Clinical Psychology Review, Vol. 21, No. 4, pp. 631±660, 2001
Copyright D 2001 Elsevier Science Ltd.
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CLINICAL AND PSYCHOLOGICAL FEATURES
DISTINGUISHING OBSESSIVE±COMPULSIVE
AND CHRONIC TIC DISORDERS
Kieron P. O'Connor
University of MontreÂal
ABSTRACT. Medical and biogenetic research has suggested that obsessive ±compulsive disorder
and chronic (multiple) tic disorder may share a common etiology. This article reviews
corresponding evidence for psychological similarities and differences between the two disorders.
There are similarities in self-management strategies, psychological traits (both report high scores
on different aspects of perfectionism) and in the ego-syntonic ± ego-dystonic cycle of the
impulsive ± compulsive behavior. Situational cues likely to elicit or worsen the problem differ
between the disorders as do associated emotions, comorbidity and background styles of action. In
both disorders, cognitive factors, such as anticipations and appraisals of the problem, can play a
role in onset and maintenance of the problem, and this raises the question as to whether cognitive
or behavioral factors are best addressed in treatment. Psychological characteristics, such as lack of
confidence, may contribute to apparent performance deficit. Psychological evaluation,
particularly functional analysis, may aid in differential diagnosis between the two disorders,
lead to improvement in treatment matching, and in understanding of the multidetermined
etiology. D 2001 Elsevier Science Ltd. All rights reserved.
KEY WORDS. Obsessions, Compulsions, Tics, Clinical psychology.
THERE HAS BEEN considerable interest recently in the diagnostic overlap between
obsessive ±compulsive disorder (OCD), chronic (multiple) tic disorder (CMT) and
Gilles de la Tourette syndrome (TS). Several researchers (e.g., Pauls, 1992) have
argued that these disorders, while appearing phenomenologically distinct, may share a
common etiology and possibly a common gene. Support for a common etiology
between OCD and CMT comes from comorbidity studies and family pedigree studies,
which suggest a genetic link between OCD spectrum disorders and CMT. But the two
Correspondence should be addressed to Dr. Kieron O'Connor, Department of Psychiatry,
Centre de Recherche Fernand-Seguin, Louis-H La Fontaine Hospital, University of MontreÂal,
7331 Hochelaga Street, MontreÂal, QueÂbec, Canada H1N 3V2. Phone: (514) 251-4015. Fax:
(514) 251-2617; E-mail address: [email protected]
631
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K. P. O'Connor
disorders of OCD and CMT have a distinct clinical phenomenology, natural history and
respond to different pharmacological and psychological interventions. This review
examines, from a psychological point of view, the similarities and differences between
CMT and OCD. The first section examines phenomenological and diagnostic issues.
The second section discusses the clinical relevance of psychological factors in the
evaluation and management of CMT and OCD. Psychological factors include emotional, behavioral, and cognitive aspects. Finally, the role of psychological variables in
the etiology of both disorders is considered alongside the genetic and neurobiological
evidence that has been very influential in molding clinician consensus about overlap.
DIAGNOSTIC FEATURES
One of the key problems in comparing OCD, CMT, and TS disorders is a lack of diagnostic
precision concerning in particular, the diagnosis of tic disorders. Shapiro and Shapiro
(1992), for example, insist that diagnostic vagueness has caused much confusion in
clinical research, and that apparent similarities between TS, CMT, and OCD may, in fact,
be an artifact of imprecise diagnoses. Comings, Himes, and Comings (1990) noted that
sampling techniques and diagnostic criteria varied so widely over epidemiological
studies that a stable prevalence rate of tic disorders is elusive. Obviously, if there are no
strict criteria as to the phenomenological distinctness of two disorders, then discussion of
their relatedness is premature, and it seems wise to focus initially on definitions.
Tics are defined, rather vaguely, in the fourth edition of the Diagnostic and Statistical
Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 1994) nosology
as a recurrent, nonrhythmic series of movements (of a nonvoluntary nature) in one
or several muscle groups. Tics are usually divided into simple and complex tics of a
motor, sensory, or vocal nature. In practice, simple tics have to be differentiated from
such behaviors as routines, automatisms, and stereotypes; from spasms of neurological or neurochemical origin, and from dystonias and torticollis of a possibly
psychoneurological origin. Complex tics, which involve sequences of several distinct
muscle movements, can visibly resemble the ritualized compulsions of OCD.
OCD prevalence rates stand at around 2 ±3% of the population and, like tic disorders,
suffer the additional problem of being hidden, underreported, and therefore underestimated (Rasmussen & Eisen, 1992). Traditionally, OCD rituals are distinguished
from tics on the assumption that they are preceded by ``intentional'' thoughts. The
person suffering from OCD experiences repetitive aversive intrusive thoughts, which
the person recognizes as his/her own but feels compelled to ``neutralize'' by either a
mental or behavioral ritual. OCD is classified in DSM-IV as an anxiety disorder, although
not all clinicians agree on this categorization (see Nelson & Chouinard, 1995).
The relationship between TS and CMT may cause another diagnostic boundary
problem. In TS, multiple tics, repetitive movements, and compulsive rituals are
frequently found together with other behavioral and attentional problems, such as
attention-deficit/hyperactivity disorder (ADHD) (Knell & Comings, 1993). TS is
recognized in the DSM-III (American Psychiatric Association, 1980) and DSM-IV
(American Psychiatric Association, 1994) as a distinct diagnostic category with
multiple tics, including vocal tics occurring several times a day, everyday, throughout
a period of more than 1 year and whose location, number, frequency, and severity
can change over time, with onset before the age of 21 years. CMT is often conceived
by clinicians as a less severe or ``light'' form of TS. On the one hand, there seems to
Obsessive-compulsive and Chronic Tic Disorders
633
be a consensus amongst researchers that CMT and TS share enough common
aspects to be considered on a continuum of severity (e.g., Spencer, Biederman,
Harding, Wilens, & Faraone, 1995). On the other hand, the diagnosis of TS is
currently dichotomous, not dimensional, and depends crucially on the existence of a
vocal tic. Although there has been controversy about current criteria for TS (e.g.,
First, Frances, & Pincus, 1995; The Tourette Syndrome Classification Study Group,
1993). One key distinction between OCD, TS, and CMT is their respective comorbidity rates with other axis 1 disorders.
CO-MORBIDITY OF OCD AND CMT WITH OTHER EMOTIONAL DISORDERS
Austin et al. (1990) looked at 18 male and 18 females aged 17 ± 66 years diagnosed
with OCD per DSM-III-R criteria (American Psychiatric Association, 1987) and YBOCS, and found that at the time of interview, 14% experienced panic attacks
(lifetime prevalence, 39%), 14% simple phobia, 19% social phobia, and 57% of
people with panic and 77% without had experienced at least one major depressive
episode. Rasmussen and Eisen (1992), in a study of 100 people with OCD (DSM-III,
56% male, aged 18 ±65 years), found 7% rate of simple phobia (lifetime 22%), a 11%
prevalence of social phobia (lifetime 18%), 6% prevalence of panic disorder (lifetime
15%), 31% current prevalence of depression (lifetime 67%) and 7% lifetime
prevalence of TS. Thomsen and Jensen (1994) studying 284 people diagnosed
OCD by ICD-8 criteria (40% male, mean age 35.0), found an 8% prevalence of
neurosis. However, it is worth recalling that the participants in these studies were
generally selected from those presenting at psychiatric clinics. Fallon and SchwabStone (1992) pinpointed several methodological problems in evaluating comorbidity
studies of tic disorders, in particular sample selection bias (e.g., the clinician's illusion
springing from the use of clinical, not community, samples). Such selection bias of
samples may also give a distorted view of associated features because clinic samples
disproportionately represent people with multiple conditions. Identifying cases
through self-report can also be problematic, especially if people are misinformed
about TS criteria. Fallon and Schwab-Stone (1992) conclude that ignorance in the
definition of tic disorders and their natural history makes clinical studies difficult,
and recommend longitudinal studies, which would allow more control for informant
bias and a more consistent assessment of premorbid function. Table 1 lists studies
that have directly compared clinical aspects of OCD, CMT/TS. There is a higher
incidence of depression, social anxiety, and phobia in OCD, but it is not clear if this
precedes, accompanies, or is a result of the OCD. The comorbidity of a tic disorder
with OCD varies across studies from 25 to 63%. But where OCD occurs with either TS
or CMT, the tics and obsessions seem to develop independently (Swedo & Leonard,
1994). In the case of tic-related OCD, the compulsions seem to resemble more
sensory-based rituals, raising the question as to whether such rituals are better
classified as impulsive than compulsive.
DISTINGUISHING IMPULSIONS AND COMPULSIONS: SENSORY TICS,
COGNITIVE TICS, AND OBSESSIONS
Shapiro and Shapiro (1992) have argued that sensory preoccupations are not to be
confused with obsessions because there seems to be no logic to the preoccupation.
562 adolescents
67% male
Age range, 16 ± 17 years
8 OCD Ð 2 M
(mean age: 44 years)
9 TS Ð 8 M
(mean age: 26 years)
54 non-TS CMT
36M
Mean age: 17 years
10 OCD Ð 6 F; mean age: 32
15 OCD + TS Ð 4 F
Mean age: 33 years
Zohar, Rayzoni, Pauls, Apter, Bleich,
Kron, Rapoport, Weizman, &
Cohen (1992)
Cath, Hoogduin, van de Wetering, van
Woerkom, Roos, & Rooymans (1992)
George, Trimble, Ring, Sallee, &
Robertson (1993)
Leonard, Lenane, Swedo, Rettew,
Gershon, & Rapoport (1992)
16 TS, 16 OCD, 16 controls
50% M
Mean age: 31.0 years
Pitman, Green, Jenike, &
Mesulam (1987)
DSM-III-R,
Y-BOCS, LOI
DSM-III-R, NIMHGS
DSM-III-R, ZDRS;
LOI, EPQ, SCID-II
DSM-III-R, Y-BOCS
DSM-III, MOCI,
EPI, STAI
OCD more depressed, lower EPQ score on
psychoticism, higher on social desirability
Symptoms in TS more related to impulse
control than anxiety
8.5% had OCD
6.5% some anxiety disorder
47% depression
OCD + TS had more obsessions involving
violent sexual, symmetrical, touching,
blinking, counting, and self-harming
OCD + TS had less obsessions concenring
OCD dirt, germs, and cleaning
OCD compulsions were more likely to be
preceded by anxious or guilty thoughts
60% of OCD had tics
63% of TS had OCD
OCD + tics more depressed, anxious, panic,
phobia, more sensory precursors to
compulsions, reported mounting tension
rather than anxiety before compulsion
25% of OCD had tics
TABLE 1. Studies Directly Comparing Clinical Features of Obsessive ±Compulsive Disorder (OCD) and Chronic Multiple Tic Disorder
(CMT)/Tourette Syndrome (TS)
634
K. P. O'Connor
13 ``pure'' OCD; 8 M;
Mean age: 32 years
13 TS + OCD; 4 M
Mean age: 29 years
35 OCD + tics
35 age gender, matched
OCD ± tics
27 M
Mean age: 30 years
177 OCD
78 M
Mean age: 39.0 years
56 had tic-related OCD
OCD + tics had more aggressive, religious, sexual
obsessions as well as more checking,
counting, touching, hoarding.
TS + OCD had more intrusive images; concern
for body part; need for symmetry; need to
touch, tap, rub and rituals involving
blinking, storing.
Pure OCD more checking and
harm-related obsessions.
DSM-III-R, Y-BOCS
DSM-III-R, Y-BOCS
OCD + tics had more compulsions, involving
touching, tapping, rubbing, checking, blinking,
staring, repeating, grooming, and less obsessions
with contamination.
DSM-III-R, Y-BOCS,
HRSD, STOBS
DSM-III = Diagnostic and Statistical Manual of Mental Disorders. 3rd ed; MOCI = Maudsley Obsessional ± Compulsive Inventory: EPI = Eysenck Personality Inventory: STAI = State ± Trait Anxiety
Inventory: DSM-III-R = Diagnostic and Statistical Manual of Mental Disorders. 3rd ed., rev.: Y-BOCS = Yale ± Brown Obsessive ± Compulsive Scale; ZDRS Ð Zung Depression Rating Scale for
Depression; LOI = Leyton Obsessional Inventory; EPQ = Eysenck Personality Questionnaire; Structured Clinical Interview for DSM diagnosis; NIMHGS Ð National Institute of Mental Health
Global Scale; HRSD = Hamilton Rating Scale for Depression; STOBS = Schedule for Tourettes and Other Behavioral Symptoms.
Leckman, Grice, Barr, de Vries,
Martin, Cohen, McDouble,
Goodman, & Rasmussen
(1994/1995)
Petter, Richter, &
Sandor (1998)
Holzer, Goodman, McDougle,
Baer, Boyarsky, Leckman, &
Price (1994)
Obsessive-compulsive and Chronic Tic Disorders
635
636
K. P. O'Connor
Cognitive content would appear to be a key distinguishing feature of tics and rituals.
