g. referential without any dominant theme Specify if: with bizarre content – agents replacing organs with artificial ones and not leaving scars; without bizarre content – ex-girlfriend breaking in to steal or displace things in the apartment. Delusional disorder – DSM V (APA, 2013) After 1 year duration – course specifiers First episode, currently in acute episode: First manifestation of the disorder meeting the defining diagnostic symptom and time criteria. An acute episode - period in which the symptom criteria are fulfilled. First episode, currently in partial remission: improvement after a previous episode is maintained and the defining criteria of the disorder are only partially fulfilled. First episode, currently in full remission: after a previous episode, when no disorder-specific symptoms are present. Multiple episodes, currently in acute episode Multiple episodes, currently in partial remission Multiple episodes, currently in full remission Continuous: Symptoms remaining for the majority of the illness course, with subthreshold symptom periods being very brief relative to the overall course. Unspecified Brief psychotic disorder – DSM V (APA, 2013) 1 day 1 month Presence of at least 1 of the following (1,2,3): 1. Delusions. 2. HallucinaIons. 3. Disorganized speech Op@onal: 4. Grossly disorganized or catatonic behavior. Onset is sudden (not gradual!) Eventual full return to premorbid level of funcIoning (!) Diﬀeren@ate with: major depressive or bipolar disorder with psychoIc features or another psychoIc disorder such as schizophrenia or catatonia, and is not aiributable to the physiological eﬀects of a substance (e.g., a drug of abuse, a medicaIon) or another medical condiIon. Note: Do not include a symptom if it is a culturally sancIoned response. Brief psychotic disorder – DSM V (APA, 2013) Increased S risk in the acute phase. 9% of all first-onset psychosis episodes (US data, APA, 2013). Onset across the whole lifespan but most typical: mid 30s. If it doesn’t end after 1 month and a full recovery does not appear à change of diagnosis (usually to schizophreniform or delusional disorder). Risk factors: schizotypal PD, borderline PD, suspiciousness (temperamental), cannabis use (5 x higher risk). Specify if: With marked stressor(s) - (brief reactive psychosis)- in response to stressful events. Without marked stressor(s). With postpartum onset - during pregnancy or within 4 weeks postpartum. Specify if: With catatonia Schizophreniform disorder – DSM V (APA, 2013) 1 month 6 months (if untreated; otherwise provisional) Inc. prodromal, active, and residual phases At least 2 of the following during a 1-month period & at least 1 of these must be (1), (2), or (3): 1. Delusions. 2. Hallucinations. 3. Disorganized speech 4. Grossly disorganized or catatonic behavior. 5. Negative symptoms Differential: Schizoaffective disorder and depressive or bipolar disorder with psychotic. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition. Lack of a criterion requiring impaired social and occupational functioning Schizophreniform disorder – DSM V (APA, 2013) Development and onset similar to schizophrenia. 2/3 of diagnosed patients at some point are diagnosed with schizophrenia or schizoaffective disorder. Risk factors: relatives diagnosed with schizophrenia. Specifiers: With good prognostic features: presence of at least 2 of the following onset of prominent psychotic symptoms within 4 weeks of the first noticeable change in usual behavior or functioning; confusion or perplexity; good premorbid social and occupational functioning; absence of blunted or flat affect. Without good prognostic features (may progress into schizophrenia) Specify if: With catatonia. Schizophrenia - DSM V (APA, 2013) > 6 months (if untreated) At least 2 of the following during a 1-month period & at least 1 of these must be (1), (2), or (3): 1. Delusions. 2. Hallucinahons. 3. Disorganized speech. 4. Grossly disorganized or catatonic behavior. 5. Negahve symptoms, For a signiﬁcant porhon of the hme since the onset of the disturbance, level of funchoning in areas, such as work, interpersonal relahons, or self-care, is markedly below the level achieved prior to the onset (or, when the onset is in childhood or adolescence there is failure to achieve expected level of interpersonal, academic, or occupahonal funchoning Anosognosia – lacking insight of the disorder. Schizophrenia - DSM V (APA, 2013) During prodromal or residual periods, the signs of the disturbance may be manifested by only negative symptoms or symptoms in an attenuated form (e.g., odd beliefs, unusual perceptual experiences). Differential diagnosis: Schizoaffective disorder and depressive or bipolar disorder with psychotic features. