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PSYB32 Final Exam Chapters 11, 12, 13, 16.docx

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University of Toronto Scarborough
Konstantine Zakzanis

Chapter 11 - Schizophrenia:  Schizophrenia – a psychotic disorder characterize by major disturbances in thought, emotion and behaviour: disordered thinking in which ideas are not logically related, faulty perception and attention, flat or inappropriate affect and bizarre disturbances in motor activity  Withdrawal from others into fantasy life with delusions  Prevalence b/w 0.2% and 2%, lifetime prevalence 1%  Asian population have lowest prevalence rates  Higher in males than females  Usually appears in late adolescence or early adulthood  Have acute episodes, in b/w episodes still have issues  10% of people with schizophrenia commit suicide  2004: 234 305 with schizophrenia in Canada, 374 deaths, costs 6.85 billion (70% productivity lost) Schizophrenia and Comorbidity:  Comorbid personality disorders (avoidant, paranoid, dependent, antisocial) are common, mood, anxiety, drug abuse  37% with substance abuse disorder also  OCD and schizophrenia often leads to suicide attempts  PTSD is highly prevalent and underdiagnosed in many military veterans  Familial association b/w schizophrenia and depression and anxiety  MDD and cannabis dependence, while developing schizophrenia Clinical Symptoms of Schizophrenia:  Disturbances in: thought ,perception and attention, motor behaviour, affect or emotion, and life functioning  Main symptoms into 2 categories: positive and negative Positive Symptoms:  Excesses or distortions, such as disorganized speech, hallucinations and delusions  Define an acute episode of schizophrenia  Presence of too much of what is present in normal people  Negative = absence of behaviour that should be evident in normal people Disorganized Speech:  Aka formal thought disorder  Problems in organizing ideas and in speaking so that a listener can understand  Incoherence - lack of clarity or organization (found in patients with schizophrenia)  Loose associations/derailment – person may be more successful in communicating with a listener, but difficulty sticking to one topic, drift off evoked by idea of the past Delusions:  Beliefs held contrary to reality  Common positive symptoms of schizophrenia o Unwilling recipient of bodily sensations or thoughts imposed by an external agency o Believe their thoughts are broadcasted or transmitted o Thoughts being stolen by an external force o Feelings controlled by an external force o Behaviour controlled by an external force o Impulses to behave a certain way by an external force Hallucinations and other Disorders of Perception:  World seems different or unreal to them  Hallucinations – most dramatic distortions of perception, sensory experiences in the absence of any stimulation from the environment o More often auditory than visual (74%) o Can be very frightening o Occur more often in schizophrenic people  Own thoughts spoken by another voice, hear voices arguing, hear voices commenting on their behaviour Negative Symptoms:  Behavioural deficits such as avolition, alogia, anhedonia, flat affect and asociality  Endure beyond an acute episode  Strong predictor of a poor quality of life  Associated with earlier onset brain damage and progressive loss of cognitive skills  Flat affect (lack of emotional expressiveness) can be result of anti-psychotic medications  Specificity also an issue hard to see differences between flat affect and depression Avolition:  Aka apathy  Lack of energy and a seeming absence of interest in or an inability to persist in what are usually routine activities  Clients become inattentive to grooming, hygiene  Difficulty persisting at work, school, household chores and sit around doing nothing Alogia:  Negative thought disorder that can take several forms  Poverty of speech: Sheer amount of speech is greatly reduced  Poverty of content speech: repetitive, long speech that is vague Anhedonia:  Inability to experience pleasure  Lack of interest in recreational activities, failure to develop close relationships, no interest in sex  Clients aware of this symptom Flat Affect:  Virtually no stimulus can initiate an emotional response  Client may seem lifeless  Speak in a flat and toneless voice  Refers only to the OUTWARD expression of emotion Asociality:  Severely impaired social relationships  More childhood social troubles, more shy, no interest in making friends Other Symptoms:  2 other symptoms don’t fit the models: catatonia and inappropriate affect Catatonia:  Several motor abnormalities – increase in activity, wild flailing of the limbs  Catatonic immobility- client adopt unusual postures and maintain them for very long periods of time  Wavy flexibility – another person can move the person’s limbs into strange positions that they can maintain or extended periods Inappropriate Affect:  Emotional responses are out of context  Likely to shift rapidly from emotional states for no reason  Symptom is quite rare, but relatively specific to schizophrenia History of the Concept of Schizophrenia: Early Descriptions:  Formulated by 2 European psychiatrists: Emil Kraeplin and Eugen Bleuler  Kraepelin: dementia praecox – early term for schizophrenia o 2 major groups of endogenous, or internally caused psychoses: manic depressive illness and dementia praecox o Dementia praecox included – dementia paranoids, catatonia and hebephrenia o They shared a common core: an early onset (praecox) and intellectual deterioration (dementia- mental enfeeblement)  Eugen Bleuler: believed the disorder did not have an early onset and believed that it did not inevitably progress towards dementia o Term: schizophrenia (schizein = split, phren =mind) o Breaking of associative threads o Attentional difficulties are a result from