On the face of it, tics are involuntary, impulsive, purposeless movements, whereas
OCD is characterized by the presence of intrusive thoughts. Miguel et al. (1995), in a
study of intentions preceding OCD and tic disorder, reported that whereas all 15
adults with OCD reported thoughts preceding rituals, only 2 of 12 TS reported
thoughts, the rest of the sample reporting sensations. However, five of the TS were
excluded exactly because they suffered intentional tics. There are two assumptions
implicit in this voluntary/nonvoluntary, cognitive/noncognitive distinction between
tics and rituals: the first assumption is that no cognitive activity precedes tic onset,
and the second assumption is that thoughts preceding rituals are indeed intentional.
But, with regard to the first assumption, tics do not occur in a void and a sensory
sensation or premonitory urge frequently precipitates the tic. This sensation is
considered a sensory tic, indicating tension in the surrounding area. Leckman,
Walker, and Cohen (1993) reported that 93% of a sample of 135 people with tics
aged 8 ± 71, reported premonitory urges prior to the tic and this, according to the
authors, challenged the conventional wisdom that tics are involuntary. Chee and
Sachdev (1997) studied 50 TS, 50 OCD, and 50 healthy controls to determine
prevalence and phenomenology of sensory tics. The sensory tics in both TS and
OCD groups were predominantly located in rostral anatomical sites. The lifetime
prevalence of sensory tics in the TS groups was 28%, compared to 10% in OCD and
8% in controls. The authors conclude that sensory tics seem to be a common feature
of TS and a subgroup of OCD predisposed to tics. It is not clear if this sensation serves
as a warning, a precipitator or is in fact part of the tic, because the sensation can
persist even when treatment alleviates the actual tic movement. One possible
interpretation of sensory tics is that they represent the subjectively experienced
component of neural dysfunction below the threshold for motor or vocal tic
production (Chee & Sachdev, 1997). Kane (1994) has suggested that urges represent
a heightened attention to physical sensations. He suggests that a particularly
heightened sensitivity of the person with tics to somatic sensation produces an
attentional focus that provokes the tic. If heightened awareness or attentional
hypersensitivity to a particular tension becomes a preoccupation, and the attempt
to suppress such preoccupation provokes a tic, then this tic-producing process
resembles the thought suppression analogue of obsessional thought patterns, where
the attempt to suppress an intrusive thought results in its resurgence (Purdon, 1999).
Regarding the second assumption: are the obsessions preceding ritual in OCD
always intentional? Earlier formulations associated obsessions with mental impulses
(Janet, 1903) and Cath et al. (1992) have recently introduced the notion of a
``cognitive tic'' as a means to clarify some of the confusion between intrusive mental
impulses and obsessional ruminations. The distinguishing factor between ``cognitive
tics'' and ``ruminations'' according to Cath et al. (1992) is that the latter are
impulsive, often resembling simple urges with no rationale behind them, whereas
ruminations are more complex. So, counting a sequence of numbers for no reason
would be classified as a ``cognitive tic,'' whereas a flash of a scene of potential
catastrophe would constitute an obsessional intrusion. However, in practice it is
difficult to separate the two. Apparent meaningful thought or rational self-statements
may be examples of mental or ``cognitive'' tics, where the mental obsession producing the neutralizing ritual is itself part of an involuntary sequence, not a voluntary
precursor of this sequence. Furthermore, obsessions may come to resemble tics in
their repetitive nonsensicalness when they become overlearned habits devoid of
Obsessive-compulsive and Chronic Tic Disorders
637
original cognitive motivation. In addition, a client may retrospectively ascribe an
intentional motivation to a tic. Cath et al. (1992) have also pointed to the fact that a
purposeless movement may sometimes be given a sense by the person post-hoc. A
head movement may be interpreted by the person as meaning there was something to
look at. But this ex-consequential logic follows from and is not prior to the movement. It is difficult in such cases to separate primary from secondary cognitions, that
is to say, to distinguish the logic behind an initial thought from the logic of
subsequent reflections on the initial thought. Although intrusive thoughts are
complex, their unwanted appearance may still be impulsive rather than intentional,
and some intrusions may be a more complex version of cognitive tics. Both cognitive
tics and obsessions need also to be distinguished from cognitive rituals. These are
mental operations, such as wiping away or suppressing or substituting intrusive
thoughts as a way of neutralizing their impact. Mental neutralization is equivalent
to the overt neutralization of compulsive rituals.
The ``just right'' phenomenon is a label applied to compulsions such as arranging
books, or performing symmetrical movements, which seem to lack an obsessional
precursor other than the need for everything to be ``just right.'' It is equally present
in OCD with and without tics, and according to Leckman et al. (1994/1995), it is a
complex mix of high activation, perceptual sensitivity, doubting, and repetitive
action. This phenomenon could fall into the category of ``cognitive tic'' in the sense
that the content is cognitive but the relief is experienced predominantly as a sensory
fulfillment, and there are no external consequences. It may straddle the border
between tic and obsession. However, a careful psychological analysis is necessary to
effect such a differential diagnosis because although there may not be observable
consequences to not performing the ``just right'' ritual, there may be consequences
in the sense of how the person feels about themselves if things are not ``just right.''
Shapiro and Shapiro (1986) argued that it is precisely the confusion between
impulsion and compulsion that results in erroneous rates of comorbidity between
OCD and CMT. Impulsions, according to Shapiro and Shapiro (1986), give pleasure;
feelings of guilt and regret only arising later, whereas compulsions cause anxiety and
tension. Shapiro's distinction between the impulsive type rituals found in TS and the
``genuine'' compulsions of OCD has been incorporated into a clinical validation of a
questionnaire to distinguish TS type compulsions from OCD compulsions (George et
al., 1993). TS rituals, according to George et al. (1993), tend to be ego syntonic,
impulsive, and directed to the self, whereas obsessional compulsions are more
elaborate, ego dystonic, and world-directed actions like cleaning or checking. Fallon
and Schwab-Stone (1992) recommend a return to the comparative clinical phenomenology of the two disorders in order to clarify some of the definitional confusion
and we now examine more closely psychological associations in TS, CMT, and OCD.
EMOTIONAL ASSOCIATIONS
Tics in common parlance are considered ``nervous'' tics, but the associated emotions
at the time of tic onset are mainly frustration and dissatisfaction rather than anxiety
(O'Connor, Gareau, & Blowers, 1993). Although a recent study did report a
correlation between number of tics and self-reported anxiety level (Woods, Milten,
& Lumley, 1996), people with CMT are not more neurotic as measured by the EPI
[defined in Table 1] (O'Connor et al., 2000a).
638
K. P. O'Connor
The feeling of guilt is seen as a prime motivator in OCD (e.g., Rachman, 1993).
Savoie (1996), in his phenomenological investigation of OCD, also notes that the role
of guilt may precede and motivate as well as be the consequence of OCD and that
such guilt is highly idiosyncratic. In OCD, clients may have negative scenarios more
readily available than positive scenarios (Tata, Leibowitz, Prunty, Cameron, &
Pickering, 1996), which could indicate a vulnerability and a low estimation of their
own abilities to cope. Hence, the extreme reactions of guilt may develop from
underlying problems with self-affirmation. Stemberger et al. (1997) reported shame
and low self-esteem in 75% of 67 clients with OCD spectrum disorders. GilboaSchectman, Franklin, Ferrarelli, and Foa (1997) reported a greater impact of
imagined negative scenario on self-esteem in OCD clients than in socially anxious
clients and controls.
Although the literature specifically addressing self-esteem is sparse, one speculative
hypothesis may be that clients with CMT are preoccupied by how they are perceived
by others, and clients with OCD have a more pervasive lack of self-confidence and are
preoccupied more by their performance in general in the world. Fava et al. (1996)
reported low self-esteem as a key prodromal symptom in OCD. Low self-esteem seems
a precursor of neurotic perfectionism (Rice, Ashby, & Preusser, 1996). Such low selfesteem may account for the low self-confidence in a variety of performance domains
in OCD (McNally & Kohlbeck, 1993).
Obsessional clients have been consistently observed to assign the self and ideal self
to opposite poles of constellatory constructs (Makhlouf-Norris & Norris, 1973).
According to Guidano and Liotti (1988), the obsessional is happier with the self as
bad, and the compulsive behavior allows the client to avoid testing this assumed
badness. The client with CMT, in contrast, rarely has such concerns about performance efficacy, but seems overly preoccupied by the judgement of others about their
appearance and self-image (O'Connor et al., 1993). Christenson and colleagues
(1994) note that in other impulsive disorders (e.g., compulsive buying), the person's
self-esteem seems to depend unduly on the response of others.
Thibert, Day, and Sandor (1995) reported TS with OCD had a higher degree of
self-consciousness coupled with social anxiety than TS without OCD. But both
groups had low self-satisfaction and self-esteem. In CMT, unlike in OCD, the very
thought of experiencing a negative self-evaluation can provoke the tic. Watson and
Sterling (1998) note, in the functional analysis of a case of a vocal tic, that social
attention was a precipitating factor. On the other hand, in OCD, it is often the selforiented interpretations placed on the obsession, for example, that the person
should control it or should not have such thoughts, which may maintain the
obsession (Rachman, 1997).
One of the key emotional distinctions between tics and OCD compulsions is related
to the emotional experience at the time of doing the tic or OCD ritual. Hoogduin
(1986), for example, is of the opinion that a person with an impulsion experiences
pleasure from the deed, whereas someone committing a compulsive act experiences
anxiety and tension that is temporarily relieved by the neutralization. Cath et al.
(1992) see this distinction as crucial to diagnosis. Evolution of emotion in simple tics
tends to follow the pattern of immediate frustration producing tension, with the tic
inducing short-term relief from tension but leading finally to renewed tension.
Shapiro and Shapiro (1986) originally noted that impulsions give pleasure with
feelings of guilt and regret only arising later. Cath et al. (1992) found that the key
differentiator between OCD and TS was indeed ``felt emotion.'' Clients with OCD,
Obsessive-compulsive and Chronic Tic Disorders
639
according to these authors, always found thoughts unpleasant, whereas clients with TS
often felt a relief from tension, and even a neutrally affective playfulness after the tic.
In trichotillomania, also, clients can report a clear sense of activation during the
hair pulling (King et al., 1995). There may be a neurochemical basis for suggesting
that tic movements stimulate the person in a milder but similar way to stimulants,
such as nicotine, and may act on the catecholamine system (O'Connor, 1989;
Peterson, Campise, & Azrin, 1994). There is some evidence of substitution between
cigarette smoking and tics. Tics can become more intense after smoking cessation
(Peterson et al., 1994) and nicotine procalix has been found somewhat effective in
reducing tic frequency (McConville & Norman, 1992; Richards, 1992). Sanberg et al.
(1997) suggest that transdermal nicotine could serve as an effective aid to neuroleptic
medication in TS.
If both tics and rituals do initially provide stimulation and positive reinforcement,
then an ``opponent process'' model (Solomon & Corbit, 1973), often applied to
other addictive compulsions, may apply equally to tics and rituals. Initially in OCD
the obsessional thought may be securitizing and autostimulating because it allows
the person to escape the aversive requirements of a more complex action and the
person becomes occupied in a familiar loop they can easily control. However, this
familiar loop becomes too compelling and the rituals become tiring and aversive;
the person begins to anticipate the fatigue and aversion, and tries to suppress the
obsessional thoughts with the result that the distress intensifies. Secondary rituals
develop and these become a way of ``neutralizing'' the now aversive ``thoughtsabout-the-thoughts.'' This is similar to opponent process theories of smoking and
drug abuse, where the initial stimulation gradually gives way to aversion-reduction
and the aim of use becomes avoidance of withdrawal symptoms. Of course, in tics
and rituals, the pharmacological component producing mood changes during
withdrawal and the contribution of these mood changes to relapse is absent. Miele,
Tilly, Frist, and Frances (1990) have argued that a number of behavioral syndromes,
especially compulsive and impulsive disorders, appear to share descriptive similarities with chemical dependence. Availability of alternative rewards to replace the ticinduced stimulation seems crucial to success in relapse prevention and even more so
in the treatment of habit disorders, such as hair pulling (Azrin & Peterson,
1988a,b). The next sections discuss, in more detail, differences in psychological
management strategies.
SELF-MANAGEMENT STRATEGIES
The problem behavior is self-managed and resisted in both CMT and OCD. Selfmanagement strategies employed in CMT and OCD are distinct but seem to serve the
same purpose of suppressing, delaying, or disguising the problem behavior and are
counterproductive in producing both increased tension and desire to perform the
tic/ritual. Clients with CMT are capable of suppressing tics completely for shorter or
longer intervals. The most common strategies adopted are: tensing of muscles
antagonistic to the tic muscles, which can block the movement; tensing of the
general area where the tic takes place; changing posture, suppressing or delaying
onset; attempting to hide the tic by disguising it with another movement (see
Wojcieszek & Lang, 1995). The result of these strategies is often extreme discomfort
and an increased desire to tic, but the tic is temporarily impeded and so the outward
640
K. P. O'Connor
impression is one of normality. Whereas a tic involves a part of the body, OCD
behavior involves complete action, and in OCD, a client is most likely to inhibit a
major compulsive ritual by self-instruction. Self-management strategies in OCD
include: thought suppression, thought elimination, thought transformation or substitution, putting time limits or other (superstitious) boundaries on the ritual,
delaying the ritual, distracting mentally and/or physically, changing routine, seeking
another's help, and avoidance (Freeston & Ladouceur, 1997).
