










































Body Dysmorphic Disorder and OCD


Graduate Student Journal of Psychology                                                                             Copyright 2009 by the Department of Counseling & Clinical Psychology 
2009, Vol. 11                                                                                                                        Teachers College, Columbia University                          
 
 

Obsessive Compulsive Related Disorders: A New Classification for the  
DSM-V 

 
Lauren M. Mancusi, M.A. 

Teachers College, Columbia University 
 

There is concern surrounding the classification of obsessive compulsive disorder (OCD) for the next 
edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM). The DSM-V workgroup 
for OCD related disorders and researchers alike suggest removing OCD from the anxiety disorders 
category of the DSM, and placing it under the heading of obsessive compulsive related disorders 
(OCRD). This paper provides a review of current literature examining three popular candidates (body 
dysmorphic disorder, trichotillomania, and Tourette’s disorder) for inclusion in the OCRD category. 
Recommendations for future research are made.  

 
The classification of obsessive compulsive disorder 

(OCD) has undergone considerable change since the initial 
compilation of the Diagnostic and Statistical Manual of 
Mental Disorders (DSM). In the DSM-II, OCD was 
categorized as “obsessive- compulsive neurosis,” while 
obsessive compulsive disorder received a new classification 
in the DSM-III as an anxiety disorder. Currently, OCD 
remains classified as an anxiety disorder in the DSM-IV-TR 
(Montgomery, 1993); however, the classification of OCD 
continues to be a topic of controversy for the DSM-V.  

Researchers have recently suggested that the current 
classification of OCD is mainly symptom based. 
Specifically, obsessive thoughts increase anxiety which is 
moderated by compulsive behaviors (Bartz & Hollander, 
2006). As such, anxiety presents as a byproduct of the 
disorder and not an underlying feature (Mataix-Cols, 
Pertusa, & Leckman, 2007). Additionally, the current 
classification fails to account for the differences among OCD 
and the remaining anxiety disorders, mainly in the sphere of 
repetitive behaviors and an inability to resist impulses. 
Several other disorders (e.g., body dysmorphic disorder, 
trichotillomania, and Tourette’s disorder) that are not 
included in the anxiety disorders category also display the 
compulsive and impulsive behaviors present in OCD. Thus, 
the Research Planning Agenda for the DSM-V Workgroup 
on obsessive compulsive-related disorders suggests 
removing OCD from the anxiety disorders category and 
placing it under the title of obsessive compulsive related 
disorders (OCRDs) (Hollander, Braun, & Simeon, 2008). 

Other recent work has proposed a multidimensional 
model of OCD that recognizes the heterogeneity among 
causes and presenting symptoms across OCD and related 
disorders (Castle & Phillips, 2006; Mataix-Cols, 2007).  It is 
suggested that OCD and related disorders be classified along 
a continuum for future editions of the DSM. The OCD 
spectrum is subdivided into three distinct clusters; (1)1 
preoccupations with body sensations or image (e.g., body 

                                                 
Correspondence: Lauren Mancusi, lmm2176@columbia.edu 

dysmorphic disorder), (2) impulse disorders (e.g., 
trichotillomania), and (3) neurological based disorders (e.g., 
Tourette’s disorder). These seemingly unrelated disorders 
display consistency across (1) symptomology (e.g., 
compulsivity and impulsivity), (2) neurobiology (e.g., fMRI 
data), and (3) responses to psychosocial (e.g., cognitive 
behavioral therapy) and pharmacological (selective serotonin 
reuptake inhibitors) treatments (Castle & Phillips, 2006; 
Rossi, 2006). Further, Hollander (1993) suggests a 
“compulsive-impulsive” dimension, with compulsive 
disorders (e.g., OCD) on one end of the spectrum 
(compulsive) and impulse control disorders (e.g., 
trichotillomania) at the other end of the spectrum 
(impulsive). In this case, compulsivity reflects harm 
avoidance, whereas impulsivity reflects risk seeking.                