a loss of purposeful direction in thought o Blocking (loss of train of thought) – complete disruption of person’s associative threads o Led to a broader concept of schizophrenia Historical Prevalence of Schizophrenia:  Rates of schizophrenia fallen since the 1960s  Kasanin: schizoaffective psychosis – describes the disturbances in clients  Concept of schizophrenia broadened by 3 additional practices: (rapid increase in US b/c) o US clinicians tended to diagnose schizophrenia whenever delusions/hallucinations were present (these people may just have a mood disorder) o People who would be diagnosed with a personality disorder now diagnosed with schizophrenia o People with acute onset of schizophrenic symptoms with rapid recovery were diagnosed with having schizophrenia DSM-IV-TR Diagnosis:  More narrow range now, 5 ways to diagnose: o Diagnostic criteria are presented in explicit and considerable detail o People with symptoms of mood disorder excluded (mix of schizophrenia and mood = schizoaffective) o Requires at least 6 months of disturbance for diagnosis (one month active phase with 2 symptoms (or just one if bizarre), remaining time can be prodromal (before active phase) or residual (after active phase)), acute episode = scizophreniform disorder or brief psychotic disorder (one day to one month) o Mild forms of schizophrenia now diagnosed as personality disorders o Differentiates between paranoid schizophrenia and delusional disorder  Delusional disorder – troubled by persistent persecutory delusions or by delusional jealousy (ie. Think spouse is unfaithful)  Somatic delusions – believe organ is malfunctioning  Delusions of erotomania – believe one is loved by another person usually a complete stranger with a higher social status  People in developing countries have a more acute onset and more favourable course than those in industrialized societies DSM-5 Proposal for psychotic risk syndrome and symptom dimensions:  Psychotic risk syndrome  Among 6 criteria: one of delusions, hallucinations or disorganized speech  9 dimensions of core symptoms: hallucinations, delusions, disorganization, abnormal psychomotor behaviour, restricted emotional expression, avolition, impaired cognition, depression, mania Categories of Schizophrenia in DSM-IV-TR:  3 types of schizophrenic disorders: disorganized (hebephrenic), catatonic and paranoid, originally proposed by Kraepelin 1) Disorganized Schizophrenia:  Speech is disorganized and hard for listener to follow  Clients invent new words speak incoherently  Flat affect or experience shifts of emotion  Behaviour disorganized and not goal directed  May completely neglect their appearance 2) Catatonic Schizophrenia:  Clients typically alternate between catatonic immobility and wild excitement but one symptom may predominate  Clients resist instruction and often repeat back the speech of others  Onset is more sudden that other forms of schizophrenia  Seldom seen today b/c drug therapy works effectively  Was misdiagnosed before with what was lethargica (sleeping sickness) 3) Paranoid Schizophrenia:  Presence of prominent delusions (persecution delusions most common)  Grandiose delusions – exaggerated sense of their own importance, power, knowledge or identity  Delusional jealousy – unsubstantiated belief that their partner is unfaithful  Vivid auditory hallucinations may accompany  Ideas of reference – incorporate unimportant events within a delusional framework and read personal significance into the trivial activities of others  Agitated, argumentative, angry and somewhat violent  Emotionally responsive  More alert and verbal than people with other types of schizophrenia  Language is not disorganized Evaluation of the Subtypes:  Subtypes have little predictive validity  Considerable overlap among the types (all forms people have delusions)  Undifferentiated schizophrenia – people who meet diagnostic category but NOT for any of the 3 subtypes  Residual schizophrenia – used when the client no longer meets the full criteria for schizophrenia but still shows some signs of the disorder  Heinrichs: primacy of cognition, link of schizophrenia to cognition strong because of influence on brain systems that have a role in information processing, cognitive factors reflect genetically determined constraints, possible influence of stress/distress on cognition in people prone to schizophrenia  Andreasen and Olsen: most people with schizophrenia show mixed symptoms (+ & -), very few were purely positive or negative  Some studies show 3 symptoms: split positive into 2 categories: delusions and hallucination AND disorganized component (bizarre behaviour and disorganized speech)  DSM-5: reject all classic types of schizophrenia and rejected alternatives take their place o Why? Because subtypes rarely used with the exception of paranoid schizophrenia and maybe undifferentiated schizophrenia o Findings do not point to a single system of subtyping Etiology of Schizophrenia: The Genetic Data:  Predisposition genetically to schizophrenia (inherited)  Identical twin very likely to have schizophrenia Family Studies:  Relatives with people with schizophrenia at a HIGH risk  Negative symptoms have a stronger genetic component  Relatives also at risk for other disorders (less severe forms of schizophrenia)  Also influence of environment as a key factor (ie. Parent influences child) Twin Studies:  Identical twins (44.4%), fraternal (12.08%)  Predisposition increases when twin more severely ill  Environment could be the main factor (intrauterine environment – share same blood supply)  Fischer: non-schizophrenic twins would have genotype for schizophrenia, just not expressed o Might pass along an increased risk for children  Negative symptoms have a stronger genetic component Adoption Studies:  Children of women with schizophrenia more likely to be diagnoses as mentally