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Volume 2 | Issue 1 | 1 of 8
Int J Psychiatry, 2017
Mechanisms of Response Prevention and the Use of Exposure as erapy for
Obsessive-Compulsive Disorder
Review Article
1Tehran University of Medical Sciences, Tehran, Iran.
2Dept of Psychology, University of Oregon, Eugene.
Abstract
The combination of exposure therapy and response prevention (ERP) is the most widely used and to date the most
effective treatment for obsessive-compulsive disorder. We review the two main theoretical mechanisms proposed to
account for the effectiveness of ERP: (1) habituation of anxiety due to exposure and (2) extinction due to withholding
reinforcement of behaviors undertaken to decrease anxiety. Both of these mechanisms have their origin in behavior
theory based upon classical and instrumental conditioning, and relate to the view that OCD is an anxiety-related or
anxiety- based disorder. DSM- 5, however, no longer lists OCD as an anxiety disorder, instead positing an obsessive
- compulsive disorder spectrum (OCDS), and emphasizing the diversity of OCD symptoms. More recent cognitive
and neuroscience approaches have also stressed mechanisms involved in the control of emotional and behavioral
responses. In this paper we review habituation and extinction accounts and attempt to integrate the newer neuroscience
perspectives, moving toward a more complete framework for understanding OCD treatment.
International Journal of Psychiatry
Habibollah Ghassemzadeh1, Mary K. Rothbart2 and Michael I.Posner2*
*Corresponding author
Michael I. Posner, University of Oregon, Eugene, OR USA, E-Mail:
mposner@uoregon.edu.
Submitted: 14 Nov 2016; Accepted: 26 Dec 2017; Published: 30 Apr 2017
Keywords: ERP, Habituation, Extinction, OCDS, Neuroscience
perspectives
Introduction
Obsessive-Compulsive Disorder (OCD) is a common, chronic
disorder in which a person has uncontrollable, reoccurring
thoughts or images (obsessions) and/or behaviors (compulsions)
that he or she feels the urge to repeat over and over– mostly in
a ritualistic manner. OCD has many subtypes or clusters of
symptoms. Rasmussen and Eisen studied 560 OCD patients in
the USA meeting DSM-III or DSM-III-R criteria [1]. The most
prevalent obsession theme in that study was contamination (50%),
and the least prevalent was sexual impulse (24%). The other themes
included pathologic doubt, somatic concerns, need for symmetry,
and aggressive impulses. The most prevalent compulsion was
checking (61%) and the least prevalent was hoarding (18%).
Other compulsive behavior included cleaning/washing, counting,
seeking exactness and expressing a need to confess.
Obsessive- compulsive disorder has been indicated as the fourth
most common psychiatric disorder and the tenth leading cause
of disability in the world (World Health Organization [2]. The
lifetime prevalence of OCD worldwide is approximately 2-3 %
and the prevalence in ve US communities ranged from 1.9 to
3.3 % [3, 4]. According to the National Institute of Mental Health
(NIMH) more than 2.2 million Americans suffer from obsessive-
compulsive disorder. It strikes men and women in roughly equal
numbers and usually appears in childhood, adolescence, or early
adulthood. One-third of adults with OCD developed symptoms
as children, and research indicates that OCD may run in families.
Although the prevalence of various symptoms tends to vary
widely across different cultures and studies, the overall pattern of
symptoms is more or less similar [5, 6].
In this paper we examine exposure therapy combined with response
prevention (ERP), one of the most widely applied psychological
treatments in anxiety-related disorders in general and obsessive-
compulsive disorder (OCD) in particular.It is important to note,
however, that in the 5th edition of the Diagnostic and Statistical
Manual of the American Psychiatric Association the disorder
was removed from the set of anxiety disorders and given its own
spectrum [7]. Because of the new diagnostic category and recent
imaging ndings we focus on relating issues of exposure to those of
response prevention to develop a common framework for therapy.
In a recent meta-analysis, different pharmacological and
psychotherapeutic interventions for OCD in adults were
systematically reviewed and analyzed [8, 9]. The three main
categories of psychotherapeutic interventions were examined:
behavioral therapy (BT), cognitive therapy (CT), cognitive
behavioral therapy (CBT) and CBT with ERP. The pharmacological
agents included clomipramine, uvoxamine, and SSRIs. The
investigators also considered the combinations of psychological
and pharmacological treatments. The criterion for efcacy was
based on Yale-Brown Obsessive Compulsive Scale and the waiting
list was taken as a control group in most of these studies.
