Schizophrenia

Seven Approaches

Edith H. Buss, George Willison

• Publisher: Routledge
• Year: 2017
• Print ISBN:
  9781138532236
• eBook ISBN:
  9781351492034
• Topic: Medicine
• Subtopic: Psychiatry & Mental Health

Seven controversial approaches to schizophrenia, each assuming a distinctive model, biological, psychological, or social, are presented by their leading exponents. Arnold and Edith Buss deal with such fundamental issues as: What is the nature of schizophrenia? What general approach does each theory represent? What does each theory assume, what evidence does it require for proof, and what follows if the theory is correct? While the various approaches covered here have many differences and few similarities, they are not all mutually contradictory, and several may be combined into a larger synthesis.

From a biological point of view, schizophrenia is a disease like any other, originating in heredity, tissue malformation, and physiological abnormality. The biological approach is represented here by a theory focusing on genetic and neurological aspects. The psychological approach treats schizophrenia as a failure of adjustment. Within this framework there is considerable disagreement. One theory emphasizes the cognitive problems of perceiving, thinking, and problem-solving; another centers on motivational disturbance, with its attendant problems of anxiety and withdrawal; and two theories focus on regressive behavior.

Schizophrenia provides a stimulating basis for discussion by presenting the etiology of schizophrenia in terms of the most significant contemporary approaches. The juxtaposition of these viewpoints enables the professor to maximize students' interest as well as their insight into the complexity of contradictory evidence and opinions.

1: Schizotaxia, Schizotypy, Schizophrenia

Paul E. Meehl

In the course of the last decade, while spending several thousand hours in the practice of intensive psychotherapy, I have treated—sometimes unknowingly except in retrospect—a considerable number of schizoid and schizophrenic patients. Like all clinicians, I have formed some theoretical opinions as a result of these experiences. While I have not until recently begun any systematic research efforts on this baffling disorder, I felt that to share with you some of my thoughts, based though they are upon clinical impressions in the context of selected research by others, might be an acceptable use of this occasion.

Let me begin by asking a question which I find is almost never answered correctly by our clinical students on Ph.D. orals, and the answer to which they seem to dislike when it is offered. Suppose that you were required to write down a procedure for selecting an individual from the population who would be diagnosed as schizophrenic by a psychiatric staff; you have to wager $1,000 on being right; you may not include in your selection procedure any behavioral fact, such as a symptom or trait, manifested by the individual. What would you write down? So far as I have been able to ascertain, there is only one thing you could write down that would give you a better than even chance of winning such a bet—namely, “Find an individual X who has a schizophrenic identical twin.” Admittedly, there are many other facts which would raise your odds somewhat above the low base rate of schizophrenia. You might, for example, identify X by first finding mothers who have certain unhealthy child-rearing attitudes; you might enter a subpopulation defined jointly in such demographic variables as age, size of community, religion, ethnic background, or social class. But these would leave you with a pretty unfair wager, as would the rule: “Find an X who has a fraternal twin, of the same sex, diagnosed as schizophrenic” (Fuller and Thompson, 1960, pp. 272–83; Stern, 1960, pp. 581–84).

Now the twin studies leave a good deal to be desired methodologically (Rosenthal, 1962); but there seems to be a kind of “double standard of methodological morals” in our profession, in that we place a good deal of faith in our knowledge of schizophrenic dynamics, and we make theoretical inferences about social learning factors from the establishment of group trends which may be statistically significant and replicable although of small or moderate size; but when we come to the genetic studies, our standards of rigor suddenly increase. I would argue that the concordance rates in the twin studies need not be accepted uncritically as highly precise parameter estimates in order for us to say that their magnitudes represent the most important piece of etiological information we possess about schizophrenia.

It is worthwhile, I think, to pause here over a question in the sociology of knowledge; namely, why do psychologists exhibit an aversive response to the twin data? I have no wish to argue ad hominen here—I raise this question in a constructive and irenic spirit because I think that a substantive confusion often lies at the bottom of this resistance, and one which can be easily dispelled. Everybody readily assents to such vague dicta as “heredity and environment interact,” “there needle no conflict between organic and functional concepts,” “we always deal with the total organism,” and so on. But it almost seems that clinicians do not fully believe these principles in any concrete sense because they show signs of thinking that if a genetic basis were found for schizophrenia, the psychodynamics of the disorder (especially in relation to intrafamilial social learnings) would be somehow negated or, at least, greatly demoted in importance. To what extent, if at all, is this true?