defective, psychopathic, neurotic  More frequently involved in criminal activity  Children reared away from schizophrenic mothers still schizophrenic (therefore strong genetic factor) Molecular Genetics:  Thaker (why hunt for schizophrenic genes is hard) o Lack of preciseness in defining boundaries of clinical phenotype o Absence of biological tests that confirm diagnostic categorization o Clinical heterogeneity and the complex nature of schizophrenia  Endophenotypic strategy – Gottesman and Shields – reflect actions of genes predisposing an ind to a disorder even in the absence of diagnosable pathology o Ind endophenotypes assumed to be determined by fewer genes o Thus complexity would be reduced  Serotonin type 2A receptor gene dopamine D3 receptor gene and chromosomal regions 6, 8, 13 and 22  Microdeletion of chromosome 22  DTNBP1  G protein signalling 4 – gene localized to chromosome lq23  Overlap between schizophrenia and bipolar disorder Evaluation of the Genetic Data:  Schizophrenia defined by behaviour  Must keep in mind diff between genotype and phenotype  Genian quadruplets – (diasthesis stress and biopsychosocial models)  Stress required to spark schizophrenia  Not been possible to specify how predisposition of schizophrenia transmitted  Exact nature of inherited diasthesis is unknown The Genain Quadruplets:  All sisters had schizophrenia by age 24  Sisters experienced very diff life outcomes  Hester – severe impairment, never completed high school  Iris and Nora – better, but never had careers/married  Myra – worked, married and raise a family  Course of disorder can vary Biochemical Factors:  Neurotransmitter – norepinephrine and serotonin  Dopamine – best researched factor Dopamine Activity:  Excess activity of dopamine  Anti-psychotic drugs produced effects of Parkinson’s disease (low dopamine)  Anti – psychotic drugs block dopamine receptors (D2 receptors)  Excess activity in dopamine nerve tracts  Dopamine theory – amphetamine psychosis – amphetamines produce state that resembles paranoid schizophrenia o Amphetmaines cause release of catecholamines including norepinephrine and dopamine into synaptic cleft to prevent inactivation o Result of increasing dopamine (not norepinephrine) o Over-sensitive dopamine receptors o Dopamine receptors in greater numbers in schizophrenics o Amphetmaines worsen positive symptoms but effect on negative is less clear o Excess dopamine activity in the mesolimbic pathway and effects of antipsOver-sensitive dopamine receptors o Dopamine receptors in greater numbers in schizophrenics o Amphetmaines worsen positive symptoms but effect on negative is less clear o Excess dopamine activity in the mesolimbic pathway and effects of antipschotics occur there (helping positive symptoms) lowering activity in the neural system o Prefrontal area thought to be linked to negative symptoms, dopamine neurons may be underactive  fail to exert inhibitory control  overactivity in dopamine system Evaluation of the Dopamine Theory:  Takes several weeks for antipsychotics to lessen positive symptoms  Strange that you need do reduce dopamine so much to create Parkinson’s  Dopamine may not be the only answer Other Neurotransmitters:  Dopamine neurons in prefrontal cortex regulate GABA neurons  Serotonin neurons regulate dopamine is mesolimbic pathway  Glutamate may also play a role  Low levels of glutamate in CSF of schizophrenics  Street drug PCP can cause schizophrenic symptoms – it interferes with glutamate receptors  Decrease in glutamate from prefrontal/hippocampus to corpus striatium can result in increased dopamine activity  Glutamate, serotonin and dopamine all factors Schizophrenia and the Brain: Structure and Function: Enlarged Ventricles:  Enlarged ventricles which imply a loss of subcortical brain cells  Structural problems in hippocampus, prefrontal and temporal cortex  Males especially have enlarged ventricles  Reduction in cortical grey matter in temporal and frontal regions and reduced volume in basal ganglia and limbic structures  Large ventricles = impaired performance on tests, poor adjustment, poor response to drug treatment  Large ventricles have neurodevelopmental origin and not progressive  Large ventricles not specific to schizophrenia (bipolar) Prefrontal Cortex:  Plays a role in behaviours disrupted in schizophrenia  Lack of awareness  Reductions in prefrontal cortex grey matter  Low metabolic rates in prefrontal cortex when performing tests  Failure to show frontal activation in MRI  Failure to show frontal activation related to negative symptoms  People with schizophrenia and anti-social and substance abuse show different functioning than those with just schizophrenia and violence Congenital and Developmental Considerations:  Consequence of damage during birth/gestation  Women delivering babies with schizophrenia show complications that lead to schizophrenia (but these only occur in kids with predisposition for it)  Virus invades brain and damages during fetal development – influenza (cell migration issues)  Reduced numbers of cells in outer layers of cortex in both prefrontal and temporal areas o Frontal cortex smaller in those with schizophrenia  Torrey Yolken: Human endogenous retro-virus attacks NS and incorporates itself into cellular genome code of infected person o Cryptic code can be activated by certain biological events (ie. Puberty) o Positive symptoms before age 12  Dalman: 50% increased risk to those exposed to viral CNS infection before age 12  Weinberger: brain injury interacts with normal brain development and that the prefrontal cortex matures late (that’s why schizophrenia is seen late) o Dopamine also peaks in adolescence Contemporary Research:  4% bilateral hippocampal volume reduction in people with schizophrenia o Bilateral medial temporal regions especially  Brambilo: reduced cerebral blood volume