Obsessive compulsive symptoms are present in various 
disorders besides OCD. These disorders include Tourette’s 
disorder (TD), body dysmorphic disorder (BDD), and 
trichotillomania (TMM) (Castle & Phillips, 2006). While 
these disorders are primary candidates for OCRDs, eating 
disorders, autism, and depersonalization disorder, along with 
certain neurological disorders such as Parkinson’s and 
Sydenham’s chorea, are also under consideration for 
inclusion within the OC domain (Castle & Phillips, 2006; 
Hollander, 1993). What is more, recent literature revealed 
that the DSM-V Workgroup on obsessive compulsive-
related disorders labored over whether or not to include 
behavioral addictions, such as pathological gambling, 
kleptomania, and pyromania within the OCRDs. The 
workgroup concluded these behavioral addictions will not be 
classified as OCRDs, but rather will be included in a parallel 
category of behavioral and substance addictions. The 
behavioral and substance addictions category will include 
existing as well as new (compulsive buying, internet 
addiction, and compulsive sexual behavior) impulse/control 
disorders as well as substance addictions (Bartz & 
Hollander, 2006).  

This paper aims to elaborate on the process of the new 
classification proposed for the OCRDs by examining the 

12 



OBSESSIVE-COMPULSIVE DISORDER 
 

 

 

13

three contending disorders (body dysmorphic disorder, 
trichotillomania, and, Tourette’s disorder) with regard to the 
symptom domain, the neurobiological and genetic domain, 
and the treatment domain. Suggestions for future research 
are recommended as well. 

 
Body Dysmorphic Disorder and OCD 

 
The Symptom Domain 
 

Body dysmorphic disorder is currently classified as a 
somatoform disorder, and is marked by an excessive 
preoccupation with a perceived body defect which is usually 
non-existent or minimal (American Psychiatric Association, 
2000; McKay, Neziroglu, & Yaryura-Tobias, 1997). The 
experienced preoccupations are believed to be similar to the 
obsessions experienced in OCD; obsessions in OCD and 
BDD tend to be intrusive and persistent. Additionally, 
individuals with these disorders recognize the obsessions as 
excessive. However, unlike individuals with OCD, 
individuals with BDD do not view their obsessions as 
unreasonable (Hollander, Braun, & Simeon, 2008). This may 
be due to the lack of global insight often seen in individuals 
with BDD as compared to those with OCD who tend to have 
more insight and recognize their obsessive thoughts as 
excessive and harmful (Phillips et al., 2007).     

As evidenced in OCD, individuals with BDD engage in 
compulsive behaviors (e.g., mirror checking) and 
reassurance seeking in attempts to reduce the stress 
surrounding the preoccupation. The repetitive behaviors 
often are expressed in a ritualized form and may follow a 
certain sequence. Furthermore, this sequence is repeated if 
interrupted or until a desired aim is achieved (Phillips, 
McElroy, Keck, Pope, & Hudson, 1994). In both groups, the 
compulsions are not inherently gratifying or pleasurable, but 
rather distressing and socially debilitating. While both 
individuals with OCD and BDD engage in compulsive 
behaviors, these activities are less likely to reduce anxiety, 
behaviors, or compulsions in individuals with BDD 
(Hollander, Braun, & Simeon, 2008), which might be 
attributed to the poorer insight observed in individuals with 
BDD.  

McKay, Neziroglu, and Yaryura-Tobias (1997) 
examined the overlapping symptom domains of OCD and 
BDD. A sample of 22 OCD outpatients and 23 BDD 
outpatients were administered a variety of psychological 
measures assessing OCD, BDD, overvalued ideation, 
depression, physical symptoms of anxiety, and cognitive 
symptoms of anxiety. The researchers found that BDD is a 
more severe variation of OCD. Participants with BDD 
reported higher levels of overvalued ideas when compared to 
those with OCD. Additionally, the BDD participants 
exhibited more severe obsessive and compulsive symptoms 
than the OCD participants. The two groups were statistically 
equivalent on other measures of depression and physical 
symptoms of anxiety; however, there was a significant 
difference between the two groups on the measure of 

cognitive symptoms of anxiety, with the OCD participants 
reporting higher incidences. These results suggest a 
difference in the experience of anxiety associated with each 
disorder, on the one hand, while, on the other, that those with 
OCD and BDD similarly experience obsessive and 
compulsive symptoms. The relatedness between the two 
disorders in the symptom domain provides evidence in favor 
of an OCD spectrum. 