Here we run into some widespread misconceptions as to what is meant by specific etiology in nonpsychiatric medicine. By postulating a “specific etiology” one does not imply any of the following:

1. The etiological factor always, or even usually, produces clinical illness.

2. If illness occurs, the particular form and content of symptoms are derivable by reference to the specific etiology alone.

3. The course of the illness can be materially influenced only by procedures directed against the specific etiology.

4. All persons who share the specific etiology will have closely similar histories, symptoms, and course.

5. The largest single contributor to symptom variance is the specific etiology.

In medicine, not one of these is part of the concept of specific etiology, yet they are repeatedly invoked as arguments against a genetic interpretation of schizophrenia. I am not trying to impose the causal model of medicine by analogy; I merely wish to emphasize that if one postulates a genetic mutation as the specific etiology of schizophrenia, he is not thereby committed to any of the above as implications. Consequently, such familiar objections as “Schizophrenics differ widely from one another” or “Many schizophrenics can be helped by purely psychological methods” should not disturb one who opts for a genetic hypothesis. In medicine, the concept of specific etiology means the sine qua non—the causal condition which is necessary, but not sufficient, for the disorder to occur. A genetic theory of schizophrenia would, in this sense, be stronger than that of “one contributor to variance”; but weaker than that of “largest contributor to variance.” In analysis of variance terms, it means an interaction effect such that no other variables can exert a main effect when the specific etiology is lacking.

Now it goes without saying that “clinical schizophrenia” as such cannot be inherited, because it has behavioral and phenomenal contents which are learned. As Bleuler says, in order to have a delusion involving Jesuits one must first have learned about Jesuits. It seems inappropriate to apply the geneticist’s concept of “penetrance” to the crude statistics of formal diagnosis—if a specific genetic etiology exists, its phenotypic expression in psychological categories would be a quantitative aberration in some parameter of a behavioral acquisition function. What could possibly be a genetically determined functional parameter capable of generating such diverse behavioral outcomes, including the preservation of normal function in certain domains?

The theoretical puzzle is exaggerated when we fail to conceptualize at different levels of molarity. For instance, there is a tendency among organically minded theorists to analogize between catatonic phenomena and various neurological or chemically induced states in animals. But Bleuler’s masterly Theory of Schizophrenic Negativism (1912) shows how the whole range of catatonic behavior, including diametrically opposite modes of relating to the interpersonal environment, can be satisfactorily explained as instrumental acts; thus, even a convinced organicist, postulating a biochemical defect as specific etiology, should recognize that the causal linkage between this etiology and catatonia is indirect, requiring for the latter’s derivation a lengthy chain of statements which are not even formulable except in molar psychological language.

What kind of behavioral fact about the patient leads us to diagnose schizophrenia? There are a number of traits and symptoms which get a high weight, and the weights differ among clinicians. But thought disorder continues to hold its own in spite of today’s greater clinical interest in motivational (especially interpersonal) variables. If you are inclined to doubt this for yourself, consider the following indicators: Patient experiences intense ambivalence, readily reports conscious hatred of family figures, is pananxious, subjects therapist to a long series of testing operations, is withdrawn, and says, “Naturally, I am growing my father’s hair.”

While all of these are schizophrenic indicators, the last one is the diagnostic bell ringer. In this respect we are still Bleulerians, although we know a lot more about the schizophrenic’s psychodynamics than Bleuler did. The significance of thought disorder, associative dyscontrol (or, as I prefer to call it so as to include the very mildest forms it may take, “cognitive slippage”), in schizophrenia has been somewhat de-emphasized in recent years. Partly this is due to the greater interest in interpersonal dynamics, but partly also to the realization that much of our earlier psychometric assessment of the thought disorder was mainly reflecting the schizophrenic’s tendency to underperform because uninterested, preoccupied, resentful, or frightened. I suggest that this realization has been overgeneralized and led us to swing too far the other way, as if we had shown that there really is no cognitive slippage factor present. One rather common assumption seems to be that if one can demonstrate the potentiating effect of a motivational state upon cognitive slippage, light has thereby been shed upon the etiology of schizophrenia. Why are we entitled to think this? Clinically, we see a degree of cognitive slippage not found to a comparable degree among nonschizophrenic persons. Some patients (e.g., pseudoneurotics) are highly anxious and exhibit minimal slippage; others (e.g., burnt-out cases) are minimally anxious with marked slippage. The demonstration that we can intensify a particular patient’s cognitive dysfunction by manipulating his affects is not really very illuminating. After all, even ordinary neurological diseases can often be tremendously influenced symptomatically via emotional stimuli, but if a psychologist demonstrates that the spasticity or tremor of a multiple sclerotic is affected by rage or fear, we would not thereby have learned anything about the etiology of multiple sclerosis.

