CHAPTER 13

Obsessive-Compulsive and Related Disorders

Darin D. Dougherty, M.D., M.M.Sc.

Sabine Wilhelm, Ph.D.

Michael A. Jenike, M.D.

In DSM-IV (American Psychiatric Association 1994) and DSM-IV-TR (American Psychiatric Association 2000), obsessive-compulsive disorder was characterized as an anxiety disorder. In the new DSM-5 (American Psychiatric Association 2013), OCD has been moved to its own section, titled "Obsessive-Compulsive and Related Disorders," and disorders that were previously classified in other sections have been included in this section. Additionally, new disorders have been added to the Obsessive-Compulsive and Related Disorders section. Currently, the new Obsessive-Compulsive and Related Disorders section includes obsessive-compulsive disorder, body dysmorphic disorder, hoarding disorder, trichotillomania (hair-pulling disorder), excoriation (skin-picking) disorder, substance/medication-induced obsessive-compulsive and related disorder, and obsessive-compulsive and related disorder due to another medical condition. The goal of this chapter is to review the new Obsessive-Compulsive and Related Disorders chapter of DSM-5 and each of the disorders contained within this new DSM-5 categorization.

Obsessive-Compulsive Disorder

Diagnosis

Obsessive-compulsive disorder (OCD) is characterized, as the name suggests, by obsessions and/or compulsions (see DSM-5 diagnostic criteria for OCD in Box 13-1). Obsessions are unwanted, repetitive thoughts that usually involve themes of harm and danger. Common obsession content includes fear of contamination, pathological doubt, violent and/or sexual intrusive thoughts, symmetry concerns, and religious scrupulosity (Table 13-1). In contrast, compulsions are the repetitive behaviors that the sufferer performs in response to the distress associated with the content of the obsessions. Common compulsive behaviors include excessive cleaning (e.g., hand washing), checking, ordering, rearranging, counting, repeating, and mental rituals (see Table 13-1). DSM-5 requires that individuals meet criteria either for obsessive thoughts or for compulsive behaviors (Criterion A) in order to receive a diagnosis of OCD. However, most patients with OCD have both obsessions and compulsions. Also, in order to meet criteria for an OCD diagnosis, the obsessions or compulsions must be time-consuming (e.g., take more than 1 hour per day) or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion B). Additionally, the OCD symptoms cannot be attributable to the physiological effects of a substance or another medical condition (Criterion C) and may not be restricted to the symptoms of another DSM disorder (Criterion D). DSM-5 includes specifiers as to insight (good or fair, poor, or absent) and as to whether the OCD is tic related (i.e., whether the individual has a lifetime history of a chronic tic disorder).

Box 13-1. DSM-5 Criteria for Obsessive-Compulsive Disorder

300.3 (F42)

  1. Presence of obsessions, compulsions, or both:
  2. Obsessions are defined by (1) and (2):

    1. Recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance, as intrusive and unwanted, and that in most individuals cause marked anxiety or distress.
    2. The individual attempts to ignore or suppress such thoughts, urges, or images, or to neutralize them with some other thought or action (i.e., by performing a compulsion).

    Compulsions are defined by (1) and (2):

    1. Repetitive behaviors (e.g., hand washing, ordering, checking) or mental acts (e.g., praying, counting, repeating words silently) that the individual feels driven to perform in response to an obsession or according to rules that must be applied rigidly.
    2. The behaviors or mental acts are aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation; however, these behaviors or mental acts are not connected in a realistic way with what they are designed to neutralize or prevent, or are clearly excessive.
    3. Note: Young children may not be able to articulate the aims of these behaviors or mental acts.

  3. The obsessions or compulsions are time-consuming (e.g., take more than 1 hour per day) or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  4. The obsessive-compulsive symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.
  5. The disturbance is not better explained by the symptoms of another mental disorder (e.g., excessive worries, as in generalized anxiety disorder; preoccupation with appearance, as in body dysmorphic disorder; difficulty discarding or parting with possessions, as in hoarding disorder; hair pulling, as in trichotillomania [hair-pulling disorder]; skin picking, as in excoriation [skin-picking] disorder; stereotypies, as in stereotypic movement disorder; ritualized eating behavior, as in eating disorders; preoccupation with substances or gambling, as in substance-related and addictive disorders; preoccupation with having an illness, as in illness anxiety disorder; sexual urges or fantasies, as in paraphilic disorders; impulses, as in disruptive, impulse-control, and conduct disorders; guilty ruminations, as in major depressive disorder; thought insertion or delusional preoccupations, as in schizophrenia spectrum and other psychotic disorders; or repetitive patterns of behavior, as in autism spectrum disorder).

Specify if:

With good or fair insight

With poor insight

With absent insight/delusional beliefs

Specify if:

Tic-related

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

Table 13-1. Frequency of common obsessions and compulsions in a clinic sample of 560 patients with obsessive-compulsive disorder

Obsessions % Compulsions %

Contamination

50

Checking

61

Pathological doubt 42 Washing 50
Somatic 33 Counting 36
Need for symmetry 32 Need to ask or confess 34

Aggressive

31

Symmetry and precision

28

Sexual 24 Hoarding

18

Multiple obsessions 72 Multiple compulsions 58

Source. Adapted from Rasmussen SA, Eisen JL: "Clinical and Epidemiologic Findings of Significance to Neuropharmacologic Trials of OCD." Psychopharmacology Bulletin 24:466-470, 1988.

Differential Diagnosis

The diagnosis of OCD is determined by the presence of obsessions and/or compulsions. Although this may seem straightforward, the differential diagnosis includes the ruminations of depression, the delusions of psychosis, anxiety symptoms associated with other anxiety disorders, and severe obsessive-compulsive personality disorder (OCPD). OCPD is defined as a rigid, perfectionistic personality type. A general rule of thumb is that whereas OCPD tends to be experienced as ego-syntonic, the obsessions and compulsions of OCD are experienced as ego-dystonic. Despite the similarity of their names, OCPD is clearly a separate disorder from OCD and does not respond to the treatments used for OCD.

