conclusion for ocd research paper

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• Published: 18 May 2009

Obsessive-compulsive disorder and related disorders: a comprehensive survey

• Michele Fornaro 1 ,
• Filippo Gabrielli 1 ,
• Claudio Albano 2 ,
• Stefania Fornaro 3 ,
• Salvatore Rizzato 4 ,
• Chiara Mattei 1 ,
• Paola Solano 1 ,
• Valentina Vinciguerra 1 &
• Pantaleo Fornaro 1  

Annals of General Psychiatry volume  8 , Article number:  13 ( 2009 ) Cite this article

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Our aim was to present a comprehensive, updated survey on obsessive-compulsive disorder (OCD) and obsessive-compulsive related disorders (OCRDs) and their clinical management via literature review, critical analysis and synthesis.

Information on OCD and OCRD current nosography, clinical phenomenology and etiology, may lead to a better comprehension of their management. Clinicians should become familiar with the broad spectrum of OCD disorders, since it is a pivotal issue in current clinical psychiatry.

Introduction

Obsessive-compulsive disorder (OCD) is a common, chronic, anxiety condition that can have disabling effects on both genders throughout the patient's lifespan. OCD can manifest with a wide range of clinical pictures [ 1 ].

The disorder is among the most disabling anxiety conditions and counts for more than half of serious anxiety cases [ 2 ]. However, no univocal clinical opinion exists about its classification. In fact, although the Diagnostic and Statistical Manual of Mental Disorders, 4th edition – text revision (DSM-IV-TR) [ 3 ] classifies OCD as an anxiety disorder, some clinicians conceptualize it as a spectrum of related disorders (OCRDs) sharing the 'anxiety/fear' coupled with 'worry' clinical feature [ 4 , 5 ].

The broad spectrum of OCRDs includes the somatoform disorders (for example, body dysmorphic disorder (BDD) and hypochondriasis), the impulse-control disorders (for example, trichotillomania (TTM), pathological gambling, skin picking and others) and the tic disorders (for example, Tourette's syndrome) but others, including drug-induced and non-psychiatric disorders, could overlap and show similar clinical pictures [ 6 ]. The National Comorbidity Survey Replication study reported more than a quarter of evaluated subjects developing obsessions and compulsions at some point in their life and possibly manifesting with a full-threshold OCD, while a higher number of patients will probably suffer from OCRDs [ 2 ].

The most common age of onset of OCD is reported to be between 22 and 35, while affected patients spend an average of 17 years before receiving a correct diagnosis and treatment, with most OCD and OCRDs often showing a waxing and waning course, frequently increasing in severity when left untreated [ 7 , 8 ].

Further increasing the burden of OCD is the fact that affected subjects, along with many psychiatric patients, often experience discrimination and stigmatization due to a non-medical perception of the phenomenon. Yet OCD and OCRDs represent relevant medical conditions. Findings provided by recent studies, mainly focusing on the role played by the amygdala and its links to the 'fear circuits' and other structural and functional abnormalities of several corticostriatal pathways, also indicate a relationship between OCD manifestations and its neurobiological basis, suggesting new therapeutic strategies [ 9 ].

Treatment of OCD typically involves the use of medications in combination with other modalities (such as cognitive behavioural therapy (CBT), psychoeducation and support groups and so on): first line treatments options include both serotonin reuptake inhibitors (SRIs) medication and CBT [ 10 ], but anxiolitics and antipsychotics, among other classes of drugs, are used as well. Finally, the identification of OCD and its appropriate treatment is essential to improve the quality of assistance and to reduce the waste of health care resources through unnecessary medical care.

Historical background and current nosography

Obsessions thoughts and compulsive urges or actions are part of everyday life. We return to check that we locked a door and switched off the light. We cannot stop thinking about the stressful event scheduled for the next week. We refuse to eat with the spoon that dropped on the floor, even if we know the chance of contamination is remote.

These events are part of the normal feedback and control loop between our thoughts and our actions, and they have an ancestral biological survival value. It is only when obsessive thoughts become frequent or intense, or unavoidable, or when these compulsive rituals become so prominent that they interfere with an individual's functioning, that the diagnosis of OCD is made.

Descriptions of the phenomena of obsessions and compulsions can be found in historical documents over the past several centuries, since OCD has a long history. A passage from the Malleus Maleficarum , the 15th century compendium of witchcraft and psychopathology, describes a priest brought to Rome for exorcism:

' [w]hen he passed any church, and genuflected in honour of the Glorious virgin, the devil made him thrust his tongue far out of his mouth when he tried to engage in prayer, [the devil] attacked him more violently' [ 11 ].

