Research and the Complex Causality of the Schizophrenias

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STATEMENT OF PURPOSE THE GROUP FOR THF. ADVANCE:'vfENT OF PSYCHIATRY has a membership of approximately 300 psychiatrists, most of whom are organized in the form of a number of working committees. These committees direct their efforts toward the study of various aspects of psychiatry and the application of this knowledge to the fields of mental health and human relations.

Collaboration with specialists in other disciplines has been and is one of GAP's working principles. Since the formation of GAP in 1946 its members have worked closely with such other specialists as anthropologists, biologists, economists, statisticians, educators, lawyers, nurses, psychologists, soci­ ologists, social workers, and experts in mass communication, philosophy, and semantics. GAP envisages a continuing pro­ gram of work according to the following aims: 1. To collect and appraise significant data in the fields of psychiatry, mental health, and human relations 2. To reevaluate old concepts and to develop and test new ones 3. To apply the knowledge thus obtained for the pro­ motion of mental health and good human relations GAP is an independent group, and its reports represent the composite findings and opinions of its members only, guided by its many consultants.

RESEARCH AJ\'.D THE COMPLEX CAUSALlTY OF THE SCHIZO­ PHRE:\"IAS was formulated by the Committee on Research.

The members of this committee are listed on the next page.

The following pages list the members of the other GAP com­ mittees, as well as additional membership categories and cur­ rent and past officers of GAP.

vii

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ŰɈŀĹȤǦʍʎǶƤ‫؂‬ɉª‫؂‬űǒȐʦǹ‫؂‬ɘɶʺŲǧǓōʏɩʻ‫؂‬ L`ñ¡ąG%ą 2ra¤à ą<b¢ø|áí¸ ąR}þ& Ĩ‫؂‬ 7- c Íù~Îâ¹­ą Ǻ Ҋ΃ս‫؂‬ȥ ‫؂‬T΄ ѯ*‫؂‬ų˨ ˩˪ҥ ‫ ؂‬Ȍʼ ‫؂‬ ǔ˫ ө‫؂ך‬ƘӪҦˬ ͛‫؂‬ƙ ҧAӫ C‫ ؂‬ȹ΅‫؂כ‬ʽ ՀчG‫ ؂‬Ⱥ ʾ ‫؂‬

XӬվ ԥϺ‫ ؂‬ƴЙտ̀ϻϼӭϏ ‫ ؂‬VΆB ‫؂‬łѿКk ‫؂‬ ‫؂‬ ǻԢ֤·ԦϽ‫ˋ ؂‬ϐ ¯ŇՁ# Â‫؂‬3 ͜Лր ҨH‫؂‬ʫМց÷‫؂‬ ǼӮ ‫؂‬ƵO‫؂‬2́ƚΈӓӔӯA à Ȅթ ‫ ؂‬Ǖ;ҩӰѓ‫׀‬єׁ,‫؂‬ǖ˭‫ל‬ˮ Н‫؂‬ ǽׂϾҪ‫؂‬ɷ͂Ͽӱ‫˯ם‬ѕ֧ >Ä‫؂‬Z ‫؂מ‬Ǘ˰‫ג‬Ήҫ ‫ ؂‬ӲҬҭ ‫؂‬ ʐxΊӳ͝ӴՂ΋‫؂‬ɸЀ˱ԧ&Ճ<K‫ ؂‬Łp‫؂ן‬ʿӵ ш ‫ ؂‬ȝˀø‫؂‬ əΌ ΍>‫؂‬ʑ˲ ϥ‫ת˳׃‬Å‫ ؂‬ȑ ւ‫ ؂‬Ŏ Ϧψ q@,‫ ؂‬Ŵ4іОϑĊ‫؂‬ ȒΎҮӶՄΏ‫؂‬ƶùƓċ‫ ؂‬ʒΐՅՆÆ‫؂‬ɹ˴ү‫ ؂‬ƷՇ˵Ұ̓{փժӏÇ‫ ؂‬ŵ˶ї8t ‫؂‬

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@ Óāą U(ą =Ôô²pleõ¥ ą0.f mÕ u q ąJ èé !ą 9 g ÖÇ ×ê ą ʮþ‫ ؂‬ɮԉ̰6Ւ ‫؂‬ŢΣ̊‫ה‬ΤՓ֍D‫؂‬Ɯ̋ѵ9̌ÓL‫؂‬ʚΥ‫צ‬0‫؂‬ ; ³ą ăHą 3 Ø h´Ąą Ք‫ו‬о͓Օ =һÔ‫؂‬Ni)ą ȗΦΧ‫؂‬ſԊґ̱ՖЦҼ͔эïLj ̍Ї̎Ғ ‫؂‬ɟЈЧѠfͥϊѶԬ${̏Õ‫؂‬ɠ̐ÿ‫؂‬ ǩ՗̑‫؂‬V ‫؂‬ƀ Ш͆}Ö‫؂‬Ŀ͇‫ˇ؂ף‬ԋ՘ъ×‫ ؂‬Ⱦðˉ‫؂‬ WՙΨm6 '͈ ‫؂‬lj ֹֺ ЩΩ̲ ‫؂‬ȘԌ֎‫ ؂‬ŕҽvϋ Ϊ Ø‫ ؂‬Ɓg пϘė‫؂‬ Xԍ֏#ԭy‫ ؂‬ɾ̒‫͉׊‬ҾÙ‫؂‬ɿ̓ҿ‫ ؂‬ƹ՚̔ ͊Ъ֐͋ Ú‫؂‬Ƃ ѡzώĀ‫؂‬

ƃɋȫːǪʛʜƪƫ‫؂‬Ɍʴ‫؂‬NJɍʩƽ1ɳÛ«ʼnȬ҄ȿʝŖǫāÜ‫؂‬ŗƄșɀƅȇ1ʀ‫؂‬ 'ѷ Ы̕ғ‫؂ ؂‬ʪ̖ ‫ ؂‬ʁֻԡ L‫؂ ̗[ ؂‬ŘѢ֬Ԏ ‫؂‬Ɔ̘ |ϕ ,‫؂‬ ÙÈ Üì ą ȁ :7 ‫؂‬ɡP‫؂‬Ƈ̙ Bp ѣÝ‫؂‬ȭԏ ֭# Ϋ‫׭‬F‫؂‬3֑֒̚ ‫؂‬ ʂЬͦӀά‫؂׮‬ʃ ‫؂‬NjԐ ͧέӁÞԑЉӂ ‫ ؂‬Ȉ ‫^؂פ‬Ԓ՛ыE‫؂ ^ ¡ ؂‬ ɁaԓҔЭ‫؂‬ǞήѸѹ6 G‫؂‬ʯ̛֓ЊЮ v֮ -‫؂‬ƝĂƈP‫؂‬ ɯԔϱ ՜‫؂‬ɢίΰ q-‫؂‬ʰ̜֔Ћ Ӄϫ ԕ M‫ ؂‬ƞ.Ɖ ‫؂‬