As in the tic case, the client with OCD will experience discomfort while refraining
from the ritual, and waiting for an opportune moment to perform the ritual. So, a
surgeon may be capable of suppressing tics during an operation, but will seek ``relief''
from the tics in private soon after. A client with OCD may defer checking for a
number of hours until others have departed, but will nonetheless feel obliged to
perform the ritual, even several hours later. Although difficulty of suppression varies
between clients in both CMT and OCD, the counterproductive effect is similar, and
suppression of the thought or action does not alleviate the desire to tic or, in the
OCD case, to ``neutralize.'' If instead of suppression, the person is encouraged to
step back and let the intrusive obsessional thoughts flow by unimpeded and without
censure, some of the associated anxiety is alleviated (e.g., Salkovskis & Warwick,
1998). The equivalent motor strategy for tics (relaxing muscles instead of tensing
them to resist the tic) can also alleviate tension in tic disorders (O'Connor, Gareau, &
Borgeat, 1995, O'Connor, Gareau, & Borgeat, 1997).
Awareness training by itself can be an effective self-management strategy in tic
disorders (Wright & Miltenberger, 1987; Woods et al., 1996), but this strategy has not
been shown to be successful in improving or alleviating symptoms in OCD. The client
with OCD is not only aware of the problem but may have made strong judgements
about it, and be, in most cases, resisting the ritual. Whereas the person with tics may
be able to carry on daily life unaware of the tic (Rosenberg, Brown, & Singer, 1994).
Successful management also depends on the situations in which the problem occurs,
as revealed by functional analysis.
FUNCTIONAL ANALYSIS AND SITUATIONAL VARIABILITY
Traditionally OCD rituals have been considered cue elicited in accordance with the
original behavioral model of OCD, developed from first principles, as a variant of a
phobic disorder (Meyer, 1966). The client sees dirt, disorder, or asymmetry and this
elicits discomfort, which in turn provokes the ritual to ``neutralize'' the discomfort.
By contrast tics, like habit disorders, are increasingly viewed as situationally elicited.
Circumstances eliciting tics are the overall state or situations (or anticipations about
situations) in which the person finds themselves. Christenson, Ristvedt, & Mackenzie
(1993) noted a series of emotional precursors to onset of hair pulling. Azrin and
Nunn (1977) recognized that different strategies need to be applied in habit
reversal depending on different situations. Several authors have noted that tics
and habits are elicited by negative states, including depression, lack of self-worth,
and boredom (Dean, Nelson, & Moss, 1992). In a clinical context, functional
analysis is frequently employed to clarify the antecedents and consequences reinforcing tic behavior (e.g., Carr, Taylor, Wallander, & Reiss, 1996; Fuata & Griffiths,
1992; Scotti, Schulman, & Hojnacki, 1994). However, few studies have systematically
examined situational factors.
Obsessive-compulsive and Chronic Tic Disorders
641
In a series of studies examining situational variables, O'Connor, Gareau, & Blowers
(1993, 1994) initially monitored high, medium and low risk situations in 13 clients
with tics and found that the clients showed idiosyncratic situation profiles, but that
these profiles showed little consistency across clients. All subjects identified situations
when the tic occurred and when it did not occur. High-risk situations could be either
high or low arousal situations, for example, one client was most likely to tic when
active at work, another when relaxing at home. However, this situational blurring was
clarified when considering cognitive constructs underlying the situations, because
whatever the physical activity level, the accompanying thoughts and feelings most
frequently concerned impatience and frustration and not performing as desired.
These findings of a cognitive and situational profile have been replicated in
subsequent studies (O'Connor, Gareau et al., 1997; O'Connor et al., 2001b).
Anticipation of a high-risk tic situation can by itself elicit the tic, suggesting a strong
potential role of cognitions (and cognitive appraisal processes) in tic production.
Despite the lack of definitive evidence about the role of situations (as opposed to
cues) as provocations in compulsive rituals, OCD symptoms tend to be domain
specific. The person does not necessarily display OCD symptoms in all walks of life. A
person who checks or cleans does so principally in one domain, although there may
be some generalization across areas. State and situation factors do, however, affect the
severity of the OCD ritual. Feelings of fatigue, insecurity, depression, and stress may
make the ritual more severe, conversely states of pleasant excitement or relaxation
and novelty may diminish ritual intensity (Emmelkamp, 1987). In some checking
rituals, the number of repetitions can be reduced if the person feels less responsible
(i.e., in the presence of another) or if they believe there will be another later chance
to check (Salkovskis & Warwick, 1998).
Compulsions can mask coping difficulties, and the compulsion could be seen as a
way of actively avoiding a more complex situation. When the time spent on
compulsions is reduced, difficulties in situational coping skills may also arise because
the person has not had the occasion to develop certain coping skills. So, for example,
a person who has avoided contact with others through fear of contamination, fears
rejection in interpersonal dealings when the contamination ritual is eliminated and
he/she resumes normal interaction. There have been reports of increases in depression in some clients after treatment of OCD (Foa & Kozak, 1996). If compulsive
rituals mask anxiety about performance, this may have implications for the psychodynamic notions of the ``securitizing'' role of a compulsion in the face of a perceived
hostile environment. The notion that OCD rituals may mask problems in initiating
complex motor actions has also been proposed as a cognitive motor theory of
etiology (Otto, 1992).
PSYCHOLOGICAL TREATMENT
The current psychological treatment of choice for tics is habit reversal (Azrin &
Nunn, 1973, 1977); while that for OCD is exposure and response prevention
(Emmelkamp, 1987; Foa & Kozak, 1996). Habit reversal essentially addresses the tic
as a behavior; while exposure addresses the discomfort driving the OCD behavior.
The principal stages in habit reversal involve relaxation and introduction of a
competing response (Peterson et al., 1994). Recently treatment of both tics and
habit disorders has addressed anticipatory thoughts and mood likely to increase
642
K. P. O'Connor
tension (Mansueto et al., 1999), whereas cognitive approaches in OCD seek generally
to alleviate anxiety associated with the obsessional conviction (Salkovskis, 1999).
Modifying beliefs about dealing with the problem may be commonly useful in both
disorders. In OCD, these focus mainly on the imagined repercussions of the
obsessional thought (e.g., I am going mad; these intrusive thoughts mean I am a
bad person). Such appraisals have been grouped into four categories: according an
overimportance to thoughts; viewing thinking as equivalent to acting (thought ±
action fusion); overestimating the significance of events and exaggerating personal
responsibility (Freeston, RheÂaume, & Ladouceur, 1996). Secondary appraisals in
CMT have not been extensively studied but can be grouped into three categories:
concern with self-image, thoughts about the judgement of others, and fear of physical
consequences of the tic (O'Connor et al., 1994). Changing appraisals as a way of
reducing compulsive behavior has been addressed in cognitive therapy for OCD
(Freeston et al., 1996) and attempted as a cognitive adjunct in a treatment of tic
disorders which addresses the anticipations and the consequences of ticing (O'Connor et al., 1997). Treatment in both OCD and CMT can lead to substantial clinical
improvement (Freeston et al., 1996; Peterson et al., 1994) and this raises questions
addressed in the following sections about the psychosocial, genetic, and neuropsychological aetiology of both disorders.
DEVELOPMENTAL ASPECTS
There are differences in the way tics and OCD rituals develop. Onset of simple tics
generally precedes complex tics, and simple tics can develop at any time in childhood
from 0 to 5 years. Vocal tics develop after motor tics and it is rare for tics to develop
post adolescence, although they can develop in adults (Cohen, Leckman, & Shaywitz,
1992). On the other hand, OCD has in the past been rarely recognized before
adolescence (Rapoport, Swedo, & Leonard, 1992), and is most likely to develop and
intensify around puberty or during early adulthood (after age 18). Age of onset
seems earlier in males and has recently been estimated at around 10 years (ACAP
Official Action, 1998; Zohar, 1999). However, whereas tics seem to wax and wane in
severity throughout life and may in the case of TS be substituted by completely
different tics or may even spontaneously remit (Nomoto, 1989), such substitution and
remission of OCD is rarely reported in the literature (Foa & Kozak, 1996). Although
intensity and generality of OCD rituals may change over time, the type of OCD, at
least in adults, tends to remain constant.
GENETIC FACTORS
Pauls, Towbin, Leckman, Zahner, and Cohen (1986) and Pauls (1992) are perhaps
the key proponents of a genetic link between TS, OCD, and CMT and in contrast to
other researchers have reported no difference in clinical features between TS with
OCD, and TS without OCD, claiming both these groups show similarities in tic
characteristics such as frequency, severity, degree of disruption, and age of onset.
Pauls (1992) suggests that OCD may be the female expression and tics the male
expression of the same genetic disorder and finds support for the claim in studies of
proband relatives which indicated that male relatives were more likely to have TS or
CMT while females were more likely to be OCD (Eapen, Pauls, & Robertson, 1993).
Obsessive-compulsive and Chronic Tic Disorders
643
Pauls (1992) has, however, noted that some forms of OCD may not be related to TS,
but that the patterns of inheritance of TS and OCD within the same families are
consistent with the transmission of an autosomal dominant genetic locus with high
penetrance. Table 2 details studies examining characteristics in families of CMT/TS/
OCD probands. Leonard et al. (1992), who examined lifetime and current prevalence of TS in child probands diagnosed as OCD and in their first-degree relatives,
found a greater incidence of OCD in male relatives, thus countering Pauls' assertion
(that OCD may be the female expression, and tics the male expression, of the same
genetic disorder). McMahon et al. (1996) found no sex differences, and also noted
that tic severity of descendants was minimal. These authors found no correlation
between the presence of OCD in individual relatives, and appearance of OCD in a
given proband, supporting again the assertion (made earlier) that even in TS with
compulsions, the tics and the OCD rituals develop independently. de Groot and
Bornstein (1994) found a correlation between Leyton Obsessional Inventory (LOI)
symptoms in parents and their expression in the offspring. But interestingly they
reported an asymmetry in their findings. If the focus was on TS probands, a high LOI
score did not predict a high LOI score in the parents, but (contrary to the Yale study),
high LOI scores of the parents did predict high LOI scores in the probands.
In the Yale Child Study Center studies (Leckman & Chittenden, 1990), statistical
modeling of genetic transmission using segregation analysis gave penetrance rates
high enough for an autosomal dominant hypothesis only if OCD, TS, CMT and
obsessive ±compulsive features (OCF) were all included. Robertson and Gourdie
(1990) agree with the Yale study that the TS phenotype has to be broadened to
include CMT and OCD criteria of ``caseness'' if an autosomal dominant penetrance is
to be supported and even then the inheritance is incomplete. Black, Noyes, Goldstein, and Blum (1992) reported that relatives of OCD probands did have higher
anxiety and some subsyndromal OCD but found no evidence of a genetic contribution for OCD spectrum disorders.
Shapiro and Shapiro (1992) criticize the clinical objective measures used in genetic
studies and suggest, for example, that the commonly used LOI, though useful for
screening a heterogeneous group of anxiety disorders, is not useful for diagnosing
OCD. This point is supported by recent psychometric comparisons between the LOI
and other obsessive ± compulsive questionnaires (Van Oppen, Hoekstra, & Emmelkamp, 1995). Shapiro and Shapiro (1992), needless to say, report no overlap between
OCD and CMT or TS, and are of the opinion that the association between OCD and
TS is spurious. Shapiro and Shapiro (1992) point to serious methodological flaws in
studies demonstrating epidemiological and genetic associations, such as: the inclusion of over general phenotypes as OCD, inadequate sampling techniques, unreliable
diagnostic criteria, lack of blind evaluation, definitional confusion of what constitutes
a tic, and the use of inappropriate controls.
Rasmussen (1993), in his critical review of genetic studies of OCD, promotes the
need for methodological improvements and suggests that diagnostic uncertainty is a
key limiting factor in genetic linkage studies. Although the diagnostic criteria for
obsessive ±compulsive disorder are clear, our understanding of what constitutes
subclinical compulsive features is far from complete, and there is a tendency for
researchers to have flexible criteria as to these sub-clinical features. Furthermore, as
Pauls, Alsobrook, Goodman, Rasmussen, and Leckman (1995) commented, clarifying the phenotypic spectrun of OCD or TS can only facilitate further genetic
studies (p. 83).
