Path: utzoo!utgpu!news-server.csri.toronto.edu!rpi!zaphod.mps.ohio-state.edu!pacific.mps.ohio-state.edu!linac!att!princeton!pucc!PSYC From: harnad@clarity.Princeton.EDU (Stevan Harnad) Newsgroups: sci.psychology.digest Subject: PSYCOLOQUY V2 #5 (Discussion Paper: Schizophrenia/Salzinger : 498 l.) Message-ID: <9104162353.AA00567@psycho.Princeton.EDU> Date: 16 Apr 91 06:13:29 GMT Sender: VMNNPOST@pucc.Princeton.EDU (Listserv to Netnews Gateway) Organization: Listserv to Netnews Gateway at pucc.Princeton.EDU Lines: 493 Approved: PSYC@PUCC PSYCOLOQUY ISSN 1055-0143 Tue, 16 Apr 91 Volume 2 : Issue 5 Schizophrenia, Vulnerability, and Behavioral Analysis / Salzinger ---------------------------------------------------------------------- From: Kurt Salzinger Subject: Schizophrenia, Vulnerability, and Behavioral Analysis / Salzinger The object of this article is to stimulate further "skywriting" in PSYCOLOQUY in this area of psychology. Both commentaries on this article and short articles by other investigators in this area are invited. The article below deals with schizophrenia, the concept of vulnerability, and behavioral analysis. It has been my experience that the increasing work on schizophrenia -- and, for that matter, other areas of psychopathology -- has concentrated on biochemical and neurological approaches to understanding the disorders without paying sufficient attention to the need to connect such findings with behavioral ones. On the other hand, behavior analysts have been concentrating on therapy without paying sufficient attention to the problem of mechanism. My hope is that this article will stimulate some discussion of the interconnections between the two. K. Salzinger, Associate Editor, PSYCOLOQUY [Editorial Note: This article has been refereed by two members of the Editorial Board of PSYCOLOQUY.] The Road from Vulnerability to Episode: A Behavioral Analysis Kurt Salzinger Polytechnic University Abstract: The object of this paper is to describe vulnerability in terms of the Immediacy Hypothesis and to indicate the role of behavioral interaction with the environment in the production of schizophrenic symptoms. There is a story of a psychologist who went to visit a colleague at a mental hospital. He approached a patient sitting near the entrance to the grounds to ask for directions. The patient proceeded to scratch his head and think, starting several times to explain how to get there, but after a number of abortive attempts, he finally said, "You can't get there from here." Examination of various theories of schizophrenia leads one to the conclusion that here too there is no way to "get there from here." How does one get from vulnerability to episode? We are told that there is a genetic predisposition that constitutes the diathesis for the disorder. It is not enough to say that there is a larger amount of dopamine in the synaptic clefts of schizophrenic patients to explain why they are suffering from various kinds of esoteric symptoms. The same, of course, goes for the finding of larger ventricles in the brains of schizophrenic patients or, for that matter, when experts in the area find a correlation between the early loss of a parent and a greater probability of having a depression at a later time. We need to specify exactly how one gets from here to there. The purpose of this paper, based in part on the vulnerability theory of schizophrenia expounded by Joseph Zubin and Bonnie Spring (1977), is to examine what we might find along the path. Let us briefly describe a model of what the vulnerability might be. Most investigators assume that vulnerability is a special sensitivity to a stressor. Although a stressor might well play an important role in moving many patients to an episode (Dohrenwend, Levav, Shrout, Link, Skodol, & Martin, 1987), an alternate route needs to be considered since all patients having an episode are not necessarily reacting to a stressor. A lock and key metaphor would seem quite appropriate for an alternative explanation. The gate barring the path to the episode is opened by keys consisting of certain classes of events. The gate to the episode would remain locked under two conditions -- if the lock (the vulnerability) did not permit any of the keys (episode-producing events) to fit it, or if the appropriate keys were not present in the environment. Zubin and Spring (1977) have constructed a theory to separate enduring trait conditions found not only in schizophrenic patients, but in all those that are vulnerable to the disease, from those fluctuating state conditions that manifest the presence of the psychosis in full bloom. This model, like its predecessors, and indeed like most of our conceptions of how one becomes mentally disturbed, appeal to the concept of a stressful life event as a cause. The point is that although this has accrued a good deal of evidence in its favor, there are also grounds for believing that episodes arise frequently without a stressor. Furthermore, we have evidence for the reverse, namely that stressors do not necessarily produce episodes. Arguments and evidence for the absence of supporting social networks and the presence of adverse family relationships in the form of excessively emotional environments (the expressed emotion variable) have been added as moderating variables on top of the genetic predisposition and stressor. What we need to do, however, is to specify in greater