Those with obsessive thoughts of a blasphemous or sexual nature were thought to be partially possessed by the devil, while 'psychotic' individuals appeared fully possessed. Obsessions and hand-washing rituals resulting from guilt were immortalized in the 17th century by the Shakespeare character Lady Macbeth:

'[...] it is an accustomed action with her, to seem thus washing her hands. I have known her continue with this a quarter of an hour' (Macbeth, V.i.28, describing the time-wasting characteristic of OCD).

With time, the explanation for obsessions and compulsions moved from a religious view to a medical one. Obsessions and compulsions were first described in the psychiatric literature by Esquirol in 1838, and, by the end of the 19th century, they were generally regarded as manifestations of melancholy or depression. By the beginning of the 20th century, the view of obsessive-compulsive phenomena had begun to shift OCD toward a psychological explanation; Janet had already described the successful treatment of compulsive rituals with what would come to be known behavioral techniques [ 12 ], and with Freud's publication in 1909 of the psychoanalysis of a case of obsessional neurosis (the Rat Man), obsessive and compulsive actions came to be seen as the results of unconscious conflicts and the isolation of thoughts and actions from their emotional components [ 13 ]. Although this shift succeeded in pointing out that actions can be motivated by factors of which the individual is unaware or unable to control, it did little to improve the outcome of patients OCD.

In the 1950s, with the rise of behavioral therapy, the learning theories that had proved to be helpful in the conceptualization and treatment of phobic disorders were applied to OCD symptoms. Although these learning theories are clearly insufficient to account for all OCD (as well as OCRD) symptoms, they did lead to the development in the late 1960s and early 1970s of effective treatments for reducing compulsive rituals. During the 1980s, research focused on the relationship of OCD and neurological problems such as epilepsy [ 14 ], memory disorders and Tourette's syndrome [ 15 ] while Westphal's early observation of an association between obsessions, tic disorders and epilepsy already presaged recent neurobiological findings in OCD.

OCD and OCRDs may also have common manifestations and, since the 1990s, they have therefore been conceptualized with a broad spectrum of related disorders [ 16 ] (Figure 1 ) [ 17 ].

The current spectrum of obsessive-compulsive disorder (OCD) and related disorders (OCRDs) . Adapted from Roan WM et al. [ 17 ].

The 1994 DSM-IV operated a split between the phobic/anxious-avoidant and obsessive dimensions, categorized by the previous DSM-III (1980) and its 1987 revised edition (DSM-III-R) with the unitary diagnosis of 'phobic-obsessive disorder' [ 18 ]. The current DSM-IV-TR describes OCD as characterized by repetitive thoughts, images, impulses that intrude on a patient unable to stop them [ 3 ].

Current nosology underlines the following three major symptom clusters for OCD and OCRDs: a 'somatic' cluster for BDD and hypocondriasis, a 'reward deficiency' cluster for TTM and other impulse control disorders (ICDs), and an 'impulsivity' one for kleptomania, compulsive shopping (CS), pathological gambling (PG), intermittent explosive disorder (IED) and others [ 19 ].

While most psychiatrists generally agree on the OCD spectrum including anxious and phobic manifestations, a greater number also focus on the need of a clear-cut definition of anxious and obsessive symptoms, as is anticipated by the research agenda for DSM-V[ 5 ]. In fact, anxious phobia differs from OCD. Both phobic and obsessive-compulsive subjects usually avoid feared objects and generally retain awareness their fears and avoidance behaviors are excessive. Phobics are usually more upset about the prospect of actually coming into contact with the thing they fear and do what they can to avoid it, while OCD patients may be more concerned about the time-consuming rituals such contacts will trigger, rather than fear of the contact itself.

Epidemiology

Obsessive and compulsive symptoms are common and not all of them may be accounted for a full-threshold OCD. Approximately 50% of the general population engage in some ritualized behaviors, while up to 80% experience intrusive, unpleasant or unwanted thoughts [ 20 ].

The 1 month prevalence of adult OCD is about 0.6% [ 21 ] while the DSM-IV 12 month prevalence ranges from 0.6% to 1%. Regardless, the prevalence of OCD, as well OCRDs, may vary depending on the source of data and the choice of diagnostic instruments. Many OCRDs may co-occur with each other and with OCD. With regard to the somatoform disorders, the estimated prevalence rate of hypochondriasis is 1% to 5% in the general population and 2% to 7% among primary care outpatients. Unfortunately, the prevalence rate of BDD is difficult to estimate given the secrecy of this severe condition [ 22 ], but estimates range from 0.7% to 2.3% in the general population and at least from 6% to 15% in cosmetic surgery settings [ 23 ]. For OCRDs the prevalence of Tourette's is 0.1%, while the exact lifetime prevalence of TTM is unknown, but rates from 1% to 2% have been reported for cases that satisfy the full threshold diagnostic criteria [ 24 ].