Riddle, Scahill, King,
Hardin, Towbin,
Ort, Leckman, &
Cohen (1990)
Leckman &
Chittenden (1990)
Robertson &
Gourdie (1990)
Pauls, Towbin,
Leckman, Zahner,
& Cohen (1986)
Study
32 families;
122 first-degree
relatives of TS
probands
Direct interview in 117
Method
Instruments
Findings
Best estimate DSM-III Probands with OCD + TS clinically and
demographically similar to OCD ± TS
12.1% of TS + OCD relatives had
TS, 17.2% CMT, 19% OCD
8.9% of TS ± OCD had TS, 20% CMT,
26.7% OCD
122 members of a
85 had diagnostic interview LOI, CCEI, GHQ
50 met criteria of caseness
family affected by TS
18 definite TS without OCB
15 without OCB
7 definite CMT with OCB
2 without OCB
The other 23 probable diagnosis
DSM-III
11 had definite TS
Self-rating used to make
103 first-degree
19 had definite CMT
``best estimate''
relatives of 27
22% had OCD
diagnoses using DSM-III
TS probands
Interview
DSM-III-R
Tics observed in 24% of sample
Parents of
15 patients had a parent with
21 children
either OCD (n = 4) or OC subclinical symptoms
and adolescents
(n = 11), but only 2 parents had mild tics
with OCD
Subjects
TABLE 2. Family Pedigree Studies Examining Prevalence of Tourette Syndrome (TS), Chronic Multiple Tic Disorder (CMT), and
Obsessive ± Compulsive Disorder (OCD) Amongst Descendants
644
K. P. O'Connor
32 probands
with OCD; 33
normal controls
Subjects
175 descendants;
16 spouses
who married
into single
TS pedigree
LOI, TSSL
Best estimate
DSM-III-R
YTS, Y-BOCS
Precoded structured
interview
Self-report
DSM-III (DIS), LOI
Instruments
All first-degree
relatives interviewed,
by diagnostic
interview schedule
Self-report
Method
No difference between probands and
controls in presence of OCD (3%) or
TS or CMT (5 ± 9%), but increased
prevalence of GAD
TS probands having parents with
elevated OC scores
also had a total OC score < 70
Rate for OCD higher in OCD
relatives (10.3%) versus
controls (9.9%) and for
subthreshold OCD
(79% vs. 0%)
Rate for tics (TS + CMT) significantly
higher in OCD proband relatives (4.6%)
67% of descendants and 44% of
married in spouses had tics
38% of descendants had OCD
Tics were minimal
Findings
DSM-III = Diagnostic and Statistical Manual of Mental Disorders, third edition; LOI = Leyton Obsessional Inventory; CCEI = Crown Crisp Experiential Inventory; GHQ = General Health Questionnaire;
DSM-III-R = Diagnostic and Statistical Manual of Mental Disorders, third edition, revised; TSSL = Tourette Syndrome Symptom Checklist; YTS = Yale Tic Schedule; Y-BOCS = Yale ± Brown Obsessive ±
Compulsive Scale.
McMahon,
van de Wetering,
Filloux, Betit, Coon,
& Leppert (1996)
31 mothers;
13 fathers of
TS probands
Pauls, Alsobrook,
100 probands
Goldman, Rasmussen, with OCD;
& Leckman (1995)
466 first-degree
relatives,
113 controls
De Groot &
Bornstein (1994)
Black, Noyes,
Goldstein, & Blum
(1992)
Study
Obsessive-compulsive and Chronic Tic Disorders
645
646
K. P. O'Connor
A direct genetic link between TS, CMT, and OCD seems tenuous, and only when the
spectrum is broadened considerably to include a range of subsyndromal traits, does
one find any acceptable correlation and predictive value through linkage studies. On
the other hand, in TS itself, genetic studies seem to favor an autosomal dominant
mode of transmission with incomplete penetrance and variable expression (Eapen,
O'Neill, Gurling, & Robertson, 1997; Mueller, Putz, Straube, & Kathmann, 1995).
Although even here there is no consensus, Barr and Sandors (1998), for example,
state that there is no convincing evidence of genetic linkage. Robertson and Stern
(1998) note that the ``presumed'' genetic substrate in TS has not been identified,
and as many as 35% of TS may not acquire the disorder genetically (Parraga, Parraga,
Spinner, Kelly, & Morgan, 1998). Genetic transmission of OCD by contrast, while
possibly familial, is more heterogeneous; there seems no equivalent pedigree in OCD
to support a direct genetic influence of parental incidence of OC on proband OC
(Pauls, Alsobrook, Goodman, Rasmussen, & Leckman, 1995). As regards non-TS
CMT disorders, there are not enough studies available to draw any conclusion on
mode, if any, of genetic transmission. Evidence is so far equivocal with Hyde and
Weinberger (1995), arguing for a common genetic basis for all tic disorders whereas
Brett, Curtis, Robertson, and Gurling (1995) reporting no evidence of common
genetic variation between TS and CMT.
PSYCHOSOCIAL AND LEARNING FACTORS
The tic, according to Commander, Corbett, Prendergast, and Ridley (1991), is a form
of startle reflex that is learned in response to an aversive event, although the
propensity to be startled and overstimulated may be biochemically determined.
However, Sachdev, Chee, and Aniss (1997) found no evidence of abnormal audiogenic startle reflex in 15 TS compared to 15 controls using stimuli at 88 and 114 db.
But more recently Gironell, Rodriguez-Fornells, Kulisevsky, Pascual, Riba, Barbanoj,
and Berthier (2000) did report on exaggerated acoustic startle reflex in 10 TS
compared to 10 controls presenting 110 db signals in a start-react paradigm.
Similarly, Azrin and Nunn (1973) view tics as developing, initially, subsequent to
physical events or injuries but thereafter developing according to the laws of learning.
There is evidence of tics developing subsequent to peripheral physical injuries and
Factor and Molho (1997) report two such cases. Tijssen, Brown, Morris, & Lees
(1999) reported 3 late onset startle-induced tics, 2 linked to physical trauma and 1
linked to emotional stress. Some tics can be traced to learned gestures (e.g.,
scratching developing after a bout of acne, blinking after an eye operation, a head
tic beginning due to the long hair worn during adolescence). This information,
clinically useful though it may be in helping the person understand the morphology
of the tic, proves nothing about the learned nature of tics because such a situation
may simply have been the occasion for the tic developing. In TS in particular, tics can
wax and wane, and be adopted on the basis of suggestion as an echo phenomenon
(Seligman, 1991). Perhaps the client with a tic may be more suggestible than normal,
more open to motor mimicry, and hence more likely amongst other things to learn to
tic. Such heightened suggestibility may manifest itself as a failure of inhibition, and
may explain why the majority of children (who may not be so suggestible) abandon
their tics in adolescence, and why tics in childhood can sometimes appear initially as
exaggerations of normal developmental activity. There is some evidence that tics may
respond to hypnotic suggestion (Walters, Boudwin, Wright, & Jones, 1988). O'Con-
Obsessive-compulsive and Chronic Tic Disorders
647
nor and PeÂlissier (1998) found that clients with OCD showed greater suggestibility to
their own self-generated narratives than anxious or nonanxious controls.
Behavioral theorists (e.g., Rachman & Hodgson, 1980) have suggested parental
influences on the development of OCD, in particular the negative effects of intrusive,
controlling parental overprotection, coupled with some degree of rejection. Perfectionism has been associated with parental rearing practices, in particular parental
criticism and lack of encouragement (Frost, Marten, Lahart, & Rosenblate, 1990).
There has at present been no intensive study into the rearing style experienced by
OCD patients, but there is some clinical evidence that the style experienced by people
with both phobia and obsessions may be characterized as ``affectionless control''
(Gerlsma, Emmelkamp, & Arrindell, 1990). So far, very few studies have examined
these hypotheses and the results are not conclusive. In one study, Hafner (1988)
found that OCD self-help group members reported higher levels of parental overprotection as compared to normal controls. In another study, Hoekstra, Visser, and
Emmelkamp (1989) found that people with OCD reported more rejection and less
caring than non-clinical controls, but findings were mixed for overprotection; those
with excessive washing reported more parental overprotection than controls whereas
those with excessive checking reported less over-protection than controls. Vogel,
Stiles, and Nordahl (1997) compared outpatients with OCD and healthy controls in
their recalled parental styles of upbringing and found no differences between the two
groups. However, the Vogel and collaborators' study did not test other anxious
control groups. Turgeon, O'Connor, and Marchand (1998) found no differences in
recalled parental protectiveness between OCD and agoraphobia but both clinical
groups recalled their parents as more protective than a nonanxious control group.
These instruments rely on retrospective accounts of the (now adult) child and
hence suffer from possible recall bias. The parenting questionnaires may not tap
important incidental learning experiences in childhood of the more dynamic aspects
of family interaction as measured by attachment profiles. For example, Zuellig,
Newman, Kachin, and Constantino (1997) reported increased feelings of anger
and vulnerability in generalized anxiety using an adult attachment interview. Similarly, Schut et al. (1997) reported that individuals with trichotillomania tended to use
hostile dominance as their primary interpersonal style and this related to perceived
childhood experiences as measured by an Inventory of Adult Attachment.
NEUROPSYCHOLOGICAL ASPECTS
Comprehensive reviews of neuropsychological findings are found in Cox (1997) and
Schultz, Carter, Schahill, and Leckman (1999) for OCD and CMT/TS, respectively.
Both tics and compulsive ± perseverative-type symptoms can occur in a range of braindamaged syndromes, which indicates that variants of both disorders can accompany
neurological loss of coherent cognitive input (Berthier, Kulisevsky, Gironell, & Heras,
1996). In view of the automatic perseverative nature of both CMT and OCD disorders,
a common etiology might be traceable to frontal lobe deficit. However, there is little
consistent evidence of such deficit, as measured directly by electroencephalograph
(EEG) or other brain mapping procedures, or indirectly by tests of central faculties
supposedly controlled by the frontal lobes (e.g., executive functioning).
In terms of direct evidence of brain abnormalities, early EEG studies seemed to
produce a plethora of abnormalities in OCD, principally increased slow wave activity,
648
K. P. O'Connor
in a number of brain regions. Silverman and Loychik (1990) noted at that time ``it is
not possible to offer an integrated explanation of the various neurophysiological
abnormalities reported in OCD patients'' (p. 322). Prichep et al. (1993) proposed
that the EEG could distinguish OCD clients who responded following 12 weeks
serotonin reuptake inhibition (SRI) medication (fluvoxamine, fluoxetine, or clomipramine). The responders were characterized at baseline by excess relative power in
the alpha band and the nonresponders showed excess theta in temporal and frontal
regions. The topographical differences were not, however, correlated with treatment
response. The authors did not measure EEG post treatment but speculated that SRI
medication decreases alpha. They do caution against treating OCD clients as
homogenous and suggest there may be organic and nonorganic subtypes.
Other studies examining regional blood flow in medicated clients have found that
such medication reduces cerebral blood flow and can itself lead to impaired
performance on frontal lobe neuropsychological tests (Hoehn-Saric et al., 1991).
Baxter et al. (1992) studied brain glucose metabolism and found decreases in local
cerebral metabolic rates in the right head of the caudate nucleus in 13 clients treated
with either medication (fluoxetine) (n = 7) or behavior therapy (n = 6). However, as
the authors themselves note, the significant findings were limited to 1 of 10 channels
studied and ``our data do not prove that caudate nucleus dysfunction is the cause of
OCD'' (p. 687), and in any case ``brain imaging studies do not prove that OCD is the
product of some specific brain lesion'' (Baxter, 1995, p. 7).
Other direct investigations include studies of neurological soft signs in OCD.
Hollander et al. (1990) compared soft signs of central nervous system function in a
group of 41 medication-free OCD and 20 control subjects. Thirty-nine of the OCD
clients had at least one soft sign, compared with 11 of the controls. The signs
principally involved minor involuntary movement, minor movements, and motor
coordination difficulties. It is not clear if the findings were specific to OCD because
there was no other clinical comparison group. Hollander et al. (1990) reported a
correlation between soft signs and severity of obsession but not compulsion. Caramelli, De Lima, Stip, and Bacheschi (1996) also found movement abnormalities in
11 out of 15 OCD clients examined, but found no correlation with clinical ratings.
There is compelling evidence of difficulties in visuomotor integration and fine
motor coordination under some complex conditions in children with TS (Schultz et
al., 1999), but few studies have examined adults. Even within the child population,
presence of attentional difficulties seems to be a confounding problem. Several
research workers have noted that apparent differences in perceptual ± motor functioning of tic disorders may be due to comorbidity of other disorders, such as
attention deficit disorder (ADD), as well as from the distracting interference of the
tics at the time of testing (Channon, Flynn, & Robertson, 1992; Silverstein et al.,
1995). Similar problems with visuospatial organization and recall have been proposed
for OCD. Zielinski, Taylor, and Juzwin (1991), comparing 21 OCD and 21 controls,
found OCD were consistently impaired on recall of visual ± spatial sequences and the
ability to learn a recurring spatial pattern but equal or better than normals on verbal
tasks and measures of frontal lobe functioning. There were no correlations between
performance and OCD symptom severity and the OCD group was more anxious and
depressed at the time of testing. Boone, Ananth, Philpott, Kaur, and Djenderedjian
(1991) also reported poor visuospatial memory in 20 nondepressed OCD as compared to 16 controls, but no deficits in frontal lobe skills, verbal memory, attention, or
intelligence. Patients with a family history of OCD scored worse and accounted for
Obsessive-compulsive and Chronic Tic Disorders
649
the overall differences with the controls, but there was no association between
performance and symptom severity.
However, Cohen et al. (1992) showed that both OCD and phobic patients showed
impairment in tasks of visual construction relative to normals. Rettew et al. (1991)
compared 21 people with trichotillomania with 12 people with OCD, 17 people with
other anxiety disorders and 16 controls on performance of the Money Road Map test
and the Stylus Maze test. There was no difference in performance between pathological subgroups, but the trichotillomania group had more route errors and rule
violations than the normals, while the OCD participants and normal participants
differed only on the number of rule breaks. Enoch, Schreier, and Barroso (1995)
reported visual field defects in OCD, TS, and major affective disorder, but the field
defects were unrelated to clinical severity and in the authors' opinion had no clinical
significance. However, Clemenz, Farber, Lam, and Swerdlow (1996) found no
difference between OCD and controls in smooth pursuit eye movements of slowly
moving targets. Conversely, Savage et al. (1994) reported abnormal evoked potentials
in OCD during low level auditory processing, but not during low level visual
processing. In a further study, Savage et al. (1994) examined recall and recognition
in 20 nonmedicated clients with OCD and 20 matched controls and found abnormalities in the OCD group affecting delayed recall of nonverbal but not verbal
information but recall, overall, was normal in OCD.