ƊɎȮ҃ęòDzʞʟƾƬ‫؂‬Ԗ‫ ؂׾؀‬ǟ‫ˎ ؂‬ļƟ Ƌřɣʄ‫؂‬ ă‫؂‬ ɂ;ծҕ̝ ‫؂‬ɰ ‫؂‬ţαիӑ֕֯β&ӄ ‫؂‬ƌ Я̞͌Ϭ ß‫؂‬ǰ (Ąà‫؂‬ :£ą+j Ú Ûëà ą 2γ‫ׯ‬s՝‫؂‬ʅQ‫؂‬nj‫׋‬Ӆְ$s՞á‫؂‬ƍ$8͍̟ϭԗâ‫؂‬DZѺѻą‫؂‬ TδA ‫ ؂װ‬ɦ‫׺‬εϖϗ͎՟̳̠‫׌‬Җã‫ ؂‬Ǡ=‫ ֖׍‬Ԙ ä‫؂‬ʠζ‫ק‬å‫؂‬ ʱ'Ѽ а̡җ‫ ؂‬ǡ ‫؂‬ʆ̢͏ M‫؂‬ɤ ՠֱ( ӆ"æ‫ ؂‬ɏաηϮR‫؂‬ ʲбѽ в̣Ҙ‫؂‬Ś ‫؂‬ʇԙӇг֗+‫ ؂‬Ťθ ι֘"̤ç‫؂ ͨ!؂‬ ǍκԚբw#‫؂‬ʡ̥գт̦ӈ ‫؂‬Ț ֙‫؂‬śӉwλ9ό֚ ‫̧ ؂‬ѤдϙĘ‫؂‬ ʢyԛ:d ‫؂‬ǎ ‫؂‬ʳμ̴ ֲν ‫ ؂‬Ќ' ϯ ӊè‫؂‬Ơ Ǝ ‫؂‬ Ǣξ լ‫؂ױ‬ǣ ‫ ؂‬դьé‫؂‬ťο π̨֛ͩê‫! ؂‬n ‫؂‬

ƏɐȯȰּ¦Ѿ§ đϝěĔ‫؂‬ɑľ‫؂‬ѥɃʣƭĜɄŜʤѦɒɅŝֽ ‫؂‬ɱƮțŞʥǬɓɆʈ‫؂‬ ƺ ̩ kр֜‫؂‬ƻĆ‫؂‬U Ӓ ֝ ‫ ؂‬Ɛ 7‫֞ ؂ײז‬ρë‫ ؂‬ȱn I‫؂‬ Ƒ ̪еեԮς?֟) ‫؂‬ ɲԜ̵σ? ‫؂‬Ȳ ‫؂‬ơԝզӋì‫׎̫]؂‬4ҙτ Ԟí‫؂‬ƒ 8Ϛ0‫؂‬ Ȃԟ$ӌ‫؂‬ʉ ‫ ؂‬Ȏ̬Ϝ *‫ ֠؁ ؂‬ж ϰֳԠ ‫ ؂‬ƢćƔĐ‫؂‬

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ŷȺˎ‫ב‬τȚυʓʔϊĂƛ‫ך‬ċ‫ ךי‬ɎɹˀŸǃǍłʕɫˇ‫ ך‬Ńȩƍ‫ך‬ɥƜȃǙƫǎȻȪ‫ך‬ ńё͂͝ԟђDK ‫ך‬Ǿ!̓ Ҭ=‫ך‬ʲӥӦ g9‫ך‬Ź̛.СϋăÑ‫ך‬ ź ̜ТԠ‫ג‬Ӻ͞ԡՒӧ ‫ך‬ ɺմÒҀxׄ͡‫ ך‬$>‫ך‬Ż&յlÓ‫ך‬Œπ /Ө04Ô‫ ך‬ĨѤ̳՜՝õ‫ך‬ Rqͳҭβ‫ךׅ‬ƥ֒ öǏǿ ‫ ך‬œ ҮֻÕ‫ ך‬ȱ ˁ‫ך ך‬ _Ë ½ Ī ŠF Š U¨ŗÌ "ŠZ©s'Š N ŕªö#ŠGč Š Ɲ̝ ѥ‫ך‬Ņ ‫ ך‬LөӪҁ Ö‫ך‬ǥ ×‫ך‬F֓ϣ֙՞ն̞Ø‫ך‬Ƭ̟‫ך‬ ħ‫׍‬ɓԢշУđүγԣ‫[ך‬ľŠȀȼˏː <‫;ך‬īĎ÷ř Šę˓¡‫ ך‬o,Š żѓ‫ʹ׆‬δ‫ ך‬ɦ ‫ך‬S ‫ ͵ׇ‬ԤÙ‫ך‬ņɏȽÚ‫ ך‬ϔ ˂ ‫ך‬ ѯєФ` ̠ρѦ‫ ך‬ɧ ‫ ̡ˉ ך‬εՓ ‫ך‬ƭ jζ ֶ ͟ЂÛ‫ך‬Ž Ұ1 ‫ך‬

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žȾțбօԯ ʖˈāƞ‫ך‬ȿȫ‫ך‬ɐɻ˃ſDŽǐŇʗɨ˄‫ˊך‬Ȭ‫ ך‬ǑȭƎʜɼʘɩ˅‫ך‬ < ĬĭÍ«Šf ŠLĮ¬Î°´ Š ďĿŇĐø$Š V ŀŁ %ŠH ÏįĖ ù5đúŠ \­ň®İŠ Ȅý‫=ך‬ıÔÜÝ&Š]¾ÐÛ ¯Þė¿Ñ Š^ -Š H!̢ ‫ך‬ɔ ‫ ך‬Dẓ̌Ϥη Ü‫ך‬ɽ4þ‫ך‬ȁ ֔ Ք ‫ ך‬Ȝ֕A‫ך‬ ɬ ‫ך‬ƟͶַ̤ԥ ‫ ך‬dž֖kϏ҂̥ Ý‫ך‬ňՕ h֧ ѧѨθÞ‫ך‬Ȯ ƀ ‫ך‬ Ə^֨ ͷ‫ך‬Ơ÷‫ך‬Oӫ Ֆ ұß‫ך‬ɑ̦ [ոХ à‫ך‬ǒ ÿ‫ך‬ Ɛ̧֩ ͸‫ך‬Ŕ ‫ך‬ɪӬ̈́ͅ ՟8‫ ך‬ƁЃ'ӻӼ̨Ԁ֗Y ‫ך‬ȯøˆ ‫ך‬ Ƃ \ iҲ͠ι‫ ך‬Q~ָ "‫ ך‬RչB‫ ך‬ɒ̩֘ѩ ‫ ך‬ȝЦ2ҳ ‫ך‬ Ǧaφϒ3)‫ך׈‬L ‫ך‬ɾӽjѪ κ á‫ ך‬ʼn λּ̪Ҵ͹ ̫ ‫ ך‬ʦ̬ ‫ך‬ J Є ‫ ך‬V̭,hϐаς ͺâ‫ך‬S̮ ̯պ ϥ̰ã‫ ך‬ƃ_ ЮόA‫ך‬

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TABLE OF CONTENTS Statement of Purpose ......... . .... .. . . ............... . ......... . . .

vii

1 Introduction ................................................................

3

2 The State of the Field ................................................

Genetic Theories ........ . . .................................... .......

