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Martin S. Willick 49/1

PSYCHOANALYSIS AND
SCHIZOPHRENIA:
A CAUTIONARY TALE

The history of psychoanalysis and schizophrenia is used as an example

of psychoanalytic theories of etiology that have not stood the test
of time. Those theories pointed to three main factors: very serious
inadequacies in the caretaking person; the presence of these inadequacies
so early, during the preverbal period, that they led to the impairment of
early object relations, the development of psychic structure, and basic
ego functions; and the absence of underlying biological abnormalities.
Today, many analysts are still reluctant to acknowledge biological
etiological factors for other psychiatric conditions. For illnesses such as
borderline conditions and various severe character disorders for which
biological factors are still much in doubt, analysts are today proposing
etiological formulations similar to those once advanced for schizo-
phrenia. These formulations may indeed prove correct for these
disturbances, but analysts are urged to heed the cautionary tale of
psychoanalysis and schizophrenia.

F ollowing is a cautionary tale, a story of how it came to pass that

two or three generations of eminent psychoanalysts writing about
schizophrenia from the 1940s to the 1970s, and even beyond, proposed
theories about the causes of that illness that have proven incorrect.
After spelling out some of the reasons for these errors, I will raise the
question whether some of these reasons might still be operating today,
leading us to make the same mistakes again with regard to other
psychiatric disorders.
We all know that the road to scientif ic discovery is often marked
by erroneous hypotheses, faulty theories, and invalid conclusions.
We accept them as inevitable parts of the scientif ic process. In many

Training and Supervising Analyst, New York Psychoanalytic Institute;

Lecturer in Psychiatry, College of Physicians and Surgeons, Columbia University.
Submitted for publication February 2, 1999.
 Martin S. Willick

instances, the very scientists who have given the world the most pen-
etrating insights have also made serious errors, errors that could not
be corrected until shifts in theory or advances in technology enabled
them or others to gather the data with which to correct them.
Errors in our own f ield, of course, start with Freud himself. When
he realized that his early belief in the universality of childhood sexual
seduction in cases of hysteria was not correct, he was able to develop
one of his most important insights—the discovery of infantile sexu-
ality and its representation in unconscious, repressed sexual fantasies.
Twenty years later, he corrected his theory of anxiety, a revision that
opened up new investigations of the processes of defense.
Freud’s corrections and revisions required not a new technology but
a reevaluation of existing clinical data, as well as the collection of
new data based on revisions of his technique. Since then we have con-
stantly been revising our views of the nature and genesis of psycho-
pathology as we gather and reevaluate clinical observations and data.
More recently, however, psychoanalysis has been confronted with
data of a different kind from the f ield of neurobiology—data that have
28
forced us to revise our formulations of the etiology of mental illnesses
such as schizophrenia, bipolar disorder, OCD, and infantile autism
(Marcus 1992). Even as we accept these revisions, it will prove useful
to examine the sources of our incorrect theories of etiology in order
both to understand how we came to believe in them and to alert our-
selves to the possibility that we might be making similar mistakes today.
There is perhaps no better example of a psychoanalytic theory that
has turned out to be incorrect than the once prevalent theory regarding
the etiology of schizophrenia. This theory, or perhaps I should say con-
viction, about the cause of schizophrenia had three components. It was
believed, f irst, that the damage to the ego and its functions took place
primarily in the f irst one or two years of life; second, that the major
cause of these ego impairments was to be found in profoundly inade-
quate caretaking; and, third, that in most cases there was no fundamen-
tal organic process responsible for the illness. As has been true of other
mistaken scientif ic ideas, the correction of these ideas had to await
the development of a technology capable of studying the brain in ways
hitherto impossible—technologies that are now about twenty-f ive
years old in the f ield of neuroscience. While it is true that powerful
genetic data obtained through family, twin, and adopted-away studies
had existed even prior to this new neurobiological information, those
 PSYCHOANALYSIS AND SCHIZOPHRENIA

studies were frequently ignored by analysts or placed far into the back-
ground of the etiological equation.
The neurobiological research of the past twenty-f ive years offers
compelling evidence that the etiology of schizophrenia is, to put it suc-
cinctly, biological rather than psychogenic. Although its exact cause, as
well as its pathogenesis, has yet to be determined, most researchers
believe that a combination of genetic predisposition and intrauterine
and birth insults are necessary for the illness to occur. If there are
environmental factors after birth that contribute to the cause of schizo-
phrenia, there is very little evidence that they take place in the f irst
one or two years of life (see Willick 1990, 1993).1
It should be noted that there are still a number of psychoanalysts
who, though they now accept the contribution of a genetic predispo-
sition, believe that a destructive early environment is involved in the
later expression of the disorder. Robbins (1993) believes that good early
mothering can prevent the emergence of the illness in otherwise predis-
posed children. Volkan (1997) proposes that schizophrenia occurs in
individuals who have an infantile psychotic self “formed during the
29
early interaction of mother and child . . . ” (p. 8).
What I intend to do in telling this cautionary tale is to f irst
review some of the forces that have led so many analysts to formu-
late these theories of the etiology of schizophrenia. Who were the
analysts who led the way to such formulations? What ideas inf lu-
enced them in that direction? And what sort of clinical data did they
use?
My purpose here is not to criticize analysts for past errors. As I
have said, errors are an inevitable part of any scientif ic endeavor. What
is important is to inquire into the reasons for them. After a brief
review of some of these reasons, I will turn to an examination of
current psychoanalytic theories about the cause of other serious psychi-
atric disorders in order to ask the question, Are we making the same
mistakes again?

1
Many studies seem to indicate that environmental factors after birth may not
be of etiological importance. A few studies (Tienari 1991; Tienari, Sorri, and Lahti
1987; Jones et al. 1994) do, however, implicate family dysfunction or poorer-than-
average mothering in the expression of the illness. Even these, however, do not
necessarily concern caretaking during the first year or two of life. In addition, the rate
of schizophrenia among African-Caribbeans in Trinidad is markedly lower than the
high rate among second-generation African-Caribbeans in London (Bhugra et al.
1996). No one knows precisely what the environmental risk factors are.
 Martin S. Willick