There do seem to be consistent problems for CMT, TS, and OCD in inhibition,
whether this be inhibiting information intake or performance. Enright and Beech
(1993) found that people with OCD do not show a negative priming effect (a
longer reaction time to the previously suppressed stimulus). The difference with
normals seems to widen with increased task complexity. This weak inhibition to
semantically related concepts in memory, could lead in OCD to increased likelihood of intrusive thoughts. Finding of reduced ability to attend to relevant and
inhibit irrelevant information seems to generalize to tests of everyday attention as
reported in 13 OCD clients compared to a group with panic disorder (Clayton,
Richards, & Edwards, 1999).
O'Connor, Serawaty, and Stip (1999, 2000b), using a countermanding paradigm
adapted to be an analogue of a high-risk tic situation, found no difference in
psychomotor speed between CMT and non-tic controls, but the authors did find
that participants with CMT showed more difficulty when inhibiting an automated
than a controlled response and showed no practice effect in performance over trial
blocks. Ziemann, Paulus, and Rothenberger (1997) report evidence of normal motor
threshold and excitability but reduced or impaired motor inhibition in TS. The
finding relates to inhibition but not to excitability, and likewise Georgiou, Bradshaw,
Phillips, Cunnington, and Rogers (1997) found no impairment in TS in fast, goaldirected movements. Cox (1997), in a recent comprehensive review of neuropsychological abnormalities in OCD, also reported that only tasks requiring inhibition of an
automatic response correlated with severity of OCD symptoms.
PSYCHOLOGICAL ACCOUNTS OF NEUROPSYCHOLOGICAL DEFICIT
Although such problems with inhibition could be subserved by orbito-frontal-subcortical circuits, differences could indicate functional rather than structural deficit
and spring from adoption of a particular information processing style. One potential
650
K. P. O'Connor
candidate linked with attentional style, among those with CMT, is style of planning
action. Such style of planning involves a particular overactive style of trying to achieve
too much at once (O'Connor et al., 2000a). The selective problems in inhibition in
CMT may be a result of deliberate overpreparation due to a perfectionist style of
personal organization which subsequently makes inhibition more difficult. Style of
action was addressed as part of tic management therapy using behavioral modification techniques and apparent differences in motor function (as measured pretreatment by Purdue Pegboard and other tests of executive function) had decreased at
post-treatment (O'Connor et al., 2001a).
One possibility for explaining incoherences in neuropsychological findings is that
the psychological aspects of the disorder simulate performance deficits. As Maki,
O'Neill, and O'Neill (1994) put it, compulsive checking may result from ``perceived
cognitive failures rather than actual deficits'' (p. 191). If the client with OCD has less
confidence in performance or shows more concern over making mistakes, or feels
obliged to inhibit thoughts or words, or becomes distracted by preoccupations, this in
itself could affect performance. Feelings of over-competitiveness may inhibit as well as
enhance motor performance (Stanne et al., 1999). Conversely, concern over the
occurrence of tics, low frustration threshold, perfectionist ideas of performing actions
could lead also to poorer performance. Reed (1985) pointed to the important role of
indecisiveness in OCD, which could affect slowness and performance inaccuracies.
Dixon, Almodovar, Bateman, DiBartolo, and Frost (1997) have noted the detrimental
effects of perfectionist concern over mistakes on performance, which can be improved
through therapy.
Maki et al. (1994) formulated an inhibitory control hypothesis and speculated that
the less efficient inhibitory control could lead to several cognitive failures, including
failure of selective attention due to distraction, inability to suppress inappropriate
word meanings, and impaired memory due to intrusion of to be forgotten material.
The point about confidence is reiterated in a study by McNally and Kohlbeck (1993).
These authors hypothesized that people who are compulsive checkers have a deficit
in reality monitoring, hence they become confused as to whether they really did
something or thought they did something. On a test comparing an imagined trace
drawing of a line with a real drawing, they found no support for the hypothesis, but
they did find less confidence in the checkers compared with washers and normals.
The client who checks excessively may not have problems with memory but rather
with confidence in memory (McNally & Kohlbeck, 1993), and it may be lack of
confidence not memory impairment which leads to checking. Lack of confidence in
setting up appropriate criteria for completing a task may lead to problems in reality
testing and evaluating feedback, which could in turn induce chronic pathological
doubt or conflict over appropriate performance. Under some circumstances, memory
in OCD may be superior to controls. Brown et al. (1994), for example, using a signal
detection paradigm, found that participants with OCD discriminated seen from
imagined words significantly more frequently than controls. Constans, Foa, Franklin,
and Mathews (1995) also reported no difference in reality monitoring, and found
that checkers reported higher levels of memory vividness but more dissatisfaction
than controls. Rubenstein, Peynircioglu, Chambless, and Pigott (1993) noted that
memory impairment was only present in areas relating to human actions but not for
more objective material.
Deficits may appear more under conditions of high emotionality. Sher, Mann, and
Frost (1984) originally noted that checkers experience more anxiety than noncheck-
Obsessive-compulsive and Chronic Tic Disorders
651
ers during memory experiment and that this anxiety may partially account for
performance deficit.
EMOTIONAL REGULATION AND PERFORMANCE
One of the key qualifiers for poor performance in OCD is the influence of
emotionality and emotional stressors on performance. Stimuli that activate differential performance between those with OCD and others tend to be threatening, may
elicit anxious overconcern or may evoke strong emotionality. Foa and colleagues
(1993), using the Stroop test, showed that people who washed excessively showed
longer latency responses to contamination words than nonwashers, but that in
general clients with OCD showed a longer latency to threat words. Wilhelm, McNally,
Baer, and Florin (1996) found that clients with OCD exhibited deficits in the ability
to forget negative material compared to controls, and they concluded that in OCD
there is a propensity to encode negative words. Radomsky and Rachman (1999)
demonstrated that memory in OCD is enhanced for threat-related stimuli. Oltmanns
and Gibbs (1995), investigating the emotionality in OCD, found that physiological
reactions to stimuli were appropriate in OCD but that facial expressions indicated
more attempt in OCD to suppress emotion and fear. Amir, Ferrarelli, Watlington,
Kozak, and Joa (1997) suggest that the negative priming effect (noted earlier) in
OCD may be due to deliberate strategies used to inhibit disturbing stimuli which can
lead to rebound effects (Clark, Ball, & Pape, 1991).
Indeed, problems in autonomic regulation in both OCD and CMT may lead to
impaired modulation of neuronal activity, so producing performance problems
(Peterson, Zhang, Anderson, & Leckman, 1998). The precise mechanism underlying
autonomic regulation is unclear, but such regulation might influence catecholamine
and dopamine levels (Tulen, van de Wetering, & Boomsma, 1998). Zahn, Leonard,
Swedo, and Rapoport (1996) reported that electrodermal activity showed consistent
positive correlations with ratings of OCD severity in a group of 55 adolescents with
OCD, both with and without tics. Clients with a comorbid CMT showed larger
electrodermal responses than those without CMT to novel stimuli, which might
reflect greater autonomic sensitivity, except the authors considered the differences
insufficient to indicate a separate aetiology for OCD with and without tics. Abberant
behavioral and autonomic regulation could contribute to changes in dopamine
activity associated both with CMT and TS (Ernst et al., 1999) and OCD (Billett et
al., 1998; Goodman et al., 1990).
In all, there is no firm evidence for uniform hard-wired deficit in either CMT or
OCD. In any case, such a pervasive deficit model would be at odds with the clinical
picture of the often domain specific and contextual nature of the problem. The person
with OCD does not necessarily ``doubt'' everything and in CMT, tic onset is situational.
A client convinced that a chair is dirty despite no visible proof and who cannot trust his
perception enough to sit down, also races cars around a track at over 100 mph.
CONCLUSION
The current review highlights the potential contribution of psychological evaluation
of CMT and OCD to differential diagnosis, to tailoring psychological treatment
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K. P. O'Connor
possibilities and to clarifying etiological factors. Because clinical phenomenology
(including psychological, behavioral, biographical, and developmental aspects) is still
the basis for diagnosis of CMT and OCD and there is as yet no neurological or
biochemical-based diagnosis available, further refinement of cognitive and emotional
associations can only aid clinical precision. In particular, further investigation into the
following six research areas shows a potential to substantially improve our psychological understanding of TS, CMT and OCD: emotional associations; systematic functional analysis; cognitive factors; distinctions between impulsive and compulsive
thoughts; childhood experiences; and clinically relevant experimental paradigms.
Further analysis of the emotional associations of both problems would likely expose
the idiosyncratic nature of associated emotions and reveal that neither disorder is
primarily an anxiety or nervous disorder. Tic onset seems mostly associated with
frustration and dissatisfaction. The anticipatory emotions in OCD seem a combination of excessive vulnerability, exaggerated menace, guilt, disgust, and the postneutralization emotions of embarrassment, shame, or stupidity. Apparent puzzling ego
syntonic/dystonic associations in both disorders are clarified when considered in the
light of a possible opponent process model usually applied to addictive behavior.
Both tics and rituals can be viewed as ego syntonic or ego dystonic at different points
in the same action. Tics are ego syntonic when first performed, but ego dystonic when
suppressed. Obsessional thoughts may initially be stimulating, but the ensuing
compulsions and associated evaluations plunge the person into major discomfort.
As regards cognitive factors, both disorders seem to entail perfectionist thoughts but
the perfectionism in tics seems more specific and related to personal standards and
organization and induces tension and frustration rather than anxiety. Tics in CMT
are also preceded by anticipations, even though the anticipations relate more to a
situational appraisal than to a specific intrusive thought. The value of attending to
cognitive factors is highlighted by the way that anticipations and appraisals may
provoke the onset and maintenance of both disorders. Cognitive techniques, such as
distraction, might alleviate the attentional focus producing the tics. Premonitory
urges, even severe coprolalia-related ones, can be modified by distraction. In a vocal
tic case treated recently by the author, distraction by thought or action was a useful
strategy for breaking the link between urge to make the noise and onset of the vocal
tic, and thereby demonstrating to the client the possibility of control. The debate on
the role of cognition also raises the intriguing possibility that what is learned or
acquired in both disorders is a cognitive structure that facilitates the emotional
experience and provokes the tic or ritual. This underlying cognitive structure rather
than the specific movement that it provokes may prove to be a clearer marker of
both disorders.
Further work clearly needs to be done on clarifying impulsive and compulsive thoughts
and distinguishing mental tics from both voluntary thoughts, worries and obsessional
intrusions. Obsessive ruminations may be distinguishable from complex cognitive tics
because the latter may be repeated in series, and may not develop as other intrusions
do, nor be accompanied by the same level of awareness, and may, like other tics, show
a situational profile. In addition, like other tics, cognitive tics may not always reach
the threshold of conscious awareness, but may need to be monitored in all their
detail through awareness exercises. Tics can be incorporated as part of obsessional
behavior. A recent client at our clinic felt the tics brought good luck and that
otherwise something ``bad'' would happen later in the day. The superstitious
thoughts were triggered by thoughts about events that would occur during the day,
Obsessive-compulsive and Chronic Tic Disorders
653
whereas the tics were provoked in situations of interpersonal frustrations. But the tics
were sometimes voluntarily induced to assuage the conviction that otherwise bad luck
would follow. Lang, Consky, and Sandor (1993) also reported a case where tics were
integrated into sign language, which blurred the division into voluntary and involuntary movement. A possible way of differentiating obsessions from mental or
cognitive tics comes from evidence of a client's ability to substitute a cognitive tic
for another type of tic. For example, a client who felt the urge to count numbers and
letters on advertising signs by the roadside was able to interchange this mental
routine with a leg tic. She felt the same immediate relief from doing either and she
could substitute one for the other depending on circumstance. The content of
obsessional ruminations, by contrast, tends not to be interchangeable although one
neutralization strategy may substitute for another.
If some obsessions are cognitive tics, one might expect to find a situational profile
associated with the cognitive tic in the same way that anticipations and beliefs
associated with tic situations are revealed through functional analysis. For example,
in the case of the lady who mentally counted and rearranged the number of letters on
roadside hoardings, the situational profile revealed a strong association between
cognitive tic onset and feelings of uncertainty and vulnerability.
Systematic application of functional analysis in both OCD and CMT would generate
data on environmental, behavioral, cognitive and affective associations. A situational
profile could help in differentiating not only between tics and obsessions, but
between tics and spasms and dystonias, which may be provoked more by physical
parameters. Also, a profile of situational associations might provide insights into the
role of psychosocial factors in acquisition of both disorders.
So far, studies employing parenting questionnaires have failed to reveal any
consistent patterns of rearing styles in either CMT or OCD but a more refined focus
on childhood experiences and attachment in childhood other than a formal exploration
of parenting characteristics may reveal more vicarious learning experiences. For
example, internalization of ambivalent messages may produce unrealistic expectations about how to accomplish an action in both OCD and CMT, particularly at the
pre-operational stage of childhood. It may be the thought patterns generated by lack
of confidence, responsibility, uncertainty or perfectionism that are learned in childhood rather than the specific behavioral patterns.