Theories of Aberrant Psychophysiologic, Perceptual, and Cognitive Function ...... .. .............. ........

Biochemical Theories ..............................................

Theories of Aberrant Psychologic Development ...

Sociocultural Theories ............... ..... ... ...... ... ..... .......

13 15 18 2I �4 30

3 Examples of Interdisciplinary Cross-Domain Research ...................................................................... 35 Assumptions .. ... .............................. .... ............ ......... 35 Selected Strategies ................................................... 37 4 Approaches to Cross-Domain Research .................... 45 A Biologic Research Study: Metabolic Abnormalities and the Schizophrenias .................. ............... 45 A Family Systems Research Study: Family Systems and the Schizophrenias ................. ..... ........ .... .... . 48 A Psychodynamic Research Study: Symbiosis and the Schizophrenias ...... ............... ... ............. .......... 51 A Longitudinal Research Study: Child Development and the Schizophrenias .............................. 56 5 Implications for Treatment and Training ....... ..... ....

63

6 Conclusion ... ......... ........ ...... ..... .... ..... .... ........ ..... ... ..... ..

67

References ....... ... . .. . .. . . . . .. . . . .. .. . .. . . . .. . .. .. . . . .. .. . . ... ... .

69

Index . ..... ....... ....... ..... ........... ...... ..... ...... ...........

81

xv

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8

Complex causality of the schi:i:ophrcnias

schizophrenias. More recently, Scheflen ( 1981) has proposed the hasic structure of a complex model with which to un­ derstand the schizophrenias.

An example of the application of a complex model to un­ derstanding disease is that described by Engel (1977, 1979).

He proposes a biopsychosocial model of disease which derives from systems theory and considers a wide range of hierar­ chically organized variables in interaction with each other.

This model not only calls for consideration of a large group of diverse variables, but also emphasizes their hierarchical interrelationships. Each subsystem of variables interacts di­ rectly or indirectly with every other subsystem, and disturb­ ance at one level may be contained at that level or affect all other levels. Engel suggests that the spread of. disturbance through many levels is a crucial factor in the development of disease. One problem involved in the use of such models is their level of abstraction. For example, terms like "positive and negative feedback" and "homeostasis" have great appeal for considerations related to the schizophrenias, but are dif­ ficult to operationalize or test, and disappointment has fol­ lowed attempts to use them.

A systems approach to the etiolog·ies of the schizophrenias can also relate to the clinical endeavors of assessment, treat­ ment, and prevention. Such an approach can help the cli­ nician decide what to assess and how to combine variables in diagnosis and treatment. In a like manner, clinical infor­ mation is equally crucial to the success of a systems paradigm.

Given the large number of possible variables and ways of combining them, clinical information should be a major feed­ back loop in the continuing elaboration of the model.

The clinician's model of causality may involve at least two levels of complexity: one for acute, potentially fatal clinical events, and a second for other situations. When faced with a crisis as, for example, in patients with diabetic coma, acute myocardial infarction, or suicidal panic, the clinician must deal with the most pressing variables and intervene promptly

Introduction

9

and incisively. In these situations the threat to life is direct and immediate, and a simple, linear model may be most appropriate. The next patient seen by the clinician, however, may be an aging person with severe rheumatoid arthritis, an adolescent with labile diabetes, or a chronically depressed individual. In these situations, the role of multiple and di­ verse variables mandate the use of a more complex model of causality. The clinician's sense of certainly growing out of a simple cause-and-effect schema may be lost, but compen­ sated for by the greatly increased range of interventions pro­ vided by the more complex model of disease. The ability of the clinician to move back and forth between levels, as the context demands, both requires and reflects a high level of clinical expertise.

It is against the background of these issues that this report is cast. Its primary goal is to encourage research efforts that clarify the patterns of relationships among groups of varia­ bles in various domains thought to be related to the etiologies of the schizophrenias. In pursuing this goal, we shall make the following assumptions about the schizophrenias: 1) The assumption of heterogeneity. This report assumes that there is a group of schizophrenias. Further, it assumes that the complex interaction of etiologic variables is different for different forms of schizophrenia. Each form displays certain characteristics that differentiate it from other forms. These characteristics may be biologic, psychologic, or social. The assumption of heterogeneity is supported by both clinical and research findings and parallels current knowledge about other disorders such as hypertension or diabetes.

2) The assumption of illness. This report assumes that the schizophrenias are illnesses, not alternative lifestyles. Al­ though there may be a risk that secondary deviance might be brought about as a result of the label of schizophrenia, this report assumes that the primary disturbance of schizo­ phrenic patients is a biopsychosocial reality.

3) The assumption of syndronie. This report assumes that the

IO

Complex causality of the schiwphrenias

present state of knowledge about the schizophrenias is con­ sistent wilh the designation of syndrome. Although the terms syndrome, reaction, illness, and disease often lack precision, this report defines syndrome as a clinical disorder in which there are certain patterns of symptoms, the etiology of which is poorly or incompletely understood. ft is useful, however, to keep in mind that syndromes are composed not only of those symptoms that various patients have in common, but also of features that reflect individual, idiosyncratic elements.

Bowers (1974), for example, suggests that although the de­ velopment of delusions is a basic feature of certain stages of some schizophrenic syndromes, the content of delusions is related to the individual's past experiences, underlying con­ flicts, developmental impasses, and other idiosyncratic ele­ ments.

4) The assumption of temporal phases. This report assumes that there are discernible phases or developmental stages in the onset and progression of the schizophrenias. These f phases dif er in the various schizophrenias, but specifying the particular phase of a particular form of schizophrenia is an important consideration in planning research. Although often described in the simple terms, acute or chronic, the as­ sumptions here are that there are other phases and that each phase may be characterized by a different combination of biologic, psychologic, and social variables. Rheumatic heart disease may serve as an example. The initial stage involves a pharyngitis caused by a virulent strain of group A strep­ tococci. A small percentage of such patients develop acute rheumatic fever. This phase may be characterized by poly­ arthritis, carditis, chorea, erythema marginatum, and sub­ cutaneous nodules. Of those patients who develop a carditis, some also develop endocarditis. During the third phase there is healing of these cardiac lesions and, for some patients, fibrous thickening and adhesion of the valve commissures resulting in the characteristic valvular deformities. The fourth phase involves a variable period (frequently many

Introduction

ll

years) in which the patient may be asymptomatic. The fifth phase involves the development of congestive heart failure secondary to the valvular deformities. This simplified outline is a useful illustration of how the investigator wishing to study rheumatic heart disease must specify which phases of the illness are to be studied. To combine patients from all five phases might well obscure data that could clarify major aspects of the illness.

Although the temporal phases of the various schizophre­ nias are less clearly understood, we wish to emphasize the need to separate and study their phenomenology. To study the schizophrenias by doing research only with chronic pa­ tients may be similar to trying to understand rheumatic heart disease by studying only those patients experiencing conges­ tive heart failure secondary to rheumatic valvular disease.

5) The assumption ofadajJtivefailure. Although schizophrenia may develop in the absence of apparent. stress, clinical ob­ servations suggest that a person is more prone to develop the syndrome during a period in which internal and external events are perceived subjectively as stressful. The assumption that the individual has failed to adapt to stress is difficult to define operationally, although the concept is central to many of the newer and more complex models of disease.