accompanies brain size decrement and chronic cerebral blood volume eventually results in neuronal loss and cognitive impairments  Widespread cortical dysfunction in schizophrenia  Wexler: smaller white matter volumes in neuropsychosocially impaired people with schizophrenia o White mater forms physical connections of functional networks o White mater plays role in cognitive impairments Psychological Stress and Schizophrenia:  Philps: only limited evidence that stress = psychotic episode: Retrospective designs, inadequate control groups, over-reliance on life events, failure to consider person’s appraisal  2 stressors: social class and family Social Class and Schizophrenia:  Areas of low socio-economic status  Sociogenic hypothesis – stressors associated with being in a lower class contribute to development of schizophrenia (degrading treatment person receives increases person who is predisposed)  Social selection theory – during course of development of schizophrenia people may go into lower class places  social selection theory favoured The Family and Schizophrenia:  relationships between mother and son crucial to schizophrenia  schizophrenogenic mother- cold, dominant, conflict-inducing parent who was said to produce schizophrenia in offspring Relapse and the Role of the Family:  expressed emotion (EE) – high then more likely to relapse  environment into which patient is discharges plays a large role on relapse o expression of unusual thoughts by client = high critical comments by family o high EE families critical comments by family led to expression of unusual thoughts  related stress to HPA axis, stress may activate HPA  cortisol release  increase dopamine activity  increase schizophrenia symptoms Developmental/High-Risk Studies of Schizophrenia:  preschizophrenic boys – disagreeable, girls – passive  both men and women were delinquent and withdrawn in childhood form school  preschizophrenic showed poor motor skills and more expressions of negative effect (compared with siblings)  negative symptoms schizophrenia – birth complications  positive symptoms schizophrenia – history of family instability, ie. Separation from parents  lower grey mater suggests onset of psychotic disorders Therapies for Schizophrenia:  Hospitalized Clients with Schizophrenia:  token economy introduced  clients in the program were in a very bad state of schizophrenia (long time)  clients matched and assigned to one of 3 wards: social learning (behavioural – token economy), milieu therapy and routine hospital management  2 treatment wards  Social-learning ward: o Operated on a token economy o Clients appearance had to pass in 11 ways to receive a token o Other good factors provided tokens o Tokens were important to purchase meals and small luxuries o Residents kept busy 85% of waking time  Milieu-Therapy Ward: o Principles of Jones’s therapeutic community o Kept busy 85% of waking hours o Act responsibly and participate in decisions on how the ward functioned o Were treated as normal ind  Routine Hospital Management: o Custodial care and heavy antipsychotic meds o 5% waking hours with activity, people were on their own otherwise  Results: both social learning and milieu worked to reduce positive and negative symptoms o 10% social learning and 7% milieu left ward and lived ind, none of hospital left o 90% started with meds, after 100% hospital used meds, and the other two groups med use dropped dramatically o Social learning program superior o No one was fully cured but much better Therapies for Schizophrenia:  Hospitalization generally shows poor outcomes  Issue: many patients refuse treatment, they don’t believe they have the disorder o Paranoid schizophrenia – may view treatment as hostile outside forces  American Psychiatric Association: o Selection and application of antipsychotic medication o Identify and treat comorbid disorders o Use psychosocial treatment approaches (ie. Family interventions, psychoeducation, social skills training, CBT, assertive community treatment and supported employment) Biological Treatments: Shock and Psychosurgery:  Sakel: 1930 induced coma with large doses of insulin  Cerletti and Bini: ECT  Moniz: 1935 prefrontal lobotomy – destroys tracts connecting frontal lobes to lower centres of the brain  Leucotomy – like prefrontal lobotomy, more specific procedure  Principal reason for leaving lobotomies was introduction of drugs Drug Therapies:  1950’s = antipsychotic drugs (neuroleptics) – produce side effects similar to neurological disease First Generation (Conventional) antipsychotic Drugs:  Phenothiazine – most frequently prescribed  Antihistamines – have a phenothiazine nucleus  Laborit: pioneered use of antihistamines to reduce surgical shock  Charpentier: chlorpromazine (Thorazine) – calmed people with schizophrenia o Rapidly became preferred treatment in US o 85% used  Phenothiazine – able to block dopamine receptors, thus decreasing dopamine effects on brain  Butytophenones (Haldol, haloperidol) and thiozanthenes (Navane) o Reduce positive symptoms, less effect on negative  NOT A CURE  30-50% do not respond to drugs  Because of side effects half of the people quit taking drugs after a year, ¾ in 2 years  Extrapyramidal side effects – stem from dysfunctions of the nerve tracts that descend from the brain to spinal motor neurons o Resemble symptoms of Parkinson’s disease o Dystonia – state of muscle rigidity o Dyskinesia – abnormal motion of voluntary and involuntary muscles o Akasthisia –inability to remain still o Tardive dyskinesia – lip smacking, make sucking, chin wagging  Neuroleptic malignant syndrome – 1% of cases, sometimes fatal o Severe muscular rigidity o May lapse into a coma Second Generation (Atypical) Antipsychotics:  Clozapine (Clozaril) – greater gains than other drugs, fewer motor side effects, reduced relapse states o Major impact on