Psychiatric comorbidity is common in OCD, with the Epidemiologic Catchment Area (ECA) study finding that two-thirds of patients with OCD met criteria for at least one other psychiatric illness during their lifetime (Karno et al. 1988). The most common comorbid psychiatric diagnosis is major depressive disorder. Approximately one-third of individuals with OCD are currently experiencing a major depressive episode, and two-thirds will have a major depressive episode during their lifetime. Other commonly comorbid psychiatric illnesses include anxiety disorders, eating disorders, and substance abuse/dependence.

Clinical Course

The average age at onset of OCD is 21 years, with average onset age varying by gender (19 years for men; 22 years for women (Rasmussen and Eisen 1992). However, earlier onset is not rare; 21% of patients report symptoms before puberty. Although onset may occur during other periods of the life span, late-onset OCD is relatively rare and may warrant a medical workup for a possible organic cause.

The clinical course of OCD is typically lifelong with waxing and waning symptomatology. A minority of patients with OCD may experience a phasic or episodic course with periods of complete or partial remission. Women are at particular risk during pregnancy and the postpartum period. One report found that 57% of women experiencing postpartum depression also experienced obsessional thoughts (Wisner et al. 1999).

Epidemiology

Although OCD was once considered a rare disorder, data from the ECA study found a lifetime prevalence of OCD of between 1.9% and 3.3% in a large sample of U.S. households (Goodman 1999). Epidemiological studies from other countries throughout the world have generally found comparable lifetime prevalence rates of OCD. The disability associated with OCD is severe enough that the World Health Organization has listed

OCD among the 10 medical illnesses most likely to cause disability (Murray and Lopez 1996).

Etiology

Psychodynamic Theory

Freud (1909/1973) postulated that obsessions were defensive reactions to unconscious impulses, especially sexual and aggressive impulses. Obsessions served as a way to mask these impulses and/or control them. Unfortunately, although psychodynamic therapy may help to reveal the origins of obsessions, there is little evidence that doing so changes OCD symptoms.

Genetics

A review of twin studies found that there is a strong heritable component to OCD, including concordance rates of between 80% and 87% in monozygotic twins and between 47% and 50% in dizygotic twins (van Grootheest et al. 2005). OCD also tends to run in families, with a recent study of 1,209 first-degree relatives of OCD probands finding an increased risk of OCD among relatives of probands (8.2%) compared with control subjects (2.0%) (Hettema et al. 2001). Candidate gene studies have found a number of genes that may be associated with OCD, including many associated with serotonin, dopamine, and glutamate. Larger-scale studies are needed to confirm these initial findings.

Neuroanatomy

While a thorough review of all that has been learned from neuroimaging studies is beyond the scope of this chapter, a general description of the neurocircuitry involved in the pathophysiology of OCD is presented. Parallel cortico-striato-thal-amo-cortical (CSTC) circuits in the brain each subserve different functions ranging from oculomotor movement to cognition and affective functions. One of these CSTC circuits, termed the ventral cognitive loop, includes the orbitofrontal cortex, the caudate nucleus, and the dorsomedial thalamus. Numerous functional neuroimaging studies have found functional abnormalities within all nodes of this circuit. Namely, these brain regions are hyperactive at rest in patients with OCD compared with healthy volunteers, this hyperactivity is amplified during OCD symptom provocation, and the hyperactivity is attenuated with successful treatment (Dougherty et al. 2010).

Treatment

Behavioral Therapy

A specific type of behavioral therapy, exposure and response prevention (ERP), has been used and refined since the 1960s for the treatment of OCD. As the name suggests, patients are first exposed to stimuli that trigger their specific OCD symptoms. For patients with contamination fears, this may involve touching a doorknob or a faucet handle that they perceive as being contaminated. Patients then prevent themselves from responding to the stimuli as they usually would (e.g., a patient who now feels contaminated will avoid washing his hands after touching the contaminated stimulus). Initially patients experience marked anxiety, and it can take a significant amount of time for the anxiety to decrease. As patients repeat their ERP exercises, both the amplitude of the anxiety and the time required for it,to diminish will gradually decrease until patients become habituated to the stimuli.

ERP is a highly effective treatment for OCD and is considered to be a first-line intervention for OCD. While a multitude of clinical trials of ERP for the treatment of OCD have been published, meta-ana-lytic approaches provide a general estimate of the response rates associated with ERP. Foa and Kozak (1996) defined "response" as a 30% or more improvement of OCD symptoms and found that across more than a dozen studies the response rate was 76%-83%. While pharmacotherapy treatment of OCD will be reviewed later in this chapter, it is noteworthy that the few studies that have compared ERP with pharmacotherapy have found that ERP is superior to pharmacotherapy (e.g., Foa et al. 2005). Additionally, some studies have suggested that combining ERP and pharmacotherapy results in lower relapse rates in patients with OCD when they discontinue pharmacotherapy.

Cognitive Therapy

Cognitive therapy (CT) is a form of psychotherapy that seeks to identify and modify maladaptive beliefs. A recent meta-analysis of psychotherapies in OCD (Rosa-Alcazar et al. 2008) found very similar effect size estimates for CT and ERP; however, the CT effect size was only based on three studies. Several recent CT studies not included in the metaanalysis (e.g., Wilhelm et al. 2009) also showed promising results. However, given that the number of CT studies is still relatively small, ERP is currently considered the psychotherapy of choice for OCD.