More recently, Phillips and colleagues (2007) conducted 
a comparison study of clinical features of OCD and BDD. 
The researchers administered the structured clinical 
interview and a variety of psychological measures assessing 
symptoms of OCD, BDD, beliefs, and depression with 210 
OCD participants, 45 BDD participants, and 40 comorbid 
OCD/BDD participants. A comparison of subjects’ 
characteristics showed OCD and BDD did not significantly 
differ in regard to demographic traits such as age, race, 
gender, age of onset, illness duration, most functioning 
measures, and most comorbidity. Findings suggest that 
subjects with BDD were more likely to suffer from lifetime 
major depression or another mood disorder. However, the 
symptom severity of these disorders did not differ 
significantly among the groups, suggesting that BDD may be 
a good candidate for the OCRDs within the symptom 
domain.    

  
The Neurological and Genetic Domain  
    

The brain circuitry within OCD patients is characterized 
by hyperactivity in the orbital frontal cortex, caudate 
nucleus, thalamus, and the anterior cingulated nucleus (Bartz 
& Hollander, 2006). Researchers have noted that the 
prefrontal regions of the brain, specifically, the frontal-
striatal region including the basal ganglia, have been linked 
with the intrusive thoughts associated with OCD (Stein, 
2000). Unfortunately, few neuroimaging studies in BDD are 
available for comparison (Mataix-Cols & van den Heuvel, 
2006). Researchers conducted a morphometric study with 8 
women with BDD and 8 female controls, and results showed 
a significantly different asymmetry in the caudate nucleus 
with a leftward shift in the BDD group. The activity in the 
caudate nucleus suggests that a similar brain region is active 
in both OCD and BDD (Mataix-Cols & van den Heuvel, 
2006); however, research in this area is sparse and requires 
replication.   

Bienvenu et al. (2000) examined the relationship among 
OCD and prospective spectrum disorders. The researchers 
found that cases of BDD were significantly higher in case 
probands than controls.  BDD was also shown to be 
transmitted in families of patients with OCD, while BDD 
rates were higher in families with patients of OCD. The 
researchers suggest developing phenotypic definitions for 
future genetic research of OCD spectrum disorders 
(Bienvenu et al., 2000).      
 
 
 



MANCUSI 
 

 14 

The Treatment Domain 
 
Obsessive compulsive disorder and body dysmorphic 

disorder both respond to psychosocial and 
psychopharmacological treatments (Hollander et al., 2008). 
The leading psychosocial treatments for OCD are cognitive 
and behavioral-based therapies that focus on exposure and 
response prevention (ERP). ERP is considered the preferred 
psychosocial treatment for OCD (Castle & Phillips, 2006; 
Wilhelm et al., 2005). One study suggests that 63% of OCD 
patients respond positively to ERPs; however, 20% to 30% 
remain resistant or refuse ERP due to the anxiety provoking 
exposure (Wilhelm et al., 2005).  

While OCD responds favorably to ERP alone, the 
cognitive component of cognitive behavioral therapy (CBT) 
has also been efficacious (Castle & Phillips, 2006). Wilhelm 
and colleagues (2005) examined the effects of a purely 
cognitive treatment for individuals with OCD. Participants 
received 12 weekly 50-60 minute individual sessions of 
cognitive therapy. The cognitive therapy included 
psychoeducation, procedures according to Beck’s cognitive 
model (e.g., Socratic dialogue and identification of cognitive 
errors), and relapse prevention strategies. The researchers 
found that all participants improved across OCD symptoms 
as well anxiety symptoms and maladaptive beliefs. While 
results support the efficacy of cognitive treatment alone, this 
was the first study to examine purely cognitive techniques 
with an OCD sample, and further work is needed to make 
more conclusive statements regarding this therapeutic 
approach.     

