Lecture 13 Schizophrenia: Etiology Psychosocial Factors Lecture Outline I. Introduction II. Vulnerability A. Developmental Dysfunction B. Social Factors C. Summary III.Psychosocial Stress Factors A. Communication 1. Double Binds 2. General Communication Patterns B. Expressed Emotion IV. Conclusion ------------------------------------------- I. Introduction In today's lecture we will look at some of the psychosocial factors that play important roles in the onset, course and treatment of schizophrenia. Most researchers today see these factors as part of an overarching diathesis-stress model - that is, there is an interaction between genetic/biological predispositions and environmental stresses. Today, we will focus on those psychological factors that have been identified as important in the development of schizophrenia. II. Vulnerability To identify psycho-social vulnerability factors (ie: personal attributes of the person and social/environmental conditions which predispose the person to schizophrenia), it is necessary to examine the person and his/her environment prior to the development of the disorder. Typically, identification of such "high-risk" people is accomplished by finding children with one or more schizophrenic blood relatives (usually a parent). It is hypothesized that such individuals are at higher risk than those without disturbed relatives (Goldstein, 1987). There is evidence that indicates this is in fact the case (eg: Erlenmeyer- Kimling, 1968): Lifetime risk of developing Schizophrenia Both parents normal: 1-2% One parent Schizophrenic: 12% Both parents Schizophrenic: 35-46% (As we shall see next lecture, there is evidence of a genetic component as well). The lives of these high-risk children are then followed, and those that go on to develop schizophrenia are compared to those who do not and to those children who are not at risk. Problems: Around 90% of schizophrenic persons do not have a schizophrenic parent (Goldstein, 1987). In addition, only about 10 - 16% of the high risk children develop schizophrenia (Goldstein, 1987). And finally, high risk children do not necessarily develop schizophrenia, many children develop other types of psychological disorders instead (Goldstein, 1987). Questions (unanswered to date): To what extent can we actually generalize from high risk studies to schizophrenia in general? To what extent have we identified people at risk for schizophrenia as opposed to people merely at risk for psychopathology in general? More research is necessary before we can answer these questions. A. Developmental Dysfunction A number of cognitive and behavioral abnormalities have been identified in children who later develop schizophrenia (Goldstein, 1987, for a review). These include: -periods of disorganized or delayed motor, visual, physical development -impaired balance, motor coordination, perception, attention -passive, unenergetic, short attention span -cognitive impairment on complex tasks These abnormalities, however, are not consistently found across studies. Results are often contradictory. Currently, these findings are suggestive at best. B. Social Factors Perhaps one of the most consistent social factors associated with later onset of schizophrenia is marked social withdrawal and generally poor interpersonal relationships (Goldstein, 1987, Parnas, Schulsinger, Schulsinger, et al., 1982). These social difficulties become particularly noticeable during later childhood and adolescence. Problem: Such social problems are seen with children who develop other psychological disorders as well. C. Summary Only a subset of schizophrenic adults manifest these early signs during their childhoods. Those children who do, however, may be at the greatest risk for schizophrenia. Nevertheless, the nonspecificity of these vulnerability factors (ie: schizophrenic persons are not the only ones to experience them) makes it impossible to use these factors to reliably identify those children who are "at risk", at least at our present level of knowledge. III. Psychosocial Stress Factors The difficulties associated with identifying high risk individuals and interpreting the findings of the vulnerability research apply here as well. Thus, we should approach the following findings as suggestive: as hypotheses regarding possible "provoking" or stress factors. The family environment as a source of chronic stress has been hypothesized to be a critical provoking factor in schizophrenic disorders. A. Communication During the 1950's there was a growing interest in the role disturbed family interactions might play in the development of schizophrenia in a family member. Of particular interest were disturbed patterns of communication. 1. Double binds: Bateson and his colleagues (eg: Bateson, Jackson, Haley & Weakland, 1956) identified a particularly insidious communication pattern that they hypothesized could play a causal role in schizophrenia. They first noted that communication occurs on multiple levels: verbal, facial, voice tone, posture. In the double bind situation, a parent gives the child simultaneous messages on more than one level which contradict each other: he/she says one thing but acts differently. For example: A schizophrenic patient, glad to see his mother "impulsively put his arm around her shoulders, whereupon she stiffened. He withdrew his arm and she asked, "Don't you love me anymore?" He blushed, and she said, "Dear, you must not be so easily embarrassed and afraid of your feelings." (Bateson, et al., 1956, p.251). No matter what the child does, he/she loses. This "crazy" type of communication, Bateson hypothesized, leads to "crazy" behavior and thought processes. Once a very popular theory of schizophrenia, there has not been a lot of empirical support for the double bind hypothesis. In addition, it has been difficult to explicitly define double bind communication. Thus, even if it does occur, it is difficult for researchers to agree on when it has occurred (Ringuette & Kennedy, 1966). 