It seems crucial in future to employ clinically relevant experimental paradigms to factor
in emotive content as a mediator of apparent dysfunction. Despite proposals to
rename OCD and TS, using neurobiological terminology (e.g., Peschel & Peschel,
1991), the scientific literature itself is very cautious and speculative when discussing
uniform neurological causes or deficits in either TS or OCD. Indeed it seems that in a
sizeable percentage of clients, there are neither clear genetic nor clearly defined
``hard'' neurological precursors. Even where baseline neurochemical differences are
established, it is unclear if they are a product of functional or structural change.
Regulation of emotion, thoughts and behavior can be the cause as well as the
consequence of neurochemical change, and a recursive psycho-neuro-biological
model seems the most appropriate to adopt when understanding the multidetermined nature of both disorders.
Neuropsychological findings may be equivocal since such research has, in the past,
sought basic organic deficit, whereas the contextual and domain-specific aspects of
both disorders suggest functional and selective deficit. Behavioral or cognitive
strategies adopted due to chronic lack of confidence (in OCD) or habitual style of
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K. P. O'Connor
planning and inhibiting action (in CMT) may produce apparent neuropsychological
impairment. Since these psychological variables can be targetted by psychological
treatment, routine testing pre- and post-behavioral treatment could help determine
the generalizability of experimental effects such as failures in selective inhibition.
Exploration of the domain-specific nature of CMT or OCD would also aid the
creation of analogue experimental paradigms where the correct situational provocation or degree of emotionality could be specified as a clinically credible high-risk
stimulus in order to elicit corresponding physiological changes, and CMT/OCD-like
behavior in both people with and without the disorders.
REFERENCES
ACAP Official Action. (1998). Practice parameters for the assessment and treatment of children and
adolescents with obsessive ± compulsive disorder. Journal of the American Academy of Child and Adolescent
Psychiatry, 3 (Suppl. 10), 27S ± 45S.
American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders (3rd ed., rev.).
Washington, DC: Author.
American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.).
Washington, DC: Author.
Amir, N., Ferrarelli, K., Watlington, C., Kozak, M.J., & Foa, E.B. (1997). The role of inhibition of threat in OCD:
negative priming. Paper presented at the 31st Annual Meeting of the Association for the Advancement of
Behavior Therapy, Miami Beach, FL.
Austin, L. S., Lydiard, R. B., Fossey, M. D., Zealberg, J. J., Laraia, M. T., & Ballenger, J. C. (1990). Panic and
phobic disorders in patients with obsessive ± compulsive disorder. Journal of Clinical Psychiatry, 51 (11),
456 ± 458.
Azrin, N. H., & Nunn, R. G. (1973). Habit reversal: a method of eliminating nervous habits and tics.
Behaviour Research and Therapy, 11, 619 ± 628.
Azrin, N. H., & Nunn, R. G. (1977). Habit control in a day. New York: Simon and Shuster.
Azrin, N. H., & Peterson, A. L. (1988a). Habit reversal for the treatment of Tourette syndrome. Behaviour
Research and Therapy, 26, 347 ± 351.
Azrin, N. H., & Peterson, A. L. (1988b). Behavior therapy for Tourette's syndrome and tic disorders. In: D.
J. Cohen, R. D. Bruun, & J. F. Leckman (Eds.), Tourette's syndrome and tic disorders: clinical understanding
and treatment ( Chap. 16, pp. 238 ± 255). New York: John Wiley and Sons.
Barr, C. L., & Sandors, P. (1998). Current status of genetic studies of Gilles de la Tourette syndrome.
Canadian Journal of Psychiatry, 43, 351 ± 357.
Baxter, L. R. (1995). Obsessive ± compulsive disorder. The Journal of the California Alliance for the Mentally Ill,
6 (1), 6 ± 7.
Baxter, L. R., Schwartz, J. M., Bergman, K. S., Szuba, M. P., Guze, B. H., Mazziotta, J. C., Alazraki, A., Selin,
C. E., Ferng, H.-K., Munford, P., & Phelps, M. E. (1992). Caudate glucose metabolic rate changes with
both drug and behavior therapy for obsessive ± compulsive disorder. Archives of General Psychiatry, 49,
681 ± 689.
Berthier, M. L., Kulisevsky, J., Gironell, A., & Heras, J.-A. (1996). Obsessive ± compulsive disorder associated
with brain lesions: clinical phenomenology, cognitive function, and anatomic correlates. Neurology, 47,
353 ± 361.
Billett, E. A., Richter, M. A., Sam, F., Swinson, R. P., Dai, X. Y., King, N., Badri, F., Sasaki, T., Buchanan, J. A.,
& Kennedy, J. L. (1998). Investigation of dopamine system genes in obsessive ± compulsive disorder.
Psychiatric Genetics, 8 (3), 163 ± 169.
Black, D. W., Noyes, R. Jr., Goldstein, R. B., & Blum, N. (1992). A family study of obsessive ± compulsive
disorder. Archives of General Psychiatry, 49, 362 ± 368.
Boone, K. B., Ananth, J., Philpott, L., Kaur, A., & Djenderedjian, A. (1991). Neuropsychological characteristics of nondepressed adults with obsessive ± compulsive disorder. Neuropsychiatry, Neuropsychology, and
Behavioral Neurology, 4 (2), 96 ± 109.
Brett, P. M., Curtis, D., Robertson, M. M., & Gurling, H. M. D. (1995). Exclusion of the 5-HT-sub (1A)
serotonin neuroreceptor and tryptophan oxygenase genes in a large British kindred multiply affected
Obsessive-compulsive and Chronic Tic Disorders
655
with Tourette's syndrome, chronic motor tics, and obsessive ± compulsive behavior. American Journal of
Psychiatry, 152, 437 ± 440.
Brown, H. D., Kosslyn, S. M., Breiter, H. C., Baer, L., & Jenike, M. A. (1994). Can patients with obsessive ±
compulsive disorder discriminate between percepts and mental images? A signal detection analysis.
Journal of Abnormal Psychology, 103 (3), 445 ± 454.
Caramelli, P., De Lima, M. A., Stip, E., & Bacheschi, L. A. (1996). Neurological examination in obsessive ±
compulsive disorder. Sao Paulo Medical Journal/RPM, 114, 1255 ± 1258.
Carr, J. E., Taylor, C. C., Wallander, R. J., & Reiss, M. L. (1996). A functional analytic approach to the
diagnosis of a transient tic disorder. Journal of Behavior Therapy and Experimental Psychiatry, 27, 291 ± 297.
Cath, D. C., Hoogduin, C. A. L., van de Wetering, B. J. M., van Woerkom, C. A. M., Roos, R. A. C., &
Rooymans, H. G. M. (1992). Tourette syndrome and obsessive ± compulsive disorder. An analysis of
associated phenomena. In: T. N. Chase, A. J. Friedhoff, & D. J. Cohen (Eds.), Advances in neurology,
(vol. 58, pp. 33 ± 41). New York: Raven Press.
Channon, S., Flynn, D., & Robertson, M. M. (1992). Attentional deficits in Gilles de la Tourette syndrome.
Neuropsychiatry, Neuropsychology, and Behavioral Neurology, 5, 170 ± 177.
Chee, K., & Sachdev, P. (1997). A controlled study of sensory tics in Gilles de la Tourette syndrome and
obsessive ± compulsive disorder using a structured interview. Journal of Neurology, Neurosurgery and
Psychiatry, 62, 188 ± 192.
Christenson, G. A., Ristvedt, S. L., & Mackenzie, T. B. (1993). Identification of trichotillomania cue profiles.
Behavioral Research and Therapy, 31, 315 ± 320.
Christenson, G. A., Faber, R. J., Zwaan, M., Raymond, N. C., Specker, S. M., Ekern, M. D., Mackenzie, T. B.,
Crosby, R. D., Crow, S. J., Eckert, E. D., Mussell, M. P., & Mitchell, J. E. (1994). Compulsive buying:
Descriptive characteristics and psychiatric comorbidity. Journal of Clinical Psychiatry, 55, 5 ± 11.
Clark, D. M., Ball, S., & Pape, D. (1991). An experimental investigation of thought suppression. Behavioral
Research and Therapy, 29, 253 ± 257.
Clayton, I. C., Richards, J. C., & Edwards, C. J. (1999). Selective attention in obsessive ± compulsive disorder.
Journal of Abnormal Psychology, 108, 171 ± 175.
Clemenz, B. A., Farber, R. H., Lam, M. N., & Swerdlow, N. R. (1996). Ocular motor responses to unpredictable and predictable smooth pursuit stimuli among patients with obsessive ± compulsive disorder.
Journal of Psychiatry and Neuroscience, 21, 21 ± 28.
Cohen, D. J., Leckman, J. F., & Shaywitz, B. A. (1992). The Tourette syndrome and other tics. In: J. F.
Cohen, & D. J. Cohen (Eds.), Clinical guide to child psychiatry ( pp. 3 ± 26). New York: Raven Press.
Comings, D. E., Himes, J. A., & Comings, B. G. (1990). An epidemiologic study of Tourette's syndrome in a
single school district. Journal of Clinical Psychiatry, 51 (11), 463 ± 469.
Commander, M., Corbett, J., Prendergast, M., & Ridley, C. (1991). Reflex tics in two patients with Gilles de
la Tourette syndrome. British Journal of Psychiatry, 159, 877 ± 879.
Constans, J. I., Foa, E. B., Franklin, M. E., & Mathews, A. (1995). Memory for actual and imagined events in
OC checkers. Behavioural Research and Therapy, 33, 665 ± 671.
Cox, C. S. (1997). Neuropsychological abnormalities in obsessive ± compulsive disorder and their assessments. International Review of Psychiatry, 9, 45 ± 59.
Dean, J. T., Nelson, E., & Moss, L. (1992). Pathologic hair pulling: a review of the literature and case
reports. Comprehensive Psychiatry, 33 (2), 84 ± 91.
de Groot, C. M., & Bornstein, R. A. (1994). Obsessive characteristics in subjects with Tourette's syndrome
are related to symptoms in their parents. Comprehensive Psychiatry, 35, 248 ± 251.
Dixon, A., Almodovar, S., Bateman, A., DiBartolo, P., & Frost, R. (1997). A laboratory procedure to inoculate
against the disruption of perfectionism on an evaluative task. Paper presented at the 31st Annual Meeting of
the Association for the Advancement of Behavior Therapy, Miami Beach, Florida.
Eapen, V., O'Neill, J., Gurling, H. M., & Robertson, M. M. (1997). Sex of parent transmission effect in
Tourette's synrome: evidence for earlier age at onset in maternally transmitted cases suggests a genomic
imprinting effect. Neurology, 48, 934 ± 937.
Eapen, V., Pauls, D. L., & Robertson, M. M. (1993). Evidence for autosomal dominant transmission in
Tourette's syndrome: United Kingdom cohort study. British Journal of Psychiatry, 162, 593 ± 596.
Emmelkamp, P. M. G. (1987). Phobic and obsessive ± compulsive disorder. In: L. Michelson, & L. M. Ascher
(Eds.), Anxiety and stress disorders ( pp. 310 ± 331). New York: Guilford Press.
Enoch, J. M., Schreier, H. A., & Barroso, L. (1995). Visual field defects in psychiatric disorders: possible
genetic implications. Biological Psychiatry, 37, 275 ± 277.
Enright, S. J., & Beech, A. R. (1993). Reduced cognitive inhibition in obsessive ± compulsive disorder. British
Journal of Clinical Psychology, 32, 67 ± 74.
656
K. P. O'Connor
Ernst, M., Zametkin, A. J., Jons, P. H., Matochik, J. A., Pascualvaca, D., & Cohen, R. M. (1999). High
presynaptic dopaminergic activity in children with Tourette's disorder. Journal of the American Academy
of Child and Adolescent Psychiatry, 38, 86 ± 94.
Factor, S. A., & Molho, E. S. (1997). Adult-onset tics associated with peripheral injury. Movement Disorders,
12, 1052 ± 1055.
Fallon, T. Jr., & Schwab-Stone, M. (1992). Methodology of epidemiological studies of tic disorders and
comorbid psychopathology. In: T. N. Chase, A. J. Friedhoff, & D. J. Cohen (Eds.), Advances in neurology,
(vol. 58, pp. 43 ± 52). New York: Raven Press.
Fava, G. A., Savron, G., Rafanelli, C., Grandi, S., & Canestrari, R. (1996). Prodromal symptoms in obsessive ±
compulsive disorder. Psychopathology, 29, 131 ± 134.
First, M. B., Frances, A., & Pincus, H. A. (1995). DSM-IV criteria for Tourette's: reply. Journal of the American
Academy of Child and Adolescent Psychiatry, 34, 402.
Foa, E. B., Ilai, D., McCarthy, P. R., Shoyer, B., et al. (1993). Information processing in obsessive ± compulsive disorder. Cognitive Therapy and Research, 17, 173 ± 189.
Foa, E. B., & Kozak, M. J. (1996). Psychological treatment for obsessive ± compulsive disorder. In: M. R.
Prien, & R. F. Prien (Eds.), Long-term treatment of anxiety disorders ( pp. 285 ± 309). Washington, DC:
American Psychiatric Press.
Freeston, M. H., & Ladouceur, R. (1997). What do patients do with their obsessive thoughts? Behavioral
Research Therapy, 35, 335 ± 348.
Freeston, M. H., RheÂaume, J., & Ladouceur, R. (1996). Correcting faulty appraisals of obsessional thoughts.