There seems to be a bimodal age of onset for OCD. The mean onset has been reported to be 19 years (21% of the cases emerged at age 10), while the mean age for adult OCD occurs between age 22 and 35. In a small number of cases the onset of the disorder occurs at age of 50 or more [ 2 ]. Usually, the earlier the age of onset, the worse the course of OCD and OCRDs; by contrast, no specific gender predominance has been reported in large samples epidemiological studies. This latter evidence is in contrast with non-OCD anxiety conditions whose gender ratios usually indicate a prevalence of female cases [ 25 ].

While economic, social and cultural effects may play a role in producing different clinical pictures of OCD, biological, immune and genetic factors and family predisposition may also contribute to the pathogenesis of the disorder. For example, streptococcal infection may be associated with an abrupt, exacerbating-remitting early-onset form of OCD, which is termed pediatric autoimmune disorder associated with streptococcus (PANDAS), but little is known about this condition, and in particular about the genesis of this OCRD [ 26 ].

OCD's burden may also vary depending on the case in question, on the course of disorder and on the fact it is almost unknown among the general population. As a consequence, many patients do not seek medical care until (originally) milder forms of OCD and OCRDs become more distressful and possibly harder to treat. Furthermore, a large number of obsessive-compulsive conditions may go under-diagnosed: studies have placed the prevalence between 1% and 3% of OCD cases, although the prevalence of clinically recognized OCD is probably much lower [ 2 ].

The fact that many individuals do not seek early appropriate treatments may be due to stigma, but also to other factors. Sometimes patients do not realize that they are affected by OCD. In some cases, the 'typically obsessive' features of intrusive, 'ego-dystonic' feelings and thoughts are absent, as in the poor-insight obsessive-compulsive disorder (PI-OCD), complicating the course and severity of the illness [ 27 ]. Including PI-OCD and other subtypes extends the range of OCD cases that are reported to afflict approximately 2% to 3% of the world's population; these show varying degrees of severity and chronic course and often also include depressive feelings (80%), major depression (MD) comorbidity (30%) and Tourette's syndrome comorbidity (5%).

Additionally, OCD patients usually present symptoms similar to those of their affected relatives. About 8% of first degree relatives have OCD, while first symptoms occur by their 20s in 75% of the patients; this may happen suddenly or slowly, generally showing an episodic course [ 28 ]. Interestingly, the episodic course is sometimes an overlap feature of the illness with MD, but it may also prompt clinicians to explore other affective comorbidities as well [ 29 ], and we urge for more vigilance for largely under-recognized entities such as cyclothymic-OCD [ 30 ].

For example, a small number of very severe OCD cases may also develop suicidal ideations or behaviors, as the patient could be perceive suicide as the only possibility of escape from their tremendous pain. In such patients, a common neurobiological and genetic basis has been hypothesized to be responsible for depressive suicidal behaviors and for severe ego-dystonic obsessive manifestations. Such a hypothesis has also been supported by the ex adiuvantibus findings of similar pharmacotherapeutic strategies being effective in both pathological dimensions.

Diagnostic criteria

The main features of OCD are the obsessions and compulsions. According to DSM-IV-TR, the obsessions and compulsions cause marked distress, are time-consuming (usually taking more than 1 h per day for a month or more) and significantly impair the normal functioning of the subject. If another Axis I disorder is present, it is mandatory that the content of the obsessions or compulsions not be restricted to it (for example, preoccupation with food or weight in eating disorders or guilt ruminations in the presence of a major depressive episode (MDE)). The disturbance should not be due to the direct effects of a substance (for example, drug or medication abuse), or a general medical condition (Figure 2 ).

Diagnostic and Statistical Manual of Mental Disorders, 4th edition – text revision (DSM-IV-TR) criteria for obsessive-compulsive disorder (OCD) .

Obsessions may also manifest with very heterogeneous clinical pictures (for example, religious scrupulosity, aggressive or intrusive thoughts, inappropriate sexual thoughts, concerns about symmetry and perfectionism, pathological doubt, contamination worries, pathological collecting and hoarding), while compulsions are defined as repetitive behaviors or mental acts (for example, washing, counting, checking, ordering, touching, cleaning, hoarding, conducting mental or physical rituals).

Obsessions are usually unwanted, unavoidable, intrusive, ego-dystonic, occasionally frightening or violent (for example, the impulse to leap before a car, the thought that you may attack your spouse, that the pateint may molest a child) and often impair functioning and quality of life (QoL) [ 31 ].