I am referring to two kinds of mistakes. One is the continuing reluc-

tance of many of us to recognize underlying biological predispositions
in such conditions as ADHD, panic disorder, recurrent depression,
dysthymia, and even perhaps some forms of borderline condition. The
other has to do with our theories about the causes of serious illnesses
for which underlying biological abnormalities may not be found. I am
referring to some of the borderline conditions and severe character
disorders. In reading the more recent literature on borderline disorders,
I am often struck by the fact that many analysts are formulating
a theory of pathogenesis similar to that once advanced for schizo-
phrenia—namely, the role of the mother’s inadequacy during the f irst
one or two years of life. In our quest to discover the causes of these
serious disturbances, are we making the same mistakes we made with
schizophrenia? Or is it precisely for these other disorders that our
theories about the consequences of impairments in the early mother-
child relationship will prove accurate?
The list of analysts who adhered to the older, erroneous view of the
etiology of schizophrenia reads like a Who’s Who in Psychoanalysis.2
30
I will be citing a number of them who seem to have been most inf lu-
ential and whose works are assigned most frequently in the psycho-
analytic institutes that still offer courses on the psychoses (only about
half of the institutes of the American Psychoanalytic Association). They
are a diverse group that includes ego psychologists, the British object
relations theorists, and the Washington school of psychiatry (the inter-
personal point of view). In reviewing them, I will take the liberty of
condensing their ideas into a sentence or two for the purpose of illus-
trating the major thrust of their formulations. Although some mentioned
the possibility in some cases of an underlying primary organic process,
most believed that the major ego impairments occurred in the f irst
year or two of life, and many emphasized profound def iciencies in the
caretaking person as primarily responsible for these impairments.3
2
A few analysts, notably Redlich (1952), did express reservations about these
etiological formulations even as they gained wide acceptance, but such instances
were rare.
3
I will be omitting the family studies of the 1950s and 1960s; though they were
inf luential in promoting these views about the etiology of schizophrenia, they did
not necessarily emphasize family diff iculties during the f irst two years of life.
They include the works of Bowen (1960; Bowen et al. 1959); Wynne (1968; Wynne
and Singer 1963a,b; Wynne et al. 1958); Bateson (1969; Bateson et al. 1956);
Jackson (1957); and Lidz (1958, 1964; Lidz et al. 1957a,b, 1965). For a review of
family studies see Howells and Guirguis (1985).
 PSYCHOANALYSIS AND SCHIZOPHRENIA

WHAT ETIOLOGICAL FORMULATIONS

DID WE PROPOSE?

Ego Psychologists

Many of the ego psychologists who wrote about schizophrenia

came to this country already inf luenced by the prevailing views of
European psychiatry, which acknowledged some organic features in the
etiology of the disorder. Nevertheless, all of them adhered to the view
that if hereditary and biological factors did in fact operate, they did
so in the very early years of life, when ego structure was being built up.
In addition, they often accepted the idea that diff iculties in the early
mother-child relationship caused impairments in object relations and
ego structure and function. Although they all stressed that such ego dis-
turbances were more important than particular kinds of dynamic con-
f lict, they still believed that severe early conf lict caused impairments
in ego function, especially in the gradual differentiation of self- and
object representations.
For Hartmann (1953), one of the most important defects in schizo-
31
phrenia was failure in the process of neutralization. Since neutralization
is rooted in object relations during child development, he placed its
failure there, rather than seeing this as occurring in the face of later
organic deterioration: “the capacity for full object relations and for neu-
tralization, and the resistivity against object loss and deneutralization,
are rooted in ego development” (p. 186); “Failure or impairment of
neutralization . . . can be studied in the child” and “these defects can be
considered relevant in the predisposition to schizophrenia,” (p.189), as
can “distorted object relations” (p. 191). Hartmann did acknowledge,
however, that for certain patients “it is not unlikely that pathognomic
features . . . may come about . . . as a consequence of later organic
impairments” (p.195).
Bak (1954, 1971) emphasized a different but related aspect—the
decathexis of object representation, which he considered a defense
against aggression. By noting that the “cathexis . . . was originally
defective” (p. 258), he too placed the origins of the disturbance in
impaired object relations early in the child’s life. Although Bak, like
Hartmann, warned against the “genetic fallacy” whereby regressive
symptoms are taken to be similar to early childhood states, he did
believe that various manifestations of loss of ego boundaries were
regressions to primitive states of poor self-object dif ferentiation.
 Martin S. Willick

Both Jacobson (1953, 1954, 1966) and Bak adhered to the view that
early ego development in schizophrenia was more disturbed than in
illnesses they considered less severe. Bak did so in comparing schizo-
phrenia to the perversions, while Jacobson did so in comparing it to
manic-depressive illness. “Manic depressives,” Jacobson (1953) wrote,
“seem, at some point, to have reached a higher level in the differenti-
ation and integration of the psychic systems. Consequently, the acute
regressive process during their episodes does not go so far as in schizo-
phrenics and is of a different type” (p. 51). She also made a number of
distinctions about schizophrenia and manic depressive illness based on
the type of regressive symptoms they manifested. Many of these mani-
festations, such as the loss of ego boundaries, and the presence of thought
insertion and thought broadcasting, are now seen to be present in both
types of patients and are therefore not useful in distinguishing between
the illnesses or between degrees of regression. Thus, both Jacobson and
Bak went along with some form of the idea that there is a chronological
timetable for the development of various psychiatric illnesses.
The proposition of a chronological timetable can to be found also
32
in Kernberg’s writings in the seventies (1975, 1976). He believes that
there are two major tasks for the early ego: the f irst is to differentiate
self- and object representations; the second is to integrate them. By
proposing that borderlines accomplish the f irst task but not the second,
while “psychotics” accomplish neither, he promotes the idea that such
defects in ego structure in schizophrenia occur during the first year of life,
while those in borderline conditions occur later in child development.
Mahler’s work (Mahler and Furer 1968; Mahler, Pine, and Bergman
1975), in laying out a developmental sequence of stages from autistic
through to symbiotic to separation-individuation on the way to object
constancy, fostered the idea that the more severe the pathology, the
earlier were its roots in development.
By and large, ego psychologists believed that symptoms such as
loss of ego boundaries or loss of self-object differentiation were mani-
festations of regression to very early normal functioning. They were
then led to the conclusion that such severe ego impairments must be
caused by some basic faults in the very laying down of psychic
structure during infancy. It was therefore not diff icult for a clinician
like Greenacre (1953) to state that “the matrix of these severe distur-
bances . . . lay in disturbances in that period at the very dawn of the ego,
roughly around six months and a little later . . .” (p. 10).
 PSYCHOANALYSIS AND SCHIZOPHRENIA

