Asian Journal of Psychiatry 3 (2010) 177–185

Contents lists available at ScienceDirect

Asian Journal of Psychiatry

journal homepage: www.elsevier.com/locate/ajp

Instinctual impulses in obsessive compulsive disorder: A neuropsychological

and psychoanalytic interface
Pritha Mukhopadhyay a,*, Sreemoyee Tarafder b, Dinaz D. Bilimoria c, Debika Paul d,
Gautam Bandyopadhyay e
a
Department of Psychology, University of Calcutta, India
b
Department of Psychology, West Bengal State University, India
c
Department of Psychology, Loreto College, University of Calcutta, India
d
Department of Psychology, University of Calcutta, India
e
Department of Psychiatry, R. G. Kar Medical College and Hospital, Kolkata, India

A R T I C L E I N F O A B S T R A C T

Article history: Psychopathology of obsessive compulsive disorder (OCD) that has been characterized by a conflict
Received 4 August 2009 between the ego and superego on one hand, and aggressive and sexual impulses emerging from the id on
Received in revised form 18 September 2010 the other, and employment of characteristic defenses to combat intense conflicts being connected with
Accepted 10 October 2010
ones’ biological disposition from the psychoanalytic school of thought now gets empirical foundation
from neuroimaging research. The findings disregard the psychological construct, exclusively establish-
Keywords: ing the neurobiology of the disorder. With the objective to study the impact of sexual and aggressive
Obsessive–compulsive disorder
impulses on the executive functions and processing speed in the patient group, 20 OCD patients (11
Sexual impulses
Aggressive impulses
males, 9 females) and 20 normal control subjects, matched for all relevant variables including age, sex,
Executive function educational level and handedness were studied. Sexual impulse and guilt was assessed on the Sex Guilt
Processing speed Rating Scale (SGRS), aggressive impulses were tested using State-Trait Anger Expression Inventory
Neuropsychology (STAXI), the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) was used to assess symptom severity,
executive functions were assessed through Wisconsin Card Sorting Test (WCST), and processing speed
was assessed by employing the Processing Speed Index (PSI) – from WAIS III. It was found that the OCD
group differed significantly from the controls, attaining significantly lower percentiles on Processing
Speed Index and for all variables of WCST under consideration, namely, perseverative response,
perseverative error, non-perseverative error, conceptual level response and number of categories
completed. They reported higher scores on subscales of STAXI, specifically related to trait anger and
lower scores on anger expression. On the items of SGRS, the OCD group significantly differed with the
controls, expressing greater sexual inhibition. In conclusion, we propose an explanation of
psychopathology of OCD, which addresses instinctual impulses, executive functions and neural
substrates. Our findings contribute to understanding instinctual impulses from the neuropsychological
perspective. The findings have implications for better eclectic understanding of the pathogenesis of OCD.
ß 2010 Elsevier B.V. All rights reserved.

1. Introduction
In 1909, psychoanalytic notions about obsessional neurosis
(later known as obsessive compulsive disorder) were delineated
with Freud’s publication of the remarkable Rat Man case. Fenichel
in 1945 concisely explained psychopathology of Obsessive
Compulsive Disorder (OCD) to be characterized by a conflict
* Corresponding author. Mailing address: Department of Psychology, UCSTA, 92,
A.P.C. Road, Kolkata 700009, West Bengal, India. Tel.: +91 943 333 1666.
E-mail addresses: pritha_m2@yahoo.com, prithamukhopadhyay@gmail.com
(P. Mukhopadhyay).
between the ego and superego on one hand, and aggressive and
sexual impulses emerging from the id on the other (Fenichel,
1945). The concept has received considerable attention in
psychoanalytic literature since a very early date (Abraham,
1924; Freud, 1909/1955; Fenichel, 1945; Nagera, 1978) and
continues to be relevant in the treatment of OCD from
psychodynamically oriented therapeutic approaches (Chessick,
2001; Esman, 1989, 2001; Gabbard, 2001; Salzman, 1980; Shapiro,
1965, 2001). The OCD symptom has been regarded as the
manifestation of the struggle of the ego against the intolerable
impulses and a ‘‘severe’’, ‘‘unkind’’ (Freud, 1926), ‘‘archaic’’
(Weissman, 1954) or ‘‘hypermoral’’ superego (Fenichel, 1945);
Kempke and Luyten (2007) have aptly pointed out that the ensuing