Behavioural Research and Therapy, 34, 433 ± 446.
Frost, R. O., Marten, P., Lahart, C., & Rosenblate, R. (1990). The dimensions of perfectionism. Cognitive
Therapy and Research, 14, 449 ± 468.
Fuata, P., & Griffiths, R. A. (1992). Cognitive behavioural treatment of a vocal tic. Behaviour Change, 9,
14 ± 18.
George, M. S., Trimble, M. R., Ring, H. A., Sallee, F. R., & Robertson, M. M. (1993). Obsessions in
obsessive ± compulsive disorder with and without Gilles de la Tourette's syndrome. American Journal
of Psychiatry, 150, 93 ± 97.
Georgiou, N., Bradshaw, J. L., Phillips, J. G., Cunnington, R., & Rogers, M. (1997). Functional asymmetries
in the movement kinematics of patients with Tourette's syndrome. Journal of Neurology, Neurosurgery and
Psychiatry, 63, 188 ± 195.
Gerlsma, C., Emmelkamp, P. M. G., & Arrindell, W. A. (1990). Anxiety, depression, and perception of early
parenting: a meta-analysis. Clinical Psychology Review, 10, 251 ± 277.
Gilboa-Schectman, E., Franklin, M.E., Ferrarelli, K., & Foa, E.B. (1997). Evaluation biases in individuals with
anxiety disorders: probability and cost estimates of interpersonal events in generalized social phobia, OCD, and
controls. Paper presented at the 31st Annual Meeting of the Association for the Advancement of Behavior Therapy, Miami Beach, Florida.
Gironell, A., Rodriguez-Fornells, A., Kulisevsky, J., Pascual, B., Riba, J., Barbanoj, M., & Berthier, M. (2000).
Abnormalities of the acoustic startle reflex and reaction time in Gilles de la Tourette syndrome. Clinical
Neurophysiology, 111, 1366 ± 1371.
Goodman, W. K., McDougle, C. J., Price, L. H., Riddle, M. A., Pauls, D. L., & Leckman, J. F. (1990). Beyond
the serotonin hypothesis: a role for dopamine in some forms of obsessive compulsive disorder? Journal
of Clinical Psychiatry, 51 (8), 36 ± 43.
Guidano, V., & Liotti, R. (1988). Complexity of the self. New York: Guilford Press.
Hafner, R. J. (1988). Obsessive ± compulsive disorder: a questionnaire survey of a self-help group. International Journal of Social Psychiatry, 34, 310 ± 315.
Hoehn-Saric, R., Harris, G. J., Pearlson, G. D., Cox, C. S., Machlin, S. R., & Camargo, E. E. (1991). A
fluoxetine-induced frontal lobe syndrome in an obsessive compulsive patient. Journal of Clinical Psychiatry, 52, 3.
Hoekstra, R. J., Visser, S., & Emmelkamp, P. M. G. (1989). A social learning formulation of the etiology of
obsessive ± compulsive disorders. In: P. M. G. Emmelkamp, W.T.A.M. Everaerd, F. Kraaimaat, & M. J. M.
van Son (Eds.), Fresh perspectives on anxiety disorders (pp. 115 ± 123). Amsterdam: Swets and Zeitlinger.
Hollander, E., Schiffman, E., Cohen, B., Rivera-Stein, M. A., Rosen, W., Gorman, J. M., Fyer, A. J., Papp, L.,
& Liebowitz, M. R. (1990). Signs of central nervous system dysfunction in obsessive ± compulsive disorder. Archives of General Psychiatry, 47, 27 ± 32.
Holzer, J. C., Goodman, W. K., McDougle, C. J., Baer, L., Boyarsky, B. Y., Leckman, J. F., & Price, L. H.
(1994). Obsessive-compulsive disorder with and without a chronic tic disorder. British Journal of Psychiatry, 164, 469 ± 473.
Obsessive-compulsive and Chronic Tic Disorders
657
Hoogduin, C. A. L. (1986). On the diagnosis of obsessive ± compulsive disorder. American Journal of Psychotherapy, 36 ± 51.
Hyde, T. M., & Weinberger, D. R. (1995). Tourette's syndrome: a model neuropsychiatric disorder. Journal
of the American Medical Association, 273, 498 ± 501.
Janet, P. (1903). Les Obsessions et la Psychasthenie. Paris: FeÂlix Arcan. [reprinted in New York: Arno Press, 1976].
Kane, M. J. (1994). Premonitory urges as ``attentional tics'' in Tourette's syndrome. Journal of the American
Adademy of Child and Adolescent Psychiatry, 33, 6.
King, R. A., Scahill, L., Vitulano, L. A., Schwab-Stone, M., Tercyak, K. P. Jr., & Riddle, M. A. (1995).
Childhood trichotillomania: clinical phenomenology, comorbidity, and family genetics. Journal of American Academy of Child and Adolescent Psychiatry, 34, 1451 ± 1459.
Knell, E. R., & Comings, D. E. (1993). Tourette's syndrome and attention-deficit hyperactivity disorder:
evidence for a genetic relationship. Journal of Clinical Psychiatry, 54, 331 ± 337.
Lang, A. E., Consky, E., & Sandor, P. (1993). ``Signing tics'' and Insights into the pathophysiology of
symptoms in Tourette's syndrome. Annals of Neurology, 33, 212 ± 215.
Leckman, J. F., & Chittenden, E. H. (1990). Gilles de la Tourette's syndrome and some forms of obsessive ±
compulsive disorder may share a common genetic diathesis. EnceÂphale, 16 (Suppl. 1), 321 ± 323.
Leckman, J. F., Grice, D. E., Barr, L. C., de Vries, A. L. C., Martin, C., Cohen, D. J., McDouble, C. J.,
Goodman, W. K., & Rasmussen, S. A. (1994/1995). Tic-related vs. non-tic-related obsessive compulsive
disorder. Anxiety, 1, 208 ± 215.
Leckman, J. F., Walker, D. E., & Cohen, D. J. (1993). Premonitory urges in Tourette's syndrome. American
Journal of Psychiatry, 150, 98 ± 102.
Leonard, H. L., Lenane, M. C., Swedo, S. E., Rettew, D. C., Gershon, E. S., & Rapoport, J. L. (1992). Tics
and Tourette's disorder: a 2- to 7-year follow-up of 54 obsessive ± compulsive children. American Journal
of Psychiatry, 149, 1244 ± 1251.
Makhlouf-Norris, F., & Norris, H. (1973). The obsessive compulsive syndrome as a neurotic device for the
reduction of self-uncertainty. British Journal of Psychiatry, 122 (568), 277 ± 288.
Maki, W. S., O'Neill, H. K., & O'Neill, G. W. (1994). Do nonclinical checkers exhibit deficits in cognitive
control? Tests of an inhibitory control hypothesis. Behaviour Research and Therapy, 32, 183 ± 192.
Mansueto, C. S., Goldfinger Golomb, R., McCombs Thomas, A., & Townsley Stemberger, R. M. (1999). A
comprehensive model for behavioral treatment of trichotillomania. Cognitive and Behavioral Practice, 6,
23 ± 43.
McConville, B. J., & Norman, A. B. (1992). Nicotine potentiation of haloperidol in reducing tic frequency
in Tourette's disorder: reply. American Journal of Psychiatry, 149, 418.
McMahon, W. M., van de Wetering, B. J., Filloux, F., Betit, K., Coon, H., & Leppert, M. (1996). Bilineal
transmission and phenotypic variation of Tourette's disorder in a large pedigree. Journal of American
Child and Adolescent Psychiatry, 35, 672 ± 680.
McNally, R. J., & Kohlbeck, P. A. (1993). Reality monitoring in obsessive ± compulsive disorder. Behaviour
Research and Therapy, 31, 249 ± 253.
Meyer, V. (1966). Modification of expectations in cases with obsessional rituals. Behaviour Research and
Therapy, 4, 273 ± 280.
Miele, G. M., Tilly, S. M., Frist, M., & Frances, A. (1990). The definition of dependence and behavioural
addictions. British Journal of Addiction, 85, 1421 ± 1423.
Miguel, E. C., Coffey, B. J., Baer, L., Savage, C. R., Rauch, S. L., & Jenike, M. A. (1995). Phenomenology of
intentional repetitive behaviors in obsessive ± compulsive disorder and Tourette's disorder. Journal of
Clinical Psychiatry, 56, 246 ± 255.
Mueller, N., Putz, A., Straube, A., & Kathmann, N. (1995). Obsessive ± compulsive disorder and Gilles de
la Tourette syndrome: Differential diagnosis of organic and psychogenic symptoms. Nervenarzt, 66,
272 ± 278.
Nelson, J., & Chouinard, G. (1995). Le trouble obsessionel ± compulsif n'est pas un trouble anxieux.
Confrontations Psychiatriques, 36, 211 ± 245.
Nomoto, F. (1989). Tourette's syndrome. Journal of Mental Health, 35, 63 ± 70.
O'Connor, K. P., Gareau, D., & Borgeat, F. (1995). Muscle control in chronic tic disorders. Biofeedback and
Self-Regulation, 20, 111 ± 121.
O'Connor, K., & PeÂlissier, M.-C. (1998). Deductive and inductive inference bias in obsessive ± compulsive disorder
(OCD). Poster, World Congress of Behavioral and Cognitive Therapies (WCBCT) Acapulco, Mexico,
July 1998.
O'Connor, K. P. (1989). Individual differences and motor systems. In: T. Ney, & A. Gale (Eds.), Smoking and
human behaviour ( pp. 141 ± 170). Chichester: Wiley.
658
K. P. O'Connor
O'Connor, K. P., Gareau, D., & Blowers, G. H. (1993). Changes in construals of tic-producing situations
following cognitive and behavioral therapy. Perceptual and Motor Skills, 77, 776 ± 778.
O'Connor, K. P., Gareau, D., & Blowers, G. H. (1994). Personal constructs associated with tics. British
Journal of Clinical Psychology, 33, 151 ± 158.
O'Connor, K. P., Gareau, D., & Borgeat, F. (1997). A comparison of behavioral and cognitive ± behavioral
management of tic disorders. Clinical Psychology and Psychotherapy, 4, 105 ± 117.
O'Connor, K. P., Serawaty, M., & Stip, E. (1999). Simple and complex motor processing in chronic tic
disorders. Brain and Cognition, 40 (1), 211 ± 215.
O'Connor, K. P., Brault, M., Robillard, S., Loiselle, J., Borgeat, F., & Stip, E. (2000a). Evaluation of cognitive
behavioral program for the management of chronic tic and habit disorders. Behaviour Research and
Therapy (in press).
O'Connor, K. P., Robert, M., Dubord, J., & Stip, E. (2000b). Automatic and controlled processing in
chronic tic disorders. Brain and Cognition, 43, 349 ± 352.
O'Connor, K. P., Brault, M., Robillard, S., Loiselle, J., Borgeat, F., & Stip, E. (2001a). Does behavior therapy
modify performance in chronic tic disorders? Poster, World Congress of Behavioral and Cognitive
Therapies, Vancouver, Canada, July 2001.
O'Connor, K. P., Brisebois, H., Brault, M., Robillard, S., & Loiselle, J. (2001b). Situational cues in chronic
tic and habit disorders. Poster, World Congress of Behavioral and Cognitive Therapies, Vancouver,
Canada, July 2001.
Oltmanns, T. F., & Gibbs, N. A. (1995). Emotional responsiveness and obsessive ± compulsive behaviour.
Cognition and Emotion, 9, 563 ± 578.
Otto, M. W. (1992). Normal and abnormal information processing: a neuropsychological perspective on
obsessive compulsive disorder. Psychiatric Clinics of North America, 15, 825 ± 848.
Parraga, H. C., Parraga, M. I., Spinner, L. R., Kelly, D. P., & Morgan, S. L. (1998). Clinical differences
between subjects with familial and non-familial Tourette's syndrome: a case series. International Journal
of Psychiatry in Medicine, 28, 341 ± 351.
Pauls, D. L. (1992). The genetics of obsessive compulsive disorder and Gilles de la Tourette's syndrome.
Psychiatric Clinics of North America, 15, 759 ± 766.
Pauls, D. L., Alsobrook, J. P. II, Goodman, W., Rasmussen, S., & Leckman, J. F. (1995). A family study of
obsessive ± compulsive disorder. American Journal of Psychiatry, 152, 1.
Pauls, D. L., Towbin, K. E., Leckman, J. F., Zahner, G. E. P., & Cohen, D. (1986). Gilles de la Tourette's
syndrome and obsessive ± compulsive disorder. Evidence supporting a genetic relationship. Archives of
General Psychiatry, 43, 1180 ± 1182.
Peschel, E., & Peschel, R. (1991). Neurobiological disorders. The Journal of the California Alliance for the
Mentally Ill, 2 (4), 4.
Peterson, A. L., Campise, R. L., & Azrin, N. H. (1994). Behavioral and pharmacological treatments for tic
and habit disorders: a review. Developmental and Behavioral Pediatrics, 15, 430 ± 441.
Peterson, B. S., Zhang, H., Anderson, G. M., & Leckman, J. F. (1998). A double-blind, placebo-controlled,
crossover trial of an antiandrogen in the treatment of Tourette's syndrome. Journal of Clinical Psychopharmacology, 18, 324 ± 331.