Klein and the British Object Relations Theorists

The British object relations theorists have given us many penetrat-
ing insights into primitive mental operations and primitive uncon-
scious fantasies, but their formulations about the origins of schizophre-
nia have to be one of the more serious errors in this cautionary tale. By
the very nature of Klein’s conception (1946) that there is a paranoid-
schizoid position in the mental life of the child during the f irst six
months, her theories set off in a direction that leads inexorably to the
conclusion that the origins of schizophrenia are laid down during these
early months.
She believed that schizophrenia, paranoid psychosis, and schizoid
personality are the outcomes of any failure to adequately overcome the
paranoid-schizoid position. If the infant is endowed with too much
aggressive drive or if an excessive amount of frustration has been
aroused during these early months, persecutory fears and primitive
defenses such as splitting and projective identif ication will persist.
Segal (1964), summarizing Klein’s view of the etiology of schizo-
phrenia, wrote, “We know that the f ixation points of psychoses lie in the 33
earliest months of infancy. . . . In so far as the psychotic regresses to
the earliest months of infancy, he regresses to a phase in development
which already possessed pathological features in his infancy. Through
a study of the case-histories of schizophrenic and schizoid patients,
and from observations of infants from birth, we are now increasingly
able to diagnose schizoid features in early infancy and foresee future
diff iculties.” (pp. 54–55; emphasis added).
Those who came after Klein propounded the view that it was not
the intensities of the aggressive drive but the inadequacy of the mother,
or at least impairments in the mother-child dyad, that made it diff icult
to overcome the paranoid-schizoid position. Winnicott’s work (1965) is
often cited with regard to schizophrenia, probably because of his
emphasis on the importance of the early dyad and his concept of the
“good enough mother.” He stated that psychopaths and some others
with severe character pathology had such mothering early in life but
subsequently lost it and consequently forever felt deprived; in contrast,
a person with schizophrenia never had good enough mothering, a
privation that took place even before it was able to be perceived by
the infant (see pp. 131–136). In a similar vein, Fairbairn (1954) pro-
posed that in infants who go on to develop schizophrenia there has
been considerable early maternal withdrawal leading to profound
 Martin S. Willick

deprivation. A sense of this deprivation leads the infant in the paranoid-

schizoid position to regard its love as bad and destructive, leading to a
withdrawal of emotional contact with the outer world and a disturbed
sense of external reality.
Rosenfeld (1965) claimed that some mothers of children who
develop schizophrenia show a diminished tolerance toward the projec-
tions of the infant; feeling disturbed and persecuted, they withdraw
their feelings from the child. The schizophrenic, he wrote, “has never
completely outgrown the earliest phase of development to which this
object relationship belongs . . . ” (1952, p. 458). While both Bion (1967)
and Guntrip (1969) are valued for their descriptions of primitive
mental operations, they formulated somewhat similar views of the
etiology of schizophrenia.
Thus, the British object relations theorists f irmly placed the roots
of schizophrenia in ego impairments brought about by various kinds of
def iciencies in the early mother-child dyad. It came as somewhat of
a surprise to me, therefore, when I found myself unable to f ind a single
well-documented case of schizophrenia in the work of Klein, Winnicott,
34
Fairbairn, Bion, or Guntrip. Only Rosenfeld seems to have actually
treated patients with this disorder. (Kernberg, who has carefully studied
the British object relations theorists, has conf irmed my observation in a
personal communication.) Many of their cases seem to be of schizoid
personalities or severe character disorders. But in truth, and this is part
of the problem with their theories about the etiology of schizophrenia,
they never make much of a distinction between schizophrenia, paranoid
personality, schizoid personality, and other severe character disorders;
rather, these conditions are all lumped together as examples of the failure
to adequately overcome the paranoid-schizoid position.

Interpersonalists
The observation that most of the British object relations theorists
who wrote about schizophrenia lacked actual experience with schizo-
phrenic patients cannot be applied to the American analysts who can be
grouped together under the name of the Washington school of psychi-
atry. Proponents of the interpersonal point of view, they published
extensive case histories of schizophrenic patients treated four or f ive
times weekly, mostly in a hospital setting.
Many analysts from this school would acknowledge that Sullivan
(1953, 1956, 1962) provided a good deal of the foundation for their for-
 PSYCHOANALYSIS AND SCHIZOPHRENIA

mulations, however much this foundation was elaborated. Sullivan’s

interpersonal model of human development is similar to that of the
British object relations theorists in that the infant is seen as motivated
primarily by the need for object-relatedness rather than drive satisfac-
tion. Like Winnicott, Sullivan believed that there is no psychology of
the infant independent of the psychology of the infant-mother dyad.
So impressed was Sullivan with the degree of anxiety and terror
frequently present in acute schizophrenic episodes that he placed the
generation of anxiety in infancy at the forefront of his etiological con-
cepts. He then concluded that anxiety is imparted to the infant primarily
by an anxious mother in the interpersonal situation. This leads to a self-
state of intolerable or, in Sullivan’s phrase, “not me” anxiety. At times
his statements about the destructive role of caretakers are extreme:
e.g., “Let us talk about the extreme poverty of favorable opportunity
that the schizophrenic has had for building a successful self-esteem
system because, early in life, the idea was in some way conveyed in-
escapably to him that he was relatively infrahuman . . .” (1956, p. 364).4
The term schizophrenogenic mother seems to have f irst been used
35
in 1948 by Fromm-Reichmann. “The schizophrenic,” she wrote, “is
painfully distrustful and resentful of other people because of the severe
early warp and rejection that he encountered in important people of his
infancy and childhood, as a rule, mainly in a schizophrenogenic
mother ” (1948, pp. 163–164). Without using that particular term, sim-
ilar conclusions were drawn by others of the interpersonalist school.5

4
From his writings it appears that Sullivan was not only an astute clinician who
did not accept easy formulations about the etiology of the disorder, but was an
empathic therapist who treated his patients with great respect. As a matter of fact, as
early as the mid-1920s he established a ward to treat young male schizophrenic
patients at the Shepard and Enoch Pratt Hospital in Maryland. The guiding principle
was to treat these patients as human beings capable of relating to others despite their
severe impairments. He did believe that in some cases of schizophrenia an heredi-
tarily determined organic process was responsible (1956, p. 309).
5
In Schizophrenia and the Need-Fear Dilemma (Burnham 1969) these con-
clusions are represented in this way: “We believe that among the various types of
schizophrenia there is at least one group of persons whose inborn psychic apparatus
is normal but whose disordered early object relations interfered with normal devel-
opment. It seems likely that another group has suffered compounding of genetically
given weaknesses as a result of unfavorable early experiences” (pp. 15–16); “We
postulate that the nature of the schizophrenic’s early object relations interferes with
the normal processes of differentiation and integration” (p. 31). These conclusions
were drawn from the study of staff-patient relationships in a group of hospitalized
chronic schizophrenic patients and from the long-term intensive treatment that was
carried out at that time.
 Martin S. Willick