The treatment approach for BDD is based on the 
treatment of OCD (Neziroglu & Khemlani-Patel, 2003), such 
as psychosocial interventions that include a cognitive 
component as well as exposure and response prevention 
treatment to lessen anxiety and ritualistic behaviors 
(Buhlmann, Reese, Renaud, & Wilhelm, 2008; Castle & 
Phillips, 2006). While the literature on BDD remains fairly 
limited, the available research suggests that BDD responds 
to similar psychosocial treatments as OCD (Neziroglu, 
2008). Neziroglu, McKay, and Yaryura-Tobias (1996) 
presented a case series in which 17 patients with BDD 
received daily 90-minute CBT sessions over the course of 1 
month. Results showed a 50% reduction in symptoms in 
more than half the participants (n = 12). Veale and 
colleagues (1996) conducted a randomized study assessing 
the effectiveness of CBT with individuals with BDD. 
Nineteen individuals with BDD were randomly assigned to 
either the treatment group or the waitlist control group. 
Participants in the treatment group attended weekly 1-hour 
sessions of CBT for 12 weeks, and those that received 
treatment improved significantly more than those in the 
waitlist condition. In a 6-week intensive treatment of BDD 
using exposure response and prevention (without a cognitive 
component), 10 participants received five 90-minute sessions 
a week. The results indicated that participants improved on 
measures of BDD symptoms, avoidance, depression, and 

anxiety, while follow-up data showed that improvements 
remained stable over a 6-week period (McKay et al., 1997).    

With regard to psychopharmacological treatments, OCD 
and BDD respond favorably to selective serotonin reuptake 
inhibitors (SSRIs) (Castle & Phillips, 2006; Hollander et al., 
2008). In a meta-analysis of treatments employing long-term 
medication for OCD, researchers found that SSRIs were, 
overall, effective over time and also helpful in relapse 
prevention. Data suggest that paroxetine, escitalopram, and 
fluoxetine are the most effective SSRIs in relapse prevention 
of OCD (Fineberg, Pampaloni, Pallanti, Ipser, & Stein, 
2007). Studies to date often report that SSRIs are also 
efficacious for BDD (Phillips, Didie, Feusner, & Wilhelm, 
2008). In a 12-week double-blind study (N = 67), fluoxetine 
was significantly more efficacious than placebo for BDD 
beginning at 8 weeks and continuing at 10 and 12 weeks and 
with participants receiving a relatively high dose of the 
medication (77.7 +/- 8.0 mg/d) (Phillips, Albertini, & 
Rasmussen, 2002). This finding is in accordance with 
previous reports that psychopharmacological treatment of 
BDD often has a longer delay in SSRI response and requires 
higher SSRI doses (Neziroglu & Khemlani-Patel, 2003). 
Literature shows similar information for the delay in SSRI 
response and effective treatment dose with OCD (Castle & 
Phillips, 2006; Hollander et al., 2008). 

 
Trichotillomania 

 
The Symptom Domain 
 

Trichotillomania (TTM) is currently classified as an 
impulse control disorder characterized by repetitive hair 
pulling (American Psychiatric Association, 2000). While 
TTM is not distinctly marked by obsessions, they are 
sometimes present in the disorder. When obsessions are 
present, they often are not associated with an intrusive 
thought, but rather with the compulsive desire to pluck one’s 
hair, and this urge is recognized as unreasonable as intrusive 
thoughts are to individuals with OCD (Hollander et al., 
2008). The ritualized and repetitive hair pulling associated 
with TTM is parallel to compulsions expressed in OCD. 
Much like compulsive behaviors exhibited in OCD, the 
compulsive hair plucking often reduces anxiety and is 
influenced by an individual’s need for symmetry in the hair 
pattern (Hollander et al., 2008). Often the compulsive 
behavior is rigid and repeated until the desired outcome is 
achieved; hair plucking is a tension reducing response to the 
urge to pluck one’s hair. Furthermore, hair plucking is 
distressing and socially debilitating as seen in OCD, and, 
while both hair pulling and OCD compulsions reduce 
anxiety, hair pulling is gratifying (Castle & Phillips, 2006).   