serotonin receptors o Serious side effects: impairs immune system function (1% clients), lowering white blood cells  Olanzapine (Zyprexa)  risperidone (Risperdal - 6mg) o improves working memory o reduces activity of serotonin sensitive receptors in the frontal cortex  Antipsychotics block D2 (dopamine) receptors Current Issues and New Directions:  Relapse prevention  Atypical seem to give patients a better quality of life, long term symptoms unknown  Ability to function in community  Developing drugs to improve cognition  NIMH with MATRICS developing study for negative symptom drugs  Olanzapine and risperidone clients improved in executive function, learning and memory ,processing speed, attention and vigilance, verbal working memory and motor functions  Risperidone – visuospatial memory improved  Haloperidol – only in learning and memory improved  Atypical antipsychotics are effective for treatment resistant schizophrenics  Children under 18 excluded from drug trials  Antipsychotic success in children quite low  MATRICS – Measurement and Treatment Research to Improve Cognition in Schizophrenia Psychological Treatments:  Increase effectiveness of medication and decrease relapse rates  Freud: people with schizophrenia incapable of establishing the close interpersonal relationship essential for analysis Social Skills Training:  Teach people techniques to help in interpersonal situations Family Therapy and Reducing Expressed Emotion:  Educate families on biological vulnerability to schizophrenia  Provide info and advice on monitoring medication  Encourage family to not blame themselves  Help with communication  Encourage family to expand social network and contact  Instill hope that things can improve  Family therapy + meds reduces relapse over periods of 1-2 years Cognitive-Behavioural Therapy:  CBT effective in positive symptoms  Group CBT not the best  CBT should be saved for patients that are medication non-responsive with positive symptoms Personal Therapy:  Broad-spectrum CBT approach  Conducted one on one and in workshops  Less emotional reaction by family = less relapse  Muscle-relaxation  Empathy with realization that life can be better  Not a short-term treatment can take up to years  Much of focus on client NOT family – teach client coping skills Treatment Focus on Basic Cognitive Functions:  Cognitive enhancement therapy (CET) – developed by Hogarty, educational and supportive aspects of personal therapy o Computer-based training in attention, memory and problem solving as well as social skills o Proved successful in improving cognition and processing speed  Utility of scaffolding – must tailor to account for person’s skill level o Look at person’s capability and assign tasks accordingly Case Management/Assertive Community Treatment:  Mobile Crisis Intervention Team (MCIT) – nurses in bulletproof vests General Trends in Treatment:  Not making family feel like it is their fault  Family oriented treatment  Early intervention  Teach client social skills The Homeless Mentally Ill:  86% of homeless mentally ill in Canada Employment and Housing:  Chronic shortage of subsidized housing  1/3 psychiatric patients face discrimination when looking for housing Destigmatization:  54% people with schizophrenia should be considered violent and dangerous  31% employee would be fired from job  Younger respondents believed in rehabilitation in community  Psychiatrists have a largely negative stereotype Early detection:  20 projects in Canada  Most treatment done in home  Goal: prevent onset of early symptoms, decline in cognitive, social and occupational functions  3 strategies: coping and stress management, medication and education  African Americans received high levels of medication Chapter 12 – Substance-Related Disorders:  2 categories: substance abuse and substance dependence Substance dependence:  At least 3 of the following: o Person develops tolerance: a) larger doses for desired effect b) effects less if usual amount taken  DSM 5: distinction b/w substance abuse and dependence dropped and replaced with Addiction and Related Disorders o Withdrawal symptoms o Uses it for longer than needed o Unable to stop using o Much of person’s time spend obtaining drug o Continues to use despite health signs o Gives up/cuts back participating in activities  DSM 5: pathological gambling be included, inclusion of behavioural addictions  Substance abuse diagnosed as accompanied by physiological dependence Substance abuse (less serious):  One of the following: o Failure to fulfil major obligations o Exposure to physical damages o Legal problems o Persistent social or interpersonal problems  Substance intoxication – ingestion of substance affects the CNS  DTs/delirium tremens – substance withdrawal from alcohol  DSM-5: quantitative severity distinction rather than qualitative b/w substance abuse and dependence; so include both disorders together o Substance use disorder symptoms less useful for severe/mild pathology Alcohol Abuse and Dependence:  Alcohol dependence – tolerance or withdrawal, those who drink early have issues in 30-40’s o Increased tolerance following heavy drinking o Body adapts to drug and can process more effectively o Tolerance results from changes in number/sensitivity of GABA or glutamate receptors o When drinking stops, receptors overactive  Often part of polydrug (polysubstance) abuse – using or abusing more than one drug at a time o 80-85% alcoholics are smokers o Nicotine and alcohol are cross tolerant o Alcohol + barbiturates lethal Prevalence of Alcohol Abuse and Comorbidity with other Disorders:  Alcohol misuse 3 in 10  Prevalence higher in men, younger, whites – often chronic (4 years)  Comorbid with mood and anxiety disorders  25% suicides Course of the Disorder:  Alcoholics Anonymous: 4 stages: social drinking  person only lives to drink  No single pattern of