Pharmacotherapy

The serotonin reuptake inhibitors (SRIs) represent the first-line pharmacotherapy intervention for OCD (Bandelow et al. 2008). The SRIs include all of the selective serotonin reuptake inhibitors (SSRIs) as well as clomipramine. Meta-analyses have generally found that 40%-60% of patients with OCD achieve response (defined as at least a 25%-35% decrease in OCD symptoms) when treated with SRIs (Greist et al. 1995). These meta-analyses, as well as a small number of head-to-head studies, have failed to demonstrate superior efficacy of any SRI over the others. When SRIs are used for treating OCD, it is important that high dosages be achieved (clomipramine up to 250 mg/day, fluoxetine up to 80 mg/day, paroxetine up to 60 mg/day, fluvoxamine up to 300 mg/day, sertraline up to 200 mg/day, citalopram up to 40 mg/day, and escitalopram up to 30 mg/day) because response rates are higher compared with treatment with low doses. Additionally, it is important for both the clinician and the patient to realize that response may not be achieved until after 8-12 weeks of treatment.

Other potential monotherapy approaches to the treatment of OCD generally involve other classes of antidepressants that affect the serotonergic system. Although data are much more limited, there is some support for the use of serotonin-norepinephrine reuptake inhibitors (SNRIs) and, possibly, the monoamine oxidase inhibitors (MAOIs). There is no evidence supporting the use of dopaminergic antidepressants (e.g., bupropion) for the treatment of OCD, and there is strong evidence from clinical trials that tricyclic antidepressants (TCAs) other than clomipramine are not effective for the treatment of OCD.

There have long been data supporting the use of dopaminergic antagonists to augment the effects of SRIs in the treatment of OCD. Although the initial studies, by necessity, included only conventional antipsychotics, studies since the advent of the atypical antipsychotics also support their use as augmenting agents with the SRIs. Because of the lower extra-pyramidal side-effect burden, most clinicians now use the atypical antipsychotics to augment SRIs for the treatment of OCD. However, the gains of lower extra-pyramidal side-effect burden with the atypical antipsychotics are somewhat mitigated by the higher rates of metabolic syndrome with the atypical antipsychotics, so clinicians should use these agents with caution and an understanding of the risks and benefits. Dosages are usually in the low to moderate range (e.g., risperidone 1-4 mg/day), and response after augmentation is typically seen within 1-4 weeks.

More recent pharmacological approaches to OCD treatment include agents that affect the glutamatergic system. Preliminary studies involving memantine, riluzole, and N-acetylcysteine are promising.

Neurosurgery

Although beyond the scope of this chapter, neurosurgical approaches may be efficacious for patients with intractable OCD that has not improved despite treatment with all conventional therapies. These approaches include ablative limbic system procedures such as anterior cingulotomy, anterior capsulotomy, subcaudate tractotomy, and limbic leucotomy as well as deep brain stimulation (DBS) electrodes placed at a number of different brain targets. The U.S. Food and Drug Administration (FDA) approved the use of DBS at the ventral capsule/ventral striatum target for treatment-refractory OCD in 2009.

Prognosis

Rates of full remission over different time lengths (although all are over years, not months) in different studies have ranged from 6% to 43%. Rates of partial remission reported in these same studies have ranged from 17% to 75% (Eisen et al. 2010). The longest-term follow-up study ever conducted (mean follow-up period of 47 years) found that almost half (48%) of patients reported clinical recovery (defined as no clinically relevant symptoms for at least 5 years). However, only 20% experienced full remission (i.e., complete absence of symptoms for at least 5 years) (Skoog and Skoog 1999).

Body Dysmorphic Disorder

Diagnosis

Body dysmorphic disorder (BDD; see DSM-5 diagnostic criteria in Box 13-2) is characterized by a preoccupation with one or more perceived defects or flaws in physical appearance that are not observable by or appear very mild to others (Criterion A). For an individual to be diagnosed with BDD, DSM-5 also requires that at some point during the course of the disorder, the individual has performed repetitive behaviors (e.g., mirror checking, excessive grooming, skin picking, reassurance seeking) or mental acts (e.g., comparing one's appearance with that of others) in response to his or her appearance concerns (Criterion B). Although there is no minimum threshold of daily time occupied by the preoccupation required to meet diagnostic criteria for BDD, the preoccupation must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). Finally, the appearance preoccupations must not be restricted to concerns with body fat or weight in an eating disorder (Criterion D). DSM-5 includes specification as to insight (good or fair, poor, absent/delusional beliefs) and as to presence of muscle dys-morphia (the belief that one's body build is too small or insufficiently muscular).

Box 13-2. DSM-5 Criteria for Body Dysmorphic Disorder

300.7 (F45.22)

  1. Preoccupation with one or more perceived defects or flaws in physical appearance that are not observable or appear slight to others.
  2. At some point during the course of the disorder, the individual has performed repetitive behaviors (e.g., mirror checking, excessive grooming, skin picking, reassurance seeking) or mental acts (e.g., comparing his or her appearance with that of others) in response to the appearance concerns.
  3. The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  4. The appearance preoccupation is not better explained by concerns with body fat or weight in an individual whose symptoms meet diagnostic criteria for an eating disorder.

Specify if:

With muscle dysmorphia

Specify if:

Indicate degree of insight regarding body dysmorphic disorder beliefs (e.g., "I look ugly" or "I look deformed").

With good or fair insight

With poor insight

With absent insight/delusional beliefs

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

The diagnosis of BDD requires the preoccupation with perceived appearance defects as described above. Patients believe they look ugly, unattractive, abnormal, or deformed. The perceived defects can involve any area of the body. Behaviors such as comparing oneself with others and mirror checking are common. Many, if not most, patients with BDD attempt to hide or camouflage their perceived defects using clothing, hair growth, cosmetics, and so forth. Many will seek care from dermatologists and/or cosmetic surgeons. As opposed to the generally good insight seen in patients with OCD, most patients with BDD have poor insight into their illness. They tend to firmly believe that the perceived defect is present and not imagined. BDD patients often suffer from delusions of reference and believe that others are laughing at them or mocking them because of the perceived appearance flaw.

Muscle dysmorphia, a form of BDD appearing almost exclusively in males, consists of preoccupation with the idea that one's body is too small or not muscular enough (Phillips et al. 2010). These individuals actually look normal or even muscular. Most diet, exercise excessively, and lift weights. These individuals are at higher risk for anabolic steroid abuse. BDD by proxy is a form of BDD where individuals are preoccupied with perceived defects in another person's appearance.