Understanding an illness often involves considering how individuals vary in their vulnerabilities to illness in general, their predispositions to specific illnesses, the quality and quantity of life stress, and the role of support groups such as family, friendship networks, and work groups in mitigating the impact of stressful life circumstances. From such an ori­ entation, the schizophrenias could not be assumed to rise de novo, but rather as attempts to deal with stress, develop­ mental impasses, or other human predicaments in a manner that is influenced significantly by overall coping capacity, genetic predispositions, developmental deviances, interper­ sonal support syste�s, and other factors. From this perspec­ tive, the development of a schizophrenic syndrome can be

12

Complex causalily of the schizophrenias

understood both as an adaptive failure and as a continuing attempt to master both internal and external experiences.

In summary, this report emphasizes that in the study of a complex syndrome such as the schizophrenias it is necessary to develop complex models. Models that best approximate a complex, open, interactive system are most likely to yield illuminating results. At the present time multivariate, inter­ disciplinary approaches appear to be the most productive and powerful means of studying such models. Systems theory holds out a promise, as yet unfulfilled, that may ultimately bring greater coherence to our understanding.

2

THE STATE OF THE FIELD

Although the schizophrenias have been a human concern since the outset of civilization, modem concepts of their na­ ture arose in the late 19th century at the confluence of psy­ chiatry's beginnings and medicine's defining the disease process (Klerman, 1978). Since that time, understanding of schizophrenic disor<lers has been influenced by changing medical viewpoints of the nature of the disease process in general. The early success of a circumscribed disease model in the understanding of infectious diseases led to an increas­ ing emphasis on biologic factors. It was in this scientific at­ mosphere that Kraepelin ( 1921, 1962, 1968) contributed his categorization of psychiatric disorders. His focus on symptom complexes, etiology, and outcome has sometimes been as­ sociated with unsuccessful attempts to elucidate a single biol­ ogic etiology for the schizophrenias, although it is well to emphasize that such an etiology is not a requirement or con­ straint of Kraepelin's model.

Bleuler (1950) provided a descriptive schema for the schizophrenias which differed from Kraepelin's by empha­ sizing the link between phenomenology and presumed un­ derlying psychologic processes. Bleuler's efforts suggested the importance of considering factors in at least two do­ mains-psychologic and biologic-in understanding the etiologies of the schizophrenias. However, the problems of such a complex approach were also reflected in Bleuler's difficulties in developing and supporting a consistent theory of psychologic and biologic contributions to schizophrenia.

Another early attempt to integrate psychosocial factors 13

14

Complex causality of the schizophrenias

with biologic variables was the work of Meyer (195 7), whose "psychobiology" had considerable influence on the field, es­ pecially in American psychiatry. However, the vast detail of assessment required by his approach and the failure to de­ velop testable etiologic hypotheses may have contributed to the waning influence of Meyer's teachings.

Freud (1953, 1954, 1955) and his followers in the psy­ choanalytic movement developed theories about psycholog­ ical conflicts and deficits that contributed to an understanding of the etiologies of the schizophrenias. Although they have been useful clinically, these theories have been difficult to test or elaborate from an empirical base. Some psychoanalysts such as Sullivan (1953) were centrally concerned with the schizophrenias, and they inspired a gr�wing emphasis on the role of psychologic factors and their interactions with family relationships in the origins and treatment of the schizophre­ nias. This approach contrasted strikingly with Kraepelin's and had a powerful effect on etiologic theory. Although not stressing an integrated psychobiologic view of the schizo­ phrenias, Sullivan's influence provides some paths for sys­ tematic inclusion of interpersonal and internalized social experience in an integrated model.

This historical perspective suggests some of the approaches taken in the past to understanding the etiologies of the schizo­ phrenias. With the exception of Meyer, there has been no major proponent of an integrated, multiple systems view.

Today the majority of research into the causation of the schizophrenias continues to occur in etiologic frameworks that can be seen as derivatives of earlier single-cause forms.

Most often such efforts are isolated from each other.

This section selectively reviews some of the advances in research about the schizophrenias that are derived from sin­ gle-domain research and emphasizes how the inclusion of variables from other disciplines _and domains might have in­ creased the yield. More comprehensive reviews of the evi-

The state of the field

15

dence concerning the etiologies of the schizophrenias exist and are recommended to the reader wishing to pursue them (Arieti, 1974; Bellak & Loeb, 1969; Weiner� 1980). For pur­ poses of this illustration, theories about the etiologies of the schizophrenias derived from the following disciplines will be examined: genetics, psychophysiology (including perception an � cognition), biochemistry, developmental psychology, and soc10logy.

GENETIC THEORIES The idea that the schizophrenias are genetically caused was in existence long before systematic studies began, as illus­ trated by the concept of "tainted families." More recently, systematic studies with increased methodological sophistica­ tion have evolved, resulting in greater understanding (Can­ cro, 1980). Consanguinity studies, beginning early in the century (Rudin, 1916) and continuing until recently (Bleuler, 1941; Kallman, 1938; Kety, Rosenthal, Wender, Schulsinger, &Jacobson, 1975; Odegaard, 1972; Schultz, 1932; Tsuang, Crowe, Winokur, & Clancy, 1978) have demonstrated that schizophrenia runs in families. However, this fact by no means guarantees that the disorder is genetically caused.

Poli�ical or religious beliefs may prevail in families for gen­ erations, yet few would suggest that such beliefs are geneti­ cally determined. Perhaps among the most interesting of the consanguinity studies are those of Karlsson ( 1970, 1973). He studied approximately lOO descendants of a woman born in 1735 and found that the family produced, in addition to a large number of psychotic (presumably schizophrenic) per­ sons, a large number of talented, gifted, and successful in­ dividuals. Recent studies of children thought to be at risk (because of having one or both parents with schizophrenia) also show that some are unusually creative (Anthony, 1974).

Karlsson interpreted this finding to mean that the schizo­ phrenic syndrome is caused by one or several combinations

