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Biopsychosocial BPS model FINAL EDITED (4).pptx
- 1. BIOPSYCHOSOCIAL MODEL OF SCHIZOPHRENIA PRESENTOR : DR.M.KANAGAPORANI 2ND YEAR PG CHAIRPERSON : DR.R.ISHWARYA,MD(PSY) ASSISTANT PROFESSOR 04.08.2023
- 2. INTRODUCTION • The biopsychosocial model is an interdisciplinary way of understanding a patient beyond simply a diagnosis or label, to being able to understand them from a holistic view. • It helps to treat and support the person , rather than just diagnose the disease. "What's going on with this person?" What's wrong with this person?"
- 3. “BIOPSYCHOSOCIAL (BPS) MODEL” • The “biopsychosocial (BPS) model” emphasizes the interconnection between biological, psychological and socio- environmental factors. • -highlights the inseparable relationships between these three factors. • When one or more of the trio is disturbed, it can have direct and often negative impacts on the others
- 4. The biopsychosocial model considers the “4 Ps” for each of the biological, psychological, and social factors: Predisposing factors that increase the risk for the presenting problem.eg: genetics, life events, or temperament Precipitating factors specific event or trigger to the onset of the current problem Eg: accident,relationship conflicts,infec etc . Perpetuating factors . those that maintain the problem once it has become established Eg: include unaddressed relationship conflicts, lack of education, financial stresses, and occupation stress. Protective factors reduce the severity of problems and promote healthy and adaptive functioning.
- 5. SCHIZOPHRENIA.. • Schizophrenia is a debilitating, lifetime illness which manifests in early adulthood. Its etiology being complex…..not a single cause.., • disease affects approximately 1% of the world's population. • the current approach to schizophrenia is the biopsychosocial model, initially articulated by Dr. George Engel in 1997 (Ader & Brown, 2004). • This model as an important ingredient in understanding the relationship between the mental and physical mechanisms of schizophrenia
- 6. BIOPSYCHOSOCIAL MODEL OF SCHIZOPHRENIA Genetic association, Brain localization and Environmental factors that trigger the onset of this disorder are discussed… Etiology Familial genetics environmental Neuro biology
- 9. LIFE TIME RISK SCHIZOPHRENIA 1 percent General population 10 percent First degree relative 50 percent Two parent with the disorder
- 10. TWIN STUDIES MONOZYGOTIC TWIN DIZYGOTIC TWIN Genes share – 100% Genes share 50% Environment – 100% Environment 100%
- 11. TWIN STUDIES • 46 percent in monozygotic twin • 14 percent in dizygotic twin Gottesman study • 42.6 percent in monozygotic twin • 0 percent in dizygotic twin Cardno et al study -108 pairs • schizophrenia is determined by individual inheriting genes. Results
- 12. LIMITATION OF TWIN STUDY – It is difficult to separate the contribution of factors in families . (environmental factors). Hence to control the environmental factors – ADOPTION STUDIES
- 13. ADOPTION STUDIES Adopted children (If it genetic ) Biological parents (similarities greater) Adopted parents. PARANOID – less familial than other types Very late onset – less genetic loading
- 14. ADOPTION STUDIES • 5 Out of 47 children – mother of schizophrenia • none out of 50 adoptees Heston and Denney study • significantly higher proportion of adopted away offspring of parents with schizophrenia – SCHIZOPHRENIA / SCHIZOPHRENIA SPECTRUM DSIORDERS , than controls Danish American study • Familial aggregation of schizophrenia is determined by INHERITING GENES > intrafamilial culture RESULT
- 15. MOLECULAR GENETIC STUDIES • To seek the gene that predispose to schizophrenia – LINKAGE STUDIES . • NO SINGLE GENE – INCREASES THE RISK OF SCIZOPHRENIA (studies) – number of susceptible genes – DM / SHTN. • Approaches Chromosome region – implicated specific gene Chromosomal rearrangements Association studies