detail just what constitutes the predisposition. This must be done, not merely in terms of differences such as those on the continuous performance test, in a distractibility task, or in reaction time, but also in terms of the underlying variable(s) that constitutes the vulnerability factor. Finally, the explanation must show just how that vulnerability interacts with the environment to produce the episode. The kind of vulnerability factor referred to may turn out to be an advantage in one environment and a disadvantage in others. It is conceivable, for example, that people with especially acute hearing could be more distractible simply because they are stimulated by more sounds than the rest of us; such a person might, on the other hand, be the beneficiary of more information than the rest of us in being able to hear things we are not privy to. Differences in sensitivity to various classes of stimuli are very important in governing the way we live and interact. Those basic stimulus-control differences have a cascade of different effects on the life of a person. A number of views of schizophrenia exist (Straube & Hahlweg, 1990; Schulz & Tamminga, 1989) that refer to differences in reactions to stimuli (with a minor motif of motor defects), and quite a number of investigators have been studying what has come to be grouped under the all purpose heading of information processing. These studies can also be viewed in terms of stimulus control -- whether the stimuli precede or follow the responses of interest. Although investigators do not agree on what the basic deficit in schizophrenia is, most deem critical a dysfunction in the way in which patients respond to their environment. It is interesting to note that those working in therapeutic intervention are beginning to home in on the specific functions thought to characterize the basic deficit, such as concept formation, abstraction abilities, recall and recognition, social perception, social skills, and problem solving skills (Brenner, Kraemer, Harmanutz, & Hodel, 1990; Liberman, Mueser, Wallace, Jacobs, Eckman, & Massel, 1990). If schizophrenic patients have a thought disorder, these investigators assume that one should attack the specific functions constituting it directly. Alternatively, one could look for an even more basic deficit. The usual characterization of schizophrenic symptomatology -- whether measured objectively or clinically -- is not a godd starting point if we are to take seriously the idea of relating behavioral data to biological deficits (Salzinger, in press). To say something meaningful about the patient's vulnerability, we must do the following: 1. state the nature of the basic deficit as clearly as possible, 2. trace its transformation into the symptoms that can be observed in the patient, and 3. do so by leaving room for the interaction between behavior and environment. If we leave no room for that, then our hypothesized deficit is overexplaining. Let us use a behavior analytic approach to include the environment in tracing the development of schizophrenia. That approach is the only one now available that allows one to conceptualize individuals' interaction with their environment. Everybody's behavior is modified by the environment. In some cases of abnormality, that process of modification itself constitutes the basic deficit (as in mentally retarded individuals), but in the case of schizophrenia there is no evidence for a deficit in learning beyond the involvement of special stimulus classes to which such patients respond. We must therefore trace how a basic deficit interacts with the laws of learning to produce the symptoms that are generally agreed to characterize schizophrenia. A number of theories of schizophrenia hypothesize a basic deficit; the argument to be presented here will therefore also be applicable to other hypothesized deficits as we trace the path from vulnerability to episode. For the sake of brevity, this paper will restrict itself to the Immediacy Theory of schizophrenia. According to the Immediacy Hypothesis, the behavior of schizophrenic individuals is controlled primarily by stimuli immediate in their environment (Salzinger, 1984). What this means is that schizophrenic patients have a tendency to respond to a subset of the stimuli to which the rest of us react. It becomes instructive to try to sketch out how the behavior of a person so limited would differ from that of a person not limited. To do that it will be useful to examine the behavioral mechanism which shows how behavior is controlled. By following the diagram in Figure. 1, below, we can see what changes might be expected. On the left are the independent variables preceding behavior. They are the physical state of the organism, the physical and social environment providing discriminative stimuli for the responses, the reinforcement history of the organism, and the current reinforcement contingencies acting on the organism. All these variables impinge directly on behavior but also on the discriminative and reinforcing stimuli that control the behavior. The latter two classes of stimuli control the behavior that produces the consequences which in turn act back on the independent variable sets, altering the physical state of the organism, the environment, the reinforcement history, and finally the current reinforcement contingency. Figure 1: The Behavioral Mechanism (from Salzinger, 