Results showed that all three psychotherapeutic interventions were
more effective than drug placebo. Comparing these 3 interventions,
cognitive behavioral therapy (CBT) was less effective than BT
Volume 2 | Issue 1 | 2 of 8Int J Psychiatry 2017
and CT and was not different from the psychological placebo
(general stress management). But excluding waiting list controls
led to a larger effect of CBT. The general conclusion was that
all 3 psychotherapies “were more likely to lead to a larger effect
than were medications” (p.7). The combined treatment of both
medication and psychological treatment was more effective than
the latter alone. This nding differs from the Foa et al. study,
which showed CBT combined with pharmacological treatment
(clomipramine) was not more effective than CBT alone [10].
Although some practitioners using cognitive models of OCD
have found cognitive methods to be the best choice for reducing
obsessions and compulsions, cognitive therapy and cognitive
behavior therapy in this review “are no more effective than
ERP”(p.145) [11]. Also as Abramowitz has indicated, “the
prognosis for individuals for OCD has changed from poor to very
good as a result of the development of ERP” (p.407) [12]. We now
consider some of the most popular theoretical models of ERP,
and results of brain imaging studies suggesting alternative views
of the effectiveness of ERP and the possibility of new treatment
approaches.
Exposure and exposure therapy
Exposure therapy and response prevention (ERP) involves a set
of psychological treatment approaches and/or techniques for
improving anxiety-related disorders, including OCD. The common
core of these approaches and techniques is asking patients to
confront their anxiety provoking situations or fearful thoughts
while controlling their usual response to the situation.
Two main theoretical mechanisms have been proposed to
account for the effectiveness of ERP: habituation due to response
exposure, and extinction due to withholding reinforcement of
the behaviors undertaken to decrease anxiety [13]. Both of these
mechanisms have their origin in behavior theory based on classical
and instrumental conditioning, and are for the most part based on
the view that OCD is an anxiety disorder. There are problems,
however, regarding the theoretical basis of this set of treatments
and the mechanism of their efcacy. As argued by Abramowitz, it
is crucial to have an up to date theoretical framework in order to
design and execute effective treatment [13].
In this paper we review the historical basis for dening the role of
habituation and extinction in ERP. In addition, we consider new
studies using imaging to identify mechanisms of control of responses
in OCD. In particular, brain systems of executive attention have
been found to exercise control over both emotional and behavioral
responses [14]. We hope this review might aid clinicians to clarify
the theory underlying existing therapies and aid in the development
of possible new therapies that could improve treatment of OCD.
Historically the application of exposure/response prevention goes
back to Meyer’s innovative work on the treatment of two patients:
one with compulsive washing and another with sexual obsessions
[15]. The main rationale for this approach was that if OCD patients
are asked and persuaded in a fear situation to withhold carrying
out the compulsive rituals, they will eventually realize that (1)
the feared consequences of not performing the ritual do not occur
and (2) their expectations of “disastrous consequences” are not
fullled [15]. Meyer reported some success in his rst study and
in a later study, used the same technique with 15 OCD patients.
In the second study ten patients were either “much improved” or
totally improved [16]. Meyer’s main conceptualization was that “a
completely successful modication of expectations would lead to
a complete elimination of ritualistic behavior” [15].
Although Meyer’s treatment was based on modication of
expectations, a likely cognitive interpretation, many researchers
and clinicians shifted their attention from a cognitive strategy
to a behavioral mechanism, attempting to explain the possible
treatment effects of ERP within the framework of conditioning
terminology [16].
At this time behavior was associated with physical reexes, for
example, Isaac Marks published an article entitled “the current
status of behavioral psychotherapy: theory and practice”,
suggesting exposure as a common principle of most behavioral
approaches to the treatment of phobic disorders and compulsive
rituals [17]. He refers to Wolpe’s desensitization in fantasy as
an early form of exposure treatment (imaginal exposure) [18].
He also explains exposure in vivo, which gives quicker results
by bringing the patient into contact with the anxiety-provoking
situation without relaxation [19].