- 16. CONTD… Chromosome region implicated with specific Chromosomal re arrangements Association studies 1 . NEUREGULIN 1 – chromo 8p21- 22 2 . DYSBINIDIN – dystrobrevin binding protein (DTNBP1)- chromo 6p22.3 1 . Chromosomal translocation (1,11)(q42;q14.3) – due to disruption of gene – DISC1 – disrupted in schizophrenia 1 . 1 . COMT GENE – role in dopamine – prefrontal cortex – due to mis sense mutation , valine to methionine substitution at codon 158 – Val158Met. Hence , unstable enzyme – reduced degradation – increase in OTHERS - G 72 (D – aminoacid oxidase activator , DAOA – schizophrenia and bipolar disorders
- 17. BIOLOGICAL ABNORMALITIES IN RELATIVES OF PEOPLE WITH SCHIZOPHRENIA STUDIES FINDINGS – obligate carriers MAUDSLEY STUDY larger lateral ventricles MCDONALD STUDY grey matter deficit in frontal and temporal Other studies delayed P300 neurological abnormalities schizotypal personality Individuals can inherit these characteristics without being psychotic, but increases the risk
- 18. IMPORTANT NOTE STUDY RESULTS SIPOS ET AL STUDY Schizophrenia is common in those whose father were old at the time they were born. This association is present in those with NO FAMILY HISTORY . REASON - accumulation of de novo mutation in paternal sperms with ageing contributes to the risk of schizophrenia
- 20. Environmental factors Pre and postnatal complications Childhood risk factors Social and geographic risk factors
- 21. PRE NATAL AND POST NATAL COMPLICATIONS • obstetric complications – Broad range of obstetric events STUDY RESULTS International study – 700 schizophrenic patients and a similar number of controls. Limitation – recall bias . Low birth weight , prematurity , resuscitation at birth , retarded foetal growth , rhesus incompatibility Increases the risk of hypoxia Minor neurological signs , cognitive and behavioural problems .(pre schizophrenic
- 22. Stefanis et al study Schizophrenia patients with affected relatives , no obstetric complications Schizophrenia with no affected relatives , but had a significant obstetric history . Hippocampal volume is reduced . Indicates hypoxia – ischaemic damage rather than genetic predisposition Normal control Compared hippocampal volume
- 23. SEASON OF BIRTH AND MATERNAL EXPOSURE TO INFECTION • Season – Late winter and spring . • Exposure – INFLUENZA RUBELLA OTHERS – herpes simplex , cytomegalovirus , toxoplasmosis (no consensus) • Severe prenatal malnutrition , appears to have an effect . Studies reported
- 24. CHILDHOOD RISK FACTORS Childhood risk factors High risk studies Follow back studies Cohort studies Schizophrenia patients show abnormalities in their early development .
- 25. HIGH RISK STUDIES • STUDY RESULTS DAVIES ET AL Done – offspring of mothers with schizophrenia . Quarter to half shows deviation from normal terms . NEONATAL PERIOD – hypotonia , decreased cuddliness INFANCY – delayed milestones EARLY CHILDHOOD - poor motor coordination LATER CHILDHOOD – deficits in attention and information processing . Later , FISH ET AL – followed their cohort – 12 high risk infants to adulthood . One – schizophrenia Six – schizotypal / paranoid personality traits LIMITATION : Only minority of people who develop schizophrenia have a mother with same illness. Follow back studie s
- 26. FOLLOW BACK STUDIES • Patients with schizophrenia – maternal recall – to document early development of adults with schizophrenia. • LIMITATION – recall bias . • Childhood home videos – reviewed – high rates of neuro motor abnormalities , RESULTS – impairment of cognitive and neuromotor development , inter personal problems . Male > female. (can also be seen in affective psychosis )
- 27. COHORT STUDIES • STUDY RESULT Dunedin birth cohort study Followed the development of 1037 children . Through the ages 3,15 and assessed them again 18, 21,26 years Poor motor development Poorer receptive language increased the risk of Lower IQ . Developing schizophrenia at the age of 26 years 16 times more likely to develop schizophrenif orm disorders by the age of 26 years
- 28. SOCIAL AND GEOGRAPHIC RISK FACTORS • STUDIES RESULTS MCGRATH ET AL Schizophrenia is 40 percent greater in men than women . FARIS AND DUNHAM Schizophrenia was found in deprived inner city – social isolation , loss of employment , estrangement from family LEWIS ET AL 1.65 times more likely to have born in urban areas than rural areas .