alcohol abuse  Difficulties with alcohol at a later age in women, tend to be steady drinkers, drink alone, more likely to binge Binge Drinking in Schools:  1 in 4 students were binge drinkers (US)  Half million US students hurt in drinking accidents  1 in 6 Canadian students binge drink  Students drink before 16 more likely to binge drink later Costs of Alcohol Abuse and Dependence:  4 leading cause of worldwide disability  Problem drinkers use mental health places 4 times more  Suicide rate much higher  Drunk drivers kill 3-4 people each day, injure 187 per day  Prototypical drinking driver: male b/w ages 25-34  No blood alcohol in 21/under  Half of all murders committed Short-Term Effects of Alcohol:  Alcohol metabolized by enzymes after swallowed and reaching stomach  Most of it goes to small intestines where it is absorbed by blood, then broken down in liver  Absorption rapid, removal always slow  Initial effect of alcohol is stimulating, but after it peaks it is depressive  Stimulates GABA receptors which may be responsible for reducing tension  Increases levels of serotonin and dopamine = pleasurable effects  Inhibits glutamate receptors Long-Term Effects of Prolonged Alcohol Abuse:  Severe biological damage + physiological decline  Almost every tissue and organ in body affected  Malnutrition  Deficiency in B complex = memory loss, amnestic symptoms, memory gaps  Cirrhosis in liver – liver cells engorged with fat and protein  Destroys brain cells – loss of grey matter in temporal lobes  Reduces effectiveness of immune system increases susceptibility for cancer/infection  Fetal alcohol syndrome – mental retardation in infants o 1 in 100 pregnancies  Light drinking (wine) decreases coronary heart disease and stroke Inhalant Use Disorders:  Peak age for inhalant use 14-15 years, initial onset at 6  Inexpensive and readily available  Gasoline sniffing – problem in Aboriginals  Most inhalants = depressants  Feelings of euphoria, psychic numbing  Damage to CNS, nausea, headaches Nicotine and Cigarette Smoking:  Nicotine – addicting agent of tobacco, stimulates nicotinic (Acetylcholine) receptors in brain  Causes neurotransmitter release (ie. Dopamine) = pleasure  Just one puff can be enough to start addiction  Females had more brain activity in cortical and subcortical prefrontal systems (linked with attention and memory)  Females have greater changes in cognition than males Prevalence of Health Consequences of Smoking:  Smoking causes 47 000 deaths each year in Canada  Risks of smoking less for cigar/pipe smokers, but mouth cancer increased  Lung cancer, emphysema, cancer of larynx and esophagus and cardiovascular diseases  Harmful components: nicotine, tar, carbon monoxide  Health risk decline 5-10 years after quitting  Daily smokers smoke 14.9 cigarettes a day, males smoke 3 more cigarettes than females  Erectile problems in men Consequences of Second Hand Smoke:  Aka environmental tobacco smoke (ETS) – contains high conc of ammonia, carbon monoxide, nicotine and tar than does smoke inhaled by smoker  2/3 smoke of cigarette not inhaled by smoker but in air around smoker  Second hand smoke has at least 2x nicotine and tar  Regular exposure increase lung disease by 25% and heart disease by 10%  No smoking in cars when passenger is under 16 Marijuana:  Dried and crushed leaves and flowering tops of hemp plant (cannabis sativa)  Most often smoked, can be chewed, tea, baked goods  Hashish – much stronger than marijuana, produced by removing/drying resin of the tops of high-quality cannabis plants  Illegal in most countries  Canada – 15g allowed campaign (NOT ANYMORE) Psychological Effects of Marijuana:  Depend on potency and size of dose  Find it makes them feel relaxed and sociable  High doses produces hallucinations  Difficult to regulate dose because effects seen after 30 min  Delta-9-tetrahydrocannabinol (THC) – major active ingredient  Cannabis receptors in brain  Chronis use = mild impairments (not severe)  4/5 seeking treatment were male The Stepping Stone Theory:  Alcohol was gateway for cannabis  amphetamine  cocaine  Marijuana associated with heavy drinking and cocaine use  Cannabis high in males, peaked at age 18-19  Network theory more appropriate than stepping-stone Somatic Effects:  CB (cannabis) receptors in various regions, believed that receptors in hippocampus account for short-term memory loss that sometimes follows smoking marijuana o Short-term side effects: itchy eyes, bloodshot eyes, dry throat, increase appetite, reduced pressure within eye, raised BP o No evidence it has effects on a normal heart  Marijuana + tobacco = increased risk for respiratory disorders  One marijuana joint = 4 cigarettes  May be addictive  Those who started before 14 more likely to be addicts, than those started after 17 Therapeutic Effects:  Can reduce nausea and loss of appetite that accompany chemotherapy for cancer patients  Also a treatment for discomfort of AIDS, glaucoma, epilepsy, MS  2% Canadians use it for medical purposes Sedative and Stimulants:  2 categories: sedative and stimulants Sedatives:  Aka downers – slow activities of the body and reduce its responsiveness Opiates:  Relieve pain and induce sleep when taken in moderate doses  Morphine – separated from raw opium, bitter-tasting powder = powerful sedative and pain reliever  Morphine converted to heroin – initially used to cure morphine addiction, however it is more addictive and harmful than morphine, acts quicker with more intensity Psychological and Physical Effects:  Produce euphoria, drowsiness, reverie and lack of coordination  Heroin has additional effect: rush, a feeling of warm, ecstasy right after injection, user forgets worries (4-6hrs) then is letdown  Produce effects by stimulating neural receptors in body’s opioid system  Heroin  morphine  opioid receptors  Body produces opioids = endorphins