Psychopathology (PSYC 4240) Day 12
Psychopathology (PSYC 4240) Day 12 PSYC 4240
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This 6 page Class Notes was uploaded by Selin Odman on Wednesday June 1, 2016. The Class Notes belongs to PSYC 4240 at University of Georgia taught by Miller in Summer 2016. Since its upload, it has received 10 views. For similar materials see Psychopathology in Psychology (PSYC) at University of Georgia.
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Date Created: 06/01/16
Psychopathology (PSYC 4240) – Day 12 6/1/16 Other Disorders with Psychotic Features Schizophreniform Disorders -Schizophrenic symptoms for a few months (less than 6; more than 1) -Impaired functioning is not required; functioning may lag behind symptoms -Some never progress on to schizophrenia or schizoaffective disorder, but many do Schizoaffective Disorder -Symptoms of schizophrenia and a mood disorder; not a mood disorder with psychotic features Must have psychotic symptoms for a few weeks even in the absence of mood symptoms -Both disorders are independent of one another -Prognosis is similar with schizophrenia -These people usually do not get better on their own -Needs to have delusions or hallucinations for at least 2 weeks in the absence of mood disorder Bipolar type: if mania is part of presentation Depressive Type: if only major depressive episodes are part of the presentation Delusional Disorder -Presence of one or more delusions that persist for at least 1 month -Lack the positive and negative symptoms of schizophrenia Types include: Erotomanic – someone else is in love with person Grandiose Jealous – spouse/partner is unfaithful Persecutory Somatic – involves bodily functions or sensations Bizarre content; clearly implausible; not understandable -rare (0.2%) -Better prognosis than schizophrenia Brief Psychotic Disorder -One or more positive symptom of schizophrenia Delusions, hallucinations, disorganized behavior/speech Lasts at least 1 day but not longer than 1 month Many of these people will not go onto schizophrenia/schizoaffective -Not due to substance use -Usually caused by extreme stress or trauma -Can go away on its own Schizotypal Personality Disorder -May reflect a less severe form of schizophrenia -Phenotypical type of a less severe form of schizophrenia Classification Systems and Their Relation to Schizophrenia Process vs. Reactive Distinction Process: insidious onset, biologically based, negative symptoms, poor prognosis Reactive: acute onset (extreme stress), notable behavioral activity, best prognosis Good vs. Poor Premorbid Functioning in Schizophrenia -Focus on functioning prior to development of schizophrenia -No longer widely used Type I vs. Type II Distinction -Type I: positive symptoms which response well to medication, optimistic prognosis, and absence of intellectual impairment -Type II: negative symptoms, poor response to medication, pessimistic prognosis, and intellectual impairments (Defunct) Subtypes of Schizophrenia Paranoid Type -Presence of prominent hallucinations and delusions (usually persecutory or grandeur) but have relatively intact cognitive skills and affect; organized around coherent theme -Does not show disorganized behavior, speech, thought, or affect -Later onset shows better prognosis -The best prognosis of all types of schizophrenia Disorganized Type (hebephrenic) -Marked disruptions in speech and behavior -Flat or inappropriate affect -Hallucination and delusions, if present, tent to be fragmented (unlike paranoid type) -Develops early, tends to be chronic, associated with a continuous course without remissions Catatonic Type -Shows unusual motor responses and odd mannerisms -Immobility -Motor negativism (resistance to instructions or attempts to be moved) -Waxy flexibility -Examples include echolalia (mimic or repeat words) and echopraxia (mimic movements) -Tends to be sever and quite rare; less and less catatonic people are presenting but they don’t know why Undifferentiated Type -Wastebasket category -Has major symptoms of schizophrenia but doesn’t fit into above categories Residual Type -Past diagnosis of schizophrenia -Absence of prominent delusions, hallucinations, disorganized speech and behavior -Continue to display less extreme residual symptoms Presence of negative symptoms common: affective flattening, alogia, avolition or attenuated positive symptoms Facts and Stats Onset and prevalence worldwide -About 0.3-0.7% -Often develops in early adulthood Onset of first psychotic episodes is early to mid-20s for men; late 20s for women; bimodal distribution for women (second onset in 40s) Many have shown “prodromal” signs earlier Better prognosis: good premorbid adjustment, acute onset, later age of onset, being female, precipitating events, immediate treatment, treatment compliance, family history of mood problems, inter-episode functioning 5-6% die from suicide; 20% make suicide attempt Schizophrenia is generally Chronic (although 20% do okay) -Most suffer with moderate-to-severe lifetime impairment Positive symptoms more treatable than negative symptoms -Life expectancy is slightly less than average Affects males and females equally; slightly higher prevalence in men -women have better long-term prognosis b/c they usually get help faster and are less threatening seeming than men -High comorbidity, especially with tobacco use disorder and anxiety disorders -Major cognitive deficits (esp. in working memory) are common and partially explain significant functional impairment Findings from Genetic Research Schizophrenia has a strong genetic component Family Studies -Inherit a tendency for schizophrenia -Do not inherit specific forms of schizophrenia: different subtypes or forms of psychotic disorders -Risk increased with genetic relatedness Twin Studies -Monozygotic