- 29. IMMIGRATION • migrants are at increased risk of schizophrenia . • risk – lower socio economic countries and for black people moving predominantly into white societies . • STUDY RESULTS BOYDELL ET AL Migrants were especially vulnerable if relatively isolated in localities where their own ethnic group were in small minority . Other Paranoid reaction to social disadvantage and discrimination may be one factor
- 30. LIFE EVENTS • Studies – there was a significant relationship between life events and onset /relapse of schizophrenia . • females are particularly prone . • families who exhibit EXPRESSED EMOTION – enhances the risk of relapse in a family member with schizophrenia .
- 31. DRUG ABUSE • Illicit substance use is more prevalent in patients with schizophrenia than in general population . • Prevalence of such co morbidity with schizophrenia – 20 -60 % • Substance – course of the illness worse , should be strongly advised to seek help to cease such behavior STUDY RESULTS ARSENEAULT ET AL Cannabis could be considered as a casual factor in case of schizophrenia .
- 32. SCHIZOTAXIA.. • Paul Meehl introduced the term “schizotaxia” in 1962 to describe the genetic predisposition to schizophrenia, He proposed that schizotaxic individuals would eventually develop either schizotypy or schizophrenia, depending on environmental circumstances. • These events stress the inability of vulnerable individuals to compensate— either behaviorally or neurobiologically—to additional challenges, sources of stress, or, possibly
- 33. GENE ENVIRONMENT INTERACTION • genetic and environmental factors acts in a addictive manner . FINNISH ADOPTION STUDY – offspring of women with schizophrenia are placed in a well adjusted family , they have a lower risk of developing schizophrenia spectrum disorder than placed in a dysfunctional family .
- 34. PSYCHO SOCIAL AND PSYCHOANALYTIC THEORIES • SIGMUND FREUD – developmental fixation early in in life –defects in ego development- -contributes to the symptoms of schizophrenia . Because ego affects – interpretation of reality and control of inner drives – impaired. This intrapsychic conflict arising from early fixation and ego defect – fuel the psychotic symptoms. • MARGARET MAHLER – unable to separate from and progress beyond , the closeness and complete dependence that characterize the mother – child relationship in the oral
- 35. FAMILY DYNAMICS • DOUBLE BIND – Formulated by GREGORY BATESON AND DONALD JACKSON Children receiving conflicting parental messages about their behaviour , attitudes and feelings . children withdraw into psychotic state to escape from the unsolvable confusion. • SCHISMS AND SKEWED FAMILIES : described by THEODORE LIDZ . Schism – schism between parents , overly close with one child of the opposite sex. Skewed – Skewed relationship between a child an one parent , involve a powerful struggle between parents .
- 36. • PSEUDOMUTUAL AND PSEUDOHOSTILE FAMILIES : Described by LYMANN WAYNEE . Family expresses emotion – pseudo hostile / pseudo mutual verbal communication Child leaves house – problems arise in relating with other people . • EXPRESSED EMOTION : Care givers – over criticism , hostility , overinvolvement towards a person with schizophrenia . Causse – RELAPSE .
- 38. DOPAMINE THEORY • DOPAMINE PATHWAYS FUNCTIONS IN SCHIZOPHRENIA MESO LIMBIC PATHWAY Emotional behaviors, Motivation , pleasure , reward HYPERACTIVITY of the pathway , causes positive symptoms , increased smoking . MESO CORTICAL PATHWAY Cognition , executive function Regulation emotion and affect. UNDERACTIVITY of the pathway , causes negative symptoms ,cognitive symptoms, working memory .
- 39. ROLE OF GLUTAMATE • Excitatory neurotransmitter . • Many glutamate pathways – CORTICO BRAINSTEM PATHWAY (imp) • Nmda hypothesis of schizophrenia • PROPOSES – glutamate activity at NMDA receptor is hypofunctional
- 40. Meso limbic pathway Regulate dopamine release in nucleus accumbens NMDA receptor on cortical GABA interneuron hypoactive VTA will be over activated Excessive release of glutamate Excess dopamine release - Positive symptoms Meso cortical pathway Regulates dopamine release in prefrontal cortex NMDA receptor on cortical GABA interneuron hypoactive VTA will be over activated Excessive release of glutamate Excessive stimulation brain stem pyramidal neuron (gaba)- indirect Decrease in dopamine release – negative symptoms This variation is due to the presence or absence of GABA interneuron in VTA.