Differential Diagnosis

Perhaps the most important factor to consider in the differential diagnosis of BDD is the possibility of normal appearance concerns or actual clearly noticeable physical defects. Concerns with bodily defects that are clearly noticeable (i.e., not slight) are not diagnosed as BDD. Weight concerns occurring in the context of an eating disorder preclude the diagnosis of BDD. Finally, the feelings of low self-worth associated with major depression may manifest physically, and delusions associated with psychosis may focus on physical appearance.

Psychiatric comorbidity is common in BDD; major depressive disorder, with a lifetime prevalence of 75%, is the most common comorbid diagnosis. Approximately one-third of patients with BDD experience comorbid OCD during their lifetime, and almost 40% have comorbid social anxiety disorder at some point. Comorbid substance use disorders are also common.

Clinical Course

BDD symptoms typically emerge during early adolescence, and the female-to-male gender ratio ranges from 1:1 to 3:2 (Phillips 2011). The course is usually chronic, with waxing and waning symptoms. The clinical features are generally similar for men and women, although some gender differences have been reported (Perugi et al. 1997; Phillips and Diaz 1997; Phillips et al. 2006a).

Epidemiology

The point prevalence of BDD in epidemiological studies ranges from 0.7% to 2%-4% (Phillips 2011). BDD is more common in patients with other psychiatric disorders, with a frequency of 8%-37% in patients with OCD, 11%—13% in patients with social phobia, 26% in patients with trichotillomania, and 39% in patients with anorexia nervosa (Phillips 2011). Individuals with BDD are more likely than individuals without BDD to report suicidal ideation and suicide attempts related to concerns about appearance (Buhlmann et al. 2010; Rief et al. 2006). Finally, as many as 55% of individuals with BDD are unmarried (Koran et al. 2008; Rief et al. 2006), and more than 20% are unemployed (Rief et al. 2006).

Etiology

Although BDD was classified as a somatoform disorder in DSM-IV and DSM-IV-TR, it has long been considered to be an OCD spectrum disorder. There are similarities between OCD and BDD in phenomenology, onset age, gender ratio, and treatment response to SRIs. However, very few neuroimaging studies have been conducted in subjects with BDD, so comparisons between the two disorders are not yet possible. Interestingly, and perhaps unique to the pathophysiology of BDD, recent functional magnetic resonance imaging (fMRI) studies have demonstrated abnormalities in brain regions associated with visual processing, with individuals with BDD showing a bias for processing details of visual images rather than focusing on the visual image as a whole (Feusner et al. 2010, 2011).

Treatment

Before reviewing cognitive-behavioral therapy (CBT) and pharmacotherapy for BDD, it is important to note that whereas many patients with BDD seek surgical and cosmetic treatment for their perceived appearance defects, patients with BDD are rarely satisfied with the results of these treatments. Therefore, surgical and cosmetic treatments should not be encouraged in patients with BDD.

Cognitive-Behavioral Therapy

As is the case with OCD, ERP appears to be a first-line treatment for BDD. For BDD, the exposures and response prevention are simply tailored to the individual's BDD symptoms. For example, exposures may involve going into social settings with the response prevention being resistance to mirror checking or excessive grooming. CBT for BDD also often involves cognitive restructuring in which inaccurate beliefs are identified and targeted. Unlike the treatment of OCD, BDD treatment often includes mirror retraining to address the distorted perception of appearance characteristic of BDD (Wilhelm et al. 2013). Although there are fewer studies of CBT for BDD than for OCD, existing studies strongly support the efficacy of CBT in the treatment of BDD (Veale et al. 1996; Wilhelm et al. 2011).

Pharmacotherapy

There are no FDA-approved medications for BDD. The SRIs have received the most study for the treatment of BDD, but the number of studies is still relatively small. There have been two controlled trials (one of clomipramine and one of fluoxetine) and four open-label trials (including fluvoxamine, citalopram, and escitalopram) of SRI treatment of BDD. Intent-to-treat analyses of these data suggest that 63%-83% of patients with BDD will respond to treatment with SRIs (Phillips 2011). As is the case with OCD, higher doses of the SRIs are generally required, and time until response may be as long as 9 weeks. Finally, although antipsychotic augmentation of SRIs is commonly utilized in clinical practice, only one controlled study of SRI augmentation for BDD has been reported (Phillips 2005). This trial found that pimozide augmentation was not more effective than placebo.

Prognosis

The largest (N=161) follow-up study of patients with BDD found that over 1 year, the probability of full remission was 9% and the probability of partial remission was 21%, even though 84.2% of participants were receiving mental health treatment during the 1-year period (Phillips et al. 2006b). However, 4-year remission rates as high as 60% have been reported following treatment with pharmacotherapy and/or psychotherapy (Phillips et al. 2005). Finally, in terms of disability, individuals with BDD have been found to be more disabled than individuals with depression, diabetes, or a recent myocardial infarction (Phillips 2000).

Hoarding Disorder

Diagnosis

Until the inclusion of hoarding disorder as a discrete illness in DSM-5, hoarding was considered a subtype of OCD. Recent evidence regarding pathophysiology and treatment response of hoarding symptoms (Mataix-Cols et al. 2010) strongly suggests that hoarding warrants its own diagnostic category separate from OCD (Box 13-3). In DSM-5, hoarding is defined as a persistent difficulty discarding or parting with possessions, regardless of their actual value (Criterion A). This difficulty is due to strong urges to save items and/or distress associated with discarding (Criterion B). This difficulty with discarding results in the accumulation of such a large amount of possessions in living areas or the workplace that the intended use of these areas is no longer possible (Criterion C). DSM-5 does allow for exceptions for Criterion C if areas are uncluttered because of the interventions of others. Although no specific quantities of time or items are required for diagnosis, the hoarding must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion D). Finally, the hoarding symptoms may not be due to another medical condition (Criterion E) or restricted to another DSM-5 disorder (Criterion F). DSM-5 includes specifiers to indicate the level of insight (good or fair, poor, or absent) and the presence of "excessive acquisition." The diagnosis of hoarding disorder is relatively straightforward, as the diagnosis relies on hoarding symptoms that result in impairment and/or distress.