1980). Variable Sets ___________________ |PHYSICAL STATE OF|<------- ------- ------ ---------- ----- |THE ORGANISM |______________ | |_________________| | ______ ___ _____ _______| | | | ______________________________ | | ___________________ | |ENVIRONMENT OF THE | |<--- |EFFECT ON CERTAIN| | |ORGANISM (SOCIAL AND | | |EVENTS WHICH ARE | |PHYSICAL) PROVIDING |__| |MORE SALIENT AND | | |MANY OF THE DISCRIMI- | | |THEREFORE MORE | | |NATIVE STIMULI FOR RESPONSES| | |SIGNIFICANT AS | |____________________________| |--->|DISCRIMINATIVE | | __________________________ | |STIMULI AND | | |REINFORCEMENT HISTORY OF|______| | REINFORCERS | | THE ORGANISM |<-- - -- |_________________| | |________________________| | |_ ___ _|__ _ __ __| | | | _________|____ | | |__|CONSEQUENCES|___ | | |____________| | | | ~ | | ___|/________________ | | _________________________ | |BEHAVIOR CON- |_| |CURRENT REINFORCEMENT | |--->|SISTING OF CHAINS | | |CONTINGENCIES ACTING ON |______| |OF RESPONSES, LINKS | | | THE ORGANISM | |OF WHICH PROVIDE | | |________________________| |RESPONSE-PRODUCED | ~ |DISCRIMINATIVE STIMULI| | | |______________________| | | | |______ ___________ _______ ______ ____ __| If we assume that "the physical state of the organism" variable set in Figure 1 is different for schizophrenic patients and normal individuals, then we can see that it would interact differently with the environment, reinforcement history, and reinforcement contingencies in making certain stimuli preceding behavior salient and in making only some consequences impinge on the behavior of these patients. Thus a greater presence of dopamine in the synapse might well mean that a larger number of impulses would travel from neuron to neuron and, therefore, to behavior. In other words, just being stimulated by a particular event would promote a response and thus tend to crowd out the responses to more remote stimuli. One would expect immediate stimuli to act more frequently as discriminative stimuli when conditioning takes place and such immediate stimuli should also be the primary reinforcers for the affected individual. That effect manifests itself as greater distractibility, as in a sorting test where stimuli not responded to by normals are responded to by schizophrenic patients, thus interfering with their correct sorting; it also lengthens their reaction time when the immediate stimuli actually controlling their behavior distract them from a less immediate stimulus to which their reaction time is measured. Schizophrenic patients generalize more to words of similar sound than similar meaning because of their tendency to respond to stimuli closer in time (sound being closer than meaning, which requires an additional response of association). By the same reasoning, we find that schizophrenic patients tend toward retinal image rather than object constancy. They also, as we have shown in our laboratory, produce speech that is less comprehensible than that of normal speakers (Salzinger, Portnoy & Feldman, 1964; 1966; 1977; Salzinger, Portnoy & Feldman, & Patenaude,1980; Salzinger, Portnoy, Pisoni, & Feldman, 1970) because the response-produced stimulus control so important in continuous speech is modified; schizophrenic patients respond primarily to the words they just uttered (as opposed to those uttered a little longer ago), thus making less sense over longer stretches of speech. In sum, experimental results appear to fit the Immediacy Theory quite well. It is perhaps even more interesting to trace a path from the underlying deficit to the symptoms. Delusions may be the clearest example in which responding to the most immediate stimulus is tantamount to responding to stimuli in isolation; responding to stimuli in isolation makes make misinterpretation easy. The same stimuli in different contexts, or in isolation, will determine different meanings. The kinds of delusions will be a function of chance factors, such as what other stimuli happen to be in the immediate environment of the patient, and they will determine whether the delusion is one of persecution or of grandeur. Response-produced stimuli, in which certain associations have been well conditioned in a particular patient, will determine what interpretation an individual gives the stimuli reacted to in isolation. Conditioning would lend stability to the symptoms because of reactions to immediate stimuli; extinction of the behavior because of changes in the immediate environment would explain termination of episodes. Hallucinations have repeatedly been shown to be response-produced by the patient (e.g., Gould, 1948, 1949). In some cases, indirect measurement of muscular movement showed the self-production; in other cases, one can demonstrate this by simply watching patients move their lips or even whispering to themselves. Here the response to immediate stimuli, albeit response-produced, makes it difficult for patients to discriminate what they say from what others are saying, and we arrive at the symptom of "hearing voices." A very important symptom of schizophrenia according to DSM III R is a "loosening of associations" or "incoherence," but here we have an incorrect attribution of cause. Our data have shown that the so-called incoherence is not a matter of loosening of associations but, on the contrary, a tightening of associations, if by that we mean responding to a briefer series of preceding words, when talking