Chat with us, powered by LiveChat psychology of personality | excelpaper.org/
+1(978)310-4246 credencewriters@gmail.com
  

Psychoanalytically Informed
Approaches to the Treatment
of Obsessive-Compulsive Disorder

G L E N O. G A B B A R D, M.D.

208


Dr. Gabbard is Bessie Walker Callaway Distinguished Professor of Psycho-

analysis, Karl Menninger School of Psychiatry, Menninger Clinic; Director and
Training and Supervising Analyst, Topeka Institute for Psychoanalysis.

As neuroscience research has uncovered the genetic/biological
basis of obsessive-compulsive disorder (OCD), a broad
consensus has been reached that behavior therapy and a selective
serotonin reuptake inhibitor are the treatments of choice for the
c o n d i t i o n . N e v e r t h e l e s s , p s y c h o a n a l y t i c a l l y i n f o r m e d
approaches still have much to offer in an overall treatment plan.
The biologically determined symptoms have unconscious
meanings to the patient that may lead the patient to be highly
invested in maintaining the symptoms. Also, psychodynamic
factors may be involved in triggering an exacerbation of the
symptoms. Moreover, the compulsions and obsessional thoughts
almost always have interpersonal meanings that need to be
addressed. Family members and others, including treaters, may
feel compelled to accommodate themselves to the illness as a
response to coercive behaviors by the patient. Finally, the
characteriological features of individuals with OCD tend to
undermine treatment efforts in many cases and may require
psychoanalytically informed therapy to deal with them.

W O C L I N I C A L E N T I T I E S , hysterical neurosis and obsessive-Tcompulsive neurosis, have historically been considered the model
conditions for psychoanalytic treatment. While psychoanalysis was
born out of experiences with hysteria, Freud’s classic 1909 paper on
the “Rat Man” brought obsessive-compulsive neurosis into the
psychoanalytic literature with a rich and compelling psychodynamic
formulation of the symptoms. Since that time, the classical
formulation, widely accepted in analytic circles, was that the anxiety
provoked by the oedipal situation led the obsessive-compulsive
neurotic to regress to an anal-phase constellation of defenses,
including reaction formation, doing and undoing, and isolation of
affect. This regression was often viewed as more likely because of
the longstanding presence of anal fixations resulting from disturb-
ances during the phase of toilet training (Nemiah, 1988).

Despite the longstanding tradition of treating obsessive-compulsive
neurosis with psychoanalysis, reports of symptomatic cures with
psychoanalytic treatment are virtually nonexistent (Zetzel, 1970;
Malan, 1979; Jenike, Baer, and Minichiello, 1986; Nemiah, 1988;
Perse, 1988).

Parallel with the realization that psychoanalysis does not alter the
obsessive-compulsive symptoms, there has been a growing tendency
within psychiatry to view the disorder as one that has a largely
biologically based etiology. Indeed, the change in nomenclature in
D S M – I I I f r o m o b s e s s i v e – c o m p u l s i v e n e u r o s i s t o o b s e s s i v e –
compulsive disorder (OCD) reflects a widely held view that neurotic
mechanisms as traditionally defined by psychoanalytic theory are
not particularly germane to the etiology of OCD.

The evidence for biological components to the etiology is
convincing. OCD patients exhibit increased metabolism (as compared
with normal control subjects) in the orbitofrontal cortex, the anterior
cingulate cortex, and the caudate nuclei (Baxter et al., 1987; Swedo
et al., 1989). Other lines of evidence include a higher rate of
concordance for OCD in monozygotic and dizygotic twins, an
increased prevalence in patients with Tourette’s Syndrome (and in
their families), and a dramatic response in some patients to
psychosurgery (Elkins, Rapopart, and Libsky, 1980; Lieberman, 1984;
Turner, Bieder, and Nathan, 1985). In addition, Luxenberg et al.
(1988) demonstrated with the use of computed tomography that the
caudate nucleus volume is significantly less in OCD patients as