It is remarkable that most OCD patients do criticize their own thoughts and would hate to practice any by choice, yet in most cases they are unable to stop such thoughts or behaviors. Nevertheless, OCD patients can ruminate endlessly ('Did I lock the door?') and most of them develop (new) compulsions to ward off unwanted happenings or to satisfy obsessions (for example, an obsession with dirt leading to hand-washing rituals).

Differential diagnosis and clinical phenomenology

The word 'obsession' derives from Latin ' obsidēre ', which means 'to take possession', 'to occupy'. In fact, most OCD patients relate to the experience of a 'Middle ages fortress besieged by strong enemies they have to surrender to without any escape possibility'. The Latin word ' compellere ' has the significance of 'to be constrained' and 'to be overpowered': OCD patients are forced to act on compulsions trying to overcome obsessions.

Most OCD patients present both, but occasionally they can manifest only obsessions or compulsions; this is sufficient for OCD diagnosis regardless.

Up to 20% of severe depression cases present obsessive symptoms and treatment maybe identical while schizophrenics often show bizarre rituals they are usually comfortable with, as in schizo-obsessive disorder (SOD) which neurological soft signs (NSS) psychopathology suggests is a severe form of OCRD [ 32 – 34 ].

Differential diagnosis is also a concern due to current OCD and OCRD classification methods. People sometimes wonder if compulsive eating, gambling, shopping or deviant sexual behaviors are forms of OCRD. Usually, these disorders are not classified as OCRDs because some pleasure is obtained by these activities and the person would not, ordinarily, wish to stop them except for the secondary problems they may cause (such as obesity, convictions for driving while intoxicated, gambling and credit card debts and criminal prosecution for sexual deviancy). Nevertheless, few individuals with these compulsive behaviors may respond to drug and behavioral treatments that are effective for OCD [ 7 ].

Obsessions usually share an increasing 'anxious tension' before acting the compulsions (both behavioral and mental), followed by a brief sense of relief as they are carried out. This kind of feeling is particularly evident in many OCRDs too, as most eating disorders (EDs) may also be considered. In fact, many bulimia nervosa (BN) patients experience a brief reaction after binge eating while anorexia nervosa (AN) patients take a form of pleasure in being able to keep away from food.

It is important to distinguish between obsessive-compulsive symptoms in the course of EDs and OCD symptoms; a distinction should also be made for 'anxious' feelings experienced in the course of ICDs when the compulsion is carried out.

Occasionally OCD thinking is bizarre, and patients could even exhibit schizotypical personality disorder (SPD) traits, usually being unaware of this (for example, 'My spouse will leave me if I do not catch the elevator').

Since the OCD spectrum phenomenology may be vary heterogeneous, many rating scales and instruments, such as the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and others also investigating OCRDs, have been developed to help clinicians make diagnoses and to score symptoms, but clinical interview by a trained psychiatrist should not be discounted in any serious case [ 35 ].

Neurobiology and genetics

There is growing evidence based on several lines of research that OCD and OCRDs involve abnormal metabolism in specific areas of the brain. Neuroimaging findings indicate OCD involves subtle structural and functional abnormalities of the orbito-frontal cortex (OFC), the anterior cingulate cortex (ACC), the caudate nucleus (Cn), the amygdala nuclei (An), the accumbens nucleus (NAc), the cortical thalamic nuclei (Tn) as well the white matter (WM), the hippocampus (HP) and other regions [ 36 ].

The OFC is involved with social consciousness regarding proper behavior. Hypoactivity in this area (whether occurring spontaneously or as a result of damage from a perinatal or head injury, temporal lobe epilepsy, infection or brain tumor and other conditions) leads to coarsening of social consciousness and behaviors. This may lead to hypersexuality (paraphilic OCRDs), overeating behavior (EDs and Prader-Willi syndrome (PWS)), personality changes and Tourette's syndrome (frequently presenting with inappropriate use of profanity) or crude jokes (sadomasochistic disorder (SMD)). Overactivity of the OFC may results in excessive social concern, meticulousness and 'nitpicking' habits, fastidiousness and avoidant behaviors and more.

Other brain structures, such as the Cn, filter information coming from the forebrain, representing a sort of hub for many elaborate stimuli. It has been hypothesized that if 'too many' messages regarding worries about 'how things should be done' reach the Cn, they are not filtered properly and spill over into (and flood) consciousness. Increased metabolism of the frontal part of the brain is concerned with order and social proprierty. The Cn, along with other striatal structures, is also involved in regular repetitive behaviors (rituals): the anterior caudatus putamen (aCPu), the ACC directly leading to the shell of the NAc, the pallidus internus and the thalamus may play a specific role in impulsive-repetitive psychic manifestations of OCD and OCRDs (for example, the verbal Tourette's symptoms).