1876-2018/$ – see front matter ß 2010 Elsevier B.V. All rights reserved.
doi:10.1016/j.ajp.2010.10.002
178 P. Mukhopadhyay et al. / Asian Journal of Psychiatry 3 (2010) 177–185
conscientiousness and perfectionism in the obsessive character are
perhaps attempts to control the warded-off aggressive and sexual
wishes.
Classical psychoanalytic views also hypothesize basic ambiva-
lence in obsessive–compulsive neurosis to be caused by a
tyrannical superego coupled with high levels of aggression
(Kempke and Luyten, 2007). Referring to relevant literature (Blatt
and Shichman, 1983; Kernberg, 1984; McWilliams, 1994) in their
critically reviewed article, Kempke and Luyten (2007) have also
mentioned that the severe superego is thought to result from
identification with critical and demanding significant others, while
the high levels of aggression are considered to be partly inborn and
partly the manifestation of an excessive repression of anger.
Esman (2001) in his review considers Freud’s dynamic concept
of obsession (1909), which involves the regression from unre-
solved oedipal conflicts to pre-genital anal-sadistic level, when
genital sexual organization had to be relinquished. He further
pointed out to the Freud’s (1913) proposition of pregenital
organization of the libido to be determined primarily by
constitutional rather than experiential factors which has later been
resonated by Freud (1966) as determinant of ‘‘intensity of the anal-
sadistic tendencies’’, and the ‘‘preference’’ for the characteristic
defense mechanisms, as well. The emphasis on constitutional
factors links OCD to one’s biological disposition.
Extensive progress made in the fields of neurobiology, neuro-
psychology and neuroimagery, has not only revolutionalized the
understanding of OCD but has also led to the neurobiological
conceptualization of the same (Chamberlain and Menzies, 2009). As
a matter of fact, Freud’s depiction of obsessive–compulsive neurosis
has been found to have parallels in recent psychobiological theories
of OCD (Katz, 1991; Brito, 2002). Katz hypothesized that serotoner-
gic processes acted as filters or suppressors of aggressive or libidinal
impulses, and since OCD patients and violent suicide attempters are
often reported to have reduced levels of serotonin in the central
nervous system, he suggested that Freudian repression is dependent
on serotonergic mechanisms. Brito (2002), however, disagreed with
the claim that serotonergic system in isolation could represent the
neurobiological basis of repression, hypothesizing the operation of
the circuitry involving the frontal cortex, hippocampus, and the
brainstem rather than only the brainstem (where serotonergic
neurons are located) as originally envisaged by Katz. According to
the model proposed by Brito, as primitive forms of behaviour are
thought to be organized in the brainstem, the neurobiological basis
of regression, he claims, could involve an imbalance in the activity of
cortico-subcortical processes such that activity in subcortical
structures overwhelms activity in cortical structures. Owing to
the emotional salience of regressive phenomena, it presumably
involves amygdalo-hippocampal circuitry in addition to cortical and
brainstem processes (Brito, 2002).
These theoretical hypotheses may well be corroborated with
neurobiological findings from the new brain imaging studies,
particularly PET-scanning. Taken together, neuroimaging studies
indicate that OCD symptoms are mediated by hyperactivity in
orbitofrontalsubcortical circuits, which may be attributable to an
imbalance of tone between direct and indirect striato-pallidal
pathways (Saxena et al., 1998a,b, 2001). The caudate nucleus,
although less consistently implicated, has been found in several
studies to demonstrate pre-treatment abnormalities (Baxter,
1992; Whiteside et al., 2004). Most recent studies now implicate
the prefrontal cortex (orbitofrontal and cingulate), the basal
ganglia and the thalamus to the pathogenesis of OCD (Pena-Garijo
et al., 2010). Rauch and Jenike (1993), however, state that it is not
clear whether the observed neurobiological deviations cause or
develop as a consequence of the disorder.
The present paper is an attempt to converge the psychodynamic
and neurobiological approaches of understanding OCD in the
context of empirical neuropsychological findings. It endeavours to
investigate the impact of instinctual impulses of sex and
aggression on performance of higher cognitive tasks, i.e., on
executive functions.
2. Methods
2.1. Sample and study design
The study comprised of two groups and was cross-sectional
with a case–control design. A clinical sample (n = 20, male = 11,
female = 9, age mean = 30.7 years, S.D.  7.98 years right handed,
urban, with at least Standard VIII education) of patients with a
diagnosis of Obsessive–Compulsive Disorder without co-morbidity as
per ICD 10 Criteria (F42) onset of illness at 17 years or later, was
selected from psychiatric services of R. G. Kar Medical College and
Hospital, Kolkata, India. A diagnosis of OCD was made through a
detailed clinical examination by trained clinical psychologists, using
semi-structured case record format used at the Department of
Psychology, University of Calcutta. The diagnosis was independently
confirmed by the consultant psychiatrist at R. G. Kar Medical College
and Hospital.
Patients with age of onset earlier than 12 years were excluded
to minimize the heterogeneity of the OCD sample, as childhood
onset OCD is purported to be a neurodevelopmental subtype of
OCD (Geller et al., 2001; Jaisoorya et al., 2003) with different
neurobiological mechanisms from those with late onset OCD (Roth
et al., 2005). Upper age-limit of the patients was restricted to 45
years, to avoid age related changes that may interfere with
assessment of cognitive functions. Patients with history of other
anxiety disorders, psychosis, bipolar disorder, or current psycho-
active substance dependence, were excluded. A total of 20 patients
fulfilled the study criteria. Patients with all varieties of obsessions
and compulsion were included with the exception of hoarding
(comprising subgroups with aggressive/somatic obsessions with
checking compulsions = 7; contamination obsession with wash-
ing/cleaning compulsions = 8; sexual and religious obsessions = 5).
Exclusion criteria included lifetime diagnosis of schizophrenia,
bipolar affective disorder, tic disorder, and substance misuse.
Patients with diagnosis of OCD with comorbid conditions other
than depression were excluded. Severity of depression was
assessed using clinician rated Hamilton Depression Rating Scale
(HDRS) (Hamilton, 1960) and patients whose scores were greater
than 8 were excluded. Organic brain disorder, neurological
disorders, or any sensory impairment was not included. Handed-
ness, which is extremely relevant in terms of neuropsychological
assessment, was determined with the 10-item Edinburgh Hand-
edness Inventory (Oldfield, 1971) and only right-handed individ-
uals were included. The demographic and clinical characteristics of
the participants are shown in Table 1.
A community sample (n = 20, age mean = 30.8 years, S.D.  7.17
years) that matched the OCD patients in terms of age, sex, educational
level, handedness, religion and mother tongue was selected through
the snowballing technique and screened on the General Health
Questionnaire (GHQ; Goldberg and Miller, 1979). Participants scoring
above the cut off value of 4 were excluded. Exclusion criteria also
included evidence of organic brain disorder/neurological disorder,
and sensory impairment. They also had no family history of major
psychiatric illnesses (psychosis, affective disorder, OCD, suicide or
alcohol and substance misuse) in a first-degree relative confirmed by
history obtained from the control subject.
The participants responded to Yale-Brown Obsessive Compul-
sive Scale, Sexual Guilt Rating Scale, State Trait Anger Expression
Inventory, Wisconsin Card Sorting Test along with Symbol Search
and Coding subtests from Wechsler Adult Intelligence Scale III that
comprised the Processing Speed Index. After describing the
 P. Mukhopadhyay et al. / Asian Journal of Psychiatry 3 (2010) 177–185 179