To the author’s knowledge, few studies exists directly 
comparing observable behavior of OCD to TTM in terms of 
symptomology. Bohne, Savage, Deckersbach, Keuthen, and 
Wilhelm (2008) compared motor inhibition abilities in TTM 
and OCD patients. Reaction times were measured using a 
GoNogo task among 25 TTM, 21 OCD, and 26 control 



OBSESSIVE-COMPULSIVE DISORDER 
 

 

 

15

participants. The researchers reported no significant 
difference in reaction times among the TTM, OCD, and 
healthy control groups; however, there was a small portion 
of the TTM group that performed either “fast and 
inaccurate” or “slow and accurate.” This portion of the TTM 
group was associated with an earlier age of onset, suggesting 
a subgroup of TTM sufferers that experience increased 
motor inhibition. With that said, overall, findings do not 
represent a significant difference in reactions between 
individuals with TTM and OCD, and further work exploring 
motor inhibition in TTM and OCD is warranted.     
 
The Neurological and Genetic Domain 
 

The neuroimaging data on TTM is limited (Mataix-Cols 
& van den Heuvel, 2006; Stein, 2000). Researchers suggest 
the caudate nucleus, a brain structure implicated in OCD, is 
not significantly involved in trichotillomania. Stein and 
colleagues (1997) compared caudate nucleus volumes in 13 
OCD participants, 17 TTM participants, and 12 healthy 
controls. Results showed no significant differences among 
the groups. In a study with 10 women with TTM, researchers 
found clomipramine (a tricyclic antidepressant often used in 
OCD) was negatively correlated with anterior cingulated and 
orbitofrontal metabolism. Additionally, findings suggest that 
symptom severity of hair pulling is correlated with decreased 
perfusion in the frontal, partial, and strautum brain regions 
Stein et al., 2002). These findings agree with prior 
neuroimaging work on OCD, suggesting that both TTM and 
OCD involve activity in similar brain regions, mainly the 
frontal regions (Mataix-Cols & van den Heuvel, 2006; Stein 
et al., 2002).    

Bienvenu et al. (2000) found that cases of TTM were 
significantly higher in case probands than controls. TTM 
was shown to be transmitted in families of patients with 
OCD, and the disorder was the most prevalent in patients 
whose family members exhibited OCD. The researchers 
provided a lifetime prevalence of OC spectrum disorders for 
patients with OCD; TTM (4%) exhibited one of the highest 
lifetime prevalences (Hollander, 1993).  
 
The Treatment Domain    
 

The leading psychosocial and psychopharmacological 
interventions for TTM are habit reversal therapy (HR), 
SSRIs, and clomipramine (Bloch et al., 2007). Bloch and 
colleagues (2007) conducted a meta-analysis assessing the 
individual effectiveness of HR for TTM participants as 
compared to controls. The researchers found a significant 
difference between the HR and waitlist/control group. These 
results are consistent with current literature concerning 
psychosocial treatment for TTM (Hollander et al., 2008). In 
another study, 22 participants with TTM were involved in an 
open trial of individual CBT with an emphasis on relapse 
prevention. Treatment was administered in two phases. The 
first phase consisted of active treatment in which individuals 
were provided with psychoeducation, strategies of 

competing responses training, and cognitive restructuring. 
This phase included CBT once a week for 8 weeks. The 
second phase consisted of four bi-weekly sessions focusing 
on relapse prevention. Results showed that 77% of 
participants were classified as “treatment responder” and 
32% were classified as “excellent responders.” Results 
remained consistent at a 6-week follow up, with 66% of 
participants classified at “treatment responders,” and 32% 
considered “excellent responders” (Tolin, Franklin, 
Diefenbach, Anderson, & Meunier, 2007). The results 
revealed that TTM, like OCD, responds positively to 
cognitive and behavioral treatments.  