- 41. NEURODEVELPMENTAL CONCEPT • GENES – dysbindin , neuregulin , DISC 1 • all affect normal synapse formation of NMDA . • leads to dysconnectivity of glutamate neurons – schizophrenia .
- 42. normally , 1. Increases AMPA 2. synaptic strengthening Genes regulating strengthening is abnormal 1. Fewer AMPA 2. weakening of synapse . Increases the risk of schizophrenia
- 43. • Role of serotonin
- 44. 5HT2A RECEPTORS 5HT 2A RECEPTORS IN STRAITUM Stimulates glutamate Triggers GABA INHIBITS DOPAMINE RELASE Act as a BRAKE 5HT 2A RECEPTORS ANTAGONISM IN STRAITUM DOES NOT Stimulates glutamate FAILS TO Triggers GABA DOPAMINE RELASE CUTS THE BRAKE
- 45. ROLE OF GABA AND ACETYLCHOLINE NEUROTRANSMITTERS ROLE IN SCHIZOPHRENIA GABA –INHIBITORY Loss of GABAergic neuron in the hippocampus , leads to hyperactivity of dopaminergic neuron ACETYLCHOLINE Decreased muscarinic and nicotinic receptors in caudate putamen , hippocampus , prefrontal cortex.(postmortem ) NOR EPINEPHRINE Selective degeneration within norepinephrine reward neural system – cause anhedonia .
- 46. FUNCTIONAL NEUROIMAGING AND CEREBRAL ACTIVITY • Cerebral activity – PET / Functional MRI 1 . Hypofrontality – decreased activity in frontal lobes 2 . Relationship between superior temporal gyrus metabolic activity and auditory hallucination is reported.
- 47. STRUCTURAL NEURO IMAGING AND MACROSCOPIC FINDING • REPLICATED POSITIVE FINDING REPLICATED NEGATIVE FINDING Enlarged lateral and third ventricle(40%). Decreased brain size and weight (3%). Decreased cortical volumes , especially temporal lobe Fewer neurons in pulvinar thalamic nucleus Decreased synaptic markers No increased incidence of Alzheimer’s disease. No gliosis – proliferation and hypertrophy of astrocytes . The structural brain damage are present in first episode patients / even before (genetic )
- 48. CONTD Selected controversial finding Increased density of cortical neurons Smaller neurons Aberrant distribution of white matter neuron Fewer glia (oligodendrocytes) Decreased dendritic markers Effects of antipsychotic drugs on brain structure . 1 . Typical antipsychotics – enlargement and synaptic structural alteration in basal ganglia 2. Chronic administration of haloperidol and olanzapine at therapeutic level led to decreased brain volume , increased neuronal density , decreased glial density
- 49. ELECTRO PHYSIOLOGY • P300 – large , evoked potential wave that occurs about 300 milliseconds after a sensory stimulus is detected. • Major source – LIMBIC SYSTEM STRUCTURES OF MEDIAL TEMPORAL LOBES . • P300 – reduced and delayed response to auditory / visual stimuli .(schizophrenia)
- 50. BPS MODEL --CLINICAL IMPLICATIONS IN SCHIZOPHRENIA…. Here we believe that optimal outcomes for people living with schizophrenia (PLWS) arise when healthcare professionals (HCPs) consider both pharmacological and psychological interventions AIM: to embed psychosocial treatment into standard care(Pharmacological) for PLWS and improve the therapeutic alliance between PLWS, their carers, and their healthcare team& improve the overall outcome.
