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Schizophrenia

Schizophrenia. Description and Etiology. Symptoms of Schizophrenia. Positive Symptoms Pathological additions to normal behavior (ie. hallucinations, delusions). Negative Symptoms Characteristics that are lacking or are reduced (ie. reduced range of emotion, reduced amount of speech).

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Schizophrenia

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  1. Schizophrenia Description and Etiology

  2. Symptoms of Schizophrenia • Positive Symptoms • Pathological additions to normal behavior (ie. hallucinations, delusions) • Negative Symptoms • Characteristics that are lacking or are reduced (ie. reduced range of emotion, reduced amount of speech) Psychomotor Symptoms • Odd gestures, excited movement, motionless stupor

  3. Hallucinations Perceptions in any sensory modality without relevant or adequate stimuli • Auditory • may hear sounds that other people do not hear • Visual • may see images that are not really there. May also have a difficult time distinguishing relevant from irrelevant information. • Tactile • strange or unusual sensations on the skin. • Olfactory • may smell smells that are not there. • Taste • may have unusual tastes that are not caused by physical objects.

  4. DelusionsBeliefs that are unfounded and contrary to reality • Persecution - the belief that others are out to get you. • Grandiosity - the belief that you have special powers or abilities. • Guilt - belief that you have committed some crime or have done something that is unforgivable. • Reference - may attach special meanings to things or the behaviors of others. • Control - beliefs that others are controlling thoughts, feelings or behaviors or that the patient has control over others’ thoughts, behaviors or feelings, or events. • Somatic - something is physically wrong with their body even if the doctor says that nothing is wrong

  5. Disorganized Thinking or Speech • Loose associations or derailment - ideas slip off track to matters that are unrelated • Tangentiality, circumstantiality – difficulty reaching answers in a succinct way. • Incoherence - thought patterns do not make sense • Conceptual difficulties - difficult to think in abstract terms • Unusual word use: • Neologisms • Word salad • Perseveration • Clang association

  6. Inappropriate Affect • Any range of emotion that does not fit the content of the situation • May laugh when describing serious events • May have unexplainable shifts in mood • May become angry in positive situations • Mood may be inappropriately intense • Might be caused by internal stimuli (hallucination)

  7. Disorganized Behavior • People may dress oddly • Act in inappropriate manners • child-like or silly • Collect odd items • Act sexually inappropriate in front of others • masturbating, exposing oneself

  8. Negative Symptoms • Avolition - lack of energy or interest in routine activities • Alogia - poverty of speech and poverty of content of speech • Anhedonia - inability to experience pleasure • Flat or blunted affect - little facial expression,patients appear dull • Asociality (social withdrawal) - impairments in social functioning

  9. Psychomotor Symptoms • Reduced spontaneous movements • Catatonia • Decrease in reactivity to environment (stupor) • Patients make repeated gestures (excitement) • Catatonic Rigidity and Posturing • Patients will keep odd postures for a prolonged period of time. • Resist efforts to be moved (negativism) • Waxy flexibility

  10. DSM Criteria A. Characteristic Symptoms. Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated): 1) delusions 2) hallucinations 3) disorganized speech (e.g., frequent derailment or incoherence) 4) grossly disorganized or catatonic behavior 5) negative symptoms (affective flattening, alogia, avolition) B. Social/occupational dysfunction. One or more major areas of functioning such as work, interpersonal relations, or self-care are markedly below the level achieved prior to the onset. C. Duration. Continuous signs of the disturbance persist for at least 6 months.

  11. Incidence • Impacts about 1% of the population • Typically occurs in males between the ages of 18-25 • Typically occurs in females between the ages of 25-30 • Can happen earlier or later than those age groups • There is thought to be a bimodal period in women - another age period where there is a high onset, typically late 30’s early 40’s • About 10-15% may commit suicide • Often more present in cities rather than rural areas • Often more common in lower SES populations

  12. Types of Schizophrenia • Catatonic • motor immobility or excessive motor activity • disorganized behavior • Repetition of words or speech • unusual postures held for a long period of time • Paranoid • presence of hallucinations and/or delusions • negative symptoms are not prominent but may be there to a very minor extent. • Disorganized • speech and behavior are disorganized and often not goal-directed • flat or inappropriate affect

  13. Types of Schizophrenia • Undifferentiated • meet criteria for schizophrenia but none of the other categories are met (no prominent hallucinations or delusions, catatonic [im]mobility) • Residual • there has been at least one episode of schizophrenia, positive symptoms are not present, negative symptoms are present. • Often seen as a transition period between an episode and remission.

  14. Etiology

  15. Walker et al (2005) • Schizophrenia is a brain disease • Its etiology involves the interplay between genetic and environmental factors • Multiple developmental pathways eventually lead to disease onset • Brain maturational processes play a role in the etiological process.