Ğ 4 ȓ +ƲǹʽSʽěʽĊóĈpEʽ5 ʽ~ǜ ±ǝ aʽ½ʽôċÿðqʽ ^ɛ ʽ ʽB5D) ¯ ʽʢ ʽ ʽ$% 2 ʽƳǧ ¬ ʽ ʽJŲƌŎ?ɜdʽ8 ʽ ʃ N9M åʽĵ +ň ʽ [ūʽ ğ c ®gǗmʽTʽFzxúpʽ ʎ=. ș° ,0Ǩ"ʽȾOʏ 8 ʽi ʽ 00 ɝ :ʽ^ ʽJȸ1 ʶ Ƚ((ʽȿ%Ƣƴʲ B - )ŏʽ Ƶ ʄ ʽ ƶ ʽ$ʽeɞķ (ʽ MƄʽȜ Z8ɀfƷ Ǻʽ ±Ɂ) ƖʽD6ųʽ Ĕ Ƹ\ʐ ʙəʽ ħK £ȝǯĸ\ŐKʽıKɂʅîʽIJ7Kʩʽ ¤kǻ ʽɟ7<ɠʽƹǼʽ ɡȞƺ +Ƀʽ ȟ ʷ Ț³ƻC9 Ɨʽ Q?Ƙ Ǟ Oʽ Pʆ( ʍ9 ʽ ʽ Ŭ ʧʽ ʑʼnǖ I ʽ Z ' ʽ ! Ƽƍ¶ & ǽ ǩ"ʽǰ Ƞ ʽŴȹȺ ȡ©ʽ ɢƣ ʽ ƽ ʽDZ ɣőƤ ʽŒA@ b^ǟ!æʽij 8 ʽ ʒƙƚ Ʉɤhʽ ɥ Ĺ/ʽɦ (ʽĺʇʈŵ ɧƾȈǾʽŭŶƎœƿɨʽǀɅʽǿ ɩʽɆŷŔȉ ĻȢʪʽɪȊʽɫƥŸʽDzȋȣŹʽƑ ƛȤļȀɬʽ ʫ dz ʽ ʽɭƦ ʽ dʬŕƧ ɮǁŖʽ ǂɇ¡; ;çʽ ĥ 7 ȥʽ Qź Ľ § Êʽ ƨ ´ ʚ Ëʽ ʓƜƝ Ɉɯʽ ® ʽ dŗƩ n¤ Ȧ *Řʽ ` ɰ , ɉʽ řʽ ľ ȁɱ 2 ʽ Ŀ:'ʽ ŀȧŻʽ ʔ =+ ʽ ʽ Ə O ʽ ;P< ɲʽ ǃ ʽ Ƈc ʽ 2 -Ȍ: ,P Ǡʽ · e »¼ʽ H ʽ ŁȨ Eʽ ɳ ȩ - Ìʽ ƒ '(Ůʽ Ŋʭʽ ¸ Ȃ Ɋ«L 8 Gŋǡ ʽ % Ȕɴe¹ʽ S &Ī ʮ _ JfÍʽ U#āñÃèʽ ĜPʽ Lɋʽ N1 ż'ʽ ƪ ʽ ʕŚ ʽ DŽ ʽ 1% .ʽ ʨ ʯʽ ʽ ɵ Nʽ ƫ ʽ +"ʽ fśł ʽ ʽB."ŜƬ Dž%ʽ l D Ȫ ʣ ïʽ ǘ_Rʽ TʽU#vûqʽ ©ȍʽ Ɍ² ƞ . ʽ 06Ń/ʽ !ŝ džʴ B a )Ş.ʽ ȫ ʽ $ țʖ / "ʽ ʉʊ @i 2 ʽ Ō ʽ %4 @Mjʽ ! &ɶʽ / ʽ Ȭ Q ɷʽ 5ªȕ şO!ʽ ʽ hi éʽ ĝ:ʽ ʽ -LJ ʽ ¢ƅʽ ° Lj 3ʽ Đg lʽ ʽ lj!ʽ I Ǫ Žɍʽ TđɎ - lʽ ʽ ġ ĕCNJ ʸ Îʽ õ#wĉrʽ ö#yUČʽ Ē« - ȎREʽ Ƌ"Ïʽ &Ė L Ǵ ȃÐʽ ʽ ėǢ ʹ Ñʽ ǣ Òʽ } < : ʤÓʽ ʽ Ĭ ƈƉʰrʽ 7 § Eʽ FzćǕčʽ Ģ > C? F{yòÄʽ ʛ ʽ , ȭ ɸ ůʽ 0ƭ4 ʽ ʽ ɏŠ n ` ; &ʽ j gʽ 4 ʽ Nj t Yʽš )Ǥ'Ȯ ʽ * ɹʽ ʽ Ɛ%*ž Xʱʽ ʽ ʜ8 H ʽ * Ɠȯ¶ nj ʼʽ ¨ȑŢ ? ʽ NƮ ʽ ńmʽ W ʽ ʽ W +ȏ Ǎţʽ $;Ǚ ;ʽ ƊȒ¥ʽ ʽ ƔȰ ʽ ¡Ɔʽ ɐŤƯ9ʵ Ȅ <êʽ 1ʽ <, ʽ I ãR ȱǚ Ȳ ʽ ¾Ġ ] ʗÔʽ ~ʘť ɑ= ǵÕʽ Ę$ C3ʽ ĭ C51ɚɒ3ʽ ʽ Į >Ǜ.Öʽ F#ĂĀÅʽ ' ʺ ɺ ʽ/ Dʽ 5/ @/¬ʽʥǎD7ʽ Ŧ6)µ_B ȳ ]*Ņʽ ʝ ʽ ʞ 4 ʽ 2 Y Űʽ ` 9 ʽ h ʽɻ ʽ $9[ʽ ʽ H ʽ ¿ ȴʽ' ¦ ɓ Æʽ ´ ʽ ?ȅ&ȵ ʽ ǏǶ1 ǐ Ȇëʽ I ʽ b 1 ʽ ʟ ʽ+ ʽ ¢ʽŪ :.L b = ʽ 5 ȇɼʽ ō k¯ʽ ʽHʋ \ Ǒ£,4ǥʽȖȻ =Ǧ 3ʽWk ʽ* ɽ ¦ ɔʽ A ʽ* ªʽ ņ ¨ ʽQ -mʽÀĤʽ ³X ɾ ſ) ×ʽ u#ăĄÇìʽ V n Ň ʽ G Jʽ X äʦ Y ȶɕʽ ÁęA µZ ]Øʽ Ĩ ŧʌ Ùʽ ʽ V Ɵưƀɖ3ʽ ÷#wüĎʽ V o ,Úʽ ĩȼ Ũɿ ¥3ʽ 2"Ûʽ Ķ ǫ Üʽ ģ Ǭ o Ýʽ ʽ Ě cʀÞʽ u|ąýÈʽ $ ʽ 6 ʽ űʽ & ǭǮƁ Ơ² ʽ Sį6 ßʽ } àʽ ʽ Ħʠ( ʁ sʽ ø|Ćþďʽ İ ơGɗ sʽ īA áʽ ʽ ēǷ âʽ ù{xvÉʽ Ʊ 2 ʽ Ǹ @ 0ȷ 0 ʽGʽ ǒ!A ʽȐ ʽƂ" ʽ Mʡ !ʽ Ǔ[ʽ ʽ­>7 ʳ ʻ 6 ƃ ũʽ ʂ j­íʽ Ĵ ʽ > ǔo ȗ a >ʽ ʽ ƕ Rɘʽ ºȘ t

30

Complex causality of the schizophrenias

drugs can decrease relapse rates when administered to schizo­ phrenic patients returning to high EE families. In contrast, the drugs appear to have no effect on relapse (at nine months following hospital discharge) for those patients who return to families rated low on E.E. More recentlv, both Falloon (Falloon & Lieberman, 1983) and Leff (Leff, Berkowitz, & Kuipers, 1983) have shown that family interventions directed at reducing the high EE can decrease relapse rates dramat­ ically.

As another example of cross-domain research, Leff ( 1976) has shown that schizophrenic persons in high EE families have a heightened autonomic responsivity compared to those in low EE families. These studies are outstanding in illus­ trating the complex interactions between social context, treat­ ment effect, and psychophysiologic variables.