Table 1 feelings. Items consist of 4-point scales that assess intensity of

Socio demographic description of the sample.
anger at a particular moment and the frequency of anger
Category Clinical sample Community control experience, expression, and control.
(n = 20) (n = 20)  Sex-Guilt Rating Scale (SGRS) developed by Paul (2004), is a 20-
Age (yrs) item Likert type scale which was used to determine feelings of
Mean 30.7 30.8 guilt and inhibition related to sexuality, reflecting either a
S.D. 7.98 7.17 mature or immature conceptualization of sex.
n % n %
Sex
Male 11 55 11 55 2.3. Statistical analysis
Female 9 45 9 45
Education (yrs) The data were tested for normative distribution using the
8–12 8 40 8 40 Levene’s test. Since most of the neuropsychological variables were
13–15 8 40 8 40
16–18 4 20 4 20
not normatively distributed, non-parametric analysis was carried
Occupation out. Mann–Whitney U test was used to assess the differences
Unemployed 2 10 0 between patients and their control counterparts. Spearman’s
Student 5 25 7 35 correlation analysis was employed to examine the relationship
House wife 6 30 6 30
between the scores on neuropsychological tests and variables
Service 5 25 5 25
Self-employed 2 10 2 10 related to aggression and sexuality, separately for the clinical
Marital status sample and the normative sample. Stepwise regression analysis
Single 9 45 11 55 was carried out to demarcate potential explanatory variables and
Married 11 55 9 45 draw conclusions about the impact of instinctual impulses on
executive functions. In this form of regression, a variable is added
as long as its addition contributes a positive increase in the R-
purpose of the study to the subjects, informed consent was square value of the model; i.e., as long as it meets the critical value
obtained. All measures were individually administered and the of the test. The critical value required for significance was set at
order of administration was kept constant. 0.05 level. Statistical Package for Social Sciences (SPSS) version
13.0 was used for analyses and all reported p values are two-tailed.
2.2. Measures
3. Results
 Yale-Brown Obsessive Compulsive Scale (Y-BOCS), a 10-item
clinician-administered scale, is a widely used rating scale to 3.1. Socio-demographic description of the sample
measure symptom severity of OCD designed by Goodman et al.
(1989). It is used extensively in research and clinical practice to The two groups were comparable in terms of age, sex, and years
determine both severity of OCD and to monitor improvement of education. The symptom severity in the clinical group, as
during treatment. This scale, which measures obsessions assessed on YBOCS, ranged from 10 to 40, with the mean being 22
separately from compulsions, specifically measures the severity which falls within moderate range. Duration of illness ranged from
of symptoms of OCD without being biased towards the type of 2 to 10 years. The socio-demographic details of the two groups are
obsessions or compulsions present. It has two general sections – provided below in Table 1.
an obsession rating scale and a compulsion rating scale.
 Wisconsin Card Sorting Test (WCST) was originally developed to 3.2. Group differences between OCD and normal controls
assess abstract reasoning ability and the ability to shift cognitive
strategies in response to changing environment contingencies The clinical group scored significantly higher on YBOCS (u = 001;
(Berg, 1948). The WCST can be considered a measure of ‘executive p < 0.01). The OCD group attained significantly lower percentiles on
function’, requiring the ability to develop and maintain an PSI (u = 17.00; p < 0.01); and all variables of the WCST under
appropriate problem-solving strategy across changing stimulus consideration, namely, perseverative response (PR) (u = 0.40;
conditions in order to achieve a future goal (Luria, 1973; Shallice, p < 0.01); perseverative error (PE) (u = 7.50; p < 0.01); non-persev-
1982). Similar to other measures of executive function, the WCST erative error (NPE) (u = 9.50; p < 0.01); conceptual level response
requires strategic planning, organized searching, utilizing envi- (CLR) (u = 9.00; p < 0.01) and number of categories completed
ronmental feedback, shifting cognitive sets, directing behaviour (NOCC) (u = 95.00; p < 0.01). They reported higher scores on
toward achieving a goal and modulating impulsive responding. subscales of STAXI, specifically related to trait anger (T-Anger and
However, unlike other measures of abstract reasoning, the WCST T/r Anger) (u = 88.00; p < 0.01 and u = 73.00; p < 0.01); and lower
provides objective scores not only of overall success, but also for scores on anger expression (u = 129.00; p < 0.05). On the items of
specific sources of difficulty on the task (e.g., inefficient initial SGRS, the study group significantly differed with the controls on
conceptualization, failure to maintain cognitive set, perseveration three statements: SGRS1 (‘‘Sitting beside a person of opposite sex
and inefficient learning across stages of the test.) while travelling by bus is problematic’’), SGRS14 (‘‘One should not
 Processing Speed Index (PSI) from Wechsler Adult Intelligence think about physical intimacy’’) and SGRS20 (‘‘Boys and girls
Scale III (WAIS III) (Wechsler, 1997). The PSI includes two tests – should maintain a safe distance from each other’’), expressing
(i) Symbol Search: which assesses visual perception and speed greater sexual inhibition. The findings are elaborated in Table 2.
and (ii) Coding: which assesses visuo-motor co-ordination, and
motor and mental speed. 3.3. Correlations between instinctual impulses and executive
 State-Trait Anger Expression Inventory (STAXI) developed by functions in clinical sample
Spielberger (1991) is a 44-item inventory which measures the
intensity of anger as an emotional state (State Anger) and the In the clinical sample, significant positive correlation was seen
disposition to experience angry feelings as a personality trait between symptom severity and anger control (AX CON on STAXI)
(Trait Anger). The instrument consists of six scales measuring the and negatively scored items reflecting inhibited sexuality, indicating
intensity of anger and the disposition to experience angry that excessive control of aggression and narrow and stereotypical
180 P. Mukhopadhyay et al. / Asian Journal of Psychiatry 3 (2010) 177–185

Table 2
Comparison of scores of the two groups on YBOCS, WCST, PSI, STAXI and SGRS.

Domains assessed Clinical (n = 20) Community control (n = 20) U-Value p

*
p < 0.05
**
Mean SD Mean SD p < 0.01

YBOCS 21.75 9.89 0.4 0.68 .001 .001**

PR 14.9 23.95 113.55 26.02 0.40 .001**
PE 15.45 25.86 112.1 31.76 7.50 .001**
NPE 36.55 30.51 102.4 10.21 9.50 .001**
CLR 18.9 24.13 92.4 20.71 9.00 .001**
NOCC 3.35 2.25 5.45 0.76 95.00 .001**
PSI 70.95 19.21 98.2 11.51 17.00 .001**
S-Anger 13.6 4.88 12.1 2.94 172.50 .461
T-Anger 22.95 5.93 16.4 5.08 88.00 .002**
T/t Anger 8.7 3.54 6.75 2.49 132.50 .068
T/r Anger 10.8 3.16 6.95 2.68 73.00 .001**
AX/IN 19.15 2.85 19.85 2.56 170.00 .429
AX/OUT 18.9 3.21 21.35 3.86 133.50 .072
AXCON 19.5 2.5 19.7 2.39 189.50 .779
AX/EX 34.55 3.35 37.4 4.26 129.00 .053*
SGRS 1 2.35 0.93 3 0.65 120.00 .030*
SGRS 2 3.1 0.79 3.35 0.49 170.50 .429
SGRS 3 2.6 0.99 2.35 0.93 168.50 .398
SGRS 4 3 1.08 3.35 0.60 144.50 .134
SGRS 5 2.5 0.99 1.95 0.22 188.00 .758
SGRS 6 2.2 0.89 2.05 0.22 187.00 .738
SGRS 7 3.1 0.85 3 0.92 186.00 .718
SGRS 8 2.7 1.13 2.9 0.79 180.00 .602
SGRS 9 2.3 1.13 2.6 0.68 154.00 .221
SGRS 10 2 0.97 1.9 0.55 193.00 .862
SGRS 11 2.2 1.06 1.7 0.47 151.00 .192
SGRS 12 2.15 0.99 1.65 0.59 144.00 .134
SGRS 13 3.35 0.99 3.65 0.49 179.50 .583
SGRS 14 2.7 1.08 1.65 0.93 92.50 .002**
SGRS 15 1.45 0.51 1.65 0.49 160.00 .289
SGRS 16 3.5 0.69 3.6 0.50 192.00 .841
SGRS 17 2.1 0.85 2.1 0.68 193.00 .862
SGRS 18 1.8 0.77 1.85 0.99 195.00 .904
SGRS 19 1.6 0.75 1.4 0.5 176.00 .529
SGRS 20 2.8 0.95 1.85 0.67 88.50 .002**
*
p < 0.05.
**
p < 0.01.