Will (1961) put it this way: “Whatever ‘defects’ or ‘weaknesses’

there may be, it is my impression that the person who eventually dis-
plays the schizophrenic reaction has been subjected early in his life to
interpersonal experiences that would be destructive to many of us, and
that he may benef it from participation in social events directed toward
less fearful and more open exchanges with his fellows. I am supported
in this view by the responsiveness—often slow and guarded—of the
patient to corrective learning experience provided in a therapeutic situ-
ation marked by acceptance and some clarity of def inition of its char-
acteristics and limits” (p. 14).
What emerges now in the writings of these analysts is the use of
transference-countertransference interactions, particularly one’s own
countertransference feelings, to understand or reconstruct the patient’s
early experience with the caretaking person. The best example of this
is to found in the work of Searles (1965), whose writings inspired a
generation of analysts. Dedicated to helping his patients by working
with them for many years in an intense and close therapeutic relation-
ship, he was one of the f irst to stress the need of the therapist to use
36
countertransference feelings in understanding the patient’s experience
and conf licts. Nowhere, he felt, was this of more importance than in
the treatment of the very severely mentally ill, whose pathology could
arouse in the therapist such intense feelings of all sorts.
Unfortunately, it was precisely the use of his own feelings that led
Searles down the path of the etiological formulations that I am calling
into question. With few exceptions, Searles believed that his subjective
responses to his patients were derived from two sources: an unconscious
effort on the patient’s part to let the therapist know what the patient had
felt in childhood; and the patient’s desire to do to the therapist what
had been done to him or her at that time. More important, he was con-
vinced that these childhood interactions of patient and parent were
causally related to the patient’s having developed schizophrenia.
His Collected Papers (1965) contain numerous examples of his
experiencing such intense emotions as anxiety, despair, feeling inhu-
man, or feeling “crazy.” In one paper, “The Effort to Drive the Other
Person Crazy—an Element in the Etiology and Psychotherapy of
Schizophrenia,” he describes a number of instances where his feeling
of being crazy helped him understand that his patient too had been
literally “driven crazy” by his parent. Searles reports being made to feel
insignif icant or to experience a lack of conf irmation of himself when a
 PSYCHOANALYSIS AND SCHIZOPHRENIA

patient consistently misidentif ies him; he concludes that this is the

way the patient had been made to feel.6 While the examples cited do
not specif ically refer to the experience of the patient as an infant, other
examples led Searles (1965) to conclude that the “schizophrenic
patient did not experience in his infancy, the establishment of, and later
emergence from, a healthy symbiotic relatedness with his mother”
(pp. 338–339).
Ping-nie Pao (1979), who became director of Chestnut Lodge
Hospital, where so many of these analysts worked with schizophrenic
patients, believed that some patients indeed suffered from an heredi-
tary organic process. For many others, though, he too searched for
early impairments in the mother-child dyad that would have played
an important role in the genesis of the illness. Relying on the infant and
child observations of Mahler (1952; Mahler and Furer 1968, Mahler,
Pine, and Bergman 1975), he came to the conclusion that the mother’s
inability to empathize with and be mutually cued to her infant’s needs
played a major role in the development of some forms of schizophre-
nia, especially in a vulnerable child. His views are an example of the
37
use of studies of normal infant development to reach conclusions about
the relationship between early development and later psychopathology.

WHY DID WE PROPOSE THEM?

As psychoanalysts look back at these etiological theories of schizo-

phrenia from our current vantage point, we should be more than curi-
ous about why we proposed them. How did we know there was such
profound maternal deprivation, anxiety, or hostility causing these future
schizophrenics to suffer such devastating ego impairment so early in
life? Before outlining the more important specif ic factors that led to
these formulations, it might be well to remind ourselves of the general
psychoanalytic climate of the late 1940s, the 1950s, and the 1960s, the
period when such psychogenic theories of the etiology of schizophre-
nia were so prominent.

6
While such intensive work with nonmedicated, actively psychotic patients must
surely be distressing, it is difficult to know whether all therapists would experience
so much uncertainty about their essential self or identity as Searles so frequently
describes. Prominent in Searles’s countertransference feelings are many that seem to
be quite idiosyncratic and raise serious questions about the accuracy of the conclu-
sions he drew from them.
 Martin S. Willick

The Climate of Psychoanalysis after World War II

Great excitement was generated by the work of the ego psycholo-
gists on this side of the Atlantic and by the Kleinians and the British
object relations theorists on the other. The belief was current that
psychoanalysis offered an opportunity to penetrate the deepest recesses
of the mind and the hope that not only the neuroses, but many of the
more serious psychiatric disorders, could be understood and treated
using a dynamic approach. It was a time when each and every psycho-
somatic illness was attributed to a specif ic dynamic conf lict (Dunbar
1948; Weiss and English 1957). In this climate, analysts were turning
their attention to the study of schizophrenia in the belief that a growing
understanding of the effect of dynamic conf lict and new knowledge
about the earliest phases of development would shed light on the genesis
of this disorder and lead to its successful treatment. Bolstering the con-
viction and hope that long-term insight-oriented therapy was the most
effective treatment was the fact that in the late forties and early fifties no
effective medications were available other than barbiturates, with their
38 merely calming effect; in addition, biological studies had failed to con-
sistently reveal any organic abnormalities in schizophrenia. Further, it
was believed by many that a psychotherapeutic approach might be both
more effective and more humane than psychosurgery or multiple
insulin shock treatments, the widespread use of which offers an example
of errors in the theories of etiology put forward by clinical psychiatry.
The awareness that people with schizophrenia were indeed capable
of transference feelings encouraged analysts to believe Freud mistaken
in his pessimism regarding analytic treatment for this condition.
Excited by the pioneering work of Anna Freud and Melanie Klein in
child psychoanalysis, many shared a growing conviction that psycho-
analytic studies of infant development could illuminate the severe con-
f licts and impairments believed to lie at the very foundation of schizo-
phrenia. It was, then, as many have put it, the “heyday” of psycho-
analysis, with few biological studies available to offer alternative views
of the development of psychopathology.