Box 13-3. DSM-5 Criteria for Hoarding Disorder

300.3 (F42)

  1. Persistent difficulty discarding or parting with possessions, regardless of their actual value.
  2. This difficulty is due to a perceived need to save the items and to distress associated with discarding them.
  3. The difficulty discarding possessions results in the accumulation of possessions that congest and clutter active living areas and substantially compromises their intended use. If living areas are uncluttered, it is only because of the interventions of third parties (e.g., family members, cleaners, authorities).
  4. The hoarding causes clinically significant distress or impairment in social, occupational, or other important areas of functioning (including maintaining a safe environment for self and others).
  5. The hoarding is not attributable to another medical condition (e.g., brain injury, cerebrovascular disease, Prader-Willi syndrome).
  6. The hoarding is not better explained by the symptoms of another mental disorder (e.g., obsessions in obsessive-compulsive disorder, decreased energy in major depressive disorder, delusions in schizophrenia or another psychotic disorder, cognitive deficits in major neurocognitive disorder, restricted interests in autism spectrum disorder).

Specify if:

With excessive acquisition

Specify if:

With good or fair insight

With poor insight

With absent insight/delusional beliefs

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

Individuals with hoarding disorder often hoard items that they feel may have perceived utility or perceived sentimental value (including, at times, animals). They may also report a fear of losing important information. If faced with the prospect of discarding items, individuals with hoarding disorder frequently experience significant distress. The volume of accumulated items is often staggering. Individuals may fill an entire home with hoarded items, sometimes to the detriment of their safety.

Differential Diagnosis

Some patients experiencing brain trauma may exhibit hoarding behavior (e.g., damage to the ventromedial prefrontal and anterior cingulate cortices has been associated with hoarding symptoms). In these cases, the hoarding behavior would not begin until after the brain injury. Some neurodevelopmental disorders such as autism and Prader-Willi syndrome are sometimes associated with hoarding behavior. If the hoarding symptoms are directly due to obsessions or compulsions associated with OCD (fear of contamination or harm), then the diagnosis of hoarding disorder should not be considered. Additionally, individuals who exhibit hoarding behavior usually find the hoarding distressing. Finally, some patients with psychiatric diagnoses other than hoarding disorder may appear to be exhibiting hoarding behavior when, in fact, their debilitated state may prevent them from appropriately discarding items.

Approximately 75% of individuals with hoarding disorder have a comorbid mood or anxiety disorder (Frost et al. 2011). Additionally, 20% of individuals with hoarding disorder have comorbid OCD (Frost et al. 2011).

Clinical Course

Although onset age is not as well characterized for hoarding disorder as it is for OCD and BDD, some studies suggest that hoarding symptoms begin around 11-15 years of age and gradually worsen until they interfere with the individual's life (Tolin et al. 2010). One study of hoarders found that symptom onset was by age 12 for 60% of participants and by age 18 for 80% (Grisham et al. 2006). As opposed to OCD, hoarding symptoms, while also chronic, are rarely associated with a waxing and waning course and are instead associated with relatively little change over time (Tolin et al. 2010).

Epidemiology

Although there are no national epidemiology data available regarding the prevalence of hoarding symptoms, community surveys estimate the point prevalence of clinically significant hoarding symptoms as approximately 2%-6% (e.g., Samuels et al. 2008). Two studies (Iervolino et al. 2009; Samuels et al. 2008) found higher prevalence in men than in women, whereas one study (Mueller et al. 2009) found no difference in prevalence between genders.

Etiology

Until DSM-5, hoarding had been considered a subtype of OCD. However, when the different OCD symptom factors are examined, hoarding is clearly distinct from the others (Bloch et al. 2008; Mataix-Cols et al. 2010). Additionally, multiple neuroimaging studies have revealed differences in the pathophysiology of OCD and hoarding (Mataix-Cols et al. 2004; Saxena et al. 2001; Tolin et al. 2009). There does appear to be a genetic component to the illness. Approximately 50% of hoarders report a first-degree relative who hoards, and twin studies suggest that approximately 50% of the variability in hoarding is attributable to genetic factors.

Treatment

One of the most difficult aspects of treating individuals with hoarding disorder is getting them to accept treatment. Although their hoarding behavior often causes great distress to those around them, individuals with hoarding disorder may not find these behaviors distressing. The first-line treatment of hoarding disorder is behavioral therapy that focuses on removing hoarded items from the environment (increasing outflow) and providing skills to decrease future hoarding (decreasing inflow) (Frost and Tolin 2008). Some data suggest that CBT (e.g., addition of motivational interviewing) may be a more effective approach to treating hoarding behavior (Steketee et al. 2010). There is little to no data regarding pharmacotherapy specifically for hoarding disorder as hoarding has been considered a subtype of OCD. Overall, in pharmacological trials for OCD, hoarding appears to exhibit a lesser response to SRIs than other OCD spectrum disorders (e.g., Mataix-Cols et al. 1999).

Prognosis

Most studies have found hoarding symptoms to be chronic and unchanging. Individuals with hoarding disorder who participate in behavioral therapy have lower response rates than individuals with OCD (Abramowitz et al. 2003; Mataix-Cols et al. 2002). This may be partly due to poor motivation to engage in treatment and higher dropout rates. Some data suggest that CBT may be more effective than behavioral therapy alone for hoarding symptoms. Because hoarding has been considered a sub-type of OCD rather than a distinct disorder until DSM-5, there is little prognostic data regarding pharmacotherapy for hoarding behavior.