Additionally, the dysregulation of the posterior caudatus putamen (pCPu) and the dorsolateral-prefrontal cortex (DL-PFC), the pallidus internus (PI) and the thalamus may account for the neurological symptoms such as tics, Tourette's motor abnormalities and other OCD spectrum motor issues [ 32 ].

Both the striatal and the frontal brain areas are richly supplied with serotonergic neurons. It is not surprising that most OCD and OCRD drugs act as modulators for the serotonergic transmission in the central nervous system (CNS). However, even though 5-hydroxytryptamine (5-HT) is a core neurotransmitter involved in OCD and OCRD manifestations, this knowledge tells us little about the ultimate causes or triggers of this psychopathology or about effective treatments.

5-HT abnormalities may be the result of rather than cause of OCD and OCRD symptoms. Additionally, changes in serotonergic transmission may have direct or indirect effects on the neuronal firing of more than 60 other neuromodulators affecting thoughts, feelings and behaviors. Thus, OCD is probably the final expression of many different kinds of abnormalities in the structure and functioning of the brain. However, this complexity helps us to understand why some treatments are helpful while others are not as effective. The 5-HT hypothesis was initially motivated by the observed differential efficacy of selective SRIs (SSRIs) in alleviating OCD symptoms. These findings, although attesting to the therapeutic versatility of serotonin transporter inhibition in OCD, do not necessarily reflect the existence of neurobiological abnormality in the central serotonergic system in OCD; a reasoning referred to as an ex juvantibus argument [ 37 ]. There is also growing evidence from both preclinical and clinical studies that the dopamine (DA) system may be involved in the pathogenesis of OCD [ 38 ]. Studies on knockout (KO) mice for 5-HT 2C receptor, already described as a model for obesity, showed increased chewing on non-nutritive clay with a distinct 'neat' pattern and a reduced habituation of head dipping activity as compared to the wild type, with the conclusion that the 5-HT 2C receptor null mutant mouse provides a putative model for compulsive behavior [ 39 ]. Tsaltas et al . have described a model based on persistence in the context of rewarded spatial alternation [ 40 ]. Using this behavior model, they have shown that 5-HT 2C receptors are implicated in the mechanisms underlying the 'compulsive' behavior in this animal model for OCD. Acute administration of meta-chlorophenylpiperazine (mCPP), a non-selective 5-HT receptor agonist mainly acting at the 5-HT 2C receptors but with some affinity also for the 5-HT 1B , 5-HT 1A and α 2 -adrenergic receptors, increased 'compulsive' behavior [ 37 ]. The selective 5-HT 1B receptor agonist naratriptan was not effective in this animal model, supporting the role of 5-HT 2C receptors underlying the effect of mCPP [ 40 ]. On the basis of electrophysiological data, Joel and Doljansky suggested that compulsive lever-pressing depends on a phasic decrease in stimulation of D 1 receptor [ 41 ]. In a pharmacological animal model for OCD, in which rats are chronically treated with the selective D 2 /D 3 receptor agonist quinpirole (QNP), a ritual-like set of behavioral acts resembling OCD checking behavior, has been observed [ 42 ]. This 'compulsive' behavior depends on QNP administration, because it rapidly returns to normal behavior when QNP administration is discontinued [ 43 ]. Postmortem analysis in these animals revealed increased DA tissue levels in the NAc and right-PFC. The DL-PFC enables temporal information processing and holding relevant information online [ 44 ]. It is believed to mediate working memory and executive functions. The basal ganglia are thought to project back to these cortical areas though the medial dorsal and anterior nuclei of the thalamus [ 45 ].

A great amount of literature evidence reports OCD and OCRD to show an inherited transmission. Some families have at least four successive generations with clear OCD cases [ 46 ]. Since family members could have 'learned' these behaviors from other relatives, the presence of OCD across generations alone is not sufficient to unequivocally prove inheritance [ 47 ]. However, successive family members often have different obsessions and compulsions, suggesting that they have not 'learned' them. What appears to be inherited is the capacity to respond to common life experiences with obsessions and compulsions. There are also studies of inheritance involving identical (homozygotic) and fraternal (heterozygotic) twins, which also provide supportive evidence for an inherited component in OCD and OCRDs [ 48 ].

Molecular genetics studies have begun to provide evidence that specific genes may play a role in the manifestations of OCD. Segregation analysis has examined familiar patterns of OCD transmission [ 49 , 50 ].

The genetic hypothesis suggests at least few major genes implicated in OCD and OCRDs, thus they are considered oligogenic disorders. Among others, the following regions have been suggested as susceptibility loci: 1q, 6q, 9p, 19q, 7p and 15q. Specifically, the chromosome 11p15 has been linked and associated with a supposed gender effect in the OCD etiology [ 51 ]. Interestingly, deletions and other abnormalities of human chromosome 15q11-q13 are associated with two developmental disorders, PWS and Angelman syndrome (AS), which may also present with psychiatric symptoms such as binging and other ICD-related and OCRD-related manifestations [ 52 , 53 ]. Detailed analysis of the 15q11-q14 sequence corrected errors and gaps in the public access sequence to fully reveal large segmental duplications at breakpoints for PWS, AS, and inv dup(15) syndromes, confirming the tight correlations between those conditions [ 54 ].