Three Conceptual Sources of the Error

Within this general climate, we can emphasize three specif ic sources
of the etiological formulations that were proposed. All are ideas still
among the most cherished by psychoanalysts today. One is the idea that
the more widespread and serious the ego pathology, the more likely it
 PSYCHOANALYSIS AND SCHIZOPHRENIA

is that the disturbance had its roots in the earliest years of growth and
development. A corollary to this idea is that if regressive symptoms
are evident, or what are considered to be primitive defenses and object
relations, we are justif ied in concluding that impairments took place
very early in life. The second idea is that we can fairly reliably use
transference-countertransference interactions in the analytic situation
to understand the nature of the early object relations of the patient. The
third is that normal infant observation studies can help us understand
how early diff iculties can lead to adult psychopathology.
The more serious the disorder, the earlier its etiological roots. The
idea that the more serious the disorder, the earlier in life may be found
its major psychogenetic inf luences was promulgated by Freud himself.
Although Freud never attributed f ixations or impairments in devel-
opment in schizophrenia to failures in the nurturing environment in the
earliest years of life, his concepts of f ixation and regression were to
have a profound effect on theories of pathogenesis (see Willick 1990).
He furthered the idea of a chronological timetable for f ixation points
and later regression by stating that dispositional f ixations to schizo-
39
phrenia and paranoia were to be found in the earliest stages of libidinal
development, in contrast to those found in the neuroses (Freud 1913).
Despite his cautionary comments about the possibility of basic ego dis-
turbances in the psychoses (Freud 1911), the foundations were laid for a
general theory of phase-specif icity holding that the more serious the
pathology, the earlier in life did the impairments in development occur.
These ideas were elaborated by Abraham (1908, 1924), who proposed
that the psychosexual phases could be subdivided, with f ixations at each
subphase leading to different illnesses, and by Tausk (1919), whose
investigation of the delusion of an inf luencing machine in a woman with
schizophrenia led him to conclude that early self-object differentiation
had been impaired in this illness.
Thus, a very powerful concept came to the fore in the thinking of
many analysts. It seemed reasonable to them that by examining the
symptomatic manifestations in patients with schizophrenia one could
see regressions not only of the libidinal drive, but also of ego, superego
functions, and object relations. It seemed to follow, then, that there had
to have been diff iculties in the actual early phases of development,
whether one used the earlier designation of fixation at a very early
infantile level or later concepts such as developmental arrest or pro-
found vulnerability to regression to that early level at times of stress.
 Martin S. Willick

However, the presence of a regressive symptom or behavior does not

necessarily indicate developmental failure, because we are dealing with
regression in a descriptive rather than etiological sense. In addition,
some of these “regressive” manifestations have no real counterpart in
normal infant development. Proponents of both defense and def icit
models still believed that the origins of the illness lay within the f irst
few years of life; proponents of the former emphasized conf licts sur-
rounding the aggressive drive, which then inf luenced ego function and
defense, while those advancing the latter stressed failure to internalize
good experiences, which led to defects in psychic structure.
Inferences drawn from transference-countertransference inter-
actions. The second idea, promoted mainly by the interpersonal school,
continues to exert an inf luence on the way we learn about the genesis
of a patient’s pathology. Analysts like Searles alerted us to the fact that
countertransference feelings are not merely an intrusion of the analyst’s
unconscious conf licts into the clinical setting, but help us understand
the interpersonal interaction there. Further, they used these transference-
countertransference interactions to comprehend important interactions
40
in the patient’s past. Searles was only one of many who began to apply
these insights to understand the early pathological object relation-
ships of schizophrenics. Inf luenced by the belief that the damaging
inf luences in schizophrenia had to have occurred very early, analysts
became even more bold, in that they began to believe they were seeing
in these interactions the residues of object relationships even from the
preverbal period.
Inferences drawn from infant observation.The third major influence,
one increasingly relied upon today, came from the application of
normal infant and child observation studies undertaken by psycho-
analysts. Hartmann had expressed the hope that such studies would
clarify the early disturbances in ego function that he believed were
present in schizophrenia. Because autism was seen as an impairment
in the basic response of the infant to the object world, it was placed
alongside schizophrenia as one of the profound mental illnesses with
etiological origins in the very earliest years of life. 7 As mentioned
7
Kanner’s original papers on infantile autism (1943, 1944) detailed, among other
things, the profound disturbance in object relatedness in those afflicted with the syn-
drome. Despite his acknowledgment that primary organic factors in its etiology may
be important, Kanner’s observations that the parents of these children were not warm
and loving, and were frequently highly intelligent and obsessional, fueled ideas about
the role of the parents’ pathology in the etiology of the disorder.
 PSYCHOANALYSIS AND SCHIZOPHRENIA

earlier, Mahler’s work on childhood psychoses and normal devel-

opment, by laying out a developmental sequence of stages from
autistic through symbiotic to separation-individuation on the way to
object constancy, unfortunately fed into the idea that the more severe the
pathology, the earlier its roots in development. Although she was careful
to say that the normal autistic phase (the f irst two months of life) was
not the same as the syndrome of infantile autism, her developmental
schema furthered the belief that the autistic symptoms of schizophrenia
were regressions back to that phase of development.8
Mahler contrasted the etiology of early infantile autism and that
of symbiotic psychosis—the former resting heavily on organic causes,
the latter on failures in the mother’s empathic responses to her infant.
However, in stating that “autism is the basic defense attitude of those
children who cannot utilize the beacon of emotional orientation” and
“is an attempt at dedifferentiation and deanimation” (1968, p. 69), she
furthered the idea that the autistic manifestations of schizophrenia
(what we now call the “negative syndrome”) are defensive as well.9
Because Mahler was describing the gradual building up of solid and
41
distinguishable self- and object representations in the mental life of
the infant, her work was also used to explain some of the dif f iculties
seen in the area of self-object differentiation in adult schizophrenics.
For example, since Mahler had indicated that one of the major impedi-
ments to developing self-object differentiation, and therefore object
constancy, was the mother’s inadequate empathic or “mutual cueing”
response toward her infant, analysts like Pao felt that they could
apply her f indings to the genesis of schizophrenia.

8
It was also problematic that Mahler chose to label the first two months of life the
“autistic” phase because in truth, other than the fact that the infant may sleep a great
deal and does not appear to be affectively engaged with its caretaker, these features
bear little resemblance to those of a child with autism. More recent work (Stern
1985) has demonstrated that there is a good deal of object-relatedness quite early,
as well as the fact that there seems to be much more capacity for differentiating self
from other than had been realized.
9
It is more likely that the neurological abnormalities in early infantile autism are
responsible for the inability to use the mother as a beacon of emotional orientation
rather than their being defenses employed by the ego. Since Mahler’s work, an abun-
dance of studies have shown that autism is a neurological illness whose etiology is
mainly genetic, most forms of which are accompanied by significant mental retarda-
tion (Piven and Folstein 1994). Studies such as Mahler’s further strengthened the
mistaken etiological concept that autism and “childhood schizophrenia” are caused
by failures in the mother-child interaction.
 Martin S. Willick

ARE WE MAKING THE SAME MISTAKES AGAIN?