TREATMENT OF OCD 209

210 GLEN O. GABBARD

compared to healthy controls. Patients with OCD also show
significantly more signs of central nervous system dysfunction than
controls (Hollander et al., 1990). One of the most striking recent
findings about OCD patients that also suggests a biological
component to the etiology is the fact that there is virtually no placebo
response (Mavissakalian, Jones, and Olson, 1990). This finding is in
stark contrast to conditions such as panic disorder that may have as
much as a 25–40 percent placebo response (Gabbard, 1992).

Animal models for OCD are now emerging that suggest that
serotonin abnormalities are significantly involved in the pathogenesis
of OCD (Greist and Jefferson, 1995). Many of these, such as canine
acral lick, a grooming behavior in large dogs that is remarkably
similar to obsessive-compulsive behavior in humans, appears to
respond to potent serotonin reuptake inhibitors (Rapoport, Ryland,
and Kriete, 1992). In addition, potent serotonin reuptake inhibitors
are also effective in the treatment of OCD in humans (Greist and
Jefferson, 1995).

Part of the difficulty in the field stems from the disentangling of
obsessive-compulsive personality disorder (OCPD), which is
eminently responsive to psychoanalysis, and OCD. Although there
has been a historical tendency to see the two conditions as part of the
same continuum of illness, the evidence is now substantial that the
two are rather distinct entities (Pitman and Jenike, 1989; Baer et al.,
1990; Stein and Hollander, 1993). In fact, only about 6 percent of
OCD patients also have obsessive-compulsive personality disorder.
In general, OCD patients view their symptoms more egodystonically
and therefore have greater suffering as a result. The traits of OCPD
patients are often egosyntonic and may cause more distress in
significant others than in the patient. This distinction does have certain
limitations, and clinicians should keep in mind that some OCD
patients also experience their symptoms as somewhat egosyntonic
(Rasmussen and Eisen, 1989; McCullough and Maltsberger, 1995).
In this paper I shall focus specifically on psychoanalytically informed
approaches to OCD rather than OCPD.

In an era in which behavior therapy and serotonin reuptake
inhibitors have become the widely accepted treatments of choice for
OCD patients (Greist and Jefferson, 1995), we now are at risk for
relegating psychoanalytically informed approaches to history and
thereby shortchanging many of our patients from a necessary and

TREATMENT OF OCD 211

valuable component to the therapeutic armamentarium brought to
bear with OCD patients. Despite the impressive research in the
neurosciences about the biological underpinnings of OCD, the
psychoanalytically informed clinician still has much to contribute to
a comprehensive treatment plan for such patients.

The treatment strategies for OCD that I shall articulate fall broadly
in the category of psychodynamic psychiatry (as opposed to psycho-
dynamic psychotherapy). Previously, I have defined psychodynamic
psychiatry as follows: “an approach to diagnosis and treatment
characterized by a way of thinking about both patient and clinician
that includes unconscious conflict, deficits and distortions of
intrapsychic structures, and internal object relations” (Gabbard,
1994b, pp. 4–5). As implied by this definition, the psychodynamic
clinician is always thinking in terms of unconscious meaning,
transference, countertransference, and resistance, even when not
involved in formal psychoanalytic psychotherapy or psychoanalysis.
For example, a psychodynamic clinician may be prescribing a
serotonin reuptake inhibitor for a patient with OCD but thinking about
the interactions with the patient from a psychodynamic perspective.
This psychoanalytically informed approach implies a particular
conceptual model for understanding the illness of OCD.