Emotional processing theory
Probably the most inuential recent theoretical approach to OCD
has been emotional processing theory. Lang’s bio- informational
theory described anxiety as an emotional memory stored within
a semantic brain network [20, 21]. The emotional memories
were hypothesized to contain three categories of information,
(1) information about the stimulus or situation that evokes
the emotional memory structure; (2) information regarding an
individual’s responses (physiological, motor and cognitive);
and (3) elaboration that denes the meaning of the stimulus and
response. Emotions are dened as stored action dispositions,
released when a fear structure is activated. Any response pattern
depends on arousal level, valence of the stimuli, and degree of
control.
Foa extended the ideas of Lang and Rachman and proposed a
processing theory, hypothesizing that anxiety occurs as the result
of a pathological “fear structure” held in memory [20-23]. A fear
structure is a propositional network of information related to a
program to escape or avoid danger.
From this perspective, in any systematic exposure therapy session,
three important events occur. The rst is activation of the fear
structure in memory. The second is introduction of corrective
information through repeated and prolonged exposure to the feared
stimulus, leading to a modication of the fear structure, allowing
habituation within the session. The third involves changes in
the meaning of the activated fear structure. This change occurs
between sessions and is more reliably associated with long-term
therapeutic change.
Foa and McNally further revised the emotional processing
approach in a more cognitive direction by suggesting that any
successful exposure therapy goes beyond the mere modication
of existing fear structures [23]. New structures are created, which
override the previous associations.
In a more recent revision, Foa, Ruppert & Cahill proposed
that symptom reduction is though modication of erroneous
associations, not through habituation per se [24]. Accordingly we
next examine habituation and extinction as the mechanisms used
Volume 2 | Issue 1 | 3 of 8Int J Psychiatry 2017
to account for effectiveness of therapy.
Habituation
Habituation may be dened as the waning of a response to a
stimulus that occurs when the stimulus is repeatedly presented
[25]. In contrast to extinction, which is explained as associative
learning, habituation is seen as non-associative learning.
Habituation as used in stress neurobiology is conceptualized as
reduction in physiological responses to a repeated stressor in
comparison with initial response to the stressor [26]. In exposure
therapy, habituation refers to reductions in fear over time as a
person encounter fear-inducing stimuli [27, 28]. Habituation is
often measured through physiological variables such as heart rate
and skin conductance or through self-report measures such as the
Subjective Unit of Distress (SUDS) [29].
Thompson indicated that the notion of habituation is as old as
humankind but that experimental studies about habituation began
at the end of nineteenth century and early twentieth century [30].
After reviewing the basic properties of habituation as described
in classic works, Thompson refers to Thompson and Spencer’s
review in which nine basic parameters or common characteristics
of habituation were identied [30, 31]. These parameters are mostly
related to short-term or within - session habituation, emphasizing
the importance of repetition, spontaneous recovery, frequency of
stimulation, and generalization. Rankin et al. reviewed and revised
some of the nine parameters of Thompson and Spencer and added
an item that is mostly related to long-term habituation [31, 32].
They proposed that some stimulus repetition protocols might result
in response decrement lasting hours, days or weeks, suggesting
between session effects that are discussed in the next section.
The problem of within-and between session habituation
One of the main problems in the formulation and application
of emotional processing based exposure therapy is the relation
between what has been called within-session habituation to
between-session habituation. Foa’s initial position was that “The
activation of affect, its reduction during exposure sessions, and its
decrease across sessions, appear positively related to treatment
outcome, denoting evocation and modication of fear memories
during therapy” [24]. In most studies, however, a direct relationship
between within-session habituation and symptom reduction has
not been found [29].
Foa’s group discussed this issue in their 2006 update [23]. They
conclude that “within-session habituation is not a reliable indicator
of emotional processing” and suggest that “ some information may
take time to be processed, such that disconrming information
that had been presented during exposure is not fully incorporated
until some time after the exposure exercise (i.e., between sessions)
rather than within the sessions”(p.9).
Foa and McLean further suggest that factors such as distraction
and cognitive avoidance may interfere with full incorporation of
new information in the structure of memory so that the true change
in the structure of memory occurs after the exposure session [33].
Therefore, they propose a “full engagement with an exposure
exercise” (without any distraction or cognitive avoidance) to reach
a lasting outcome.
Reviewing the research on initial fear activation, within-session
habituation, and between-session habituation, Craske et al.
conclude that there is not any established relation between these
indices and therapeutic outcome [34]. Their suggestion is that we
need to move away from immediate fear reduction toward longer
term fear tolerance as a primary goal of exposure therapy. As an
explanation of exposure therapy they emphasize the inhibitory
learning central to extinction as an alternative account of what
happens in therapy. We now consider the concept of extinction.