or listening (Salzinger, Portnoy, Pisoni, & Feldman, 1970). If what you say is dependent almost exclusively on the neighboring words but not necessarily on the words just a little further back, then your speech will appear to show a loosening of associations, but the loosening will pertain only to the more remote response-produced stimuli. It is the kind of language behavior that normal individuals can produce if they speak while attending to each word alone as they utter it, rather than to a whole string of words as we normally do. Gertrude Stein demonstrated this phenomenon in a master's dissertation on automatic writing and later in some of her professional writing. The point of this very brief review of the significant symptoms of schizophrenia is to show how their great variety can be traced to a common source, in this case, to a tendency to respond to those stimuli that are immediate in the patient's environment. A word is in order here concerning the basic deficit -- responding primarily to a subset of the stimuli to which normal people respond. One can see how such people would have a peculiar conditioning history, having been conditioned to some stimuli, but not to others. One would expect people greatly dependent on immediate stimuli to have their responses extinguished more quickly since the effect of reinforcement would dissipate more quickly than for normal individuals (Salzinger & Pisoni, 1960). It follows that psychotherapy should be less successful and that behavior modification which uses concrete stimuli such as food, candy, cigarettes should be more effective. One would infer from this also that only after such patients had been conditioned for a long time could one begin to get social reinforcers to control their behavior. Only after pairing concrete reinforcers with the social ones would the therapist be in a position to utilize the social and verbal reinforcers. Let us return to the original premise of this paper, that one has to make use of concepts other than that of a stressor to explain the occurrence of episodes. We can now see that a person in a job requiring responding to immediate stimuli might survive, but when the same person has to respond to abstract and other remote stimuli, as in long range planning, one would expect problems to arise. In the first case, the person's behavior would be positively reinforced, whereas in the latter condition, the same person would be placed on extinction. It has long been known that extinction elicits emotional behavior and so we would expect the lack of fit between what individuals are capable of doing and the requirements of their environment to be involved in precipitating an episode. Thus, the tendency to respond to immediate stimuli and the relationship of that response to an environment hostile to such functioning may cause an episode. The beginning of this paper suggested that we consider a path other than the stress route to the episode. In the lock and key model, the lock is the vulnerability to a schizophrenic episode. According to the Immediacy Theory, the lock consists of the predisposition to respond to stimuli immediate in the environment, whether external or response-produced. The keys that fit into this lock in that they produce an episode are those immediate stimuli that open the gate to the symptoms we refer to as schizophrenia. Some examples of these keys are such stimuli as the remarks made to the vulnerable individual in jest, or the social reinforcers that might be delivered to that individual for remarks that sound like puns but which, because of conditioning out of context, develop into the bizarre behavior often found in schizophrenia. If one is likely to respond to immediate stimuli, one can easily misinterpret what people are going to do. A vulnerable individual's superiors might express high regard for an idea to begin with, adding a warning that they are still thinking about it, but because the first and, therefore, immediate consequences of presenting the idea consitute a positive reinforcer, the vulnerable person is likely to have that response conditioned. If the vulnerable person acts on the basis of the preliminary consequences, a problem might well ensue. Taking the conditioning by immediate reinforcers seriously, we can see also how a patient's thoughts could be reinforced by chance external events that become linked to some thoughts the patient might happen to have at the time. Symptoms such as "thought broadcasting" might also be explained in terms of the likelihood of being reinforced by chance events. The potential of this kind of behavioral analysis for determing the extent to which such stimulus control and such conditioning take place in schizophrenic patients should already be apparent. What about the role of stressful life events ? They may well constitute a route to an episode, but here too a behavior analytic concept comes into play, namely, extinction, that is produced by stressful life events (Salzinger, 1980). It does not take too much imagination to realize that the effect of stressful life events is best explicated in terms of an extinction effect. Loss of a job, for example, involves deprivation of some concrete reinforcers such as money but also of some social reinforcers that people, with whom one ordinarily spends eight hours a day for at least five days a week, provide; the loss of a dear one results in the