Now fast forward to the year 2000. Are we making the same kind of
mistakes again? I do not really know the answer to this question, but
I would like to extend this cautionary tale to our current work. I believe
it is fair to say that the very ideas that led to erroneous notions of the
etiological determinants in schizophrenia are still very much with
us and may be causing us to be too certain about the causes of other
disorders.
As I have said, the mistakes that concern me are of two kinds.
One is the reluctance that many analysts still feel in acknowledging
biological predispositions in major psychiatric syndromes other than
schizophrenia. The other involves the etiological role accorded various
disturbances in the mother-child relationship during the preverbal
period. These are often viewed as crucial determinants for the devel-
opment of borderline conditions and very severe character disorders
such as schizoid and paranoid personality.
42
As to the f irst concern: Because I have become somewhat knowl-
edgeable about the use of medications, I have often been called on by
colleagues to consult with patients who have been in analysis for a
number of years but have not suff iciently responded to the treatment.
Most of these patients have been suffering from moderate low-grade
chronic depression, low self-esteem, and severe self-critical feelings,
and are often considered masochistic. In clinical psychiatry today
they are classif ied as having dysthymia. Some, but by no means all,
respond to antidepressant medications. In addition, studies show
that some of the personality traits found in depressed patients are
often altered when medication is successful in lifting the depression
(Black and Sheline 1997). The main point I wish to make is that in
discussing these patients with their analysts I often found a reluc-
tance to prescribe medication because suff icient “dynamic” conf licts
seemed to be present to explain the illness. In other words, these
analysts were working with an etiological model that made them doubt
that medication was needed. Recall that it was not so long ago that
psychoanalysts treating schizophrenia at hospitals like Chestnut Lodge
and Austin Riggs acted similarly (McGlashan and Nayfack 1988).
I should state here that for a number of psychiatric disorders the
decision to use medication need not rest on an understanding of
etiology. It is, rather, a clinical judgment supported not by convictions
 PSYCHOANALYSIS AND SCHIZOPHRENIA

about etiology but by clinical empirical studies that have shown the
usefulness of medication for particular disorders. I should state also
that in this “heyday of biological psychiatry” mistakes are often
made in the other direction as well—some patients are mistakenly
given medication out of the conviction of a biological etiology, and
psychotherapy is neglected.
More broadly, I believe that analysts are still reluctant to consider
the role of biological predispositions or even abnormalities in deter-
mining “choice of neurosis,” a problem we are in no way near solving.
Thus, while we can note many crucial dynamic conf licts, even common
ones, in people suffering, say, from panic disorder, OCD, or eating dis-
orders, these conf licts may not be suff icient to cause expression of the
syndrome. The signif icant etiological factor in many cases of schizoid
and paranoid personality disorder may turn out to be not a def iciency
in the mother-child dyad but the patient’s position on a biologically
based schizophrenia spectrum.
The second kind of potential mistake that concerns me involves
serious character disorders such as the borderline conditions. In a
43
previous publication (Willick 1990) I pointed out that when analysts,
in the 1970s and 1980s, began to investigate the borderline group of
disorders, they often stated that their etiology could be traced back
to diff iculties in childhood development occurring later than in the
psychoses but earlier than in the neuroses. Thus, they were proposing
a developmental continuum on which inadequate caretaking played a
major role in pathogenesis. At times their ideas along these lines were
quite specif ic, as in the following statement by Modell (1968): “For
those children who have been subjected to massive neglect . . . the
outcome is likely to be a form of childhood schizophrenia. . . . What
can be reconstructed from the history of adult schizophrenia and
borderline patients is not the absence of a maternal environment
but a relative failure of the maternal environment” (p. 84).
Led by Kernberg’s seminal work on borderline personality organi-
zation, many analysts stresssed impairments in ego structure, object
relations, and defense organization occurring before object constancy
could be achieved. For many analysts it made sense that diff iculties
in the mother-child interaction during the early part of the separation-
individuation phase were the crucible for borderline functioning in
adulthood (Masterson 1976; Frosch 1983; Buie and Adler 1982; Adler
1985; Volkan 1987). Needless to say, the fact that such theories of
 Martin S. Willick

etiology are not correct for the major psychoses does not mean that
they are not correct for the borderline group of disorders. Nevertheless,
I believe that the same three ideas that earlier drove the etiological con-
cepts for schizophrenia have been operating here as well. Increasingly,
these ideas are contributing also to conclusions about patients with
other serious forms of character disorder. I am concerned about the
adequacy of these formulations, especially as they invoke the mother-
child interaction during the preverbal period. One reason for this
concern is my belief that we cannot reach such conclusions from our
work in the analytic or psychotherapeutic setting. Second, I agree with
Gunderson (1984) that “developmental theories that attempt to explain
the pathogenesis of borderline personality disorder on the basis of
a phase-specif ic, parent-child interactional failure are bound to be
inadequate. The nature of the borderline patient’s psychopathology is
such that the shaping inf luences extend to multiple phases of develop-
ment” (p. 42). This was also the conclusion that my coauthors and I
put forward in our book about borderline patients (Abend, Porder, and
Willick 1983). A similar caution about the origins of borderline condi-
44
tions is to be found in the remarks of Fonagy (1996a), one of the most
respected analysts doing infant observation research. “The identif ica-
tion of what are presumed to be primitive modes of mental functioning
in individuals with severe personality disorders . . . is often regarded as
evidence for the persistence or regressive recurrence of early patho-
genic developmental experiences. Yet, even if horizontal splitting or
identity diffusion were representatives of early modes of thought, an
issue highly controversial in any case, . . . their reemergence in adult
mental functioning may be linked to later persistent trauma” (p. 405).

Example One
An interesting example of a formulation of very early ego impair-
ment is to be found in Gerald Adler’s Borderline Psychopathology and
Its Treatment (1985.) He believes that Kernberg’s formulation, which
traces the roots of the disorder to the very young child’s inability to
integrate self- and object representations, does not suff iciently explain
the terror of utter aloneness, feelings of inner emptiness, and a sense
of panic that feels like annihilation of the self, symptoms he believes
are the cardinal ones of this disorder. His own theory of the cause of
these symptoms and of the disturbance is that even prior to the integra-
tion of self- and object representations there is a relative developmental
 PSYCHOANALYSIS AND SCHIZOPHRENIA