conceptualization of sexuality may be directly related to severity of
OCD. Trait anger domains (T-Anger and T/t Anger) and anger control
as assessed on STAXI were found to be negatively correlated to
conceptual level responses and perseverative errors, signifying that
trait anger and anger control are inversely correlated to set shifting.
Items pertaining to sexual guilt were found to be inversely
correlated to set-shifting and cognitive flexibility (reflected through
NOCC and NPE). Perseverative responses, on the other hand were
found to be directly correlated to stereotypical conceptualization of
sexuality. The findings are detailed in Table 3 as follows.
3.4. Correlations between instinctual impulses and executive
functions in control sample
In the control group, unlike the clinical sample, there was no
correlation observed between the neuropsychological test scores
and domains of aggression. However, similar findings were
obtained in the control group with respect to perseverative
responses, which were found to be directly correlated to
stereotypical conceptualization of sexuality. Reverse correlation
was seen between items reflecting inhibited sexuality and NPE,
indicating that narrow and stereotypical conceptualization of
sexuality may be inversely correlated to random trial and error
response pattern during set-shifting. Similar to the clinical group,
the control group also reflected inverse correlation between items
pertaining to sexual guilt and cognitive flexibility, reflected
through categories completed on the WCST. The findings are
detailed in Table 4 as follows.
3.5. Impact of instinctual impulses on executive functions in the
sample
Step-wise Multiple Regression Analysis was computed sepa-
rately for both the clinical and control group. In the clinical group it

Table 3
Correlations between scores on YBOCS and WCST and STAXI and SGRS in the clinical sample.

Correlated variables T anger T/t anger Ax con SGRS 2 SGRS 8 SGRS 11 SGRS 13 SGRS 16 SGRS 18 SGRS 19

YBOCS .600* .498* .531** .667**

PR .471*
PE .490*
NPE .591**
CLR .521* .449* .516*
NOCC .528** .492* .705**
*
p < 0.05.
**
p < 0.01.
 P. Mukhopadhyay et al. / Asian Journal of Psychiatry 3 (2010) 177–185 181

Table 4
Correlations between scores on YBOCS and WCST and STAXI and SGRS in the control group.

Correlated variables SGRS 2 SGRS 3 SGRS 4 SGRS 7 SGRS 8 SGRS 13 SGRS 18 SGRS 19
*
PR .471
NPE .539* .501* .453* .534*
* * **
NOCC .528 .492 .705
*
p < 0.05.
**
p < 0.01.

Table 5
Step-wise Multiple Regression Analyses between the independent variables (instinctual impulses) and the dependent variables (neuropsychological domains) in both the
groups.

Sample Dependent variable Predictors Adjusted R2 Std. error of estimate

OCD group PSI SGRS16 0.216 17.0011

SGRS16 + SGRS20 0.363 15.3319
CLR AXCON 0.233 21.1353

Control group PR SGRS18 0.233 22.7836

NPE SGRS3 0.259 8.7907
SGRS3 + SGRS5 0.467 7.4545
SGRS3 + SGRS5 + T-Anger R/R 0.604 6.4222
SGRS3 + SGRS5 + T-Anger R/R + SGRS12 0.786 4.7232
CLR SGRS4 0.219 18.3094
NOCC SGRS3 0.165 0.6938