loss of that person's reinforcers and also that person's discriminative stimuli that evoke some of the social responses the remaining person might not otherwise emit. Finally, the tendency to respond to immediate stimuli in addition to stress undermines the very kind of behavior needed to cope with such events. Planning to do things differently because of a stressful life event is just one example of how the deficit discussed would exacerbate the effect of the event and is the factor that separates the effect of the same life event on a vulnerable and a nonvulnerable individual. In sum, the vulnerability model has been fleshed out, first by allowing for more than one way to precipitate an episode and second by showing how that process of precipitation actually might take place. The lock and key model of vulnerability is very much like the greater susceptibility of some people to a particular disease than to others. The lock is viewed as an allergy or sensitivity to certain kinds of events such as pollens (the keys), for example, that cause sneezing or other untoward responses to occur. In schizophrenia, the lock consists of a greater sensitivity to immediate stimuli and the keys to the episode consist of stimuli that produce behavior (the symptoms that we call schizophrenia) injurious to the person affected. The fact that not all immediate stimuli produce behavior ultimately considered to be abnormal may well be the cause of the great variability seen in schizophrenic patients. References Brenner, H.D., Kraemer, S., Harmanutz, M. & Hodel, B. (1990) Cognitive treatment in schizophrenia. In Straube, E. R. & Hahlweg, K. (Eds.) Schizophrenia: Concepts, vulnerability, and intervention. New York: Springer-Verlag. Dohrenwend, B. P., Levav, I., Shrout, P. E., Link, B. G., Skodol, A. E., & Martin, J. L. (1987) Life stress and psychopathology; Progress on research begun with Barbara Snell Dohrenwend. American Journal of Community Psychology, 15, 677- 715. Gould, L. N. (1948) Verbal hallucinations and activity of vocal musculature: An electromyographic study. American Journal of Psychiatry, 105, 367-372. Gould, L. N. (1949) Auditory hallucinations and subvocal speech: Objective study in a case of schizophrenia. Journal of Nervous and Mental Disease, 109, 418-427. Liberman, R. P., Mueser, K. T., Wallace, C. J., Jacobs, H. E., Eckman, T. & Massel, H. K. Training skills in the psychiatrically disabled: Learning coping and competence. In Straube, E. R. & Hahlweg, K. (Eds.) Schizophrenia: Concepts, vulnerability, and intervention. New York: Springer-Verlag. Salzinger, K. (1980) The behavioral mechanism to explain abnormal behavior. Annals of the New York Academy of Sciences, 340, 66-87. Salzinger, K. (1984) The Immediacy Hypothesis in a Theory of Schizophrenia. In W. D. Spaulding & J. K. Cole (Eds.) Nebraska Symposium on motivation: Theories of Schizophrenia and psychosis. Lincoln: Nebraska Univ. Salzinger, K. (in press) Connections: A search for bridges between behavior and the nervous system. In D. Friedman and G. Bruder Eds. Psychophysiology and experimental psychopathology: A tribute to Samuel Sutton. Annals of the New York Academy of Sciences. Salzinger, K. & Pisoni, S. (1960) Reinforcement of verbal affect responses of normal subjects during the interview. Journal of Abnormal and Social Psychology, 60, 127-130. Salzinger, K., Portnoy, S., & Feldman, R. S. (1964) Verbal behavior of schizophrenic and normal subjects. Annals of the New York Academy of Sciences, 105, 845-860. Salzinger, K., Portnoy, S. & Feldman, R. S. (1966) Verbal behavior in schizophrenics and some comments toward a theory of schizophrenia. In P. Hoch & J. Zubin (Eds.) Psychopathology of schizophrenia. New York: Grune & Stratton. Salzinger, K., Portnoy, S., & Feldman, R. S. (1977) Intrusions in schizophrenic speech: The immediacy hypothesis vs. the lapse-of-attention hypothesis. Comprehensive Psychiatry, 18, 255-261. Salzinger, K., Portnoy, S., & Feldman, R. S. & Patenaude-Lane, J. (1980) From method to madness. In R. W. Rieber (Ed.) Applied psycholinguistics and mental health. New York: Plenum. Salzinger, K., Portnoy, S., Pisoni, D., & Feldman, R. S. (1970) The immediacy hypothesis and response-produced stimuli in schizophrenic speech. Journal of Abnormal Psychology, 76, 258-264. Schulz, S. C. & Tamminga, C. A. (1989) (Eds.) Schizophrenia: Scientific progress. New York Oxford University Press. Straube, E. R. & Hahlweg, K. (Eds.) (1990) Schizophrenia: Concepts, vulnerability, and intervention. New York: Springer-Verlag. Zubin, J. & Spring, B. (1977) Vulnerability -- A new view of schizophrenia. Journal of Abnormal Psychology, 86, 103-126. This paper was presented at the American Psychological Association meetings, in August 1990 in Boston. ------------------------------ PSYCOLOQUY is sponsored by the Science Directorate of the American Psychological Association (202) 955-7653 Co-Editors: (scientific discussion) (professional/clinical discussion) Stevan Harnad Perry London, Dean, Cary Cherniss (Assoc Ed.) Psychology Department Graduate School of Applied Graduate School of Applied Princeton University and Professional Psychology and Professional Psychology Rutgers University Rutgers University Assistant Editors: Malcolm Bauer John Pizutelli Psychology Department Psychology Department Princeton University Rutgers University End of PSYCOLOQUY Digest ******************************