Stress Diathesis Model of OCD

Increasing evidence suggests that many of the major psychiatric
disorders can best be understood based on a stress diathesis model
(Gabbard, 1992, 1994a). While there are clearly genetic processes at
work in the etiology and pathogenesis of OCD, psychosocial stressors
appear to be important as well. Clinicians have long observed that
increased stress or the recurrence of original precipitating problems
can worsen symptoms of OCD while reduction in tension can improve
them (Black, 1974). Some provocative research suggests that OCD
symptoms may be significantly influenced by issues involving
childcare and pregnancy. For example, Buttolph and Holland (1990)
found that 69 percent of patients with OCD could relate the
exacerbation or onset of their symptoms to parental care of their
children, pregnancy, or childbirth. In a study of 106 female patients
suffering from OCD, Neziroglu, Anemone, and Yaryura-Tobias (1992)
noted that pregnancy was associated with the onset of OCD symptoms

212 GLEN O. GABBARD

more than any other life event. In fact, 39 percent of those patients
with children first experienced symptom onset during pregnancy. Five
women in the study had had an abortion or a miscarriage, and four of
those five noted exacerbation or onset of OCD symptoms while they
were pregnant.

In my own clinical experience with OCD patients who are young
mothers or who are pregnant, I have often noted a link between
increased intensity of the OCD symptoms and a rise in unconscious
or barely conscious aggression toward the child. For example, one
OCD patient who was a new mother of a 6-month-old said that she
immediately turned off the television whenever a news story or talk
show featured a discussion of child abuse by parents. In the course
of psychotherapy, she recognized the extent to which she struggled
with overwhelming murderous wishes toward her child. While the
form the obsessional thoughts took often suggested that a disaster
from the outside would strike down the child, dynamic exploration
helped the patient understand that the threat she feared really came
from within rather than from external sources.

Part of this conceptual model is that symptoms, no matter how
biologically influenced, nevertheless have meanings, conscious or
unconscious, to the patient. As I noted in a previous communication
(Gabbard, 1992), psychodynamic conflicts frequently appropriate the
biochemical forces within the brain and use them as a vehicle of
their expression. In that communication I described a young man
who had completely controlled his mother’s life to the point where
she quit her job to stay home with him and cater to his every need.
Meanwhile, the father was forced by the young man to stay in a
separate room in the house so that the father would not contaminate
his son with “germs” from the outside world. In this regard, the OCD
symptoms served as a way of facilitating an unconscious oedipal
triumph in which the young man had his mother all to himself while
his father was out of the picture.

Of great significance in this case was the patient’s resistance to
any kind of psychiatric treatment. He had refused to go to psychiatrists
and had refused medications with some proven efficacy for OCD.
Only when his resistance could be addressed and understood was the
patient capable of collaborating in an overall treatment program.
Hence, the discovery of his intense dependency on his mother and
his wish to continue in his conflictual oedipal triumph had to be taken

TREATMENT OF OCD 213

up with him through psychodynamic understanding before he finally
agreed to take clomipramine.

Treatment Implications

In considering treatment implications for OCD, the foregoing case
vignette underscores an extraordinarily crucial point—namely, that
many OCD patients tenaciously hang on to their symptoms because
of their special meanings and because of the interpersonal control
they exert on others. They thus may be uninterested in doing the
work of behavior therapy or complying with medication regimens.
Indeed, many controlled trials exclude such problematic patients
because of their poor motivation or refusal to comply, and therefore
empirical research on OCD may not adequately address this subgroup
of patients.

Even when OCD patients are compliant with standard treatment
regimens, the results are less than ideal. For example, in the
c o m p r e h e n s i v e m u l t i c e n t e r p r o j e c t t o s t u d y t h e e ff i c a c y o f
clomipramine, after 10 weeks of treatment the mean reduction of
symptoms was only 38–44 percent (Clomipramine Collaborative
S t u d y G r o u p , 1 9 9 1 ) . M o r e o v e r, m a n y p a t i e n t s r e l a p s e o n
clomipramine or other serotonin reuptake inhibitors if they do not
have associated behavior therapy (Zetin and Kramer, 1992). Behavior
modification involving in vivo exposure combined with response
prevention appears to have the best results (Barlow and Beck 1984),
but a high relapse rate also occurs with this modality, which requires
extensive cooperation from the patient (Marks, 1981).