2. General Communication Patterns: Other lines of research have looked at general patterns of communication within the family as a whole. Families of schizophrenics tend to have deviant communication patterns. For example, parents are unable to establish a focus of attention and instead communicate with each other and other family members in an incoherent manner (Wynne, Singer, Bartko & Toohey, 1975). Verbal exchanges are often confused, vague, or incomplete. For example (Wynne & Singer, 1963, quoted in Neale & Oltmanns, 1980, p.315): Daughter (presenting patient), complainingly: Nobody will listen to me. Everybody is trying to still me. Mother: Nobody wants to kill you. Father: If you're going to associate with intellectual people, you're going to have to remember that still is a noun and not a verb. One hypothesis is that such communication patterns teach the child the disturbed thinking associated with schizophrenia. In addition, these communication disturbances are often occurring in the context of marital conflicts, thus making the home environment even more stressful for the child. The child is caught between his parents (Neale & Oltmanns, 1980), in a situation that makes very little sense. It seems clear that deviant communication occurs in these families, but such deviance may not be causally related to schizophrenia. For instance, both the schizophrenia disorder and the deviant communication patterns may be due to some third variable, such as a family genetic defect (Reis, 1974, Goldstein, 1987). Alternatively, we may just have our causal arrows pointing the wrong way: the presence of a schizophrenic person in the family may give rise to the disturbed communication. Perhaps such communication is how the family learned to cope with the schizophrenic child. For example, in one study (Liem, 1974), 11 families with schizophrenic sons were compared with 11 families with normal sons. Results: disorder was not observed in the communications of parents of schizophrenic sons - there was no significant difference between the two sets of parents normal and schizophrenic sons were not differentially affected by the communications of normal and schizophrenic parents both sets of parents were adversely affected by the communications of schizophrenic sons Finally, we must ask: Why do not all the children in the family develop schizophrenia? In any event, the communication variables that are hypothesized to be stressful and thus provoke a schizophrenic episode also appear to contribute to its exacerbation. Interventions that teach family members more adaptive communication methods have lead to substantial reductions in relapse rates. Indeed, family based communication skills training appears more effective than individual psychotherapy or drug treatment in reducing relapse rates over a 1 year period (Goldstein, 1987). B. Expressed Emotion Another family variable associated with schizophrenia is a negative emotional climate, or more generally, a high degree of expressed emotion (EE). Of particular interest are things like critical comments, hostility and emotional overinvolvement (high levels of tension and emotion). It has been claimed by some that families with high EE seem more likely to have a member who develops a schizophrenic disorder (Goldstein, 1987). Nevertheless, the problems with interpreting communication deviance discussed above, apply here as well. The most consistent evidence is that EE modulates relapse (Falloon, 1988): A patient returned to a family with high EE is much more likely (eg: 76%) to relapse, than a patient whose family is low in EE (eg: 28%) (Brown, Monck, Carstairs & Wing, 1962; see also Brown, Birley & Wing, 1972). What seems to then happen is that the negative emotional climate (eg: hostility and criticism) in these families raises the patient's arousal and stress beyond his or her already impaired coping mechanisms. An alternative explanation: patients in high EE families are initially more disturbed than patients in low EE families - ie: severe pathology is the key variable for both the negative emotional climate and the increased relapse rate. The data, do not support this, however: neither relapse rate nor level of EE is related to the degree of disturbance. Indeed, relapse rates have been found to be related to the extent to which the patient is actually exposed to the EE climate: In one study (see Neale & Oltmanns, 1980), relapse rates were examined not only for low EE and high EE groups, but also within the high EE groups based on the amount of time the patient spent in face-to-face contact with family members. The results (N=128): Relapse rates Low EE 13% (n=71) High EE 51% (n=57) a)with less than 35 hours per week contact: 28% b)with more than 35 hours per week contact: 69% Family based therapies, already shown to be particularly effective in reducing relapse rates, also typically decrease (Doane, Goldstein, Miklowitz & Falloon, 1986). In fact, whatever the therapy method (family based, individual...), when family members shift to low EE patterns, relapse rates are as low as 0%; if EE stays high, relapse rates stay high (Hogarty, Anderson, Reiss, et al., 1986). IV. Conclusion Today we have looked at a few of the psychosocial factors identified as important in the etiology of schizophrenia: developmental dysfunctions, social factors, communication deviance, and expressed emotion. The picture is still far from complete, of course. It is difficult to specify the direction of causality in these findings. Nevertheless, family factors appear to play some important role in the course of schizophrenic disorders. [Note: "Cause" vs "Course" - as we saw with Expressed Emotion, a variable can have importance in the course of a disorder (its duration, severity, prognosis, etc), if not in its initial cause]. The deviant communication patterns and high EE undoubtedly have complex origins. We are talking about individuals, within a family context, who are attempting to cope with the many overwhelming demands of a relative with schizophrenia (Goldstein, 1987). A purely psychosocial explanation of schizophrenia, however, is probably unlikely. In our next lecture we shall examine some of the biological factors that are associated with the development and course of schizophrenia.