Extinction
Extinction refers to the gradual weakening of an instrumental
response that results in the behavior decreasing or disappearing.
Extinction can occur if the trained behavior is no longer reinforced
or if the type of reinforcement used is no longer rewarding.
As has been shown in extensive empirical work, extinction may
be characterized as a form of inhibitory learning rather than an
erasure of acquired fear [35]. In other words, it is not simply an
unlearning or forgetting but rather a new process that changes the
relation between the conditioned stimulus and the unconditioned
stimulus. The amygdala has been suggested as the main area that
controls such a process [36]. Another area active in extinction
learning is the medial prefrontal cortex including the anterior
cingulate cortex (ACC), thought to regulate the function of the
amygdala [36]. The idea that exposure therapy is an automatic,
low-level process, has been challenged and it is believed today that
exposure therapy is based on extinction and involves many high-
level cognitive elements [37].
In studies of mice, the ability to extinguish fear by extinction has
been improved by a reinstatement procedure [38]. Reinstatement
involves repeating a fear-inducing stimulus. If after such a
reinstatement one introduces a drug that blocks norepinephrine
(e.g. propranolol) or carries out extinction trials within a short
period of time after reinstatement of the fear, the effectiveness in
reducing fear is increased. A recent mouse study has found that
stimulation of a circuit from the amygdala to the striatum either
optogenetically or by inducing a reward may improve extinction
of fear by reducing the tendency for it to spontaneously recover
[39].
These ndings in mice t with the importance of the production of
anxiety as a predictor of the effectiveness of exposure therapy in
patients with OCD [33]. However, subsequent studies of patients
with anxiety have shown that extinction may not always occur
and we do not know if the reduction of fear by itself will result
in improvement of the OCD symptoms [40]. However, the use
of reinstatement or simultaneous stimulation of reward pathways
may result in improvement of the existing exposure techniques as
a treatment for OCD.
Neuroscience approaches to OCD
In the new classication of psychiatric disorders (DSM-5), OCD
has been integrated within an obsessive-compulsive disorders
spectrum (OCDS). Although some psychologists have criticized
this approach, it has led investigators to pay more attention to
the different kinds of OCD that may involve different biological
mechanisms, including those involved in response prevention [41,
42]. Thus using the term OCD spectrum may be helpful both in
research and clinical practice. Imaging studies have led to a better
understanding of the regulatory mechanisms by which responses
are prevented and we discuss these mechanisms in relation to
different OCD symptoms.
OCDSs in this new system have been characterized by three
features:(1) compulsivity, which includes body dysmorphic
disorder (BDD), anorexia nervosa (AN), hypochondrias is, and
depersonalization disorder; (2) impulsivity, including sexual
compulsions, self-injuring behavior, trichotillomania (obsessive
hair pulling), kleptomania, compulsive buying, and pathological
gambling (PG); and (3) OCDSs with signicant neurological
symptoms, including Sydenham’s chorea, Tourette’s syndrome
(TS), and autism [43].
Graybiel and Rauch in search of a neurobiological basis for OCD
have indicated some key features of OCD which makes their
approach very similar to the concept of OCDSs [44]. They have
mentioned ve features summarized as follows:
• OCD patients are usually aware that their compulsions and
obsessions are senseless, but they cannot control them despite
effort;
• The symptoms usually are not bizarre;
• There is a considerable degree of consistency in the themes
of OCD across cultures, with some degree of heterogeneity in
specic symptoms;
• Some patients suffer mainly obsessions or compulsions
and others both. In some cases the disorder shows itself as
cognitive- affective and in others as executive- behavioral.
The two concepts may in fact be related as executive attention
serves as a control over affect [14, 45].
• The obsessions as thoughts, images and urges and the
compulsions, including washing , cleaning, checking, and
doing things right may continue for hours and the only way to
stop them is to get enough assurance from others.
These features of OCD suggest that there are neural circuits that
trigger repetitive and resistant behaviors and thoughts, and that
most often the patient is aware of the existence of these intrusive
events [44]. It is important to note that exposure therapy is not
applicable for most of the conditions classied under the title of
OCDSs. Abramowitz and Jacoby believe this is because “exposure
is derived from a specic psychological mechanism involving
excessive fear that is maintained by avoidance and ritualistic
behavior [41]. This pattern is present in OCD and body dysmorphic
disorder, but not in hair pulling, compulsive skin picking, or
hoarding” (p.282).