failure in the formation of introjects that provide the self a function

of holding-soothing security.
What informs Adler that there is such a profound impairment
early in the infant’s life? What clinical data did he use? Throughout the
book appear case vignettes taken from his clinical work. The most thor-
oughly discussed is that of a young man who came to treatment in his
twenties because of a lifelong sense of emptiness, diffuse anxiety, and
a lack of true close friends. We learn that his mother was emotionally
involved with the patient in terms of her own needs, rather than his
as a separate person. She was, alternately, either intensely close to him
or preoccupied with herself to such an extent that she appeared to have
forgotten him. She involved him in sensuous closeness, only to repel
him in disgust when he responded.
We then learn the following things about the patient’s life after age
three: He was repeatedly sent by his mother to an emotionally distant
aunt and uncle for periods of several weeks up to one year, presumably
to ease the mother’s burden after a sibling was born. Later, his parents
made a practice of sneaking of f in the evenings after he had fallen
45
asleep. To ensure that he would remain in the house, they removed the
doorknobs and took them with them. Repeatedly he awoke, found
himself alone, trapped and panicky. He described the times of close-
ness with his mother as heavenly, but when sent away from her he felt
he had been abandoned on a frozen desert. Further, he believed her
when she was angry with him and would declare that she had made him
and could kill him. His mother also suffered from episodes of depres-
sion, during which she would take to her bed and become relatively
unresponsive to everyone.
It seems to me that if we accept this history as accurate we have
enough to account for this patient’s severe pathology without postulat-
ing a failure in the development of soothing introjects early in infancy.
We often forget how vulnerable a child of three is, let alone one of
f ive or seven. A parent’s soothing and caring understanding is required
throughout child development.
Adler, of course, did not rely on history alone; he drew his conclu-
sions also from his work with the patient in the clinical setting, where
two things particularly impressed him. One was that as rage at the
therapist appeared in the face of separations, the patient could not
summon up the image of the therapist and felt indeed that Adler no
longer existed. Thus, as Adler says, the patient lost “evocative memory.”
 Martin S. Willick

The second was that along with this rage came fears that he might “fall
into the chest of the therapist and disappear,” or that if the therapist
leaned forward in his chair he might fall into the patient’s chest and be
totally absorbed. Adler interprets the presence of “merger” fantasies
and the failure of evocative memory as ref lections of developmental
failure in the f irst year. His conclusions about the failure of “evocative
memory” in the clinical setting are derived in part, just as they were
for some of those who investigated schizophrenia, from the application
of normal child observation studies, in this case those of Mahler, Pine,
and Bergman (1975) and Fraiberg (1969).Since Adler felt that his patient
had a very serious borderline disorder, he assumed that the roots of
the disturbance had to lie in the preverbal period.

Example Two
Another example, more recent, is taken from an issue of the
Journal of Clinical Psychoanalysis devoted to the topic “The Talking
Cure and the Preverbal Period: Developmental Facts or Genetic
Fallacies?” In this example, an analyst uses her own countertrans-
46
ference response to a patient, along with an application of current
infant research, to draw conclusions about the early roots of the
patient’s diff iculties (Lally 1996).
The analyst reports on the f irst twelve sessions of an analysis in
which the patient, a young women in her late twenties, is afraid to lie
on the couch: “As we talked about her fears regarding analysis during
the second session, I started to have visual images of caring for an
infant. My off ice felt like ‘the nursery,’ the couch was ‘the crib.’ I was
aware of the intense desire to soothe her anxiety. Her anxieties struck
me like infant cries of distress. As she revealed her fears, and as
I understood them and interpreted them, I felt like a mother minister-
ing to a distressed baby. . . . I felt as if I were using words to rock, pat,
and envelope her, to soothe her inner distress” (p. 11). “I was distinct-
ly aware of feeling as if I were with a crying baby, talking as adults
do in such situations, ref lecting back the feeling state of the infant as
they see it” (p. 13).
Interestingly, this patient did not seem to be very disturbed, although
the analyst did feel she was like a “fragile bird or lost waif.” What we
learn about her history is that the patient’s mother was frequently
hospitalized for depression beginning in the patient’s infancy. She
was often cared for by an aunt, and she had many memories of lonely
 PSYCHOANALYSIS AND SCHIZOPHRENIA

hours at the aunt’s house, waiting for her father to arrive. During her
mother’s absence, the patient felt desperate with loneliness and self-
blame. She believed that if she were very good, she would be able to
bring her mother home.
In order to understand her intense countertransference reaction,
the analyst turns to the infant observation research of Stern, Emde,
Brazelton, and Bebe and Lachmann, especially the latters’ work on
reciprocal responsiveness. She believes this research bolsters her con-
viction about the usefulness of her countertransference reactions in
understanding her patient and offers justif ication for her therapeutic
interventions. It is clear that she believes (although this was not the
focus of her presentation) that the mother, because of her depression,
was unable to be adequately empathic toward her infant. “I deciphered,”
writes the analyst, “an aspect of Joan’s experience in infancy, when her
depressed mother was unable to be responsive to her ” (p. 21).
In this example, conclusions are drawn about the patient’s
preverbal development from both the transference-countertransference
interaction and from the application of infant-mother observation
47
research. Remember that this patient had many memories of lonely
hours at the aunt’s, waiting for her father to arrive, feeling desperate
with loneliness and self-blame. Her analyst’s emotional response, while
perhaps intuitively empathic toward the patient’s pain, could just
as well have ref lected those later childhood years when the patient,
as noted, had the capacity for self-blame.
Not present in this formulation is the idea that since the patient is
so disturbed there must have been early failures. As a matter of fact,
there is nothing in the presentation of the case that would indicate that
the patient was “borderline” or had signif icant impairments in her
object relations or ego functioning, a fact pointed out by a discussant
of the paper (Olesker 1996).

Discussion
In both these examples we have etiological formulations that trace
the patient’s psychopathology to various disturbances in the develop-
ment of object relations in infancy, much as was done earlier with schizo-
phrenia. Indeed, had either of these patients been schizophrenic, many
analysts writing in the 1950s, 1960s, or 1970s might well have argued
for the causative role of the failure of soothing or holding introjects in
the first case, and the lack of reciprocal responsiveness in the second.
 Martin S. Willick

With regard to the second case, I have heard a number of colleagues cite
the presence of serious depression in the mother during a child’s infancy
as playing an important role in the development of schizophrenia.
I think we all realize that we analysts, perhaps like other scientists,
tend to look for data that will conf irm our own theories. If one is a self
psychologist, there will be ample data to reveal lack of empathy in the
mother. If one is a classical analyst, there will be enough to indicate that
conf lict and compromise formation, especially around the drives and
their derivatives, are decisive. And so on. Likewise, if one is commit-
ted to seeing the effects on the individual of the profoundly important
preverbal period, there will be ample material in case studies to support
that proposition. McGlashan (1984), who conducted a long-term follow-
up study of patients treated for psychoses at Chestnut Lodge from 1950
through 1975, says that when social workers did the intakes on schizo-
phrenic patients during those years, they found the things they were
looking for—impairments in early relationships with caretakers (per-
sonal communication).
It is important to bear in mind that our recent knowledge about
48
schizophrenia has come not from the clinical situation but from other
ways of studying the disorder—brain imaging and genetic epidemiolo-
gy studies of families. The same can be said about recent advances
in our knowledge of bipolar disorder, autism, ADHD, and OCD. There
is also some indication that some borderline patients may have a form
of af fective illness and others a form of thinking disturbance; that
is to say, some may have a biological diathesis that interacts with
the environmental milieu, early or even later in life (see, e.g., Siever
and Davis 1991).
Let us, however, leave biological considerations aside and turn our
attention to the psychological milieu. If biological predispositions are
not playing a role, we must have some other explanation to account
for the etiology of the more severe character disorders and borderline
conditions, as against the neuroses or less severe disturbances. It seems
reasonable to assume that these sicker patients have had greater diff i-
culties earlier in life, when basic ego structure and function are devel-
oping. Surely all of us believe that not only are the f irst two years of
life extremely important, but that the mother-child dyad is one of the
most crucial determinants of the infant’s development during that time.
Nevertheless, if history is to be a guide, we must proceed cautiously
when we formulate etiological theories invoking the inf luence of those
 PSYCHOANALYSIS AND SCHIZOPHRENIA