SOCIOCULTURAL THEORIES The impact of cultural and broad environmental variables has been particularly difficult to explore rigorously. How­ ever, a biopsychosocial model of disease necessitates consid­ eration of sociocultural variables. These broad areas may be the richest veins yet to be mined, particularly as sociologic and epidemiologic methods become more sophisticated.

A central question concerns whether the prevalence of the schizophrenias changes across national boundaries, among races, and over long periods of time. The available evidence indicates that the schizophrenias are ubiquitous and do not appear to occur with significantly different prevalences in different cultures, nations, or races (Goldhamer & Marshall, 1953). Some studies have suggested that national origin may influence the type of symptoms in affected individuals, but prevalences remain remarkably similar (Opler & Singer, 1956). There is, however, growing evidence that the course of schizophrenic illnesses is more benign in nonindustrial

The state of the field

31

societies (Satorious, Jablensky, & Shapiro, 1977) and in re­ porting a study in Sri Lanka, Waxler (1979) has discussed the ways in which family structure, multiple treatment sys­ tems, and systems of belief may account for the lessened prevalence of chronicity.

A related question, also dealing with various social envi­ ron?1ents, is whether prevalences change over long periods of t111;1e. The answer is uncertain because of reporting dif­ _ fic �lues �nd �he cha�ging diagnostic systems used during vanous h1stoncal periods. However, references to psychotic, presun:iably schizophrenic, individuals such as the man pos­ sessed m the Apostle Mark's tale of the Gadarene swine (Mark 5:9) have been common since human existence has been re­ corded.

C learly_, stress can arise from mai:iy sources within a per­ , son s environment, and such stress mcreases individual vul­ nerability to illness (Brown & Birley, 1968; Holmes & Rahe, 1967; Paykel, Prusoff, & Myers, 1975; Rahe, Mahan, Arthur, & Gunderson, l 970; Selye, 1956). A number of investigators (Bro:wn & Birley, 1968; Jacobs & Myers, 1976; Rogler & Ho)lmgshead, _1965) have demonstrated that schizophrenic pat�er �ts expenenced more stressful life events preceding their illnesses than socioeconomicallv matched normal con­ trols. Also focusing on environmental variables, several stud­ ies (Malzberg & Less, 1956; Odegaard, 1932) have implicated crosscu �tural migration as a stress that increases the preva­ le�ce of t?e sc�izophrenias. These studies show a higher rate of illness m emigrants than in those who remain in their place of birth.

Res earch on socio�conoi:nic variables has shown that being _ poor 1s correlated with a higher prevalence of schizophrenia (Clark, 1948; Faris & Dunham, 1939; Hollingshead & Red­ lich, 1958). Some authors suggest that poor persons' abilities to cope with stress are diminished (Langer & Michael, 1963).

A higher prevalance of schizophrenia in the lowest social class

32

Complex causality of the schizophrenias

in large cities has been demonstrated, although this finding diminishes when studying cities of less than 500,000 popu­ lation (Clausen & Kohn, l 959).

Such findings about social class raise perplexing questions.

Do people with schizophrenia drop into lower social classes because of their various disabilities? Or do poor and disor­ ganized neighborhoods increase the chance of a person's becoming schizophrenic because of higher rates of repro­ ductive casualties, the lack of availability of good general health care and nutrition, the lack of social supports, or other characteristics of such neighborhoods? These questions can­ not be answered at present, but even a brief review suggests that both socioeconomic and urban geographic variables have impact on the. pathogenesis of the schizophrenias. Such re­ ports, by themselves, however, are limited. The studies of socioeconomic variables, for example, have not involved fam­ ily characteristics in order to understand whether being poor remains a risk factor when controlled for family competence.

Many treatment studies examine socioeconomic status only as a variable to be controlled, rather than examining its re­ lationship to treatment, course, and outcome.

Cross-domain research involving sociocultural variables might be very fruitful, but it has been rare. One example in the realm of theoretical linkage is Murphy's catalog of studies in which changes in the incidence of schizophrenia over time correlate with stressful changes in social conditions such as war, geographic displacement, or role definitions (Murphy, 1967). He develops a theory of the nature of stresses that are evocative of schizophrenia and cites four qualities of such stresses: I) the stress demands an unlearned response, 2) the stress is perceived as important, 3) there is no simple solution, and 4) it is chronic. He elaborates on these criteria by noting that the stress demands action or at least decisions by the individual and that the correct (i.e., satisfying) action is dif­ ficult to recognize because of the complexity or ambiguity of the information available. Under these circumstances, Mur-

The swre or the field

33

phy feels that the incidence of schizophrenia can increase two- or threefold, but rarely more. There is an obvious par­ allel between these defining charaCLeristics of the cultural stressors evocative of schizophrenia and the double-bind the­ ory of families of schizophrenic individuals.

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46

Complex causality of the schizophrenias

role of such metabolites is that various studies have conflict­ ing findings. As one example, several researchers (Murray, Oon, Rodnight, Birley, & Smith, 1979; Rodnight, Murray, Oon, Brockington, Nicholls, & Birley, 1976) report increased excretion of the hallucinogen dimethyltryptamine (DMT) in psychosis, while others (Carpenter, Fink, Narasimhachari, & Himwich, 1975) find no difference between schizophrenic patients and normal subjects. Although differences in bio­ chemical techniques may explain these conflicting reports, much of the variance may be accounted for by the interaction of psychological or social variables with the abnormal met­ abolic process. The studies have grouped patients solely on the basis of diagnosis or current symptoms which alone pro­ vides insufficient differentiation among potential subgroups of schizophrenic patients. The importance of endogenous hallucinogens or other metabolic variables in some forms of schizophrenia may thus be lost.

In a cross-domain approach the biologic investigator who has identified a group of schizophrenic subjects with an ab­ normal metabolite might next consider other biologic factors, such as genetic loading or diet, then select specific psycho­ social variables from other domains. In this example, we sug­ gest that variables such as genetic loading, family competence, life stress, and treatment response might be productive fac­ tors to include. A series of preliminary questions could be asked. Examples are: Do schizophrenic subjects with an ab­ normal metabolite demonstrate genetic loading for schizo­ phrenia? Are they members of families that share particular interactional characteristics? Are their psychotic episodes as­ sociated with high levels of life stress? Do they respond to certain psychotropic agents? Are they accessible to particular psychotherapeutic modalities?

More specific hypotheses could be tested, for example, that schizophrenic subjects with high genetic loading for schizo­ phrenia, from families with relatively high levels of family competence, who experience high levels of life stress prior

Approaches to cross-domain research

47

to the onset of psychotic symptomatology will demonstrate the highest levels of the abnormal metabolite. Further, one could hypothesize that such subjects will respond to pheno­ thiazines, but will be difficult lO engage in traditional forms of individual psychotherapy.

In testing the hypotheses, the criteria for inclusion must be considered carefully. In this example subjects should be included only if they have a DSM-III diagnosis of Schizo­ phrenic Disorder for two years or more, have been free of neuroleptic drugs for at least two weeks, have a normal CAT scan, and demonstrate the absence of exogenous hallucino­ genic drugs in the urine and the absence (by history) of the use of such drugs during the preceding month.