Abramowitz and Jacoby discuss the use and misuse of exposure
therapy in OCD and related disorders [41]. The aim of exposure
is to facilitate extinction-related reduction in the conditioned
anxiety/fear response associated with the feared stimulus. If this is
the case, a broadened view of the disorder may help in developing
additional treatment approaches to control obsession, impulsivity
and compulsivity that are likely to share a common neurobiological
basis [44]. Even in these cases, however, preventing response in
the presence of relevant stimuli may be important.
Self-Regulation and OCD
One of the main problems in OCD seems to be related to an
inhibitory mechanism reected in the difculty patients have in
stopping the behavior or thoughts. Attention helps the individual
to select stimuli that are most relevant and disregard or ignore
irrelevant informational sources [46]. In set shifting and exibility
in problem solving, OCD patients show lower performance than
controls [47-49]. This decit is supported by a meta-analysis of
110 previous studies of OCD patients showing a broad impairment
in executive functions [50]. The brain system most likely central
to these decits is the executive attention network that includes the
anterior cingulate (ACC) and underlying striatum [14].
Compulsivity in OCD has also been associated with addiction.
In a review article, Figee et al. demonstrated that compulsivity
is not only a central feature of OCD but it is also a key element
in addiction [49]. The term addiction in this context includes
behavioral addiction along with non-drug - related disorders that
have compulsivity as their common feature, such as pathological
gambling, and compulsive eating or buying.“Receptor-binding
studies indicate hyperactivity of the striatal dopaminergic system
in OCD, with decreased striatal availability of dopamine D1
receptors and D2-like receptors in [OCD] patients versus controls,
which is also found in individuals with substance-use disorders
and in some studies with obese patients”[49]. Compulsivity in
addictions and OCD may both be related to negative reinforcement.
Negative reinforcement in this case may involve avoidance or
relief of many kinds of distress based on abnormalities in brain
reward and anxiety circuits. The main brain areas responsible
for this include bed nucleus stria terminals, amygdala, habenula
and medial prefrontal cortex. Moreover, compulsivity in OCD
and addictions entails cognitive and behavioral inexibility,
which may be rooted in a shared impairment of ACC and ventro
medial prefrontal top-down regulation, along with serotonergic
defects and excessive dopamine and glutamate signaling. Finally,
habitual responding regardless of its consequences is an aspect of
compulsivity that may be related to imbalances between ventral
and dorsal frontostriatal activity [49]. As in addictions the OCD
patient appears forced to carry out particular behaviors even when
resistance is desired. By examining recent efforts to understand the
neurobiology of addictive disorders we may gain some perspective
on the diagnosis and treatment of OCD.
One view of addictions is to regard them as involving a decit in
self- regulation [51]. The ability to voluntarily regulate behavior
including both emotion and memory retrieval has been thought
to involve the executive attention network, including the anterior
cingulate cortex [14, 51]. There is an anatomical distinction
between more dorsal cingulate areas involved in cognitive control
and more ventral areas related to emotion regulation [45, 51]. Brain
systems of executive attention have been found to exercise control
over both emotional and behavioral responses [14]. Abnormalities
of these areas are clearly involved in OCD as recognized in meta-
analyses of grey and white matter [52, 53].
It is known that craving for drugs often involves the limbic circuit,
including the anterior cingulate and ventral striate cortex [54].
One recent study recruited smokers and nonsmokers who were
interested in reducing stress. No mention was made of a desire
to quit or reduce smoking. Smoking status was one of many
variables assessed after recruitment. The study found that tobacco
consumption was reduced by 60% in those smokers assigned to
two weeks of meditation training, even among those not seeking
to reduce smoking [55]. There was no change in smoking among
those given relaxation training (the control).The mechanism for this
Int J Psychiatry 2017 Volume 2 | Issue 1 | 4 of 8
reduced smoking appears to involve less craving through a change
in ventral ACC activity and connectivity to the striatum. Before
training, smokers showed reduced activity in the ACC compared to
non-smokers. After training, ACC activity and connectivity to the
striatum was increased for those smokers assigned to meditation,
but not for smokers in the control condition. The smokers’ desire
to quit smoking was unrelated to the reduction found in smoking
behavior.
A meta-analysis of activation studies of OCD patients using
functional imaging concludes that there is a consensus that
a dysregulation of the frontostriatal circuit is involved in the
psychopathology of OCD [8. 9]. A meta-analysis of resting state
MRI data conrmed that compared to other anxiety disorders there
was a unique abnormality in frontal-striatal pathways in OCD [56].