Trichotillomania (Hair-Pulling Disorder)

Diagnosis

In DSM-IV and DSM-IV-TR, hair-pulling disorder was referred to as trichotillomania. While the term trichotillomania is retained in DSM-5, the descriptor hair-pulling disorder is now included parenthetically (see DSM-5 diagnostic criteria in Box 13-4). Additionally, the diagnostic requirement in DSM-IV and DSM-IV-TR of a buildup of tension before hair pulling followed by a sense of gratification after hair pulling has been removed in DSM-5 because it became clear that a large number of individuals do not experience these emotional states in association with their hair pulling. Currently, the core diagnostic criterion of hairpulling disorder has been simplified to "recurrent pulling out of one's hair, resulting in hair loss" (Criterion A). In addition, the individual must have made repeated attempts to decrease or stop the hair pulling (Criterion B). There are no specified lower limits regarding time spent hair pulling or degree of hair loss, but the hair pulling must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). Finally, the hair pulling or hair loss may be not due to another medical condition (Criterion D) or better explained by the symptoms of another mental disorder (Criterion E).

Box 13-4. DSM-5 Criteria for Trichotillomania (Hair-Pulling Disorder)

312.39 (F63.3)

  1. Recurrent pulling out of one's hair, resulting in hair loss.
  2. Repeated attempts to decrease or stop hair pulling.
  3. The hair pulling causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  4. The hair pulling or hair loss is not attributable to another medical condition (e.g., a dermatological condition).
  5. The hair pulling is not better explained by the symptoms of another mental disorder (e.g., attempts to improve a perceived defect or flaw in appearance in body dysmorphic disorder).

The primary symptom of hair-pulling disorder is, of course, hair pulling with loss of hair. Individuals may be drawn to pull hairs with particular characteristics (e.g., "coarse" or "kinky"). They may pull from any part of the body, including scalp, eyebrows, eyelashes, arms, legs, and pubic area (Table 13-2; Christenson et al. 1991a). Most individuals with hairpulling disorder pull from multiple sites (see Table 13-2). Whereas some patients report pulling hair when distressed, others report hair pulling during states of relaxation; most report pulling during both conditions. Many patients report mirror-checking behaviors, although they may or may not pull in front of a mirror. Some will use utensils instead of or in addition to their fingers for hair pulling. Some patients with hair-pulling disorder will eat their hair after pulling, resulting in a risk for trichobezoars that sometimes require surgical intervention. There is significant shame associated with both hair loss and the inability to stop the hair pulling. As a result, many individuals with hair-pulling disorder hide their hair loss with hats, scarves, and long clothing.

Percentage of patients

Table 13-2. Phenomenology of hair pulling in a sample of 60 patients with chronic trichotillomania

Percentage of patients

Hair pulling at specific sites

Scalp 75
Eyelashes 53
Eyebrows 42
Pubic area 17

Beard and face

10

Arms

10

Legs 7

Total number of pulling sites

One 38

Two or more

62

Three or more 33

Four or more

10

Source. Adapted from Christenson et al. 1991a.

Differential Diagnosis

Most important, of course, is not to mis-attribute hair loss caused by a medical condition to hair pulling. It is also possible that OCD or BDD may manifest with symptoms consistent with hair-pulling disorder. For example, patients may pull their hair because they feel it is contaminated (OCD) or because it is perceived as a physical defect (BDD). If this is the case, hair-pulling disorder should not be considered as a diagnosis. In these instances it may be difficult to ascertain whether patients have hair-pulling disorder instead of or in addition to OCD or BDD. Finally, individuals with psychotic disorders may remove hair as a result of a delusion or hallucination. In this case, the diagnosis is not hair-pulling disorder.

The most common psychiatric comorbidities associated with hair-pulling disorder are major depressive disorder and skin-picking disorder (Stein et al. 2008; Woods et al. 2006a).

Clinical Course

Onset of hair pulling frequently occurs around the onset of puberty, although it may begin before or after puberty as well (Mansueto et al. 1997). Some studies have found that with early childhood onset, the duration of hair pulling may be brief and not require treatment. However, if the hair-pulling symptoms are of longer duration, the usual course is chronic with some waxing and waning of symptoms (Keuthen et al. 2001). Finally, perhaps related to the high female prevalence, females sometimes report worsening of symptoms during perimenstruation.

Epidemiology

A 12-month prevalence rate of 0.6% for hair-pulling disorder has been reported in both community-based and college student samples (Christenson et al. 1991b; Duke et al. 2009). Most studies have found that females are much more commonly affected than males, with some studies estimating that 93% of individuals with hair-pulling disorder are female (Christenson et al. 1991a).

Etiology

Hair pulling is more common in persons with OCD and their first-degree relatives (Bienvenu et al. 2000, 2011), and genetic studies have shown a genetic vulnerability to hair-pulling disorder (Novak et al. 2009; Stein et al. 2010). Compared with healthy volunteers and patients with OCD, patients with hair-pulling disorder demonstrate impaired ability to inhibit motor behaviors on tasks such as the Stop-Signal Task and Go/No-Go Task (Bohne et al. 2008; Chamberlain et al. 2006). Finally, because very few neuroimaging studies have been conducted in subjects with hair-pulling disorder, comparison with OCD and other related disorders is not yet possible.

Treatment

Before seeking treatment for hair pulling, many individuals with the disorder will attempt to stop the hair pulling on their own, often using barrier methods such as covering the pulling site or their fingers so that they are unable to pull. It is not clear how successful this approach is because, if successful, these individuals will not present for treatment. Nonetheless, once an individual presents for treatment, the treatment of hair-pulling disorder can include behavioral therapy, pharmacotherapy, or both. The accepted type of behavioral therapy for the treatment of hairpulling disorder is informed by habit-reversal therapy (HRT) (Azrin et al. 1980). This therapy has several components, including self-monitoring, awareness training, stimulus control, and competing response training. Three randomized, parallel-group studies have demonstrated superior efficacy for HRT over placebo (Ninan et al. 2000; van Minnen et al. 2003; Woods et al. 2006b), providing strong evidence for HRT as the first-line treatment for hair-pulling disorder. Pharmacotherapy studies have shown mixed results with SRIs, with a meta-analysis failing to show any evidence of improvement with SRIs compared with placebo (Bloch et al. 2007). Encouraging initial results with antipsychotic medications (both as SRI augmentation and as monotherapy) have been reported. Finally, one controlled trial each for naltrexone (Christenson et al. 1994) and N-acetylcysteine (Grant et al. 2009) demonstrated efficacy superior to placebo.