Patients with OCD often have considerable difficulties in
interpersonal relationships, both with family members and with those
at work or in social settings. The diagnosis of OCD is associated
with a high risk of separation or divorce (Zetin and Kramer, 1992).
Psychodynamic approaches are extremely useful to help clarify and
address the relationship problems encountered by the illness.
Identification of the stressors and their particular meanings to patients
may also help both the patient and family members to be aware of
precipitating events and try to reduce their impact or avoid them as
much as possible.

The neurobiological substrate of OCD leads to certain kinds of
unconscious patterns in relationships that ultimately become

214 GLEN O. GABBARD

internalized as the patient’s characteristic object relationships. These
are then reexternalized in familial and extrafamilial relationships to
create a host of problems. The advantage of a psychodynamic
orientation in treatment is that the transference–countertransference
developments can be systematically examined as a way of helping
patients understand their relationship problems in other contexts.

Mr. A was a 26-year-old single man who was admitted to a
psychiatric hospital unit because his symptoms had become virtually
d i s a b l i n g a n d b e c a u s e h e h a d r e f u s e d t o c o o p e r a t e w i t h
pharmacotherapy and behavior therapy approaches. He was
preoccupied with the possibility that his mother and father had stepped
on the AIDS virus on their way home from their respective jobs and
was convinced that the house needed to be sprayed with disinfectants
thoroughly to prevent his coming into contact with the virus. His
parents had colluded with his insistence that every item of furniture
in the house needed to be sprayed and scrubbed down. Each evening
they would systematically go through the ritual of spraying and
wiping off much of the household under the direction of the patient.

When Mr. A came into the hospital unit, he asked his primary nurse
for details about the previous occupant of his room. The nurse
explained that such information was confidential and could not be
shared with him. Nevertheless, he persisted in asking questions,
particularly regarding the previous occupant’s masturbatory habits.
He became obsessed with the notion that there might be semen stains
in his room that could transmit HIV infection to him. In my daily
interviews with him, much of the time of our discussions was
consumed with this possibility. Despite the absurdity of his fear, his
insistence that we discuss the possibility of HIV contamination was
powerfully coercive to the point that I found myself engaging in
extensive efforts to argue from a rational, logical standpoint that his
fears were essentially irrational. Mr. A’s demand that I participate
with him in a dialogue about HIV had an obligatory quality associated
with it. I felt invaded by it and “bullied” into a kind of folie à deux in
which nothing else was important to the two of us. In short, I had
become an extension of Mr. A.

On one morning, while making rounds, I walked into his room to
find Mr. A’s primary nurse with disinfectant spray in one hand and a
paper towel in the other, “decontaminating” the furniture in Mr. A’s
room. The nurse appeared rather ashamed that he had been caught
colluding with the patient’s fear of contamination.

TREATMENT OF OCD 215

When I met with the nurse later, I explained to him that I could
empathize with his dilemma—namely, that Mr. A’s need to discuss
his obsession and to engage in rituals to assure himself that the room
was decontaminated was so powerfully compelling that one could
easily get drawn into colluding with it. I pointed out to the nurse,
that via projective identification, he had become tyrannized by the
patient in the same way that the patient’s parents had been tyrannized
by Mr. A at home. I shared with the nurse the time-honored view of
the psychoanalytic hospital as a place where a patient recreates his
family situation (more precisely, his internal object world) in the
milieu of the hospital with various staff members (Gabbard, 1988).

When the nurse refused to engage in such collusion following that
incident, Mr. A became highly indignant. The extent of his entitlement
was truly remarkable. He clearly had the expectation that others in
his environment should behave as narcissistic extensions of himself.
He massively denied the autonomy and subjectivity of anyone else
in his life. They existed only to respond to his needs, and his
omnipotent control was highly dehumanizing.