As with addictions, OCD has been reported to show abnormalities
in functional connectivity between midline frontal areas,
including connections between the ACC and striatum. However,
unlike tobacco and some other addictions [57]. the abnormality
sometimes appears as hyper- rather than hypo-connectivity
[58]. This dramatic difference in connectivity and the absence
of anxiety in early stages of addiction suggests that OCD might
not be an addictive disorder despite the possibility of considering
compulsive thoughts as being addictions.
The Tian et al. study showed that functional connectivity, that is the
correlation among selected brain areas, is increased in patients with
OCD compared to controls [58]. This nding suggests stronger
connectivity between the ACC and striatum in OCD. However a
meta-analysis of studies using Diffusion Tensor Imaging (DTI)
to study abnormalities in this circuitry showed hypoconnectivity
related to the dorsal more cognitive areas of the cingulate and
hyperconnectivity to the more ventral emotional control areas
[59]. Moreover altered white matter abnormalities in both hypo
and hyper connectivity occurred more widely than just in the ACC
striatal connections [59].
A later DTI study of 231 OCD patients compared to controls
showed reduced Fractional Anisotropy (FA) thus indicating
weaker connectivity of the ACC [60]. This nding was extended
in a family based approach which had similar ndings for un
medicated OCD patients and their siblings compared to normal
controls [61]. Another DTI study in children [62]. found reduced
fractional anisotropy (FA), suggesting reduced connectivity in
some of the same regions in which the Tian et al. study found
stronger functional connectivity [58]. Overall, the ndings indicate
evidence for abnormal white matter in the cingulate to striate
connections, but studies differ on whether the connections are
stronger or weaker. It is certainly possible that some connections
are stronger in OCD than controls while in others they are weaker.
We discuss this possibility below.
While there remains uncertainty about the direction of the
connectivity abnormalities in OCD, the studies are consistent
with abnormal connectivity between the anterior cingulate and
striatum in OCD patients. Recent meta-analysis studies of OCD
patients have veried abnormalities in white and gray matter in the
dorsal and ventral ACC [52, 53]. These ndings are supported by
another meta-analysis showing that problems in ACC connectivity
with the striatum are central to the symptoms found in OCD [63].
The importance of the striatum and its connections has also been
supported by the success of some forms of deep brain stimulation
in treatments, which have generally targeted areas of the ventral
striatum in efforts to relieve the symptoms of OCD [64].
In monkeys the ACC involves multiple connections to other brain
areas including the ventrolateral prefrontal cortex which has been
involved in the inhibition of motor and posterior areas in the go-
no-go task [65].
A recent paper has examined the response of OCD patients to
making an error. The study found that while patients showed a
normal response to error, they were less likely than controls to slow
their responses on the next trial. Thus in this study OCD patients
seem to have impaired ability to control response output [66]. One
paper has specied a specic cognitive role for the ACC in the
etiology of OCD [63]. According to this view dysfunctioning of
the ACC generates an inappropriate signal related to the expected
value of stimuli, which favors the compulsion in comparison with
long term goals. Over-valuation of stimuli related to the compulsion
leads to repetitive behaviors by giving priority to stimuli related to
the compulsion. This idea is compatible with an important role for
the ACC in OCD and provides a possible explanation of that role.
Direction of connectivity
Another approach to ACC function is based on the idea that some
pathways to and from the ACC are abnormal in connectivity.
For example, pathways carrying information about compulsive
events from the striatum (e.g. itching or dirty hands) could be
hyper connected, while others such as used for slowing responses
following an error could be hypoconnectivity (these pathways
could be involved in controlling motor response of scratching
or hand washing). We speculate based on the symptoms of OCD
that medial frontal pathways involved in self-regulation may be
hypoconnected, while those involved in frontal striatal loops are
hyperconnected.
Even though more research is clearly needed regarding the
direction of connectivity abnormalities in OCD found in various
pathways, recent neurobiological studies might point the way
toward methods of improving control of compulsive symptoms.
Oligodendrocytes are involved in increasing connectivity though
increased myelination. Thus activating oligodendrocytes as has
been done with motor learning in mice could perhaps be used
to increase connectivity and thus provide improved response
prevention in OCD treatment [67]. Recent studies in mice and
humans have shown improved connectivity following various
forms of learning, providing some support for this possibility [68].