twins: risk for schizophrenia if 1 twin has: 48% -Fraternal (dizygotic) twins: risk for schizophrenia if 1 twin has: 17% -Both parents: 46% -One parents: 17% Adoption studies: risk for schizophrenia remains high in cases where a biological parents has schizophrenia -Appears to be significant overlap in the genes that contribute to SZ, schizoaffective disorder, and manic syndromes Summary of Genetic Research -Risk for schizophrenia increases with genetic relatedness -Risk is transmitted independently of diagnosis -Strong genetic component doesn’t explain everything -Can be a “carrier” of schizophrenic genes without displaying disorder (i.e. a stressor never “activated” the disorder) Neurotransmitter Influences The Dopamine Hypothesis -among most prominent theories of schizophrenia -Drugs that increase dopamine (agonists; amphetamines; L-Dopa) result in SZ-like behavior -Drugs that decrease dopamine (antagonists) reduce schizophrenic-like behavior Produces side effects that look like Parkinson’s disease which is related to too little dopamine ***-Dopamine hypothesis is problematic: 1) didn’t find excess dopamine metabolites in fluid form SZ patients; 2) some not helped by dopamine antagonists; 3) do not impact negative symptoms very much; 4) new “atypical antipsychotic” work with some SZ not helped by other drugs and are not powerful dopamine antagonists Current theories: emphasize many neurotransmitters -higher density of dopamine receptors -may make and release more dopamine -excessive stimulation of Dopamine D2 receptors in the striatum (positive symptoms?) -deficient stimulation of prefrontal Dopamine D1 receptors (negative symptoms?) Structural and Functional Abnormalities in the Brain Enlarged later ventricles (50 studies) -real problems is that the areas next to the ventricles may never have developed fully or atrophies -Not found in all SZ (men; older individuals; duration of SZ) -Found in “healthy” siblings of SZ patients Less active frontal and temporal lobes Less frontal, temporal and whole-brain volume -small hippocampus: most reliable difference ***Brain dysfunction appears before onset of SZ Dysfunction in general appears before onset of SZ Children -lower intelligence and achievement scores than healthy siblings as children -abnormalities in social behaviors, less socially response, show less positive emotions, poorer social adjustment -delays and abnormalities in motor development (i.e. crawling or walking) Adolescents -subclinical signs of psychosis (unusual ideas and sensory experiences); eccentric behavior – signs of Schizotypal Personality Disorder) Viral infections during early prenatal development -Mothers exposed to influenza in second trimester may have children more predisposed for SZ -Other prenatal problems: toxemia/preeclampsia; birth complications associated with hypoxia. Cognitive dysfunctions are substantial and are linked with functional impairment -episodic memory -executive functioning: deficits may appear before onset of psychosis and found in non-SZ relative (i.e. planning, sticking to a task…) *** No abnormality shown to be specific to SZ, AND no abnormality to characterize all SZ patients Abnormalities in neural density, structure, and interconnections. No signs of postnatal injury. Benes: mis-wiring in circuits within certain brain regions (microcircuitry) and between two or more regions within a network (macrocircuitry) Psychological and Social Influences The Role of Stress -may activate underlying vulnerability -may also increase risk of relapse Family interactions -Mothers originally blamed (i.e. being cold, dominant, rigid; schizophrenogenic or giving mixed messages – called “double bind”) -High expressed emotion: associated with relapse Family members being critical, hostile, or emotionally over-involved Medical Treatment of SZ Historical Precursors -wrap in wet sheets; electric shock; insulin comas; frontal lobotomies -Institutionalized: what are the rules now? What should they be? Development of Antipsychotic (Neuroleptic) Medications -Usually the first line treatment for SZ -Began in 1950s: Thorazine (early 1950s), Haldol (1957) A-typical, new antipsychotics: Risperdal; Zyprexa; Seroquel; Clozaril; Abilify -Most reduce or eliminate positive symptoms The newer drugs don’t really treat better, they just have fewer side effects -Compliance with medication is often a problem (3/4 of patients stop taking meds for at least 1 week in a two-year span) Acute and permanent side effects are common Extrapyramidal Side Effects: movement problems -Parkinsonian symptoms: expressionless face, slow motor activity, shuffling gait) -Akathisia: feeling restless and a need to move -Dystonia: abnormal muscle tone; muscle spasms -Tardive dyskinesia: involuntary movement of the tongue, face, mouth and jaw (i.e. tongue sticking out, chewing motions); usually irreversible Caused by “typical” antipsychotics Atypical: less EPS but more weight gain and some can cause life-threatening problems -agranulocytosis: severe reduction in white blood cells caused by Clozaril New methods for reducing noncompliance -injections -psychosocial interventions Psychosocial Treatment of Schizophrenia Historical Precursors -Psychanalytic/dynamic approaches: address early experiences with parents or other traumas -No evidence of efficacy Psychosocial Approaches: Overview and Goals -Behavioral (i.e. token economies) on inpatient units; operant conditioning (response are met with reinforcement or punishment) -Community care programs -Social and living skills training -Behavioral family therapy; reduce EE, supportiveness, didactics -Vocational rehabilitation *Necessary part of medication therapy Documentary: Full documentary on how schizophrenia effects individuals and relationships
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