Each independent variable could be arranged in scalar form. Genetic variables can be rated by assessing the degree of genetic loading for schizophrenia. Approaches Lo obtain­ ing reliable genetic data and defining genetic loading are far from settled issues. At the minimum, specific questions must be addressed as, for example, how is schizophrenia in rela­ tives to be determined? Should both first- and second-degree relatives be included? What other diagnoses in relatives should be counted as part of the index of genetic loading?

Even within an otherwise homogeneous sample of schizo­ phrenic patients, considerable variation in the duration and severity of the schizophrenic syndrome can be expected.

Scales to measure duration and severity can be used to assess

their relationship to other independent variables as well as to the dependent variables.

Family system variables can be assessed in a similar manner.

One possibility would be measuring the level of family com­ petence (Lewis et al., 1976) with a global rating of the family's level of psychological functioning. Measures of life stress can be quantified using available scales (Holmes & Rahe, 1967) for stressors operating during a fixed period prior to either illness onset or hospitalization.

Treatment-response variables also may be important as

48

Com plex causalit)' of lhe schizo phrenias

they relate to the biologic dependent variable. Whether or not the subject has improved promptly with neuroleptics during prior psychotic periods and whether relapses occur if neuroleptic treatment is stopped can both be rated in scalar form. Participation in psychotherapy can be rated along a number of dimensions as, for example, attendance, accessi­ bility for a working alliance, and therapist's status reports.

The dependent variable chosen for this brief example is the urinary excretion of an abnormal metabolite, an endog­ enous hallucinogen. The major difference between this ex­ ample and earlier published studies is the use of a small number of specific variables from biologic, psychologic, and social domains as independent variables. Multivariate regres­ sion analyses permit a determination of the contribution of each independent variable to the measure of the dependent variable. Such analyses could both clarify the nature of spe­ cific subgroups of schizophrenic patients and lead to more focused and specific hypotheses to be tested in subsequent investigations.

A FAMILY SYSTEMS RESEARCH STUDY Family systems and the schizophrenias

The investigator in the area of family systems also needs to consider ways in which nonfamily variables may increase un­ derstanding of the role of family factors in the etiologies of the schizophrenias. Reiss (1975), for example, reported that there had been no investigations into the etiologies of the schizophrenias published by a family researcher that focused on the interaction of family and nonfamily variables.

Several conceptual issues may have impeded progress in understanding the etiologic role of family variables. One issue is the need for clarification regarding the role of family var­ iables specific to the development of the schizophrenias as opposed to the development of psychopathology in general.

Approaches to cross-donrnin research

51

a specific factor predisposing to a type of schizophrenic dis­ order.

A final dependent variable will be a measure of family expressed emotion (EE) that has been demonstrated to have predictive power regarding relapse in schizophrenic patients (Leff, l 976; Leff & Vaughn, 1980; Vaughn & Leff, 1976).

High levels of family EE will be considered a variable that sustains a family member's schizophrenic disorder.

In this type of family research, the inclusion of nonfamily variables can lead to a better understanding of the ways in which family variables may play a variety of roles in predis­ posing, precipitating, or sustaining certain types of schizo­ phrenic disorders in family members. In particular, the patterns of interaction of family and nonfamily variables could illuminate additional, more specific hypotheses to be tested in subsequent investigations.

A PSYCHODYNAMIC RESEARCH STUDY Symbiosis and the schizophrenias

The investigator whose primary interest is psychodynamics can further understanding of the role of such factors in the etiologies of the schizophrenias by designing investigations that include variables from other disciplines and domains.

In the following example, the role of symbiosis in the etiol­ ogies of the schizophrenias is explored.

The concept of symbiosis, developed in studies of early child development, describes that period in which the child is intensely and dependently attached to its object world while still unable to discriminate the boundary of self from that of the object. This concept has been applied to adult schizo­ phrenia, most notably by Searles ( 1965) who posited that a developmental impasse in the symbiotic phase was pivotal in the development of adult schizophrenia and was essential in understanding the transference relationship that develops

54

Complex causality of the schizophrenias

between more frequent and traumatic early separation from mothers and other caregivers and disturbed autonomic pat­ terns (Mednick & Schulsinger, 1970). The hypothesis pre­ dicts that a history of such events will predict symbiotic schizophrenia.

The second group of hypOLheses involves the subjects' re­ sponses to hospitalization and the subliminal stimulation of "Mommy and I are one." The subliminal stimulation is based on the work of Silverman and co-workers (Silverman, Lach­ mann, & Milich, 1982) which suggests that "better differ­ entiated" schizophrenic patients respond to repetitive exposure to the subliminal stimulus, "Mommy and I are one," by re­ duction in their thought disorders.

The first hypothesis reflects the belief that separation from the symbiotic object, as occurs at the time of hospitalization, increases thought disorder; it predicts that a greater baseline thought disorder f ollowing admission to the hospital will pre­ dict symbiotic schizophrenia.

A second hypothesis, based on the report that the sublim­ inal stimulus provides only better differentiated schizo­ phrenic subjects with a form of symbiotic gratification (Silverman et al., 1982) is that failure in reduction of thought disorder in response to the subliminal stimulation, "Mommy and I are one," will predict symbiotic schizophrenia.

The third group of hypotheses involves the relationship between intervention efforts and the dependent variables and are based on the belief that patients with symbiotic schizo­ phrenia are particularly vulnerable to issues of separation.

One hypothesis predicts that separation from the symbiotic parent will extend the period of initial cognitive disruption which wilf be less responsive to neuroleptic treatment. Im­ provement in the thought disorder will occur only insofar as the institution or therapist substitutes as a symbiotic object f or the patient. The hypothesis is that slower resolution of psychotic symptomatology will predict symbiotic schizophre­ nia. Other hypotheses are: A recurrence of psychotic symp-

Approaches to cross-domain research

57

There is an open-ended exploratory component to devel­ opmental studies that extend over long periods of time even though they require a mo<lel of human development and, in this instance, a model of the development of schizophrenia, as well as focused hypotheses. That is, data indicating the interaction of variables at either one or several points in the time can be useful in establishing more restricted hypotheses to be tested in smaller, cross-sectional studies.

The most general statement of the model of human de­ velopment involves the interplay of biologic, psychologic, and social variables in this progressive unfolding of the child's ego integrity and sense of self. Deviation in one variable (or system of variables) influences all other variables and, in turn, is influenced by the response of those variables to the initial change. Developmental models focus particularly on the se­ quence of events and processes and rely often on the concept of critical periods. A large number of developmental varia­ bles have ample theoretical or empirical data to warrant their inclusion in designs investigating the etiologies of the schizo­ phrenias. Selection of variables is complex and, in this ex­ ample, we wish merely to illustrate the range of variables rather than to suggest a complete list.

In keeping with the assumptions about the schizophrenias noted earlier, we expect to find that there are multiple de­ velopmental pathways to the schizophrenias and that differ­ ent domains of variables play critical roles in the different developmental pathways. Although such research empha­ sizes the complex interaction of etiologic variables, the de­ velopment of some patients' schizophrenic syndromes may be more heavily influenced by biologic deviations, and other patients' syndromes more by psychologic or social variables.