and enkephalins  Addictive  Withdrawal within 8 hours for heroin, symptoms resemble influenza (more severe in 36 hours)  More than a million heroin addicts in US  Dependence high in physicians and nurses, than any other educated background  5% street youth use heroin every day  Today heroin 25-50% pure  $200/day for opiates Synthetic Sedatives:  Barbiturates – major sedative, aids for sleeping and relaxation  Addictive  Benzodiazepine (Valium) – more commonly used and abused  Methaqualone – street drug  Sedatives relax the muscles, reduce anxiety and in small doses produce a euphoric state  Stimulate GABA system like alcohol  Large doses fatal, frequently chosen as means of suicide Stimulants:  Aka uppers – act on brain and sympathetic NS to increase alertness and motor activity  Cocaine = natural stimulant, amphetamines = synthetic stimulants Amphetamines:  Isolated alkaloid from Ephedra  ephedrine  treat asthma  Amphetamines – synthetic o First amphetamine = Benzedrine – inhalant for stuffy nose o Control mild depression/appetite o Treat hyperactive children o Benzedrine, Dexedrine, Methedrine – causing release of norepinephrine, dopamine and blocking reuptake of these o Taken orally or injected and can be addictive o Wakefulness increased, appetite decreased (Weight loss) o Boundless energy/confidence o Large dose = schizophrenia  Tolerance develops rapidly  Methedrine = strongest of all (esp when injected)  Increased use in workplace to stay awake Cocaine:  Extracted from the leaves of coca plant  Has been used as a local anesthetic  Acts rapidly on brain blocking reuptake of dopamine in mesolimbic area  Increases sexual desire, feeling of self-confidence, well-being  Chronic use leads to personality changes  Severe withdrawal symptoms  Causes blood vessels to narrow  Crack – another form, cheap, appealing to younger generation  0.3% for people ages 18-34  Most dangerous illicit drug in society Caffeine:  Two cups of coffee with 150-300mg of caffeine affect people within 30 min LSD and Other Hallucinogens:  Hofmann created D-lysergic acid diethylamide  Thought to be psychotomimetic because it showed sim symptoms to psychosis  LSD = hallucinogen  Mescaline, psilocybin and synthetic compounds MDA and MDMA  Mescaline – alkaloid, active ingredient peyote cactus  Psilocybin – crystalline powder, isolated from mushroom  All stimulate serotonin receptors  Tolerance develops rapidly, no withdrawal symptoms known, cheap  Psilocybin (ingredient in magic mushrooms) given to OCD patients – substantial decreases in OCD  Also decreases in depressions  Ecstasy – 2 closely similar synthetic compounds, MDA and MDMA o Produced via chemical synthesis o Drug enhances intimacy, improves relationships, elevates mood and promotes aesthetic awareness Effects of Hallucinogens:  Setting in which drug experienced important  Bad trip – flow blown panic attack from taking LSD (more likely to occur in anxious person)  Flashbacks – reoccurrence of effects after drug has worn off Etiology of Substance Abuse and Dependence:  Generally a developmental process  Baker: 2 elements a) intense negative effect from withdrawal b) urges to take drug  Process of becoming a substance abuser:  positive attitude  experimentation  regular use  heavy use  physical dependence/abuse Social Variables:  highest alcohol consumption rates: France, Spain, Italy – where drinking is accepted  readily availability also a factor  if both parents smoke: child 4x more likely to smoke  exposure to parents drinking increases child’s risk of drinking  protective factors: high self-esteem, family member with post-secondary education  dominant family influence from older siblings to younger especially if siblings 2 years/less apart  stronger than like between parents and children Psychological Variables:  3 classes of variables Mood Alteration, Situations and the Role of Cognition:  2 dimensions: valence of reinforcement and locus  4 combinations of these 2 possible  Cooper: scale to assess drinking motives: o Positive internal reasons measured with enhancement scale o Negative internal reasons measured with coping scale o Positive external reasons assess via social scale o Negative external reasons assess via conformity scale  Conclusion: young people drink for social motives, less likely to drink for enhancing/coping motives  Social use = moderate, coping use = alcohol related problems, enhancement motive = heavy drinking  Dalhousie: important to distinguish link between daily anxious mood and alcohol consumption Cognitive Factors in Drinking:  Reduce tension  Steele and Josephs: alcohol myopia – intoxicated person has less cognitive capacity to distribute b/w ongoing activity and worry  Positive alcohol expectations = higher levels of consumption  Negative expectations = inhibit consumption  Most people believe alcohol has a stronger effect on other people, than on themselves  Alcoholic parent + child abuse while growing up = negative expectations  Wiers and Stacy: model of addictive behaviour that distinguishes b/w controlled, reflective behaviour and automatic impulsive processing  Drug Stroop Task – requires individual to say whether a word matches a particular colour and ignore content of word itself o People with addiction respond slower to reading the word addiction in task o Stroop interference affect – people with addiction have this Beliefs about Prevalence and Risks:  Abuse lowers when people think the drug is harmful Personality and Drug Use:  Personality variables are stable and can be detected in childhood  Cloninger and Eyesneck: 3 genetically inherited dimensions of personality: novelty seeking, harm avoidance and reward dependence o Novelty seeking most relevant to alcohol dependence o 3 key dimensions of personality: extroversion-introversion, neurocriticism vs emotional stability, psychoticism o Association in