was observed that processing speed was predicted to the extent of
36% by combining two items of the SGRS, and aggression control
predicted conceptual responses by 23%. The nature of the
predictions was quite different in the control group. Perseverative
responses, conceptual responses and categories completed were
predicted to the extent of 23%, 22% and 16% respectively by items
of SGRS. Sexual guilt revealing statements in combination with a
domain of trait anger predicted NPEs to the extent of 79%. The
findings are tabulated in Table 5.
4. Discussion
4.1. Group differences between OCD and normal controls in terms of
set-shifting capacity
Impairment in set-shifting capacity in the OCD, as is evident
from the results of perseveration (PE and PR; Table 2) and number
of category completion (NOCC; Table 2) on Wisconsin Card Sorting
Test (WCST), indicates their poor feedback utilization capacity,
which is in conformity with previous research reports (Boone et al.,
1991; Christensen et al., 1992; Lucey et al., 1997; Tarafder et al.,
2006; Olley et al., 2007; Moritz et al., 2009). Their failure to attain
category completion is an indication of their difficulty in concept
attainment, hypothesis testing and cognitive flexibility. Im-
pairment of set-shifting capacity in OCD is an index of their
difficulty in making decisions regarding response selection
(Aycicegi et al., 2003) and shifting of attention (Okasha et al.,
2000; Veale et al., 1996), which may be considered to be an
increased function of underlying neural substrate of caudate
nucleus in consonance with anterior cingulate and orbito frontal
cortices (OFC) (Arciniegas and Beresford, 2001). Dysregulation in
OFC in OCD has been reported by Saxena et al. (1998b), Friedlander
and Desrocher (2006).
In contrast to normal controls, in whom strategy based on trial
and error method on WCST is a search for the way to shift between
sets utilizing the provided feedback, greater NPE in the OCD
indicates their restricted response selection which perhaps blocks
their way to select appropriate response to attain a new category.
Inference may be drawn on the basis of the evidence that execution
of a novel response as well as improvement of ongoing
performance is a result of utilization of feedback to one’s response
when the stimulus – response task is based on trial and error
mechanism (Mc.Donald and White, 1994). Increased NPE in the
OCD, therefore, could also be explained as the error in feedback
utilization, resulting in poor response selection, and culminating in
poor conceptual level response and poor category completion. Poor
conceptual level response in OCD further signifies that their
psychopathology is most likely to prevent them from developing
an effective strategy to deal with the task, which seems to be the
function of the Dorso Lateral Pre Frontal Cortex (Goldstein et al.,
2004; Haut et al., 1996; Stuss et al., 2000) in conjunction with other
cortical, subcortical and cerebellar regions (Mukhopadhyay et al.,
2008) of the brain.
4.2. Group differences between OCD and normal controls in terms of
processing speed
Taking into consideration the PSI, their slowness observed in
this study could be attributed to their quest for perfectionism
(Rhéaume et al., 1995; Lee et al., 2009). It is evident as well from
our observation of their test behaviour during digit symbol task,
where they took a lot of care in copying the symbols, concentrating
on accuracy, and compromising upon the speed aspect in order to
complete the task within the specified period of time. Impairment
in processing speed in OCD is explicable with the psychopathology
of obsessive slowness and may be attributed to their characteristic
ambivalence (Fenichel, 1945). The ambivalence may be attribut-
able to shallow processing of information regarding the given
stimulus, which causes a continual conflict in decision making
(here, symbol to be selected as right or wrong) due to inability to
keep action plan in memory (Kuelz et al., 2004) which gets
reflected in delayed response selection.
The accuracy aspect of the task dubbed as maladaptive
perfectionism (Moretz and McKay, 2009) was so prioritized by
the OCD that their scanning was restricted to the task-demand of
accuracy alone without consideration of the time factor. Their
overemphasis of the accuracy aspect perhaps symbolically
strengthens their schemata of compliance by giving extra effort
and time towards accuracy, which perhaps delays the fronto-
striatal function for motor execution of the task.
182 P. Mukhopadhyay et al. / Asian Journal of Psychiatry 3 (2010) 177–185
It may be inferred that non-conformity to rule would
supposedly induce guilt in OCD, the deficit in the OCD to respond
to feedback from the examiner regarding enhancement of speed
could be so guilt arousing that they might defensively deny the
time aspect of the instruction, which not only serves as an avenue
to release their aggression passively, but also reduces apparent
feelings of guilt in them.
This may be understood considering their setting of an internal
rule to which they conform, thereby, disregarding the external rule
is not appraised as non-conformity. Such rigidity and a strong need
for control and autonomy result in anal character traits in them
(Blatt and Shichman, 1983; Shapiro, 1965). Since they prioritize the
bottom-up processing through assimilation, they accept it only
when that set of data is congruent with their existing cognitive
structure or prevailing set. This, in turn, strengthens their set to act
upon conceptually driven but rigid top-down mechanism, ignoring
the environmental demand or feedback, which ultimately becomes
ego-syntonic in nature. Presumably, maintenance of their slow-
ness without any guilt in their life situation subsequently makes it
their character trait. The finding of slowness may be corroborated
with recent reports of bradykinesia to be correlated with mental
slowness and nonverbal performance impairment in OCD support-
ing the possibility of dysfunction of basal ganglia in OCD patients
(Pasquini et al., 2009).
The slowness also can be explained by their inability to change
the focus of attention (Martı́nez-González and Piqueras-Rodrı́guez,
2008), making it likely that they prioritize serial processing,
evident from focusing their attention onto one aspect of the task
(accuracy), with their failure to handle both the aspects of the task
(i.e., speed and accuracy) simultaneously, which again may
underlie their cognitive inflexibility.
4.3. Group differences between OCD and normal controls in terms of
aggressive instincts
With respect to the aggressive instincts, OCD shows higher
predisposition of trait anger (T-Anger) with significantly higher
sensitivity for aggression and impulsivity (T/r Anger) and lower
anger expression (AX/EX). Several studies have noted that
individuals with both clinical and subclinical levels of OCD report
elevated levels of anger compared with individuals without an
anxiety disorder (Rubenstein et al., 1995; Spinella, 2005; White-
side and Abramowitz, 2005) which is consistent with our findings.
The results may also be corroborated with research reports by
Radomsky et al. (2007) who found greater T-Anger but lower anger
expression, among OCD checkers than the student control group.
The anger expression score in the OCD group under consideration
in our study, being significantly lower than the controls coupled
with their equal status with normal on anger control (on STAXI),
suggests their excessive exertion of anti-cathexis force to prevent
the expression of anger. The finding gets strength from earlier
observations that OCD patients have strongly repressed aggressive
impulses, while normal individuals develop less maladaptive ways
of dealing with these impulses (Kempke and Luyten, 2007).
Due to fear of being aggressed upon by the authority figure, the
perception of environment as punitive (Fenichel, 1945) results in a
predisposition for narrowed response selection. It makes
responses, which would not generate any punitive consequences
that may be considered to be detrimental to one’s survival, highly
predictable. Perhaps this apprehension causes one not to produce
any novel, experimental or divergent responses which could
possibly lead to negative consequences, resulting in repetitive
cognitive or motor behaviour owing to deficit in learning of gating
and recombining divergent information of intermediary level at an
output layer (Graybiel and Saka, 2004; Parthsarathy and Graybiel,
1997). The pathology is restricted to inflexible thought or action-
reflected in perseverative responses which makes the striatum
rigidly follow a specific modular pattern of neuronal activation
based upon the information coming from within (Saka and
Graybiel, 2003).
4.4. Group differences between OCD and normal controls in terms of
sexual instincts
Regarding sexual impulse, their significantly higher scores on
few items of the SGRS indicates the over-sensitivity of the OCD to
the items that contains even a mild indication of man–woman
relationship which is within the range of social acceptability. This
can well be understood from the fact that forbidden thoughts
regarding aggression and sexuality emerged as one of the four
significant factors in a meta-analysis of the symptom structure of
OCD including 21 studies which involved 5124 participants (Bloch
et al., 2008). Our findings are also in agreement with research
reports of sexual obsessions being fairly common among
individuals with OCD (Grant et al., 2006).
4.5. Association between symptom severity, instinctual impulses and
executive functions
Symptom severity (as assessed on YBOCS) being significantly
correlated with aggression control (AX Con on STAXI) and three
statements related to sexuality (SGRS 16, SGRS 18, SGRS 19) (Table
3), reiterates the high degree of association between maladaptive
control over both sexual and aggressive impulses exerted by the
OCD group. The findings go hand in hand with previous reports of
positive correlations between contamination fear from sexual
activity and the severity of OCD symptoms (Abbey et al., 2007).
Association of the instinctual impulses with the perseverative
response in the OCD group might be attributed to the ability of
forbidden sexual and hostile thoughts to occupy Memory space,
with minimum chances of the same to get expressed or
acknowledged by the patient due to its capacity to arouse guilt.
They do not acknowledge their T-Anger because of a desire to
portray to others that they are docile by nature and do not lose
control over anger. This is consistent with clinical reports that
individuals diagnosed with OCD are often preoccupied with how
others perceive them (Newth and Rachman, 2001).
4.6. Impact of instinctual impulses on executive functions
Impact of items pertaining to sexuality on processing speed in
the OCD group (Table 5) may be associated with Brito’s (2002)
assumption that the activity of cerebral structures associated with
cortex and striatum overrides the activity of cerebral structures
associated with limbic-subcortex. This regression of sexual
impulses on the variance of conceptual responses of the OCD
substantiates the potency of the dysfunctional preoccupation to
interfere with the executive function by occupying the working
memory-space and preventing the same from acting upon the
relevant task.
4.6.1. A neuropsychological and psychoanalytic interface
The preoccupation of the patients of OCD with unresolved ego-
dystonic intrusive instinctual thoughts explains the dysexecution
in organizing and processing new thoughts giving rise to
perseveration, as one’s attentional system is occupied by the
aforementioned potent thoughts which necessitates the continu-
ous exertion of anticathexis force to ward off the thoughts from
consciousness. This observation is in conformity with the previous
research report (Mukhopadhyay et al., 2006) that claims that
obsessive thoughts predict one’s deficit in the set shifting aspect of
executive function. Psychopathology formulation of OCD from the
[()TD$FIG] P. Mukhopadhyay et al. / Asian Journal of Psychiatry 3 (2010) 177–185 183

Forbidden Thoughts of Inability to Modulate

Sexuality Hostile Thoughts

Unresolved Ego-Dystonic
Intrusive Instinctual
Thoughts

Continuous exertion of Anticathexis

Force to ward off the thoughts from
Consciousness.