Prognosis

One older long-term follow-up study after treatment with HRT found an 87% reduction in hair pulling at 22-month follow-up compared with pretreatment (Azrin et al. 1980). A more recent study found that hair-pulling symptoms did not significantly worsen over a 2.5-year follow-up period, but there was significant worsening in self-esteem (Keuthen et al. 2001).

Excoriation (Skin-Picking) Disorder

Definition

The diagnostic features of excoriation disorder (refer to DSM-5 diagnostic criteria in Box 13-5) (Wilhelm et al. 1999) are identical to those of hair-pulling disorder with the exception that the bodily focused repetitive behavior is skin picking rather than hair pulling. Although patients may pick from anywhere on their bodies, the most common sites are the face, arms, and hands. Some people will pick healthy skin; others will pick real or perceived imperfections. Once picking has resulted in a scab, the scab will frequently become a recurrent target for picking. Most persons with excoriation disorder use their fingernails, but as is the case with hair-pulling disorder, some will use utensils such as tweezers or knives. Some patients with the disorder may rub, squeeze, or bite their skin, and some will eat their skin after picking. Most persons with excoriation disorder report mirror checking, and many will pick in front of a mirror. As is the case with hair pulling, there is usually considerable shame regarding the wounds from picking as well as the inability to stop the skin picking. Finally, persons with excoriation disorder often attempt to conceal their skin-picking sites with clothing or cosmetics.

Box 13-5. DSM-5 Criteria for Excoriation (Skin-Picking) Disorder

698.4 (L98.1)

  1. Recurrent skin picking resulting in skin lesions.
  2. Repeated attempts to decrease or stop skin picking.
  3. The skin picking causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  4. The skin picking is not attributable to the physiological effects of a substance (e.g., cocaine) or another medical condition (e.g., scabies).
  5. The skin picking is not better explained by symptoms of another mental disorder (e.g., delusions or tactile hallucinations in a psychotic disorder, attempts to improve a perceived defect or flaw in appearance in body dysmorphic disorder, stereotypies in stereotypic movement disorder, or intention to harm oneself in nonsuicidal self-injury).

Differential Diagnosis

Many individuals with BDD pick their skin in an attempt to improve their appearance. Skin picking may also occur in individuals with a primary psychotic disorder (e.g., parasitosis, formication) and can be associated with substance-induced disorders (e.g., cocaine); the diagnosis of excoriation disorder would not apply in these scenarios.

Clinical Course

As is the case with hair-pulling disorder, the onset of excoriation disorder is generally in adolescence around the onset of puberty. The usual course is chronic, with waxing and waning features.

Epidemiology

Although few studies of the prevalence of excoriation disorder have been conducted, the existing studies suggest a lifetime prevalence of 2.0%-5.4%, with females more commonly affected than males (Grant and Odlaug 2009).

Etiology

Skin picking is more common in individuals with OCD and their first-degree relatives (Bienvenu et al. 2000, 2011), and there is evidence of familial transmission of excoriation disorder (Bienvenu et al. 2009; Grant and Odlaug 2009).

Treatment

The behavioral therapy treatment of excoriation disorder is identical to the treatment of hair-pulling disorder (i.e., based on HRT). The only randomized trial of HRT for skin picking found superior efficacy for HRT compared with a waitlist control condition (Teng et al. 2006). To date, three double-blind, placebo-controlled trials of pharmacotherapy treatment of skin picking have been published. One trial with fluoxetine resulted in 80% of patients assigned to fluoxetine being classified as responders (as measured with the Clinical Global Impression—Improvement scale) versus only 27.3% of those treated with placebo (Simeon et al. 1997), and two other trials failed to demonstrate efficacy with citalopram (Arbabi et al. 2008) or lamotrigine (Grant et al. 2010).

Prognosis

There are no published long-term followup studies involving subjects with excoriation disorder. However, given the close relationship of excoriation disorder with other body-focused repetitive behavior disorders such as hair-pulling disorder, one would assume similar prognoses for excoriation disorder and hair-pulling disorder.

Substance/Medication-Induced Obsessive-Compulsive and Related Disorder

Substance/medication-induced obsessive-compulsive and related disorder can be defined as the presence of obsessive-compulsive and related symptoms that are judged to be due to the effects of a substance, including a drug of abuse, a medication, or a toxin (refer to DSM-5 diagnostic criteria in Box 13-6).

Box 13-6. DSM-5 Criteria for Substance/Medication-Induced Obsessive-Compulsive and Related Disorder

  1. Obsessions, compulsions, skin picking, hair pulling, other body-focused repetitive behaviors, or other symptoms characteristic of the obsessive-compulsive and related disorders predominate in the clinical picture.
  2. There is evidence from the history, physical examination, or laboratory findings of both (1) and (2):
    1. The symptoms in Criterion A developed during or soon after substance intoxication or withdrawal or after exposure to a medication.
    2. The involved substance/medication is capable of producing the symptoms in Criterion A.
  3. The disturbance is not better explained by an obsessive-compulsive and related disorder that is not substance/medication-induced. Such evidence of an independent obsessive-compulsive and related disorder could include the following:
  4. The symptoms precede the onset of the substance/medication use; the symptoms persist for a substantial period of time (e.g., about 1 month) after the cessation of acute withdrawal or severe intoxication; or there is other evidence suggesting the existence of an independent non-substance/medication-induced obsessive-compulsive and related disorder (e.g., a history of recurrent non-substance/medication-related episodes).