Dhossche et al . suggested an association between autism, PWS, AS, catatonia and GABA dysfunction, and this appears to be particularly interesting considering the clinical and partial phenomenic overlap between those conditions, which indeed may appear with OCD and OCRD-related symptoms too [ 55 ]. PWS may present with atypical psychotic features and motor dysfunctions characterized by ritualistic, stereotyped and compulsive behaviors, which may be treated with GABA mimetic compounds such as lorazepam, valproic acid and possibly topiramate [ 56 ]. Many of the known genetically-based neurodevelopmental disorders are associated with distinctive behavior phenotypes such as this; behavioral phenotypes have been elucidated by clinical research, from distinctive profile or social traits, or have emerged as prominent syndromic features. Social phenotypic findings exist for fragile X syndrome, Down syndrome and PWS, Smith-Magenis syndrome, Turner syndrome, Williams syndrome and velocardiofacial syndrome, all possibly associated with autism [ 57 ].

OCD candidate genes have been studied based on their function and also their position in the genome. Serotonin-related genes in OCD include those coding for the 5-HT transporter (5-HT T ) and receptors (5-HT 2A , 5-HT 2B , 5-HT 2C and 5-HT 1B ) as well the 5-HT enzyme tryptophan hydroxylase [ 58 ].

DA-related genes supposed to be implicated in OCD include DA transporter (DA T ) genes and the D 2 , D 3 and D 4 receptors [ 59 , 60 ], as well as the catechol- O -methyltransferase (COMT) and monoamine oxidase A (MAO-A) enzymes [ 61 ]. Glutamate-related genes (GRIK and GRIN 2B ) and transporters (SLC1A1) have also been investigated in OCD along with the neurotrophic tyrosine kinase type 3 (NTRK3) and other genes such as the white matter genes OLIG 2 and MOG [ 62 ].

However, given the complexity of OCD phenotype, it is unlikely that a single candidate gene will have a major impact on the disorder. Additionally, many individuals suffering from OCD have no family members presenting obsessive-compulsive symptoms.

Treatment and management

The past 20 years have seen the emergency and evaluation of two major effective forms of treatment for OCD and OCRDs: CBT and drug therapy. Additionally, many other modalities, including physical treatments as electroconvulsive therapy (ECT) and ablative neurosurgical procedures have been proposed as well and should not bet disregarded even today [ 63 ].

Drug treatment using medications with marked effect on serotonergic neurotransmission has been shown to be effective in decreasing both obsessions and compulsions, while combining this pharmacological approach with CBT has been reported as the most effective strategy for most OCD and OCRDs cases [ 64 ].

Yet, regardless the adopted therapeutic strategy, results vary depending on many factors including the age of onset of the disorder, how long it has been left untreated, the OCRD subtype and/or comorbidity, the patient's insight and compliance and others [ 8 ]. Additionally, the therapeutic strategy should be 'tailored' for each single case.

CBT helps patients learn how to quell the discomfort arising from obsessions and how to reduce or eliminate compulsive rituals and it includes exposure and response prevention (ERP) and also cognitive therapy (CT).

Behavior therapy is not something done to a patient: it is a structured set of techniques the patient learns to employ whenever anxiety, discomfort, or dysfunction arise because of obsessions or rituals. Basically, patients are asked to find and face the things they fear ('exposure') and then to refrain from carrying out compulsive rituals ('rituals or response prevention'), but other techniques may be employed as well [ 65 ]. Various degrees of success ratio for CBT as OCD or OCRD monotherapy have been reported depending on many factors: the source and method of the study, the session frequency, the OCRD subtype and others [ 10 , 66 ]. Also, CBT has been hypothesized to be associated with brain glucose metabolism improvements for OCD patients [ 67 ].

Since the combination of CBT and SRI drugs seems to achieve the best results in clinical settings, this has been proposed as first-line approach in most of cases [ 64 ].

Effective SRI treatments for OCD include SSRIs and tricyclic antidepressants (TCAs), especially clomipramine, a tertiary amine. Relatively weak serotonergic TCAs, such as the predominantly norepinephrergic secondary amines, do not tend to be as effective in OCD and OCRD treatment [ 64 ]. SRIs also include the serotonergic-norepinephrergic reuptake inhibitors (SNRIs), the serotonin antagonist-reuptake inhibitors (SARIs) and others, but stronger evidence is needed to support their use as effective monotherapy for OCD and OCRDs or, as for the anti-MAOs, relevant clinical side effects may discourage or limit their use [ 68 ].