I spent a good deal of time in my meetings with him pointing out
his pattern of object relatedness, both in his relationship with the
nurse and with me on the unit and with his parents at home. I clarified
with him that his sense of urgency about the catastrophic nature of
his thoughts regarding contamination by HIV caused others to feel
that they must do his bidding or there would be dire consequences.
While this approach did not directly reduce his obsessive-compulsive
symptoms, it was of extraordinary value in helping him develop
greater empathy for others and to view them as subjects rather than
objects under his omnipotent control. In the social worker’s sessions
with the parents and Mr. A, a great deal of progress was made in
h e l p i n g t h e p a r e n t s s e e t h a t c o l l u d i n g w i t h h i s n e e d s f o r
“decontamination” were not in his best interests in the long run. The
parents felt extraordinary relief in gaining permission from the social
worker, and eventually from Mr. A, to act out of their own needs
rather than to subject themselves to Mr. A’s controlling behavior.

Another cogent reason to incorporate psychodynamic strategies
w i t h O C D p a t i e n t s i s t h e f a c t t h a t m a n y h a v e s i g n i f i c a n t
characterological issues that serve as powerful resistances to forms
of treatment such as behavior therapy or pharmacotherapy. In fact,
Baer et al. (1990) found that the presence of schizotypal, borderline,
and avoidant personality disorders predicted poor treatment outcome

216 GLEN O. GABBARD

in patients with OCD treated by clomipramine. Moreover, even when
patients fall short of meeting DSM-IV criteria for a personality
disorder, they still may have prominent characterological features
that interfere with the implementation of a comprehensive treatment
program.

In another study (Aubuschon and Malatesta, 1994), 31 patients
with OCD who were comorbid for a personality disorder were treated
with comprehensive behavior therapy. Their outcomes were compared
with a group of OCD patients without comorbid personality disorders.
Those patients with personality disorders were rated as more difficult
to treat, were more likely to terminate behavior therapy prematurely,
and required more psychiatric hospitalizations than the OCD patients
without personality disorders.

Mr. B was a 38-year-old divorced man who had been successful
in a management position until he became unable to function
effectively at work because of obsessional thoughts and compulsive
rituals. Although he had a longstanding paranoid personality disorder
and some mild symptoms of OCD, his functioning had never been
impaired until his father’s illness and death 2 years prior to seeking
t r e a t m e n t w i t h m e . H i s o b s e s s i o n s a n d r i t u a l i s t i c b e h a v i o r
dramatically worsened at the time of his father’s death, to the point
where he found he could not function effectively at work.

The patient had been angry at his father the last time he saw him
before his death and felt extraordinarily guilty about the fact that
their last meeting had been an angry one. The day preceding the
father’s funeral, Mr. B had strained his back playing baseball, and
during the funeral he experienced such severe low back pain that he
needed to take narcotic medication. Although he stopped the narcotics
after several days, his back pain continued in conjunction with his
worsening obsessional thoughts. The content of these thoughts was
primarily focused on his potential to hurt others. For example, he
was afraid that if he went to work, he would open the door to the
men’s room and seriously injure someone who was coming out as he
walked in by hitting him with the swinging door.

As a child, Mr. B had attempted to undo his anger toward his
parents with various forms of ritualistic behavior. His gradually
worsening rituals since his father’s death reflected his unconscious
conviction that he had caused his father ’s death because of the
intensity of his anger. A variety of rituals, including driving to work

TREATMENT OF OCD 217

and back as many as eight or ten times, were designed to undo the
death by increasingly escalating the rituals.

He had seen two previous clinicians prior to coming for help from
me. He had initially tried cognitive-behavior therapy that focused
exclusively on his symptoms. He finally quit because he felt the
cognitive-behavior therapist was not helping. He told me that he had
repeatedly explained to this therapist that he was aware of how
ridiculous the cognitive distortions were, but the awareness of their
irrational nature did not help him change the thoughts.