In terms of psychopharmacological treatment, SSRIs 
appear to be an effective treatment for TTM. In a 12-week 
open-label trial of treatment with escitalopram, (SSRI), 20 
women were administered 10-30 mg/d of the medication. 
Researchers found a 50% reduction from baseline in 
symptom severity (Gadde, Wagner II, Connor, & Foust, 
2007). However, based on a meta-analysis, Bloch and 
colleagues (2007) suggest that there is little evidence for the 
efficacy of SSRIs for TTM when compared to controls. 
Additionally, these researchers examined the effectiveness of 
clominpramine (a medication often used in the treatment of 
OCD) when compared to placebo control groups. Results 
suggest that clominpramine is more effective when 
compared to the placebo control group. On whole, research 
has yielded mixed results regarding the similarities and 
differences of TTM and OCD in their response to SSRI 
treatments.    

 
Tourette’s Disorder 

 
The Symptom Domain 
 

Currently, Tourette’s disorder (TD) is classified based 
on diagnosis in infancy, childhood, or adolescence. TD is 
marked by multiple motor and/or one or more vocal tics 
(American Psychiatric Association, 2000). The most familiar 
associated symptoms of TD are obsessions and compulsions. 
Obsessions are not present in all diagnosis of TD; however, 
when present, obsessions tend to be similar to OCD, and 
might include obsessions of symmetry or exactness. 
Compulsions are more persistent and, as in OCD, they are 
not pleasurable, but rather, are experienced as distressing and 
socially debilitating (American Psychological Association, 
2000; Hollander et al., 2008). In addition to a shared 
symptomology, motor stereotypy, a defining feature of TD, 
is frequently also manifested in OCD (Korff, Stein, & 
Harvey, 2008).  
 
The Neurological and Genetic Domain   
 

The frontal-striatal cortex has been indicated in various 
disorders, including OCD and other perspective OCRDs, 
such as TD (Mataix-Cols & van den Heuvel, 2006; Stein, 
2000). The basal-ganglia, caudate nucleus, and thalamus 
have been implicated in OCD and TD (Bartz & Hollander, 



MANCUSI 
 

 16 

2006; Mataix-Cols & van den Heuvel, 2006). Peterson and 
colleagues (2003) measured basal ganglia volumes using 
structural MRIs in 154 participants with TD, including 
individuals with comorbid OCD under the condition that TD 
preceded OCD, and 130 healthy controls. The researchers 
assessed regional specificity and abnormal asymmetries in 
the basal ganglia. Results showed reduced volume in the 
caudate nucleus of the basal ganglia in participants with TD 
when compared to controls. Furthermore, individuals with 
comorbid TD and OCD exhibited even smaller caudate 
nucleus volume than those with TD alone. Participants with 
comorbid TD and OCD also showed an increase in tic 
symptom severity, suggesting that a similar brain region may 
be active in both OCD and TD. Using structural MRIs, 
Peterson and colleagues (2001), examined prefrontal, 
parieto-occipital, and inferior occipital brain regions in 155 
TD and 131 health control participants. Results were 
consistent with the previously mentioned study, showing 
decreased volume in the prefrontal region of the brain in 
participants with TD. Additionally, increased symptom 
severity was correlated with decreased volume in these 
regions.          

One of the most pertinent comparisons of TD and OCD 
may be with respect to the neurochemistry of these disorders. 
Research often points to the effectiveness of SSRIs and the 
role of the serotonin neurotransmitter system in OCD, 
however, the dopamine neurotransmitter system offers 
insight into the relationship between TD and OCD, 
especially in regard to stereotypic behaviors (Stein, 2000). 
Korff, Stein, and Harvey (2008) examined stereotypic 
behaviors in deer mice to assess the role of the serotonin and 
dopamine neurotransmitter systems in OCD. The stereotypic 
behaviors were observed and baseline data was recorded. 
Deer mice were then administered high and low doses of 
fluoxetine (an SSRI). Dopamine D2 receptor agonists were 
administered as well. Results showed a significant decrease 
in stereotypic behavior in deer mice that received both high 
and lose doses of fluoxetine; the dose of the SSRI was 
positively correlated with the decrease in symptom severity. 
Additionally, states of spontaneous stereotypic behavior 
were lessened by dopamine D2 receptor agonists. On whole, 
results indicate that both the serotonin and dopamine 
neurotransmitter system may have an effect on the 
stereotypic behavior expressed in OCD and often in TD. 
These results may also aid in psychopharmacological 
treatment of these disorders.     