The decision to initiate treatment with SSRI alone, CBT only or a combination, depends on individual patients variables. Non-drug compliance, pregnancy, breastfeeding, very young or very old or mild OCD patients may prefer CBT alone. SSRI treatment should represent the desirable approach in most of the drug-treated cases because of the side effects associated with the TCA clomipramine.

Clomipramine still represents an effective treatment for severe OCD and OCRDs [ 69 ], but as the classification of OCD and OCRDs changed with the past editions of DSM so did the therapeutic approaches.

An ex adiuvantibus confirmation of partial phenomenic overlap in OCD-related clinical manifestations is historically provided by clomipramine's effectiveness in treating such conditions, also leading researchers focusing on serotonergic mechanism [ 70 ]. The pharmacological finding that serotonergic agents are more effective for obsessions and compulsions rather than non-serotonergic antidepressants, and that their anti-obsessive benefit it is independent of the antidepressant action, also contributed to the separation of OCD from mood disorders [ 71 ].

When considering the SSRI class, the choice of a specific drug depends on evidence-based medicine but also on the pharmacokinetic and pharmacodynamic properties of the biologically active agent. To mention few, a long-half life (T1/2) should be preferred for very anxious patients, reducing the risk of rebound syndrome (RS) and allowing fewer daily administrations, but it may be not suitable for older patients. Likewise, pharmacodynamic aspects should suggest anticholinergic (anti-Ach), anti-hystaminic type-1 (Anti-H 1 ) and/or anti-alpha norepinephrergic type-1 (anti-α 1 ) side effects to be preferred when a higher sedation is sought (for example, for very severe ICDs, Tourette's and other OCRDs), while the mild pro-DA agonistic action of others (such as the weak one provided by high-dosage sertraline) should be considered for BDD, binging, craving and other OCRD-related pleasure-seeking behaviors.

Indeed the SSRIs are an almost 5-HT 'selective' class of drugs: weak pharmacodynamic actions could represent a powerful clinical tool when properly managed.

Because many OCD patients respond to treatment with SRIs, usually requiring and tolerating higher doses compared to affective patients, OCD is often deemed a serotonergic dysfunctional disorder. However, despite the 'selective' efficacy of (S)SRIs, many OCD and OCRD patients fail to respond ('non-responders') to adequate doses and time exposures (for example, 20 to 60 mg/day of paroxetine for 12 weeks or 150 to 300 mg/day of clomipramine for 12 weeks), or may require augmentation strategies, usually performed by employing different classes of drugs [ 64 , 72 ]. Additionally, higher doses and the delay in the onset of action can be accounted for by the greater delay in downregulation of serotonergic 5-HT 1B receptor in the OFC and the subsequent stimulation of 5-HT 2A receptor antagonists (such as atypical antipsychotics (AA) also known as 5-HT 2A >D 2 receptor antagonists) can hasten or augment the effects of SRIs [ 73 ]. Consequently, the clinical management of resistant OCD and OCRDs may first consider a hyperdose of SRIs, especially for hard-to-treat forms of OCRD (for example, hoarder-collector patients), prior to augmentation strategies [ 74 ]. The augmentation of SSRIs with clomipramine showed significant improvements in Y-BOCS scores compared to SSRI monotherapy, but pharmacokinetic interactions and higher risk for serotonergic malignant syndrome (SMS) may discourage this kind of procedure [ 75 ]. Also, SRI anti-obsessive drugs have occasionally been reported to be associated with birth defects, and they should therefore be avoided in pregnant or breastfeeding women (while young or old patients may require lower doses).

Alternative augmentations for resistant OCD and OCRD cases may include the use of low doses of dopaminergic antagonists (haloperidol and pimozide or other typical antipsychotics (TA) or the AA class), especially for poor-insight patients (when compliant). AA may also contribute to mood stabilization in drug-induced manic patients or true bipolars [ 76 ]. Also, AAs are less likely to cause extrapyramidal symptoms (EPS) or neuroleptic malignant syndrome (NMS) in sensitive subjects.

The efficacy of adjunctive TAs or AAs to SRIs in refractory OCD may be due to direct dopaminergic D 2 blockade separate (TA) or together (AA) with 5-HT 2 receptor antagonism. Additionally, SRI-refractory OCD and OCRDs patients may have additional dysfunctional abnormalities in dopaminergic pathways that may require augmentation with DA-blocking drugs.