- 51. IMPLEMENTING PSYCHOSOCIAL TREATMENTS IN SCHIZOPHRENIA Establishing and Addressing a Need for Open Conversations and Strong Relationships Recognizing the Role of Carers Recognising and Addressing the Barriers in making strong relationship • VIA Psychoeducation(PE) & shared decision making(SDM)
- 52. TO BUILD A STRONG THERAPEUTIC ALLIANCE • : IMPROVE OUTCOME TRUST OPEN CONVERSATION RESPECT Symptom severity, hospitalizations, rates of drop-out from psychosocial treatment, & adherence to medication
- 53. RECOGNIZING THE ROLE OF CARERS • the role carers play should not be undervalued. • Carers can give important information about how the PLWS is coping, how is his daily activities , and whether any change in wellness or behavior has occurred. • carers may or may not be family members
- 54. BARRIERS TO ESTABLISH STRONG RELATIONSHIPS 1) Patient Barriers to Strong Relationships 2) Psychiatrist Barriers to Strong Relationships 3) Outdated Attitudes 4) Carer Barriers to Strong Relationships 5) Socioeconomic Barriers •
- 55. PATIENT BARRIERS TO STRONG RELATIONSHIPS Poor insight stigma impaired insight can hinder relationship. can lead the person to distrust the help provided by carers & professionals stigmatization causes embarrassment, insecurity and stress. PLWS often use social withdrawal as a mechanism for coping with stigma delay in seeking help Worsens outcome..
- 56. PSYCHIATRIST BARRIERS TO STRONG RELATIONSHIPS Poor Provision of Information • Hesitancy from HCPs • insufficient training on PE technique • poor understanding of cultural context may inhibit a HCP’s ability to form an open, honest and transparent relationship with their patient
- 57. Lack of Patient-Centered Outcomes • HCP’S views PLWS views • , outcomes are usually symptom relief or relapse prevention acceptance by their family or peers, or a return to school or work. Improves outcome
- 58. OUTDATED ATTITUDES • important aspects of personal life, like sexual activity and illicit drug use to be taken into account if avoided in clinical discussions, can create- distrust. Patient-related outcomes should be valued and considered(prioritize life goals and real-world problems) than other clinician’s outcome measure like symptom reductions(hallucinations)
- 59. CARER BARRIERS TO STRONG RELATIONSHIPS • Carers’ behaviors and attitudes can have significant effects on social functioning and treatment success • EE can refer to positive or negative communication strategies used by a carer towards PLWS. Higher levels of negative EE poorer social functionin g poorer compliance
- 60. SOCIOECONOMIC BARRIERS frequent changing of facilities and staff, high caseloads for clinicians, unstable living situations for PLWS, unavailability of accessible transport to get to appointments A availability of well-organized outpatient and outreach mobile services can improve early detection that is crucial for treatment adherence.
- 62. PSYCHOEDUCATION(PE) • PE involves providing accurate, relevant and up-to-date information to PLWS as well as to their carers and family. • focuses on improving insight and giving practical support • Include schizophrenia-specific information • how to recognize symptoms, the impact of the illness on real-life functioning and the importance of treatment for optimal outcomes
- 63. PE … • PLWS may benefit more from an approach that enhances problem-solving skills and promotes the identification and achievement of life goals • For carers, greater importance may be placed on the symptoms of schizophrenia, with a focus on promoting acceptance
- 64. SHARED DECISION-MAKING • contribution that each (PLWS&carers)can bring to the decision-making process should be recognized and considered. • factors that can be Incorporated into consultations to help facilitate SDM. honesty, (regarding treatment options and potential side effects) trust, respect politeness from all parties
- 65. • Open discussion of treatment options should happen as early as the patient is ready, • discussions should always include the pros and cons of different options, • Everyone should be open to the idea of revisiting treatment discussions to find the best option for the patient.
- 66. FORMULATION,, For diagnostic formulation the steps in the above flowchart are followed Step 1: Identification of biological factors from the history given Step 2: Identification of Social factors from the history given Step 3: Identification of predisposing social factors from the history given Step 4, 5, 6, 7: Identification of Psychological factors in accordance with the following domains – Predisposing, Precipitating, Perpetuating and Protective
- 67. CONCLUSION Today, the presentation of schizophrenia going beyond biological factors addressing psychological and social factors as well. ( Kotsiubinskii, 2002)
- 68. we need to ensure that PLWS, carers and clinicians are properly equipped with the knowledge and skills to provide reciprocal support, increase the flow of communication, and allow PLWS to take greater ownership of their illness and its treatment. Equipped with knowledge Increase flow of communicationtan Take ownership of illness & treatment
- 69. REFERNCES • oxford text book of psychiatry • synopsis of psychiatry • stahl’s essential psychopharmacology – 4 th edition • comprehensive textbook of psychiatry • etiology of schizophrenia and therapeutic options – gordana rubesa , lea gudelj
Editor's Notes
- #7: Cumulative effects of number of risk factors