early years. First, we may not be able to conf irm such theories from
our work in the clinical situation. Second, we must be careful when we
use countertransference responses to reconstruct very early conf licts
in object relations. Third, we should be cautious in moving too easily
back and forth from normal child observation studies to the clinical
situation. (For similar caveats regarding the conclusions that can be
drawn from infant observation, see Wolff 1996.) There is reason to
believe that sexual and/or physical abuse occurring after the f irst
two years of life might be the crucial determinants for serious psycho-
pathology. In other cases, such as the two cited here as examples,
cumulative trauma or ongoing diff iculties in caretakers may be more
important than what takes place during the preverbal period.
To address questions about the role of preverbal development in the
etiology of various disturbances, we may have to turn from the clinical
situation to prospective studies that follow infants through childhood
and into the adult years. We have had a serious problem in psycho-
analysis due to the absence of any system for testing and then accept-
ing or dismissing hypotheses. As Cooper (1993) has said, “Without
49
empirical studies we have no way ever to discard a hypothesis. . . .
Psychoanalysts have leaned heavily on clinical experience to give
us conf idence in our activities, although the history of medicine is
replete with tenaciously held false beliefs based on clinical experience”
(pp. 383–384).
An example of prospective empirical studies in psychoanalysis is
the research being undertaken by Fonagy and his colleagues (1996b) on
the implications of the quality of early infant-mother relationship for
later development. Working with the Adult Attachment Interview and
the Strange Situation assessment, Fonagy seems able to predict which
children will develop insecure attachments at one year. Some effects
seem to be present at f ive years as well. Now what are needed are long-
term follow-up studies of these same children to see what they will look
like as adults. Whatever these studies show, we must keep in mind what
we all know—that development is not static. Subsequent to the prever-
bal period, we enter into later phases with all of their conf licts, and
these too can have a profound inf luence on personality development.
The inf luence of later phases of development was taken up by
McDevitt (1997) in a twenty-f ive-year follow-up of the subjects of
Mahler’s original child observation studies. McDevitt questions the
“validity of inferences about inner life, about intrapsychic experiences
 Martin S. Willick

and meanings, that are drawn from largely behavioral data” during
infancy (p. 123). In one case followed up after many years, the inf lu-
ence of conf lict and compromise formation taking place after the
preverbal period is carefully described by McDevitt.
As we work toward an integration of data from the psychoanalytic
situation, from normal infant and child observation studies, and from
neurobiological research, we will have to broaden our understanding
of the complexities of the concept of etiology. It may very well turn out
that in some psychiatric syndromes, like PTSD, psychological trauma
has produced actual brain changes and abnormalities. A recent example
of the possible effect of impaired early mothering on the brains of
infants and toddlers comes from Dawson et al. (1997). They found that
at the age of 13–15 months, the infants of depressed mothers exhibit
reduced left frontal EEG activity. The long-term consequences of such
changes remain to be seen.
For analysts who still believe that the mother’s inadequacies during
the f irst year or two of life contribute to the development of schizo-
phrenia or other psychoses, such f indings will support their belief that
50
the presence of biological abnormalities in the adult do not necessarily
indicate that the etiology of the disturbance is primarily “biological” or
“organic.” However, just as with the results of the studies of “attach-
ment” disorders, the long-term consequences of neurobiological
changes in the brains of infants have yet to be determined. As I have
mentioned, we now have the opportunity to achieve an integration of
the results of studies from our own f ield, whether conducted on the
couch or in the nursery, with those of neurobiological research.

DO THEORIES OF ETIOLOGY MATTER?

Finally, we might ask whether it matters what theories of etiology we

believe. Do they really inf luence our clinical work with patients? Of
course, it matters to those of us interested in knowing what inf luences
normal and pathological development. For those of us who believe
that an understanding of those inf luences can inform our treatment,
it certainly matters. We teach analytic courses on psychopathology,
ego development, symptom formation, and character structure in the
hope that understanding how mental illness develops will guide us in
treatment. The history of psychoanalysis and schizophrenia should
alert us to the fact that at times our theories of etiology can lead us to
 PSYCHOANALYSIS AND SCHIZOPHRENIA

withhold medication in the belief that one must get to the psychological
roots of the problems, roots that might be obscured by medication.
However, with cases in which medication is already being used,
or in which it is clearly not necessary, do our theories of the origins of
the disturbance necessarily get in the way? This is diff icult to answer.
Evidently, analysts from very different persuasions, with very different
views of pathogenesis, are convinced of the correctness of their formu-
lations and are guided in their treatments by that conviction. But since
we do not yet know what is truly mutative in the psychotherapeutic
experience, it may very well be that for many patients the analyst’s
views of etiology are indeed not so crucial. I am reminded of a case
I presented at a panel on conf lict and def icit. My patient had been
unable to talk in a previous treatment, and I was therefore being more
actively helpful and supportive, talking to her at the beginning of every
session because she could not begin. One of the panelists, a self
psychologist, not only complimented me on my work, but indicated
that I had treated the patient much as he would have. He said, how-
ever, that my intuitive need to alter my therapeutic stance should have
51
led me to a conclusion regarding the cause of her psychopathology—
namely, the inadequacy of the mother’s empathic responsiveness. I will
often alter my therapeutic stance, not out of some conviction about
the origins of the patient’s psychopathology, but based on what I think
will facilitate the psychotherapeutic or psychoanalytic process.
I know there are many analysts who analyze transference, and con-
f lict and defense in all their ramif ications, without necessarily thinking
about etiological factors. However, even for some of them, as well as
for myself, reconstructions of patterns of relationship reenacted in the
transference are often an important part of the therapeutic work. I have
in general, I must say, become much more cautious in providing such
reconstructions. And, when they concern the preverbal period, I believe
we enter into a much more diff icult area, one we have visited before,
often to our detriment, an area in which verif ication is extremely hard
to come by.
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