Other glial cells including the astrocytes have been implicated in
remodeling connections through reduction of myelin [69]. Thus
biological ndings support the possibility of adjustments to both
increase underconnectivity and reduce overconnectivity.
Since medial frontal pathways involved in self-regulation may be
hypoconnected, while those involved in frontal striatal loops are
hyperconnected, it is possible that methods can be constructed
to improve both of these tendencies A preliminary report with
OCD patients suggests that transcortical magnetic stimulation
with a coil designed for deep stimulation and repeated 20 times
per second induced EEG changes in the anterior cingulate and
increased responses to error in the Stoop task [70]. If methods
Int J Psychiatry, 2017 Volume 2 | Issue 1| 5 of 8
could be found to carryout remodeling of myelin connections
in humans, they might prove useful in the treatment of OCD by
strengthening the mechanisms of self- regulation while reducing
repetitive activation. Approaching OCD through changes in
connectivity as suggested in this section, would not necessarily
be incompatible with the view that the disorder involves errors in
ACC computation of expected value [63].
Since the ACC to hippocampus pathway has been identied as
a possible route for control of retrieval from memory, increased
activity and connectivity of the ACC could result in improved
ability to control obsessive thoughts as well as behaviors [71]. One
caution about this approach, however, is that although theoretical
models and empirical studies suggest that OCD is caused by
functional and structural abnormalities in orbitofrontal and ACC
to striatal circuits, there is also evidence that other brain areas may
be involved [59,72].
Future directions for understanding the theoretical basis of
psychological treatment of OCD
As stated earlier, exposure therapy and response prevention
(ERP) involves a set of psychological treatment approaches and/
or techniques for improving anxiety-related disorders, including
OCD. The common core of these approaches and techniques is
asking patients to confront their obsessive or fearful thoughts while
controlling their response to the situation. Exposure therapy alone
or in combination with response prevention has been identied as
the rst and most effective psychotherapy for some OCD patients
and there is no doubt that Foa and her group has had enormous
effect on the evaluation, treatment and investigation of OCD in the
past 30 years [73]. The main problem with this set of approaches
and techniques is its mechanisms of action on the one hand and
the theory underlying this treatment approach on the other [13,74,
75]. By incorporating the neurobiological approaches this paper
has attempted to both specify mechanisms and move toward an
improved theory of treatment.
In all explanations the most characteristic feature of habituation
has been identied as repetition of stimulation. But in exposure
therapy in general and exposure therapy applied in OCD in
particular, something new happens that goes beyond mere
repetition or adaptation. It is the patient’s deliberate and systematic
confrontation with a supposedly threatening situation. That is, the
patient is actively involved in the process of exposure therapy.
First, the person wishes to be relieved of OCD symptoms and
seeks help. Second, the patient trusts the therapist and generates
positive expectations about the effects of therapy. Third, in CBT
approaches, the patient is presented with a rationale for the ERP
treatment and given assurances that the therapy will work.
These cognitive features and their emotional consequences have
in part been addressed by an improved understanding of the
mechanisms of attentional control of emotions, thoughts and
behavior. Improved self-regulation may thus be a key to response
prevention during exposure as well as between therapeutic
sessions. The use of meditation training has proven effective in the
control of some addictions and may be one of several mechanisms
to foster improved response prevention.
We are still in need of a fully satisfactory theoretical and explanatory
basis of exposure therapy. Although the new classication
of an OCD spectrum may cause some practical problems for
clinicians, it can also foster research on neurobiological and
cognitive commonalities of different impulsive and compulsive
disorders, providing us with new ways of looking at the nature
and psychopathology of OCD. In this review we have found clear
evidence of abnormal pathways involved in the disorder. These
include the ACC and its connections to the striatum. Moreover,
at least some results allow speculation concerning methods of
improving self-regulation by altering connectivity. This work
may help clinicians nd new insights about treatment. Most
importantly, moving in this direction of connecting cognition and
neuroscience with exposure therapy may throw light on the whole
area of psychopathology and phenomenology of disorders that
involve difculties in self-regulation [76].
✳This work was begun by HG and evolved into the current paper
while he served as a visitor at the University of Oregon Institute
for Cognitive and Decision Sciences. We express our thanks to
Prof. Dennis Galvan, Vice Provost for International affairs, and
to Peter DeFazio, and Ron Wyden for their help in arranging this
visit.
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