Preoccupation of Attentional System

with Potent Instinctual Thoughts

Inadequate Resources available in

Working Memory Space

Rigid Response Selection

Dysexecution in Organising and

Processing new thoughts

Perseveration Slowness

Fig. 1.

dynamic perspective focuses upon the inability of the obsessional
subject to express their own will against superior hostile forces
directly, making one learn to express hostility through stubborn-
ness (Fenichel, 1945). Although it apparently helps them to vent
out anger, this display of passive aggression perhaps does not help
to absolve the feeling of guilt in them. Consequently, this
resistance against superior forces, perhaps being guilt-arousing
in the unconscious, later results in a continual struggle with their
own superego (Fenichel, 1945). Since the conflict is significant, the
attentional resources, out of their own accord focus onto it, which
perhaps causes reverberation of the same in the available working
memory space.
Thus OCD, being the disorder of response selection, perhaps is
associated with increased activity in the caudate nucleus, cingulate
and orbitofrontal cortices (Graybiel and Rauch, 2000; Graybiel and
Saka, 2004), culminating in an imbalance between the direct
striatopallidal pathway responsible for selection of a given
response and concurrent suppression of unwanted response via
indirect pathways (Arciniegas and Beresford, 2001), behaviourally
being manifested as ‘slowness’ in their pathology.
Considering the psychopatholgy of OCD, it may be stated that
behaviour selection can be influenced by one’s own experience,
which being mediated by the striatum, activates the rest of the
basal ganglia to participate strongly in the control of motor and
cognitive behaviours to meet the adaptive demand of the
environment (Graybiel et al., 1994). Maintaining relevance to this
formulation, the narrow response selection in the OCD, owing to
early experience of being dominated upon by powerful others,
possibly acts through the striatum (Saka and Graybiel, 2003) in
activating rest of the basal ganglia to participate strongly in the
control of motor and cognitive behaviours, in accordance with the
adaptive demand of the prevailing environment of the OCD.
The findings may be summarized schematically in Fig. 1 below
5. Conclusion
Divergent information perhaps overwhelms the OCD subject
with a plethora of response choices, which results in rigid
cognition and motor response rather than them selecting a
response from number of available alternative options. It makes
them feel that they can exercise cognitive control only in this
manner, and this for them, is an index of ensuring their safety.
Literature on empirical validation of theoretical psychoanalytic
constructs is limited. Our findings contribute to understanding
instinctual impulses from the neuropsychological perspective. The
findings have implications for better eclectic understanding of the
pathogenesis of obsessive–compulsive disorder.
184 P. Mukhopadhyay et al. / Asian Journal of Psychiatry 3 (2010) 177–185
Limitations
A heterogeneous clinical sample (comprising OCD subgroups
with aggressive and somatic obsessions with checking compul-
sions; contamination obsession with washing/cleaning compul-
sions; sexual and religious obsessions) and small sample size were
some of the study’s major limitations. However the understanding
may be extended to a larger study with a homogenous sample.
Conflict of interest
None.
References
Abbey, R.D., Clopton, J.R., Humphreys, J.D., 2007. Obsessive–compulsive disorder
and romantic functioning. J. Clin. Psychol. 63 (12), 1181–1192.
Abraham, K., 1924. A short study of the development of the libido in the light of
mental disorders. I. Melancholia and obsessional neurosis.In: Selected Papers.
Basic Books, New York, pp. 422–433, 1953.
Arciniegas, D.B., Beresford, T.P., 2001. Neuropsychiatry: An Introductory Approach.
Cambridge University Press.
Aycicegi, A., Dinn, W.M., Harris, C.L., Erkmen, H., 2003. Neuropsychological function
in obsessive–compulsive disorder: effects of comorbid conditions on task
performance. Eur. Psychiatry 18 (5), 241–248.
Baxter, L., 1992. Neuroimaging studies of obsessive–compulsive disorder. Psychiatr.
Clin. N. Am. 15, 87–884.
Berg, E.A., 1948. A simple objective test for measuring flexibility in thinking. J. Gen.
Psychiatry 39, 15–22.
Blatt, S.J., Shichman, S., 1983. Two primary configurations of psychopathology.
Psychoanal. Contemp. Thought 6, 187–254.
Bloch, M.H., Landeros-Weisenberger, A., Rosario, M.C., Pittenger, C., Leckman, J.F.,
2008. Meta-analysis of the symptom structure of obsessive–compulsive disor-
der. Am. J. Psychiatry 165 (12), 1532–1542.
Boone, K.B., Ananth, J., Philpott, L., Kaur, A., Djenderedjian, A., 1991. Neuropsycho-
logical characteristics of non depressed adults with obsessive compulsive
disorder. Neuropsychiatry, Neuropsychol. Behav. Neurol. 4, 96–109.
Brito, G.N.O., 2002. Mind from genes and neurons: a neurobiological model of
Freudian psychology. Med. Hypotheses 59 (4), 438–445.
Chamberlain, S.R., Menzies, L., 2009. Endophenotypes of obsessive–compulsive
disorder: rationale, evidence and future potential. Expert Rev. Neurother. 9
(8), 1133–1146.
Chessick, R.D., 2001. OCD, OCPD: acronyms do not make a disease. Psychoanal.
Inquiry 21, 183–207.
Christensen, K., Kim, S.W., Dyksen, M.W., Hoover, K.M., 1992. Neuropsychological
performance in obsessive compulsive disorder. Biol. Psychiatry 31, 4–18.