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition. earlypsychosis.ca Life-time prevalence: approx. 1% S risk: 20% attempts S; 5-6% dies from S. Highest risk - depressive symptoms, being unemployed, period after a psychotic episode or hospital discharge. Schizophrenia - DSM V (APA, 2013) Gender differences: males express more negative symptoms, longer duration, poorer prognosis. Onset - between late teen years and mid 30s - av. Early-mid 20s for men and late 20s women - earlier onset – worse predictor (e.g. childhood). Prognosis – 20% get periods of well recovery, small % live symptom free with medication, but most need living support. Symptoms diminish over the life course, - probably effect of normal age-related decline in dopamine earlypsychosis.ca activity. Comorbidity: substance-related disorders >50% tobacco dependence; anxiety, OCD, undiagnosed chronic diseases (e.g. cancer) and reduced life expectancy. Schizophrenia - DSM V (APA, 2013) Specifiers after a 1-year duration: First episode, currently in acute episode: First manifestation of the disorder meeting the defining diagnostic symptom and time criteria. First episode, currently in partial remission: improvement after a previous episode is maintained and the defining criteria of the disorder are only partially fulfilled. First episode, currently in full remission: after a previous episode, when no disorder- specific symptoms are present. Multiple episodes, currently in acute episode Multiple episodes, currently in partial remission Multiple episodes, currently in full remission Continuous: Symptoms remaining for the majority of the illness course, with subthreshold symptom periods being very brief relative to the overall course. Unspecified Specify if: With catatonia Subtypes of schizophrenia- no longer listed in DSM V Paranoid – hallucinations & delusions in the center Disorganized/Hebephrenic – symptoms concentrate on disruption in speech and behavior, less delusions and hallucinations. Catatonic – core symptom is due to catatonia. Undifferentiated - do not meet the criteria for paranoid, disorganized, or catatonic types. Residual – after at least one episode of schizophrenia, when residual symptoms remain only („residual leftovers”). Schizoaﬀeccve disorder – DSM V (APA, 2013) An uninterrupted period of illness during which there is a major mood episode (major depressive or manic) concurrent with schizophrenia major symptoms. Delusions or hallucinations for 2 or more weeks in the absence of a major mood episode (depressive or manic) during the lifetime duration of the illness. Symptoms that meet criteria for a major mood episode are present for the majority of the total duration of the active and residual portions of the illness. The disturbance is not attributable to the effects of a substance (e.g., a drug of abuse, a medication) or another medical condition. Functioning impairment is not a defining criterion (v. schizophrenia!). Differentiate: with mood disorders comorbid with schizophrenia, bipolar and depressive disorder with psychotic symptoms. Schizoaffective disorder – 4 concepts Current Psychiatry Journal (Strakowski, 2003) Concept 1: a type of schizophrenia. Concept 2: a type of mood disorder. Concept 3: a heterogeneous combination of patients with schizophrenia, mood disorder, and “real” schizoaffective disorder; may include patients with severe psychotic mood disorders and either good-prognosis schizophrenia or schizophrenia with numerous affective symptoms. Concept 4: as part of a continuum of psychotic disorders from worst prognosis (schizophrenia) to best prognosis (major depression). Sharing a genetic vulnerability. Schizoaffective disorder – DSM V (APA, 2013) After 1 year duration – course specifiers Specify if: First episode, currently in acute episode: First manifestation of Bipolar type: a manic episode is the disorder meeting the defining diagnostic symptom and part of the presentation. Major time criteria. depressive episodes may also occur. First episode, currently in partial remission: improvement More common in young people. after a previous episode is maintained and the defining criteria Depressive type: only major of the disorder are only partially fulfilled. depressive episodes are part of the First episode, currently in full remission:

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