  16. Genetic Factors

  17. Diathesis-Stress Model • But… • Concordance rate is never more than 50% • Unexpressed genetic vulnerability is common • Combination of physiological vulnerability and life stresses may be needed • Adoption studies indicate an interaction between genes and environment • Tienari et al. (1994) adoption study • Rate of schizophrenia significantly higher than in the matched control adoptees • However, genetic vulnerability was mainly expressed in association with disruptive adoptive environments • Elevated rate of schizophrenia was not detected in adoptees reared in healthy family environments

  18. Prenatal and Postnatal Factors • Prenatal • Obstetrical complications (OCs) • Pregnancy, labor, and delivery complications • Hypoxia (fetal oxygen deprivation) most strongly linked to Schz • Maternal infection • Flu during second trimester (brain development) • Maternal stress during pregnancy • Effects on HPA Axis • Postnatal (Brain Injury) Do these act independently or interact with a genetic vulnerability (i.e., do genetics increase response to brain damage)?

  19. Premorbid Development • What happens prior to onset of symptoms? • Childhood • Lower IQ, grades in school (difference greatest as age increases) • Less responsive in social situations, less positive emotion, and have poorer social adjustment • Delays and abnormalities in motor development, • deficits in the acquisition of early motor milestones such as bimanual manipulation and walking

  20. Environmental Stressors • Stressful life events • Family environment predating onset of symptoms increases risk • Neglect/abuse • Institutional settings • HPA Axis (elevated cortisol levels) • Structural brain changes (reductions in hippocampal volume) • More severe symptoms and cognitive deficits • Exacerbate symptoms by augmenting dopamine activity • Increase risk for relapse • Worsen the course of schizophrenia • Number of stressful life events increases in the months immediately preceding relapse • More likely to relapse if they live in homes where family members express more negative attitudes and emotion

  21. Family Environment Early Theories • Schizophrenogenic Mother • Mother as rejecting, cold, domineering • Double-bind Theory • Parents present ideas, feelings, and demands that are mutually incompatible. Contemporary Family Studies • Expressed Emotion

  22. Camberwell Family Interview • Interview conducted with family member (spouse, parent, sibling). • Broad discussion about ill relative • Coded • Criticism • Hostility • Emotional Overinvolvement • Warmth

  23. EE & Relapse(Butzlaff & Hooley, 1998) Meta-analytic effect size r=0.31. HOW IMPORTANT ARE THESE FINDINGS? • For a hypothetical sample of 200 patients (high EE=100; low EE=100), an effect size r=0.30 translates into a high and low EE relapse rate of 65% and 35%, respectively. • In this model, EE is associated with approximately one third of the relapses that do occur and with two thirds of the relapses that do not occur.

  24. EE & Relapse • Found across cultures • Not merely a consequence of overall symptoms or illness severity • Not merely a reflection of lower tolerance for symptoms • Some relation to chronicity

  25. What gives rise to Hostility/Criticism? • Attributions • If family member believes that patient has control over behavior (internal attribution) they may show greater criticism (Hooley) • Some symptoms may give rise to such attributions Negative symptoms were more frequently criticized than positive sxs. Hi-EE relatives criticized negative Sxs more than Lo-EE relatives (Weisman et al., 1998)

  26. Causal Attributions in EE(Yang et al., 2004)

  27. Brain Abnormalities • Enlarged brain ventricles, especially increased volume of the lateral ventricles • Decreased frontal, temporal, and whole-brain volume • Reductions in the size of thalamus and hippocampus • Brain abnormalities predate onset of illness • Present in adolescent studies

  28. Malfunction of neural circuits • Possible abnormal function of “cortico-striatal circuits” that link various regions of the cortex and the limbic system with the striatus • Brain regions that distinguish these circuits mature at different rates • It is possible that disruption in one or more of the circuits characterized by neuromaturation in adolescence/early adulthood may subserve the onset of symptoms.

  29. Neurotransmitters • Dopamine • Enables communication in the circuits that link subcortical with cortical brain regions • Early evidence that • drugs that reduce dopamine activity also serve to diminish psychotic symptoms • drugs that heighten dopamine activity exacerbate or trigger psychotic episodes • antipsychotic drugs have their effect by blocking dopamine receptors

  30. Dopamine (continued) • Early studies of dopamine in schizophrenia failed to find evidence of excess dopamine or its metabolites • However, they found some evidence of increased densities in dopamine receptors • Augmented dopamine synthesis and release

  31. Glutamate • Excitatory neurotransmitter that connect the hippocampus, prefrontal cortex, and thalamus, all regions that have been implicated in the neural circuitry of schizophrenia • Evidence of diminished activity at glutamatergic receptors among schizophrenia patients in these brain regions • One of the chief receptors for glutamate in the brain is the NMDA receptor • Blockade of NMDA receptors produces negative symptoms and cognitive impairments. • Administration of NMDA receptor antagonists induces schizophrenic-like symptomatology • Conversely, drugs that indirectly enhance NMDA receptor function can reduce negative symptoms and improve cognitive functioning

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