Tourette’s disorder is genetically transmitted through 
families (American Psychiatric Association, 2000). Stein 
(2000) makes note that there is a strong genetic overlap 
between OCD and TD. Tics are seen more frequently in 
families of OCD probands, and OCD is more common in 
families with individuals with TD than in control subjects. 
Another study presents three case studies in which 
individuals with comorbid OCD and TD expressed a similar 
chromosome 18 breakpoint; the breakpoint localized to the 
same chromosomal band in each of the cases presented 
(Cuker, State, King, Davis, & Ward, 2003).While the sample 

size (18) used in this study was small, the data provide a 
promising start, and further research with individuals with 
comorbid OCD and TD seems appropriate. 

      
The Treatment Domain   
 

While psychopharmacological treatments have been 
shown effective and are most often employed in the 
treatment of TD, many patients refuse or discontinue 
medication (Wilhelm et al., 2003). Researchers have 
examined the effectiveness of psychosocial therapeutic 
approach such as habit reversal therapy. A randomized 
controlled study assessed the effectiveness of habit reversal 
therapy versus supportive therapy. Participants with TD were 
randomly assigned to 14 sessions of either habit reversal 
therapy (n = 16) of supportive therapy (n = 13). Habit 
reversal contained awareness training, self-monitoring, 
relaxation, competing response training, and contingency 
management. All participants received weekly individual 
therapy sessions for the first 8 weeks, while the remaining 
sessions were administered bi-monthly. HR patients 
exhibited significantly lower tic severity scores than 
supportive therapy patients; tic symptoms in the supportive 
therapy group remained largely unchanged, while symptom 
severity was significantly reduced in the HR group. 
Furthermore, HR participants showed significantly less 
functional impairment at 10-month follow-up compared to 
the supportive therapy group (Wilhelm et al., 2003). In a 
replication of this study, Deckersbach and colleagues (2006) 
found results similar to the initial experiment, further 
evidencing the effectiveness of HR for individuals with TD. 
While HR is not explicitly employing all the components of 
CBT, it does implement behavioral strategies (e.g., self-
monitoring) utilized in CBT and ERP. Thus, both TD and 
OCD respond well to treatments with a behavioral 
component.       

The leading psychopharmacological treatment for TD is 
dopamine agonists, including haloperidol and pimozide; 
however, other dopamine antagonists, such as 
metoclopramide have proven efficacious in double-blind 
studies as well (Nicolson, Craven-Thuss, Smith, McKinlay, 
& Castellanos, 2005). More recently, researchers examined 
the effects of aripiprazole, a partial dopamine agonist. In a 
pilot study, 14 children and adolescents with TD were 
administered aripiprazole over the course of 8 weeks starting 
with a dose of 5 mg and increasing the dose by 5 mg every 1 
to 2 weeks. Results showed that more than half of the 
participants experienced at least a 30% improvement in tic 
severity, providing a positive foundation for future work 
which might also include other age groups. As mentioned 
above (TD-The Neurobiological Domain), the stereotypic 
behaviors displayed in OCD appear to be related to the 
dopamine neurotransmitter system, and it does respond well 
to dopamine agonists, especially in the reduction of TD like 
behaviors.  

  
 



OBSESSIVE-COMPULSIVE DISORDER 
 

 

 

17

Discussion 
 

The proposal of an Obsessive Compulsive Related 
Disorders category for the next edition of the DSM has 
significant implications for treatment and classification 
(Castle & Phillips, 2006). There exists a systematic approach 
in examining the proposed disorders in relation to OCD, 
mainly assessing similarities and differences in the (1) 
symptom domain, (2) the neurobiological domain, (3) and 
the treatment domain. While this approach elucidates 
similarities among OCD and the prospective OCRDs, 
conclusive research is lacking.                 