Esman, A., 1989. Psychoanalysis and general psychiatry: OCD as paradigm. J. Am.
Psychoanal. Assoc. 37, 319–336.
Esman, A.H., 2001. Obsessive–compulsie disorder: current views. Psychoanal. Inq.
21, 145–156.
Fenichel, O., 1945. The Psychoanalytic Theory of Neurosis. 3 Volumes. W. W. Norton
and Co., New York.
Freud, A., 1966. Obsessional neurosis: a summary of psychoanalytic views as
presented at the congress. Int. J. Psychoanal. 47, 116–122.
Freud, S., 1909. Notes Upon a Case of Obsessional Neurosis. Hogarth Press, London,
Standard Edition, 10, 155–318, 1955.
Freud, S., 1913. The Disposition to Obsessional Neurosis. Hogarth Press, London,
Standard Edition, 12, 317–326, 1958.
Freud, S., 1926. Inhibitions, Symptoms and Anxiety. Hogarth Press, London, Stan-
dard Edition, 20, 87–175, 1959.
Friedlander, L., Desrocher, M., 2006. Neuroimaging studies of obsessive–compulsive
disorder in adults and children. Clin. Psychol. Rev. 26, 32–49.
Gabbard, G.O., 2001. Psychoanalytically informed approaches to the treatment of
obsessive–compulsive disorder. Psychoanal. Inq. 21, 208–221.
Geller, D.A., Biederman, J., Faraone, S., Agranat, A., Cradock, K., Hagermoser, L., Kim,
G., Frazier, J., Coffey, B.J., 2001. Developmental aspects of obsessive compulsive
disorder: findings in children, adolescents, and adults. J. Nerv. Ment. Dis. 189,
471–477.
Goldberg, D.P., Miller, V.E., 1979. General Health Questionnaire: a scaled version of
general health questionnaire. Psychol. Med. 9, 139–146.
Goldstein, B., Obrzut, J.E., John, C., Ledakis, G., Armstrong, C.L., 2004. The impact of
frontal and nonfrontal brain tumor on Wisconsin Card Sorting Test perform-
ance. Brain Cogn. 54, 110–116.
Goodman, W.K., Price, L.H., Rasmussen, S.A., 1989. Yale-brown obsessive compul-
sive scale-I: development, use and reliability. Arch. Gen. Psychiatry 46, 1006–
1010.
Grant, J.E., Pinto, A., Gunnip, M., Mancebo, M.C., Eisen, J.L., Rasmussen, S.A., 2006.
Sexual obsessions and clinical correlates in adults with obsessive–compulsive
disorder. Compr. Psychiatry 47 (5), 325–329.
Graybiel, A.M., Rauch, S.L., 2000. Towards a neurobiology of OCD. Neuron 28, 343–
347.
Graybiel, A.M., Saka, E., 2004. The Basal Ganglia and the Control of Action, in the
Cognitive Neurosciences III Gazzaniga, M.S. (editor in chief). A Bradford Book.
The MIT Press, London, England.
Graybiel, A.M., Asosaki, T., Flaherty, A.W., Kimura, M., 1994. The basal ganglia and
adaptive motor control. Science 265, 1826–1831.
Hamilton, M., 1960. A rating scale for depression. J. Neurol. Neurosurg. Psychiatry
23, 56–62.
Haut, M.W., Cahill, J., Cutlip, W.D., Stevenson, J.M., Makela, E.H., Bloomfield, S.M.,
1996. On the nature of Wisconsin Card Sorting Test performance in schizo-
phrenia. Psychiatry Res. 65, 15–22.
Jaisoorya, T.S., Janardhan Reddy, Y.C., Srinath, S., 2003. Is juvenile obsessive–
compulsive disorder a developmental subtype of the disorder? Findings from
an Indian study. Eur. Child Adolesc. Psychiatry 12, 290–297.
Katz, R.J., 1991. Neurobiology of obsessive–compulsive disorder – a serotonergic
basis of Freudian repression. Neurosci. Biobehav. Rev. 15, 375–381.
Kempke, S., Luyten, P., 2007. Psychodynamic and cognitive-behavioral approaches
of obsessive–compulsive disorder: is it time to work through our ambivalence?
Bull. Menninger Clin. 71 (4), 291–311.
Kernberg, O., 1984. Object-relations Theory and Clinical Psychoanalysis. Jason
Aronson, New York.
Kuelz, A.K., Hohagen, F., Voderholzer, U., 2004. Neuropsychological performance in
obsessive–compulsive disorder: a critical review. Biol. Psychol. 65, 185–236.
Lee, J.C., Prado, H.S., Diniz, J.B., Borcato, S., da Silva, C.B., Hounie, A.G., Miguel, E.C.,
Leckman, J.F., do Rosário, M.C., 2009. Perfectionism and sensory phenomena:
phenotypic components of obsessive–compulsive disorder. Compr. Psychiatry
431–436.
Lucey, J.V., Burness, C.E., Costa, D.C., Gacinovic, S., Pilowsky, L.S., Ell, P.J., Marks, I.M.,
Kerwin, R.W., 1997. Wisconsin card sorting task (WCST) errors and cerebral
blood flow in obsessive–compulsive disorder. Br. J. Med. Psychol. 70, 403–411.
Luria, A.R., 1973. The working brain. In: Heaton, R.K., Chelune, G.J., Talley, J.L., Kay,
G.G., Curtiss, G. (Eds.), Wisconsin Card Sorting Test manual. Basic Books, New
York (Revised and expanded. New York: Psychological Assessment Resources,
Inc., 1993).
Martı́nez-González, A.E., Piqueras-Rodrı́guez, J.A., 2008. Neuropsychological update
on obsessive–compulsive disorder. Rev. Neurol. 46 (10), 618–625.
Mc.Donald, R.J., White, N.M., 1994. A triple dissociation of memory systems:
hippocampus, amygdale and dorsal striatum. Behav. Neurosci. 107, 3–22.
McWilliams, N., 1994. Psychoanalytic Diagnosis: Understanding Personality Struc-
ture in the Clinical Process. The Guilford Press, New York.
Moretz, M.W., McKay, D., 2009. The role of perfectionism in obsessive–compulsive
symptoms: ‘‘not just right’’ experiences and checking compulsions. J. Anxiety
Disord. 23 (5), 640–644 (Epub 2009 Feb 10).
Moritz, S., Hottenrott, B., Randjbar, S., Klinge, R., Von Eckstaedt, F.V., Lincoln, T.M.,
Jelinek, L., 2009. Perseveration and not strategic deficits underlie delayed
alternation impairment in obsessive–compulsive disorder (OCD). Psychiatry
Res. 170, 66–69.
Mukhopadhyay, P., Das, S., Nandi, S., Bandopadhyay, G., 2006. Executive ability at
different levels of severity of obsessive–compulsive disorder. J. Personality Clin.
Studies 22 (1&2), 7–11.