He next went to a psychiatrist who offered to prescribe him
clomipramine. He read every piece of material he could get his hands
on regarding the medication but consistently refused to take it.
Because of his basic paranoid orientation toward the world, he was
convinced that the medication would somehow destroy him or at the
very least cause unmanageable side effects.

When he finally came to see me, I spent a good deal of time
working with him about his resistance to taking medication. I
observed that he seemed to be terribly concerned that his anger had
damaged his father. In response to that observation, he would
repeatedly assert that he was not, in fact, an angry person. His anger
would often escalate as he insisted on the notion that he had
transcended any problem with anger. Finally, after a good deal of
work on his paranoid character features, he agreed to take the
clomipramine. He took it for about 1 year at maximal therapeutic
doses but experienced no change whatsoever.

He then went through a period of months obsessing about whether
it would be advisable for him to try fluoxetine. He again read
extensively about fluoxetine and worked with me around his paranoid
ideas involving side effects. After a few months of discussing it, he
tried taking fluoxetine but felt that he was getting progressively worse
on it after 2 months and discontinued it.

Despite his lack of success with pharmacotherapy and cognitive-
behavior therapy, he did persist in his individual psychodynamic
therapy and gradually made gains in many areas of his life. While
his symptoms were manageable, they did not disappear. On the other
hand, his paranoid personality improved in a number of significant
ways. He became much less rigid and more open to entertaining ideas
that he had previously rejected. He became able to form a reasonably
trusting therapeutic alliance with me and, in association with that

218 GLEN O. GABBARD

trust, became much less hostile. He was also able to have a mutually
gratifying and meaningful sexual relationship with a woman, which
had previously been virtually unthinkable because of his paranoia.
He became much less isolated and formed other relationships as well.
He even began to return to work part time as his anxiety about his
OCD symptoms became less bothersome to him. In short, he had
made an adaptation to his symptoms that greatly enriched the quality
of his life.

Conclusions

These brief clinical illustrations point out the continued role of
psychoanalytically informed treatment with patients suffering from
obsessive-compulsive disorder. Regardless of the presence of
biological determinants that may generate OCD symptoms, these
symptoms nevertheless are rich in unconscious meaning that may
cause patients to be highly invested in maintaining their symptoms.
Psychodynamic understanding of the meaning of those symptoms
may be of enormous assistance in improving compliance with
pharmacotherapy or behavior therapy treatment programs.

OCD is an illness that fluctuates in its severity, and a dynamic
understanding of psychosocial triggers may assist in managing the
patient with OCD. For example, in the case of Mr. B, it became clear
that the onset of his symptoms was closely linked to concerns about
aggression toward others. In other patients, anxieties about injuring
children or babies may be contributory. In still others, sexual anxieties
may serve as a trigger.

The symptoms of OCD almost always have interpersonal meanings
that must be addressed. Biologically determined symptoms may serve
as the ideal vehicle to express psychodynamically based conflicts.
Hence, family members and others in significant relationships with
the patient may find themselves controlled and coerced into behaviors
that are highly dysfunctional. The transference–countertransference
dimensions of the treatment relationship with OCD patients may
provide a window into these recurring patterns that can be fruitfully
addressed as part of treatment.

The characterological features of individuals with OCD tend to
undermine treatment efforts in many cases. Confronting and
interpreting the characterological dimensions of the patient may have

TREATMENT OF OCD 219

a significant impact on the overall management of the patient.
Moreover, personality features of individuals with OCD may respond
dramatically to dynamic psychotherapy so that these patients can
lead much more gratifying lives. The case of Mr. B demonstrates an
instance in which the patient’s adjustment to life improved greatly
despite the fact that the OCD symptoms persisted.