general use and anti-social personality disorder o Studies are cross sectional rather than longitudinal =  o Cannot be assumed that personality factors create vulnerability to substance abuse o Depression was related to the initiation of smoking o Associated with nicotine addiction and DRD2 A1 allele o Maturing out phenomenon – overall tendency for peak drinking levels to occur when people are in their mid-20’s and there is a sharp drop in their late 30’s Biological Variables:  Genetic predisposition for drinking suggested  Greater concordance for identical twins in alcohol abuse, smoking, heavy use or abuse of cannabis, and drug abuse  Genetic component may be stronger for males  Ability to quit smoking has a genetic heritable component  Heritability estimates for alcohol dependence range b/w 50-60% o However environmental factors also important  OPRM1 receptor gene linked with early onset problem drinking during adolescents  Asians have a low tolerance in gene that metabolizes alcohol  2 variables predict alcohol abuse in men: self report of a low level of intoxication after alcohol use, and less body sway after drinking  Alcohol dependence leads to long-term neuro-adaptations that create a negative emotional state; alcohol ingested to relieve emotional state  Alcohol ingestion reflects negative reinforcement  Amygdala is the factor in changes that accompany problem drinking  Spanagel: complex gene-environment model: cumulative response to alcohol exposure, genetic composition and environmental perturbations over time o Chronic alcohol: brain physiology to alter gene expression and synaptic plasticity  Siegel: Conditioning theory of tolerance – underscores the need to jointly consider biological processes and environmental stimuli that may be involved in the acquisition and maintenance of addictive behaviours o Based that tolerance is a learned response o Environment = cues  Siegel: feedforward mechanisms: anticipatory regulatory responses made in anticipation of a drug , we learn to anticipate drug effects before they actually occur Therapy for Alcohol Abuse and Dependence: Admitting the Problem:  Ogborne: only 2% of lifetime drinkers reported seeking help  Heavy drinkers less likely than moderate drinkers to believe they need treatment  Heavy drinkers estimate the extent in the general population  Enabling drinker to take first step = contemplation stage Traditional Hospital Treatment:  Detoxification – withdrawal from alcohol  Tranquilizers sometimes given to ease the pain  Also need carbohydrates, vitamin B and sometimes anticonvulsants Biological Treatments:  Diselfiram, Antabuse – drug that discourages drinking by causing violent vomiting of the alcohol if ingested  Blocks the metabolism of alcohol  However can cause serious side effects  Naltrexone – continues to last only as long as person takes it  Clonidine Alcoholics Anonymous:  Largest most widely known self-help group  Instilled in alcoholics that alcohol abuse is a disease that can never be cured o Al-Anon Family Groups and Alateen (children)  AA has high drop-out rates Poundmaker’s Lodge:  Many drug abuse place for and run by Aboriginals  Addiction is viewed as disease  Crucial to treat the entire person o Balance in 4 dimensions: spiritual, mental, emotional and physical  12-17 years old (Adolescent Treatment Centre) 90 days o Treatment centre not a correctional institution o Family program vital (1 week) – to support child Couples and Family Therapy:  May live solitary lives  Often physically abusive in relationships  Husbands and wives generally both drink lots Cognitive and Behavioural Treatment: Aversion Therapy:  Problem drinkers shocked or made nauseous while looking at or reaching for alcohol  Cover sensitization – problems drinkers instructed to be violently and disgustingly sick by their drinking Contingency-Management Therapy:  Teaching clients and those close to them to reinforce behaviours inconsistent with drinking  This approach includes being more social and couples therapy  Behavioural self-control training: o Stimulus control – one narrows the situations in which one allows oneself to drink o Modification of the topography of drinking – sips rather than gulps, mixed drinks o Reinforcing abstinence Moderation in Drinking:  Controlled drinking – moderate pattern of alcohol consumption that avoids the extremes of total abstinence and inebriation (Sobellis) o Given shocks to reinforce treatment – when drank “Wrong” o Video tapes of themselves  Most experience a relapse over a 4 year period  Guided self-change: outpatient approach emphasizes responsibility and control  Harm reduction therapy – alternative approach that focuses on complete abstinence Clinical Contributions In Treating Alcohol Abuse:  Clinical assessment of what place drinking has in a person’s life  Client treatment matching – aptitude-treatment interaction (AIT) – critical issue in the development of better interventions for problem drinking  Project Match – certain kinds of treatments good for problem drinkers Harm and Reduction Therapy:  Marlatt: Harm reduction therapy (HRT) – deals with high risk behaviours in addictions o Addiction not a crime, it deserves treatment not punishment o Abstinence not the only outcome o Bottom up approach more in line with needs of addict o People can easily gain access o Based on principle of compassionate pragmatism rather than moralistic idealism – acknowledges struggles of people  Campbell: Four Pillars Drug Strategy: harm reduction, prevention, treatment and law enforcement  Managed Alcohol Project – HRT invention for homeless people with alcoholism Matching Client to Treatment: Project Match:  ATI – focuses on characteristics of people with the same disorder that might make them more suitable candidates for a treatment o 10 matching
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