Consequent upon our general assimilation of the insights given us by psychoanalysis, there is today a widespread and largely unquestioned assumption that when we can trace out the motivational forces linked to the content of aberrant behavior, then we understand why the person has fallen ill. There is no compelling reason to assume this, when the evidence is mainly our dynamic understanding of the patient, however valid that may be. The phrase “why the person has fallen ill” may, of course, be legitimately taken to include these things; an account of how and when he falls ill will certainly include them. But they may be quite inadequate to answer the question, “Why does X fall ill and not Y, granted that we can understand both of them?” I like the analogy of a color psychosis, which might be developed by certain individuals in a society entirely oriented around the making of fine color discriminations. Social, sexual, economic signals are color mediated; to misuse a color word is strictly taboo; compulsive mothers are horribly ashamed of a child who is retarded in color development, and so forth. Some color-blind individuals (not all, perhaps not most) develop a color psychosis in this culture; as adults, they are found on the couches of color therapists, where a great deal of valid understanding is achieved about color dynamics. Some of them make a social recovery. Nonetheless, if we ask, “What was basically the matter with these patients?” meaning, “What is the specific etiology of the color psychosis?” the answer is that mutated gene on the X chromosome. This is why my own therapeutic experience with schizophrenic patients has not yet convinced me of the schizophrenogenic mother as a specific etiology, even though the picture I get of my patients’ mothers is pretty much in accord with the familiar one. There is no question here of accepting the patient’s account; my point is that given the account, and taking it quite at face value, does not tell me why the patient is a patient and not just a fellow who had a bad mother.

Another theoretical lead is the one given greatest current emphasis, namely, interpersonal aversiveness. The schizophrene suffers a degree of social fear, distrust, expectation of rejection and conviction of his own unlovability which cannot be matched in its depth, pervasity, and resistance to corrective experience by any other diagnostic group.

Then there is a quasi-pathognomonic sign, emphasized by Rado (1956; Rado and Daniels, 1956) but largely ignored in psychologists’ diagnostic usage; namely, anhedonia—a marked, widespread, and refractory defect in pleasure capacity which, once you learn how to examine for it, is one of the most consistent and dramatic behavioral signs of the disease.

Finally, I include ambivalence from Bleuler’s cardinal four (1950). His other two, “autism” and “dereism,” I consider derivative from the combination of slippage, anhedonia, and aversiveness. Crudely put, if a person cannot think straight, gets little pleasure, and is afraid of everyone, he will of course learn to be autistic and dereistic.

If these clinical characterizations are correct, and we combine them with the hypothesis of a genetic specific etiology, do they give us any lead on theoretical possibilities?

Granting its initial vagueness as a construct, requiring to be filled in by neurophysiological research, I believe we should take seriously the old European notion of an “integrative neural defect” as the only direct phenotypic consequence produced by the genic mutation. This is an aberration in some parameter of single cell function, which may or may not be manifested in the functioning of more molar CNS systems, depending upon the organization of the mutual feedback controls and upon the stochastic parameters of the reinforcement regime. This neural integrative defect, which I shall christen schizotaxia, is all that can properly be spoken of as inherited. The imposition of a social learning history upon schizotaxic individuals results in a personality organization which I shall call, following Rado, the schizotype. The four core behavior traits are obviously not innate; but I postulate that they are universally learned by schizotaxic individuals, given any of the actually existing social reinforcement regimes, from the best to the worst. If the interpersonal regime is favorable, and the schizotaxic person also has the good fortune to inherit a low anxiety readiness, physical vigor, general resistance to stress and the like, he will remain a well-compensated “normal” schizotype, never manifesting symptoms of mental disease. He will be like the gout-prone male whose genes determine him to have an elevated blood uric acid titer, but who never develops clinical gout.

Only a subset of schizotypic personalities decompensate into clinical schizophrenia. It seems likely that the most important causal influence pushing the schizotype toward schizophrenic decompensation is the schizophrenogenic mother.

