I
COMING TO TERMS WITH DEFINITIONS

    ‘Culture’ and  ‘schizophrenia’ share much: they are both poorly defined, highly reified and sloppily used concepts within and without their professional applications. The acceptance of these reifications produces the mirage of drawing clear boundaries where only arbitrary distinctions exist. One such boundary can be seen in the contrast between the individual phenomenon (schizophrenia) and the aggregate phenomenon (culture) and the relationship generally posited when the two are mentioned together. Such a relationship is illustrated by both Lidz (Lidz 1963; Lidz, Fleck and Cornelison 1965) and Bateson (Bateson, Jackson, Baley and Weakland 1972; Bateson 1972) who typify two of the more prominent approaches to the psychosocial input into schizophrenia.¹  They use what might be considered as modified forms of Harry Stack Sullivan's well-known interpersonal theory.
    Theodore Lidz focuses on a deprivation in the interpersonal environment which is generally manifested in the family. The family is seen as a kind of local expression of culture charged with imparting the values of the larger system. Consequently, the culture, mediated by its sub-unit, the family, is seen as the seminal source of this deprivation.

• Now, it is clear that in the families with schizophrenic offspring the three parameters that have to be considered--the failures of the family to provide adequate nurturance to permit the child to develop autonomy, to achieve the essential structure required to direct the structure of the personality, and to convey the basic adaptive techniques of the culture--are all manifestations of the same core situation deriving from marked deficiencies in the parents personalities, their faulty marital interaction, and parental behavior (Lidz, Fleck and Cornelison 1965: 375).

Lidz's portrayal of the context of the schizophrenic situation recasts the unit of consideration from the individual to the family. Lidz extends his argument (1963: 13ff) by positing the deterioration of the family as symptomatic of rapid cultural change and this culture change is equated with a response to traumatic culture contact. However, he begs several questions which typify deficiencies often encountered in theories of schizophrenia. First, he does not account for those cases which do not conform to his sample of interesting but rather bizarre families. Second, he fails to account for 'normal' development within such circumstances. A third problem, which I will emphasize in a later discussion, is the behavioral isomorphism that exists between schizophrenia and various known reactive syndromes (e.g., drug toxicity, trypanosomiasis). Fourth, Lidz does not account for between-culture variations in manifest symptomatology or for the existence of the syndrome in cultures not in the throes of  rapid culture change.
    In a somewhat simplified depiction, Gregory Bateson’s double bind is based on “the hypothesis that schizophrenia is learned and becomes habitual” (Bateson 1972: 245). He further proposed that “to get confused about logical type, one presumably has to be intelligent enough to know that there is something wrong, and not so intelligent as to be able to see what it is that is wrong” (1972: 197). Bateson, like Lidz, focuses on the family as the context of this learning process. However, the family is not central to his hypothesis. The double bind is a learned relational definition and though family examples are used, they are more illustrative than restrictive. All of the criticisms of Lidz apply to Bateson as well. The double bind is depicted as a ubiquitous phenomenon. What differentiates the special reaction of schizophrenia? Neither the problem of isomorphy nor intercultural variation is touched on.
    From these two examples, a more general comment can be made concerning one of the implications of using -- either explicitly or implicitly -- the concept ‘culture’ and ‘schizophrenia’ in an etiological construct. In Bateson, one sees a situation in which the schizophrenic learns autistic responses in his exposure to culture. In Lidz, the schizophrenic is seen as not having learned to operate within culture by from his family experience. In both cases and virtually all others I have encountered within the social psychiatric and psychiatric anthropological tradition, (e.g., Opler 1967; Rennie, Srole, Langner, Michael and Opler 1962; Leighton 1959; Scheff 1966; Hollingshead and Redlich 1958), one finds a causal imputation going from culture to the individual and stopping there rather abruptly. Rennie elucidates this posture in explicating the theoretical basis of the Midtown Manhattan Study in his introduction:

• The formula finally arrived at places psychiatric disorder and intra-psychic malfunction as a set of dependent variables. The independent variables or relatively fixed variables are those of cultural background, socioeconomic status, ethnic identification, and the attributes of urban-rural living  (Rennie, Srole, Langner, Michael and Opler 1962: 6).

    The direction of this causal connection is implied by the nature of the concepts themselves. Since schizophrenia is not held to cause culture and a connection is imputed, culture is seen as the independent variable in relating the aggregate and the individual phenomenon.² Yet culture, classically defined as “that complex whole which includes knowledge, belief, art, law, morals, customs, and any other capabilities and habits acquired by man as a member of society”, (Tylor 1871: 1) does not easily lend itself to the interpretation of any relationship with events on an individual level. Goodenough’s definition is more useful: “A society’s culture consists of whatever it is one has to know in order to operate in a manner acceptable to its member” (1957: 167) However, Goodenough’s focus on the individual leaves us without a term for the knowledge pool held collectively by the members of a group. The definition I will be using is similar to Goodenough’s but focuses attention on the individual as a member of an information system.
    The dependent variable in this causal imputation is an even more troublesome concept. In careful use, schizophrenia is a description of a set of behaviors. There is no established physiological component--only the tautology of saying that this type of behavior is schizophrenia and schizophrenia is this type of behavior. The Modern Synopsis of Comprehensive Textbook of Psychiatry define schizophrenia as a:

• Mental disorder of psychotic level characterized by disturbances in thinking, mood, and behavior. The thinking disturbance is manifested by a distortion of reality, especially by delusions and hallucinations, accompanied by fragmentation of associations that results in incoherent speech. The mood disturbance is manifested by inappropriate affective responses. The behavior disturbance is manifested by ambivalence, apathetic withdrawal, and bizarre activity (Freedman, Kaplan and Sadock 1972).