Mukhopadhyay, P., Dutt, A., Das, S.K., Basu, A., Hazra, A., Dhibar, T., Roy, T., 2008.
Identification of neuroanatomical substrates of set-shifting ability: evidence from
patients with focal brain lesions. In: Progress in Brain Research Volume 168 Models
of Brain and Mind: Physical, Computational and Psychological Approaches Rahul
Banerjee and Bikas Chakrabarti (Editors). Elsevier, Amsterdam, pp. 95–104.
Nagera, H., 1978. Obsessional Neurosis: Developmental Psychopathology. Aronson,
New York.
Newth, S., Rachman, S., 2001. The concealment of obsessions. Behav. Res. Ther. 39,
457–464.
Okasha, A., Rafaat, M., Mahallawy, N., Nahas, G., Dawla, S.A., Sayed, M., Kholi, S.,
2000. Cognitive dysfunction in obsessive–compulsive disorder. Acta Psychiatr.
Scand. 101, 281–285.
Oldfield, R.C., 1971. The assessment and analysis of handedness: the Edinburgh
inventory. Neuropsychologia 9, 97–113.
Olley, Malhi, Sachdev, 2007. Memory and executive functioning in obsessive
compulsive disorder: a selective review. J. Affect. Disord. 104, 15–23.
Parthsarathy, H.B., Graybiel, A.M., 1997. Cortically driven immediate early-gene
expression reflects modular influence of sensory motor cortex on identified
striatal neurons in the squirrel monkey (1997). J. Neorosci. 7, 2477–2491.
Pasquini, M., Fabbrini, G., Moretti, G., Berardelli, I., Mandarelli, G., Delle Chiaie, R.,
Leone, C., Biondi, M., Berardelli, A., 2009. Bradykinesia and mental slowness in
patients with obsessive–compulsive disorder. Eur. Psychiatry 24 (Suppl. 1),
S1035.
Paul, D., 2004. The impact of instinctual impulses on executive function in Obses-
sive Compulsive Disorder. Unpublished Dissertation of Master’s in Medical
Psychology. Department of Psychology, University of Calcutta.
Pena-Garijo, J., Ruipérez-Rodrı́guez, M.A., Barros-Loscertales, A., 2010. THE neuro-
biology of obsessive–compulsive disorder: new findings from functional mag-
netic resonance imaging (I). Rev. Neurol. 50 (8), 477–485.
Radomsky, A.S., Ashbaugh, A.R., Gelfand, L.A., 2007. Relationships between anger,
symptoms, and cognitive factors in OCD checkers. Behav. Res. Ther. 45, 2712–
2725.
Rauch, Jenike, M., 1993. Neurobiological models of obsessive–compulsive disorder.
Psychosomatics 34, 20–32.
Rhéaume, J., Freeston, M.H., Dugas, M.J., Letarte, H., Ladouceur R, 1995. Perfection-
ism, responsibility and obsessive–compulsive symptoms. Behav. Res. Ther. 33
(7), 785–794.
 P. Mukhopadhyay et al. / Asian Journal of Psychiatry 3 (2010) 177–185
Roth, R.M., Milovan, D., Baribeau, J., O’Connor, K., 2005. Neuropsychological func-
tioning in early and late-onset obsessive–compulsive disorder. J. Neuropsychi-
atry Clin. Neurosci. 17, 208–213.
Rubenstein, C.S., Altemus, M., Pigott, T.A., Hess, A., Murphy, D.L., 1995. Symptom
overlap between OCD and bulimia nervosa. J. Anxiety Disord. 9, 1–9.
Saka, E., Graybiel, A.M., 2003. Pathophysiology of Tourette’s syndrome: striatal
pathways revisited. Brain Dev. 25 (Supply), S/55–S/519.
Salzman, L., 1980. Treatment of the Obsessive Personality. Jason Aronson, New York.
Saxena, S., Brody, A.L., Schwartz, J.M., 1998a. Baxter LR Neuroimaging and frontal-
subcortical circuitry in obsessive–compulsive disorder. Br. J. Psychiatry Suppl.
(35), 26–37.
Saxena, S., Brody, A.L., Schwartz, J.M., Baxter, L.R., 1998b. Neuroimaging and
frontalsubcortical circuitry in obsessive–compulsive disorder. Br. J. Psychiatry
Suppl. 35, 26–37.
Saxena, S., Bota, R.G., Brody, A.L., 2001. Brain-behavior relationships in obsessive–
compulsive disorder. Semin. Clin. Neuropsychiatry 6 (2), 82–101.
Shallice, T., 1982. Specific impairments in planning. In: Broadbent, D.E., Weiskar-
antz, L. (Eds.), The Neuropsychology of Cognitive Function. The Royal Society,
London, pp. 199–209.
Shapiro, D., 1965. Neurotic Styles. Basic Books, New York.
Shapiro, D., 2001. OCD or obsessive–compulsive character? Psychoanal. Inq. 21,
242–252.
Spielberger, C.D., 1991. State-Trait Anger Expression Inventory (STAXI). Revised
Research Edition Psychological Assessment and Resources, Inc., Florida.
185
Spinella, M., 2005. Mood in relation to subclinical obsessive–compulsive symptoms.
Int. J. Neurosci. 115, 433–443.
Stuss, D.T., Levine, B., Alexander, M.P., Hong, J., Palumbo, C., Hamer, L., Murphy, K.J.,
Izukawa, D., 2000. Wisconsin Card Sorting Test performance in patients with
focal frontal and posterior brain damage: effects of lesion location and test
structure on separable cognitive processes. Neuropsychologia 38, 388–402.
Tarafder, S., Bhattacharya, P., Paul, D., Bandyopadhyay, G., Mukhopadhyay, P., 2006.
Neuropsychological disposition and its impact on the executive functions and
cognitive style in patients with obsessive–compulsive disorder. Indian J. Psy-
chiatry 48 (2), 102–106.
Veale, D.M., Sahakian, B.J., Owen, A.M., Marks, I.M., 1996. Specific cognitive deficits
in tests sensitive to frontal lobe dysfunction in obsessive–compulsive disorder.
Psychol. Med. 26, 1261–1269.
Wechsler, D., 1997. Wechsler Adult Intelligence Scale, 3rd ed. The Psychological
Corporation, Harcourt Assessment Company, UK.
Weissman, P., 1954. Ego and superego in obsessional character neurosis. Psycho-
anal. Quart. 23, 529–543.
Whiteside, S.P., Port, J.D., Abramowitz, J.S., 2004. A meta-analysis of functional
neuroimaging in obsessive–compulsive disorder. Psychiatry Res. 132 (1), 69–
79.
Whiteside, S.P., Abramowitz, J.S., 2005. The expression of anger and its relationship
to symptoms and cognitions in obsessive–compulsive disorder. Depress. Anxi-
ety 21, 106–111.