  5. The disturbance does not occur exclusively during the course of a delirium.
  6. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

Note: This diagnosis should be made in addition to a diagnosis of substance intoxication or substance withdrawal only when the symptoms in Criterion A predominate in the clinical picture and are sufficiently severe to warrant clinical attention.

Specify if (see Table 1 [p. 482] in the DSM-5 chapter "Substance-Related and Addictive Disorders" for diagnoses associated with substance class):

With onset during intoxication

With onset during withdrawal

With onset after medication use

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

Clearly, it must first be determined that the individual was exposed to a substance. Once this is established, the next step is to link the onset of symptoms with exposure to or withdrawal from the substance. Additionally, once exposure to the substance has ceased, the symptoms should usually resolve over time.

The substances most commonly reported as potentially causing obsessive-compulsive and related symptoms (Table 13-3) are amphetamines, cocaine, and stimulants. Heavy metals have also been reported to cause obsessive-compulsive and related symptoms. Finally, atypical antipsychotics, when used as monotherapy, can result in the onset of OCD symptoms or exacerbate existing OCD symptoms.

Table 13-3. Substances that may cause obsessive-compulsive symptoms

Amphetamines

Cocaine

L-Dopa

Other stimulants/dopamine agonists

Heavy metals

Atypical antipsychotics

Table 13-4. Medical conditions that may cause obsessive-compulsive symptoms

Cerebrovascular accident

Central nervous system (CNS) neoplasm/tumor

Head injury

CNS infection (usually, but not always, streptococcal)

Obsessive-Compulsive and Related Disorder Due to Another Medical Condition

The definition of obsessive-compulsive and related disorder due to another medical condition is the presence of clinically significant obsessive-compulsive and related symptoms that are judged to be best explained as the direct effects of another medical condition (e.g., cerebrovascular accident, neoplasm) (Table 13-4; also refer to DSM-5 diagnostic criteria in Box 13-7).

Box 13-7. DSM-5 Criteria for Obsessive-Compulsive and Related Disorder Due to Another Medical Condition

294.8 (F06.8)

  1. Obsessions, compulsions, preoccupations with appearance, hoarding, skin picking, hair pulling, other body-focused repetitive behaviors, or other symptoms characteristic of obsessive-compulsive and related disorder predominate in the clinical picture.
  2. There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct pathophysiological consequence of another medical condition.
  3. The disturbance is not better explained by another mental disorder.
  4. The disturbance does not occur exclusively during the course of a delirium.
  5. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

Specify if:

With obsessive-compulsive disorder-like symptoms

With appearance preoccupations

With hoarding symptoms

With hair-pulling symptoms

With skin-picking symptoms

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

The most important step in making this diagnosis is temporally linking the onset of obsessive-compulsive and related symptoms with the onset of an illness.

Obsessive-compulsive and related symptoms have been reported following viral and bacterial encephalitis. Additionally, there have been enough reports of the onset of obsessive-compulsive and related symptoms following streptococcal infection that a syndrome called pediatric acute-onset neuropsychiatric syndrome (PANS) has been defined. In PANS, children affected by streptococcus may exhibit obsessive-compulsive and related symptoms that sometimes (but not always) resolve after effective treatment of the streptococcal infection. Studies have found that the basal ganglia must be affected by the infection in order for PANS to occur.

Also, brain lesions due to a cerebrovascular accident (CVA), head injury, or tumor have been associated with obsessive-compulsive and related symptoms.

Other Specified or Unspecified Obsessive-Compulsive and Related Disorder

The categories other specified obsessive-compulsive and related disorder and unspecified obsessive-compulsive and related disorder may be applied to presentations that are characteristic of an obsessive-compulsive and related disorder and cause clinically significant impairment but that do not meet full criteria for any of the disorders in this diagnostic class. For an "other specified" diagnosis, the clinician provides the specific reason that full criteria are not met; for an "unspecified" diagnosis, no reason need be given.

DSM-5 describes seven examples of presentations for which an "other specified" designation might be appropriate:

Conclusion

DSM-5 marks the separation of OCD from the anxiety disorders with the creation of a new chapter for Obsessive-Compulsive and Related Disorders, which includes OCD and associated disorders that in DSM-IV were placed in other diagnostic categories. There is strong evidence supporting this change, including phenomenological similarities across OCD and related disorders, neuro-biological evidence suggesting differences in pathophysiology between OCD and related disorders and anxiety disorders, and efficacy of similar treatment approaches across OCD and related disorders. The diagnoses included in Obsessive-Compulsive and Related Disorders all involve unwanted thoughts and/or repetitive behaviors. The pathology of these disorders does not primarily lie within the fear circuitry implicated in the pathophysiology of anxiety disorders. Several behavioral interventions, such as ERP and HRT, are relatively specific to OCD and related disorders. Finally, although SRls, commonly used to treat a variety of psychiatric illnesses, are the primary first-line pharmacotherapy intervention for OCD and some of the OCD-related disorders, the efficacy of neuroleptic augmentation and of newer glutamatergic agents also appears to differentiate OCD and related disorders from the anxiety disorders. Future studies should focus on furthering our understanding of the pathophysiology of the OCD-related disorders to the level attained regarding OCD itself, all while continuing to advance the knowledge base for the pathophysiology of OCD. Additionally, continued development of new treatments for OCD, including modifications of behavioral interventions and assessment of new therapeutic targets for psychopharmacology, should be fruitful in the coming years.

Key Clinical Points

 

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Suggested Readings and Online Resources

Hudak R, Dougherty DD (eds): Clinical Obsessive-Compulsive Disorders in Adults and Children. New York, Cambridge University Press, 2011

International OCD Foundation (IOCDF): http://www.ocfoundation.org

Steketee G (ed): The Oxford Handbook of Obsessive Compulsive and Spectrum Disorders. New York, Oxford University Press, 2012