Roland Fischer observes that “the only facts relevant to schizophrenia are of a psychological or sociological nature, for the simple reason that schizophrenia is disordered social or psychological behavior”  (1972: 84). Schizophrenia is not a disease in the medical sense of the term ‘disease’ and its meaning (or the lack of it) is an oft discussed topic (cf. Menninger 1970; Cancro 1970; 1972; Kubie 1972; Patterson and Kaebling 1972). However, as Altschule observes “the word [schizophrenia], I’m sorry to say, will probably last forever for two reasons. One is that it is meaningless and the other is that it’s euphonious. The combination of euphony and lack of meaning is unbeatable” (Cancro 1970: 86). The conclusion generally arrived at in considerations of the meaning of ‘schizophrenia’ is that one is dealing with a syndrome or reaction pattern.
    The isomorphy of the condition, the fact that the cluster of symptoms which define schizophrenia can be produced by many known agents coupled with its occurrence with unknown etiology cast many of the genetic and biochemical studies in a rather queer light (e.g. Slater 1972; Abelin 1972; Hurst 1972; Karlsson 1972; Heath et al. 1957; Wooley 1962; Boulton et. al. 1968). The linear causation model on which such approaches are based is invalidated by even a cursory knowledge of the clinical literature. Kety (1967) and Fischer (1972) both conclude in reviews of the bio-chemical hypotheses that have been offered that the explanations lack reliability. Fischer comments that:

• Despite these meager results, the public, of course, is informed mainly about that type of research which attains the status of an article of faith, not by evidence but by wishful thinking and the constant repetition of a “plausible and simple” explanation. How, otherwise, could the remarkable misconception of the average man on the street, that “schizophrenia is due to chemical imbalances”, be explained?  (1972: 84)

    The genetic evidence suffers from a similar deficiency. Just as there unquestionably is a bio-chemical component in at least some cases of schizophrenia, there also seems to be a genetic input into the disorder. However, though speculation on whether this input be “monogenic involving intermediateness”, “single-locus recessive”, or a “major partially dominant gene” may provide a valuable exercise for the researcher, the nature of the evidence does not justify such distinctions. In a review of these procrustean efforts at model application, Anderson comments that:

• There have been a number of efforts to find hypotheses which “fit the data”. The trouble, of course, is that a number of different models fit or can be made to fit (1972: 490).

    To summarize, the isomorphy of the schizophrenic syndrome suggests that anything that defines the requisite conditions, i.e., establishes a particular state or context, will determine a ‘schizophreniform’ reaction. The implication is also that whether the etiology be trypanosomiasis (Opler 1967; Wallace 1972), influenza (Cancro 1970), various types of drug toxicity, or unknown (which restrictively defines the medical category) in some way the responses are connected. In consequence, I will be concentrating on the reaction itself and the behavior it engenders in attempting to develop a model to explain it. It is appropriate at this point to return to the earlier consideration of ‘culture’, and to redefine the term for the purpose of this problem.
    Rather than viewing culture as the traditional, rather static construct of Tylor, or as the individuated learning concept of Goodenough, I will be using a concept of an information system in which individuals actively participate. Behavior in this context is a result of information and a source of information both to the individual and to the group. In any given situation, one is both determining a response of some kind and concomitantly reporting the success of past responses to others through ones present disposition. The information system is built out of these experiences and pieces of information which are reported to one another. Unless the information flowing back into the system is the same as what it predicted it would be, one need not visualize a static, functional model but a system of articulation which the continuous “reality test” of individuals attempting to apply the information.
    In conclusion, the necessarily limited nature of  “mapped” information is a “given”. The process of responding to “gaps” in the information system and of developing and using information is critical to understanding both group and individual behavior and specifically to appreciating how schizophrenia fits into the larger picture.

NOTES

1. In considering theories of schizophrenia I have chosen an illustrative rather than an exhaustive approach. Extensive literature reviews and discussion are available in Van Pragg (1976) and Arieti (1974).

2. Again, as in the discussion of schizophrenia, contrasting concepts of culture were chosen in lieu of a review of its many uses in the anthropological literature (cf. Kroeber and Kluckhohn 1952). More elaborate arguments concerning the utility and danger of using the concept of culture are presented by Keesing (1974) and Bennett (1976).