I hope it is clear that this view does not conflict with what has been established about the mother-child interaction. If this interaction were totally free of maternal ambivalence and aversive inputs to the schizotaxic child, even compensated schizotypy might be avoided; at most, we might expect to find only the faintest signs of cognitive slippage and other minimal neurological aberrations, possibly including body image and other proprioceptive deviations, but not the interpersonal aversiveness which is central to the clinical picture.

Nevertheless, while assuming the etiological importance of mother in determining the course of aversive social learnings, it is worthwhile to speculate about the modification our genetic equations might take on this hypothesis. Many schizophrenogenic mothers are themselves schizotypes in varying degrees of compensation. Their etiological contribution then consists jointly in their passing on the gene, and in the fact that being schizotypic, they provide the kind of ambivalent regime which potentiates the schizotypy of the child and raises the odds of his decompensating. Hence the incidence of the several parental genotypes among parent pairs of diagnosed proband cases is not calculable from the usual genetic formulas. For example, given a schizophrenic proband, the odds that mother is homozygous (or, if the gene were dominant, that it is mother who carries it) are different from those for father: since we have begun by selecting a decompensated case, and formal diagnosis as the phenotype involves a potentiating factor for mother which is psychodynamically greater than that for a schizotypic father. Another important influence would be the likelihood that the lower fertility of schizophrenics is also present, but to an unknown degree, among compensated schizotypes. Clinical experience suggests that in the semicompensated range, this lowering of fertility is greater among males, since many schizotypic women relate to men in an exploited or exploitive sexual way, whereas the male schizotype usually displays a marked deficit in heterosexual aggressiveness. Such a sex difference in fertility among decompensated cases has been reported by Meyers and Goldfarb (1962).

Since the extent of aversive learnings is a critical factor in decompensation, the inherited anxiety readiness is presumably greater among diagnosed cases. Since the more fertile mothers are likely to be compensated, hence themselves to be relatively low-anxiety if schizotaxic, a frequent parent pattern should be a compensated schizotypic mother married to a neurotic father, the latter being the source of the proband’s high-anxiety genes (plus providing a poor paternal model for identification in male patients, and a weak defender of the child against mother’s schizotypic hostility).

These considerations make ordinary family concordance studies, based upon formal diagnoses, impossible to interpret. The most important research need here is development of high-validity indicators for compensated schizotypy. I see some evidence for these conceptions in the report of Lidz and coworkers, who in studying intensively the parents of 15 schizophrenic patients were surprised to find that “minimally, 9 of the 15 patients had at least one parent who could be called schizophrenic, or ambulatory schizophrenic, or clearly paranoid in behavior and attitudes” (Lidz, Cornelison, Terry, and Fleck, 1958, p. 308). As I read the brief personality sketches presented, I would judge that all but two of the probands had a clearly schizotypic parent. These authors, while favoring a “learned irrationality” interpretation of their data, also recognize the alternative genetic interpretation. Such facts do not permit a decision obviously; my main point is the striking difference between the high incidence of parental schizotypes, mostly quite decompensated (some to the point of diagnosable psychosis), and the zero incidence which a conventional family concordance study would have yielded for this group.

Another line of evidence, based upon a very small sample but exciting because of its uniformity, is McConaghy’s report (1959) that among nondiagnosed parent pairs of ten schizophrenics, subclinical thought disorder was psychometrically detectable in at least one parent of every pair. Rosenthal (1962) reports that he can add five tallies to this parent-pair count, and suggests that such results might indicate that the specific heredity is dominant, and completely penetrant, rather than recessive. The attempt to replicate these findings, and other psychometric efforts to tap subclinical cognitive slippage in the “normal” relatives of schizophrenics, should receive top priority in our research efforts.

Summarizing, I hypothesize that the statistical relation between schizotaxia, schizotypy, and schizophrenia is cl...

Table of contents

• Cover Page
• Halftitle Page
• Title Page
• Copyright Page
• Contents
• Introduction
• 1 : Schizotaxia, Schizotypy, Schizophrenia
• 2 : Disorders of Attention and Perception in Early Schizophrenia
• 3 : A Learning Theory Approach to Research in Schizophrenia
• 4 : The Process-Reactive Continuum: A Theoretical Proposal
• 5 : A Comparative-Developmental Approach to Schizophrenia
• 6 : Toward a Theory of Schizophrenia
• 7 : Cultural Isolation and the Schizophrenic Personality
• Author Index
• Subject Index