Finally, we must be mindful that a certain percentage of patients
will respond to neither pharmacotherapy nor behavior therapy. A
psychodynamic treatment approach may be necessary to deal with a
treatment-refractory situation, even though the clinician must have
modest goals for the improvement of the symptoms per se. OCD
serves as a model illness to demonstrate the value of an integrated
a p p r o a c h t o t h e t r e a t m e n t o f m a j o r p s y c h i a t r i c d i s o r d e r s .
Psychodynamic strategies will continue to have a major role in
psychiatry as illustrated by the many ways in which psychodynamic
thinking is applicable to conditions such as OCD.

REFERENCES

Aubuschon, P. G. & Malatesta, V. J. (1994), Obsessive-compulsive patients with
comorbid personality disorder: Associated problems and response to a
comprehensive behavior therapy. J. Clin. Psychiat., 55:448–453.

Baer, L., Jenike, M. A., Ricciardi, J. N., Holland, A. D., Seymour, R. J., Minichiello
& W. E., Buttolph, M. L. (1990), Standardized assessment of personality disorders
in obsessive-compulsive disorder. Arch. Gen. Psychiat., 47:826–830.

Barlow, D. H. & Beck, J. G. (1984), The psychosocial treatment of anxiety disorders:
Current status, future directions. In: Psychotherapy Research: Where Are We and
Where Should We Go? ed. J. B. W. Williams & R. L. Spitzer. New York: Guilford,
pp. 29–69.

Baxter, L. R., Phelps, M. E., Mazziotta, J. C., Guze, B. H., Schwartz, J. M., Selin,
C. E. (1987), Local cerebral glucose metabolic rates in obsessive-compulsive
disorder: a comparison with rates in unipolar depression and in normal controls.
Arch. Gen. Psychiat., 44:211–218.

Black, A. (1974), The natural history of obsessional neurosis. In: Obsessional States,
ed. H. R. Beech. London: Methuen, pp. 19–54.

Buttolph, M. L. & Holland, A. D. (1990), Obsessive-compulsive disorders in
pregnancy and childbirth. In: Obsessive-Compulsive Disorders: Theory and
Management, ed. M. A. Jenike, L. Baer & W. E. Minichiello. Chicago, IL: Year
Book Medical, pp. 89–95.

Clomipramine Collaborative Study Group (1991), Clomipramine in the treatment
of patients with obsessive-compulsive disorder. Arch. Gen. Psychiat., 48:730–
738.

Elkins, R., Rapoport, J. L. & Libsky, A. (1980), Obsessive-compulsive disorder of
childhood and adolescence: A neurobiological viewpoint. J. Amer. Acad. Child
Psychiat., 19:511–524.

220 GLEN O. GABBARD

Freud, S. (1909), Notes upon a case of obsessional neurosis. Standard Edition,
10:155–318. London: Hogarth Press, 1955.

Gabbard, G. O. (1988), A contemporary perspective on psychoanalytically informed
hospital treatment. Hosp. Comm. Psychiat., 39:1291–1295.

 (1992), Psychodynamic psychiatry in the “decade of the brain.” Amer. J.
Psychiat., 149:991–998.

 (1994a), Mind and brain in psychiatric treatment. Bull. Menn. Clin., 58:427–
446.

, ed. (1994b), Psychodynamic Psychiatry in Clinical Practice: The Second
Edition. Washington, D.C., American Psychiatric Press.

Greist, J. H. & Jefferson, J. W. (1995), Obsessive-compulsive disorder. In:
Treatments of Psychiatric Disorders: The Second Edition. Washington, D.C.,
American Psychiatric Press, pp. 1625–1649.

Hollander, E., Schiffman, E., Cohen, B, Rivers-Stein, M. A., Rosen, W., Gorman,
J. M. & Fyer, A. J. (1990), Signs of central nervous system dysfunction in
obsessive-compulsive disorder. Arch. Gen. Psychiatry, 47:27–32.