In this example, the independent variables will be certain genetic, constitutional, family system, and phase-specific in­ fant and childhood interactional processes within their social context (such as attacRment behavior, separation-individua­ tion, initial school experiences, pubertal experiences, and

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Implications for treatment and training

65

most profitable base for developing better models about the nature of the schizophrenias.

The central thesis of this report has implications also for those whose primary involvement is training psychiatrists and other professionals. What has been said about the complexity of the schizophrenias underscores the importance of teaching a way of thinking about the etiologies of these disorders that reflects the role of multiple domains and many variables.

Therefore, students need to be introduced to the complexity of these syndromes without either oversimplification or focus on a single domain. Present gaps in our knowledge need to be presented with equal clarity. Competing theoretical models of the schizophrenias should be presented; they stimulate thought and study.

The schizophrenias often have an unclear onset and a long course, which makes it helpful to the trainee to have a clear understanding of the basic concepts of child and adolescent development as well as clinical experience with intensive, long-term treatment modalities of individuals with these syn­ dromes by which to observe the interactions between life events, relationships, and fluctuations in symptoms.

Many training programs are located in institutions or de­ partments in which there is a major emphasis upon biology, psychology, or sociology. Trainees in such institutions or de­ partments, in particular, need to be introduced to a broadly based understanding of the biopsychosocial factors involved in the etiologies of the schizophrenias. In a parallel manner, trainees need to become comfortable with using a wide va­ riety of treatment modalities. Biologic, psychologic, and social treatments are each useful and necessary in the treatment of many patients with Schizophrenic Disorders. Reliance on a single treatment modality is usually inadequate.

Finally, it should be emphasized to trainees that there is no incompatibility between the development of clinical skills and the ability to conceptualize research hypotheses. The curiosity of clinicians dealing with patients with such disor-

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82

Complex causality of the schizophrenias

Environmental factors,30-32. See also Home environment Escalona,S. K.,26,56 Etiology, 3-4,5,8, 13-33,67 biochemical theories,21-24 rnltural variables in,!l0-3 l,33 developmental theories,21,24-30 genetic theories,5,15-18, 20-21 "magic bullet " view of,21-22, 67 perinatal factors in,24-25,60 psychophysiologic theories,18-21 sociocultural theories, 30-33 socioeconomic variables in, 31-32

Evaluation, patient, 63. S,e also Diagnosis Eye movement disorders,19-21

Falloon,I. R.H.,30 Family (-ies),14,15-16,See also Parents competence of, 29,47,49,50 communication in,28-29,38-39,49, 50-51 development within,24,27-30 high expressed emotion (EE),29-30, 49,51 longitudinal study of,42,56-61 rating, 29-30 Family relationships,14,15-16 Familv studies,27-30 Family systems,18-51 Family svstems research,5,47 Faris,'R.·E. L,31 Father, communication dysfunction

and,28. See also Parents "Feedback,positive/negative," 8 FeedbackJoops,4,8 Fink, E. B.,46 Fischer,M.,16 Fish, B.,21, 26,56 Fish,B.,et al.,21,26 Fleck,S., 28 Forrester,J. W.,4 Freud, S., 14 Fromm-Reichmann,F.,25

Galvanic skin response, 27 Garmezy,N.,25 Genetic loading,46,47,50,53,60 Genetic studies,5, 15-18,20-21 Glazer,W.,7 Goldhamer,H.,30

Goldstein. \I. J., 38 Gossett,J. T.,et al., 50 Gonesman,I. l.,16 Gunderson,E. K. E.,31 Hagin,R., 21, 26, 56 Haier, R., 7 Halev J 28 Hall��i1;:Jgem,endogenous,45-46,48 Halpern,F., 21 Hertzig, M.,25 Heston,L. L,16 Himwich,H. E.,46 Hoffer,A.,16 Hollingshead,A. B.,31 Holmes,T.H.,31,47,50 Holzman,P.S.,19 Holzman. P. S.,et al.,19,�0 Home environment,29. See also Family "Homeostasis," 8 Hrubec,Z.,!6 Hughes,D.S.,19 Hun,S. W.,19 Individual development,24-26 Infant/mother relationship, 25-26, 40, 54 Infants, "temperamental types," 26 Jablensky,A.,31 Jackson,0.,28 Jacobs,S.,3 I Jacobson,B,,15 Jerauld,R.,26 Jones, J. E., 38 Jung,C. G.,18 Kafka,J. S.,28 Kallman,F. G., 15 Kallman,F. J., 16 Kandel,E. R.,7 Kaplan,A.,37 Karlsson,J. L., l 5 Kayton,L., 20 Kennell,]. H.,26 Kety,S.S.,17,18 Kety,S.S.,et al. (1968), 16,17 Kety,S.S.,et al. (1975),15,17 Klaus,M. H.,et al.,26 Klerman, G. L.,13 Knobloch,H., 24

Index

univariate, 3, 4 f Stef a, :Vf., 26 Steffy,R. A.,19 Steinglass, P., 4

Steinschneider,A., 26 Stierlin, H.,52 Stott, D. H.,24 Strauss,J.,et al.,7 St.reitman,S., 25 Stress,11 autonomic over-responsiveness to, 27 in evoking schizophrenia,31,32-33 measurement of,47 Subjects, research,selection of, 23, 3739,4i-48, 50 Subliminal stimulation, 54-55 Sullivan,II.S.,14,25 Support systems, I I Symbiosis,51-56 Syndrome,schizophrenias as,9-10 Systems theorv,4,8,12. See also . Family systems Terry,D., 28 Thomas,A.,26 Thomas,A.,et al., 26 Tiernari, P.,18 Toohey, '-·!. L., 29 Training, 65-66 Transference relationship,51-52 Transmethvlation, disorders of,22 Treatment,' of schizophrenic patients, 63-65 Treatment-response variables,40-41, 47-48 Tsuang,M. T., et al., 15 Twin studies,16,17,21

85

Vaillant,G. E.. 41 Van Dyke, J. L., 53 Variables constant/intermittent,40 familv/nonfamily, 48-S I gene(ic, 17 hierarchical interrelationships arnong, 8

measurement of,39-40 model of causalitv and,8-9 process, 2'1 selection of, 6-7,39-41 Vaughn, C.,30 Vaughn,C. E.,29,51 Visual disorders, 19-21 Vulnerability, l l,25. 26,27,28,'.ll Waxler, I\'. E.,3!

Weakland,.J.H., 4,28 Weiner,H.,7, 15, 16 Wender,P.H.,16,17,18 Wender,P. H.,et al.,17 West, K. L., 38 Weston,D. R.,2S Wille. R.,21 Wimberly. F., 56 Wilson,E. 0.,7 Wiug,J. K.,29 Winokur,G.,15 Wohlberg,C. W., 19 Wyatt.,R.,7 Wynne,L. C.,28-29 \Vynne, L. C., et al.,29, 50 Yasillo,N. .J.,19 Zahn,T. P.,53 Zax,M., 38,40,56

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