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PSYCOLOQUY   ISSN 1055-0143     Tue, 16 Apr 91       Volume 2 : Issue   5
      Schizophrenia, Vulnerability, and Behavioral Analysis / Salzinger

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From: Kurt Salzinger <KSALZING@POLYVM.BITNET>
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.

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