Petter, T., Richter, M. A., & Sandor, P. (1998). Clinical features distinguishing patients with Tourette's
syndrome and obsessive-compulsive disorder from patients with obsessive-compulsive disorder without
tics. Journal of Clinical Psychiatry, 59, 456 ± 459.
Pitman, R. K., Green, R. C., Jenike, M. A., & Mesulam, M. M. (1987). Clinical comparison of Tourette's
disorder and obsessive-compulsive disorder. American Journal of Psychiatry, 144, 1166 ± 1171.
Prichep, L. S., Mas, F., Hollander, E., Liebowitz, M., John, E. R., Almas, M., DeCaria, C. M., & Levine, R. H.
(1993). Quantitative electroencephalographic subtyping of obsessive ± compulsive disorder. Psychiatry
Research: Neuroimaging, 50, 25 ± 32.
Purdon (1999). Thought suppression and psychopathology. Behaviour Research and Therapy, 37, 1029 ± 1054.
Rachman, S. (1993). Obsessions, responsibility and guilt. Behaviour Research and Therapy, 31, 149 ± 154.
Rachman, S. (1997). A cognitive theory of obsessions. Behaviour Research and Therapy, 35, 793 ± 802.
Rachman, S., & Hodgson, R. (1980). Obsessions and compulsions. New York: Prentice Hall.
Radomsky, A.S., & Rachman, S. (1999). Memory bias in obsessive ± compulsive disorder (OCD). Behaviour Research and Therapy, 37, 605 ± 618.
Rapoport, J. L., Swedo, S. E., & Leonard, H. L. (1992). Childhood obsessive compulsive disorder. Journal of
Clinical Psychiatry, 53 (Suppl.), 11 ± 16.
Rasmussen, S. A. (1993). Genetic studies of obsessive ± compulsive disorder. Annals of Clinical Psychiatry, 5,
241 ± 247.
Obsessive-compulsive and Chronic Tic Disorders
659
Rasmussen, S. A., & Eisen, J. L. (1992). The epidemiology and differential diagnosis of obsessive ± compulsive disorder. Journal of Clinical Psychiatry, 53 (Suppl.), 4 ± 10.
Reed, G. F. (1985). Obsessional experience and compulsive behavior: a cognitive structural approach. Orlando,
FL: Academic Press.
Rettew, D. C., Cheslow, D. L., Rapoport, J. L., Leonard, H. L., Lenane, M. C., Black, B., & Swedo, S. E.
(1991). Neuropsychological test performance in trichotillomania: a further link with obsessive ± compulsive disorder. Journal of Anxiety Disorders, 5, 225 ± 235.
Rice, K. G., Ashby, J. S., & Preusser, K. J. (1996). Perfectionism, relationships with parents, and self-esteem.
Individual psychology. Journal of Adlerian Theory, Research and Practice, 52, 246 ± 260.
Richards, E. H. (1992). Nicotine gum in Tourette's disorder. American Journal of Psychiatry, 149, 417.
Riddle, M. A., Scahill, L., King, R., Hardin, M. T., Towbin, K. E., Ort, S. I., Leckman, J. F., & Cohen, D. J.
(1990). Obsessive compulsive disorder in children and adolescents: Phenomenology and family history.
Journal of the American Academy of Child and Adolescent Psychiatry, 29 (5), 766 ± 772.
Robertson, M. M., & Gourdie, A. (1990). Familial Tourette's syndrome in a large British pedigree associated
psychopathology, severity, and potential for linkage analysis. British Journal of Psychiatry, 156, 515 ± 521.
Robertson, M. M., & Stern, J. S. (1998). Tic disorders: new developments in Tourette syndrome and related
disorders. Current Opinion in Neurology, 11, 373 ± 380.
Rosenberg, L. A., Brown, J., & Singer, H. S. (1994). Self-reporting of behavior problems in patients with tic
disorders. Psychological Reports, 74, 653 ± 654.
Rubenstein, C. S., Peynircioglu, Z. F., Chambless, D. L., & Pigott, T. A. (1993). Memory in sub-clinical
obsessive ± compulsive checkers. Behavioural Research and Therapy, 31, 759 ± 765.
Sachdev, P. S., Chee, K. Y., & Aniss, A. M. (1997). The audiogenic startle reflex in Tourette's syndrome.
Biological Psychiatry, 41, 796 ± 803.
Salkovis, P. M. (1999). Understanding and treating obsessive compulsive disorders. Behavior Research and
Therapy, 37, S29 ± S52.
Salkovskis, P. M., & Warwick, H. M. C. (1998). Cognitive therapy of obsessive ± compulsive disorder. In:
C. Perris, I. M. Blackburn, & H. Perris (Eds.), Cognitive psychotherapy: theory and practice ( pp. 48 ± 74).
New York: Springer-Verlag.
Sanberg, P. R., Silver, A. A., Shytle, R. D., Philipp, M. K., Cahill, D. W., Fogelson, H. M., & McConville, B. J.
(1997). Nicotine for the treatment of Tourette's syndrome. Pharmacological Therapy, 74, 21 ± 25.
Savage, C. R., Weilburg, J. B., Duffy, F. H., Baer, L., Shera, D. M., & Jenike, M. A. (1994). Low-level
sensory processing in obsessive ± compulsive disorder: an evoked potential study. Biological Psychiatry,
35, 247 ± 252.
Savoie, D. (1996). A phenomenological investigation of the role of guilt in obsessive ± compulsive disorder.
Journal of Phenomenological Psychology, 27, 193 ± 218.
Schultz, R. T., Carter, A. S., Scahill, L., & Leckman, J. F. (1999). Neuropsychological findings. In: J.
F. Leckman, & D. J. Cohen (Eds.), Tourette's syndrome Ð tics, obsessions, compulsions. Developmental
psychopathology and clinical care (pp. 80 ± 103). New York: John Wiley and Sons.
Schut, A.J., Pincus, A.L., Castonguay, L.G., Bedics, J., Walling, F., Yanni, G., & Truckor, D. (1997). Attachment and interpersonal problems in non-clinical hair pulling. Paper presented at the 31st Annual Convention
of the Association for the Advancement of Behavior Therapy, Miami Beach, Florida.
Scotti, J. R., Schulman, D. E., & Hojnacki, R. M. (1994). Functional analysis and unsuccessful treatment of
Tourette's syndrome in a man with profound mental retardation. Behavior Therapy, 25, 721 ± 738.
Seligman, A. (1991). Echolalia. Duarte, CA: Hope Press.
Shapiro, A. K., & Shapiro, E. (1992). Evaluation of the reported association of obsessive ± compulsive
symptoms or disorder with Tourette's disorder. Comprehensive Psychiatry, 33, 152 ± 165.
Shapiro, A., & Shapiro, E. (1986). Clinical dangers of psychological theorizing. Psychiatry Quarterly, 45,
159 ± 171.
Sher, K. J., Mann, B., & Frost, R. (1984). Cognitive dysfunction in compulsive checkers: further explorations. Behaviour Research and Therapy, 22, 493 ± 502.
Silverman, J. S., & Loychik, S. G. (1990). Brain-mapping abnormalities in a family with three obsessive
compulsive children. Journal of Neuropsychiatry and Clinical Neurosciences, 2, 319 ± 322.
Silverstein, S. M., Como, P. G., Palumbo, D. R., West, L. L., et al (1995). Multiple sources of attentional
dysfunction in adults with Tourette's syndrome: Comparison with attention deficit ± hyperactivity disorder. Neuropsychology, 9 (2), 157 ± 164.
Solomon, R. L., & Corbit, J. D. (1973). An opponent-process theory of motivation: II. Cigarette addiction.
Journal of Abnormal Psychology, 82, 158 ± 171.
Spencer, T., Biederman, J., Harding, M., Wilens, T., & Faraone, S. (1995). The relationship between tic
660
K. P. O'Connor
disorders and Tourette's syndrome revisited. Journal of the American Academy of Child and Adolescent
Psychiatry, 34, 1133 ± 1139.
Stanne, M. B., Johnson, D. W., & Johnson, R. T. (1999). Does competition enhance or inhibit motor
performance? A meta analysis. Psychological Bulletin, 125, 133 ± 154.
Stemberger, R.M.T., McCombs Thomas, A., Carter, J., Delahanty, J., Jones, D., Mansueto, C.S., & Goldfinger
Golomb, R. (1997). Trichotillomania, interpersonal relationships, and self-perceptions. Paper presented at the
31st Annual meeting of the Association for the Advancement of Behavior Therapy, Miami Beach, FL.
Swedo, S. E., & Leonard, H. L. (1994). Childhood movement disorders and obsessive ± compulsive disorder.
Journal of Clinical Psychiatry, 55 (Suppl.), 32 ± 37.
Tata, P. R., Leibowitz, J. A., Prunty, M. J., Cameron, M., & Pickering, A. D. (1996). Attentional bias in
obsessional compulsive disorder. Behaviour Research and Therapy, 34, 53 ± 60.
The Tourette Syndrome Classification Study Group. (1993). Definitions and classification of tic disorders.
Archives of Neurology, 50, 1013 ± 1016.
Thibert, A. L., Day, H. I., & Sandor, P. (1995). Self-concept and self-consciousness in adults with Tourette
syndrome. Canadian Journal of Psychiatry, 40, 35 ± 39.
Thomsen, P. H., & Jensen, J. (1994). Obsessive ± compulsive disorder: admission patterns and diagnostic
stability. A case-register study. Acta Psychiatrica Scandinavica, 90, 19 ± 24.
Tijssen, M. A. J., Brown, P., Morris, H. R., & Lees, A. (1999). Late onset startle induced tics. Journal of
Neurology, Neurosurgery and Psychiatry, 67, 782 ± 784.
Tulen, J. H., van de Wetering, B. J., & Boomsma, F. (1998). Autonomic regulation during rest and mental
load in Gilles de la Tourette syndrome. Psychological Reports, 83, 515 ± 529.
Turgeon, L., O'Connor, K., & Marchand, A. (1998). Recollections of parent ± child relationships in OCD outpatients compared to panic disorder outpatients and normal controls. World Congress of Behavioral and
Cognitive Therapies (WCBCT) Acapulco, Mexico.
Van Oppen, P., Hoekstra, R. J., & Emmelkamp, P. M. G. (1995). The structure of obsessive compulsive
symptoms. Behaviour Research and Therapy, 33, 15 ± 24.
Vogel, P.A., Stiles, T.C., & Nordahl, H.M. (1997). Recollections of parent ± child relationships in OCD outpatients
compared to depressed outpatients and healthy controls. Paper presented at the Anxiety Disorders American
Association, New Orleans, LA.
Walters, A. S., Boudwin, J., Wright, D., & Jones, K. (1988). Three hysterical movement disorders. Psychological Reports, 62, 979 ± 985.
Watson, T. S., & Sterling, H. E. (1998). Brief functional analysis and treatment of a vocal tic. Journal of
Applied Behavior Analysis, 31, 471 ± 474.
Wilhelm, S., McNally, R. J., Baer, L., & Florin, I. (1996). Directed forgetting in obsessive ± compulsive
disorder. Behaviour Research and Therapy, 34, 633 ± 641.
Wojcieszek, J. M., & Lang, A. E. (1995). Gestes antagonistes in the suppression of tics: Tricks for tics.
Movement Diosrders, 10, 226 ± 228.
Woods, D. W., Miltenberger, R. G., & Flach, A. D. (1996). Habits, tics, and stuttering: prevalence and
relation to anxiety and somatic awareness. Behavior Modification, 20, 216 ± 225.
Woods, D. W., Miltenberger, R. G., & Lumley, V. A. (1996). Sequential application of major habit-reversal
components to treat motor tics in children. Journal of Applied Behavior Analysis, 29, 483 ± 493.
Wright, K. M., & Miltenberger, R. G. (1987). Awareness training in the treatment of head and facial tics.
Journal of Behaviour Therapy and Experimental Psychiatry, 18, 269 ± 274.
Zahn, T. P., Leonard, H. L., Swedo, S. E., & Rapoport, J. L. (1996). Autonomic activity in children and
adolescents with obsessive ± compulsive disorder. Psychiatry Research, 60, 67 ± 76.
Zielinski, C. M., Taylor, M. A., & Juzwin, K. R. (1991). Neuropsychological deficits in obsessive ± compulsive
disorder. Neuropsychiatry, Neuropsychology, and Behavioral Neurology, 4, 110 ± 126.
Ziemann, U., Paulus, W., & Rothenberger, A. (1997). Decreased motor inhibition in Tourette's disorder:
evidence from transcranial magnetic stimulation. American Journal of Psychiatry, 154, 1277 ± 1284.
Zohar, A. H., Ratzoni, G., Pauls, D. L., Apter, A., Bleich, A., Kron, S., Rappaport, M., Weizman, A., & Cohen,
D. J. (1992). An epidemiological study of obsessive-compulsive disorder and related disorders in Israeli
adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 1057 ± 1061.
Zohar, A. H. (1999). The epidemiology of obsessive-compulsive disorder in children and adolescents. Child
and Adolescent Psychiatric Clinics of North America, 8 (3), 334 ± 460.
Zuellig, A. R., Newman, M. G., Kachin, K. E., & Constantino, M. J. (1997). Differences in parental attachment
profiles in adults diagnosed with generalized anxiety disorder, panic disorder, or non-disordered. Poster presented at the 31st Conference of the Association for Advancement of Behavior Therapy, Miami
Beach, FL.