Jenike, M. A., Baer, L. & Minichiello, W. E., eds. (1986), Obsessive-Compulsive
Disorders: Theory and Management. Littleton, MA: PSG Publishing Co.

Lieberman, J. (1984), Evidence for a biological hypothesis of obsessive-compulsive
disorder. Neuropsychobiology, 11:14–21.

Luxenberg, J. S., Friedlander, R. P., Rapoport, J., Swedo, S. E., Flament, M. R. &
Rapoport, S. I. (1988), Neuroanatomical abnormalities in obsessive-compulsive
disorder detected with quantitative X-ray computed tomography. Amer. J.
Psychiat., 145:1089–1093.

Malan, D. (1979), Individual Psychotherapy and the Science of Psychodynamics.
London: Butterworths.

Marks, I. M. (1981), Review of behavioral psychotherapy, I: Obsessive-compulsive
disorders. Amer. J. Psychiat., 138:584–592.

Mavissakalian, M. R., Jones, B. & Olson, S. (1990), Absence of placebo response
in obsessive-compulsive disorder. J. Nerv. Ment. Dis., 178:268–270.

McCullough, P. K. & Maltsberger, T. (1995), Obsessive-compulsive personality
disorder. In: Treatments of Psychiatric Disorders: The Second Edition.
Washington, DC: American Psychiatric Press, pp. 1851–1861.

Nemiah, J. C. (1988), Psychoneurotic disorders. In The New Harvard Guide to
Psychiatry, ed. A. M. Nicholi. Cambridge, MA: Belknap Press of Harvard
University Press, pp. 234–258.

Neziroglu, F., Anemone, R. & Yaryura-Tobias, J. A. (1992), Onset of obsessive-
compulsive disorder in pregnancy. Amer. J. Psychiat., 149:947–950.

Perse, T. (1988), Obsessive-compulsive disorder: A treatment review. J. Clin.
Psychiat., 49:48–55.

Pitman, R. K. & Jenike, M. A. (1989), Normal and disordered compulsivity:
Evidence against a continuum. J. Clin. Psychiat., 50:450–452.

Rapoport, J. L., Ryland, D. H. & Kriete, M. (1992), Drug treatment of canine acral
lick: an animal model of obsessive-compulsive disorder. Arch. Gen. Psychiat.,
49:517–521.

Rasmussen, S. A. & Eisen, J. L. (1989), Clinical features and phenomenology of
obsessive-compulsive disorder. Psychiatric Annals, 19:67–73.

Stein, D. J. & Hollander, E. (1993), The spectrum of obsessive-compulsive related
disorders. In: Obsessive-Compulsive Related Disorders, ed. E. Hollander.
Washington, DC: American Psychiatric Press, pp. 241–270.

TREATMENT OF OCD 221

Swedo, S. E., Cheslow, D. L., Leonard, H. L., Kumar, A., Friedland, R., Shapiro,
M. B. & Grady, C. L. (1989), Cerebral glucose metabolism in childhood-onset
obsessive-compulsive disorder. Arch. Gen. Psychiat., 46:518–523.

Turner, S. M., Biedel, D. C. & Nathan, R. S. (1985), Biological factors in obsessive-
compulsive disorder. Psychol. Bull., 97:430–450.

Zetin, M. & Kramer, M. A. (1992), Obsessive-compulsive disorder. Hosp. Comm.
Psychiat., 43:689–699.

Zetzel, E. R. (1970), The Capacity for Emotional Growth. New York: International
Universities Press.

The Menninger Clinic
P.O. Box 829
5800 SW 6th Avenue
Topeka, KS 66601-0829

Copyright of Psychoanalytic Inquiry is the property of Taylor & Francis Ltd and its content may not be copied

or emailed to multiple sites or posted to a listserv without the copyright holder’s express written permission.

However, users may print, download, or email articles for individual use.

error: Content is protected !!