While ample research ties together the similarities 
between OCD, BDD, TTM, and TD, as outlined above, 
findings rely heavily on observable symptoms. A variety of 
disorders not included in the prospective OCRDs (e.g., 
impulse control disorder) display obsessions, compulsions, 
or both, and yet, are not under consideration for OCRD 
classification (Hollander et al., 2008). Similarly, as noted 
above, two of the more popular contenders for the OCRDs, 
TMM and TD, rarely include obsessions in their clinical 
presentation. Additionally, demographic parameters, such as 
comorbidity and age of onset, may lack sufficient strength as 
a defining OCRD criterion. While OCD shares these features 
with many of the perspective OCRDs, they are present with 
other anxiety disorders as well (Bartz & Hollander, 2006; 
Hollander, et al., 2008).    

Neurobiological studies lend to the comprehensive 
review of OCD and related disorders. However, a variety of 
brain regions are affected in OCD, and while OCD shows 
brain region abnormalities similar to BDD, TTM, and TD, it 
shares abnormalities with existing anxiety disorders as well. 
For example, both OCD and social phobia express 
abnormalities in the limbic region of the brain (Mataix-Cols 
& van den Heuvel, 2006). Similarly, effective treatments for 
OCD such as CBT, ERP, and SSRIs, have also proven to be 
efficacious for other anxiety disorders (Bartz & Hollander, 
2006).              

The future classification OCRDs proposes a spectrum 
model. Yet, a more productive approach may be to consider 
symptomology, neurobiology, and treatment on a continuum 
as opposed to categories in which similarities and differences 
with OCD are dichotomously placed (Castle & Phillips, 
2006). The current method of studying OCRDs is to examine 
the similarities and differences between OCD and another 
disorder, and place the results into a “fix” or “no fix” 
category. If a continuum of symptomology, neurobiology, 
and treatment responses were created prior to conducting 
further research studies, perhaps data on the OCRDs for the 
DSM-V would be more conclusive.     

 
Conclusion 

 
The classification of OCD has undergone considerable 

changes over the past editions of the DSM. In fact, 
classification remains a concern for future editions of the 
DSM. Researchers have offered evidence both in support of 

and against a new classification of this disorder (Mataix-Cols 
et al., 2007). However, the majority of current research is 
heavily focused on the prospective OCRDs. In order to 
conclusively and confidently remove OCD from the anxiety 
disorders category, research comparing and contrasting OCD 
to both anxiety disorders and OCRDs is warranted.  

Further research on the classification of OCD as a 
spectrum disorder is recommended, especially since the 
literature remains preliminary and inconclusive. Researchers 
have found similarities among OCD and the proposed OC 
spectrum disorders across various domains. While OCD and 
BDD appear to share the most putative symptoms, there still 
lacks conclusive evidence for the inclusion of this and other 
disorders such as, trichotillomania and Tourette’s disorder in 
the OC spectrum. To develop a spectrum of disorders based 
on the symptom domain alone appears to be an 
oversimplification which neglects other possibilities.           

 The existing research serves as a phenomenal starting 
point and needs to be built upon, especially in the areas of 
psychological and psychopharmacological treatment. For 
classification as a spectrum disorder, researchers need to 
replicate the studies that find biological, neurological, and 
treatment response similarities between OCD and the 
recommended OCD spectrum disorders. Currently, there are 
few research studies directly comparing OCD to an OCRD. 
Rather, OCD and OCRDs are often indirectly connected 
through the comparison of separate research studies, and 
future work should employ samples consisting of both OCD 
and OCRD patients. A consistent methodology would offer a 
more accurate comparison of OCD and OCRDs. Continued 
research is needed to explore the many aspects of OCD and 
how these features are expressed across other potential OCD 
spectrum disorders.     

 
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