Recent neuroimaging findings have also proposed riluzole and other glutamatergic modulators as a possible SRI augmentation strategy for OCD-refractory patients, but further evidence is needed [ 77 – 81 ]. The antiepileptic mood stabilizers such as carbamazepine, topiramate, gabapentin and others, due to the neuroinhibitorial CNS action of GABA in OCD circuits, norepinephrergic α2 (for example, clonidine) and β1 blockers (for example, propanolol), selective 5-HT 1A partial agonists (buspirone), clonazepam and other benzodiazepines (BDZ), opioid agents (for example, tramadol), antiandrogens and adrenal steroids (for example, flutamide), peptides (for example, oxytocin), hallucinogenetic agents (for example, lysergic acid diethylamide (LDS) and other drugs also acting as 5-HT 2A partial antagonists), inositol and more, have been proposed, but no univocal opinion on their efficacy for non-responder OCD and OCRDs patients exists (Figure 3 ).

Drug management of obsessive-compulsive disorder (OCD) and related disorder (OCRD) non-responders .

While a high number of drugs is available for rational OCD therapy, less literature evidence exists about OCRD non-responders management, possibly due to a lower prevalence and clinical recognition of this group; this is why a good pharmacological background should never be missed by the prescriber.

The concept of non-responders also implies a mismatch between a diagnostic classification and treatment, and this may prompt researchers and clinicians to revise current nosography and biological hypothesis [ 5 , 82 ].

A better understanding of the clinical phenomenology, etiology and therapy of obsessive-compulsive-spectrum disorders will provide clinicians with important information about the effective management of these conditions.

Most OCDs and OCRDs may go underdiagnosed or may be not promptly treated. As a consequence, many patients and their families may suffer unduly, while a delayed therapeutic intervention may mean they do not recover as effectively as an early dagnosis would allow.

Specifically, we suggest the following:

1. An early recognition of OCD and OCRDs will improve outcome and reduce burden.

2. Following current diagnostic criteria may be a useful approach in most cases, but a knowledge of OCD and OCRD phenomenology is a unique opportunity to better address the patient's needs. It also may lead to better compliance between the caregiver and the patient through a deeper understanding of each other goals.

3. To date, no univocal opinion exists about the neurobiological basis of OCD spectrum disorders. Regardless, it is important to know current literature evidence, as this is a core mechanism to proposing a rational therapeutic strategy.

4. Spreading knowledge of OCD and OCRD phenomena may also lead to overcoming the stigma it is associated with, and may finally lead to a greater comprehension of such disorders.

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Fornaro, M., Gabrielli, F., Albano, C. et al. Obsessive-compulsive disorder and related disorders: a comprehensive survey. Ann Gen Psychiatry 8 , 13 (2009). https://doi.org/10.1186/1744-859X-8-13

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6 Conclusion

• Published: May 2007
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This volume has covered the phenomenology, psychobiology, pharmacotherapy, and psychotherapy of obsessive-compulsive disorder (OCD). We have also briefly considered some of the OCD-related conditions. We have attempted to synthesize the growing research literature, with the aim of providing practical guidance to clinicians.

Significant advances have been made in describing the complex phenomenology of OCD, and this has important practical implications. First, given the high prevalence of OCD and related conditions there is growing consensus that there is value in screening patients with simple questions, such as those listed by Zohar and Fineberg. A high index of suspicion for OCD is justified in a number of contexts, including dermatology clinics, patients with tics, and pregnancy. Additional work is needed to reverse the underdiagnosis and undertreament of OCD.

Second, there is again a good deal of consensus that only a few symptom dimensions capture much of the variance in OCD symptoms. Of course, it is important for clinicians to remain on the lookout for rarer forms of OCD. However, instruments such as the dimensional Yale–Brown Obsessive Compulsive Scale (DY-BOCS), which focus on four key symptom dimensions, appear to be useful in the clinical setting. Instruments are also available for the assessment of OCD symptoms in children and adolescents.

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• Published: 01 December 2018

Living with obsessive-compulsive disorder (OCD): a South African narrative

• Kirsten Celeste Kohler 1 ,
• Bronwynè Jo’sean Coetzee 1 &
• Christine Lochner 2  

International Journal of Mental Health Systems volume  12 , Article number:  73 ( 2018 ) Cite this article

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Obsessive–compulsive disorder (OCD) is a highly prevalent and debilitating psychiatric disorder known to interfere with several life domains. Yet little is known about the subjective experiences of living with OCD amongst South Africans and more so, the ways in which it impacts daily functioning and quality of life (QOL).

The aim of this study was to explore daily functioning and QOL among South African adults living with OCD. Qualitative semi-structured interviews were conducted with 20 adults with a primary diagnosis of OCD. We used ATLAS.ti v7 to analyse the data, thematically. The study was conducted at the SU/UCT MRC Unit on Risk and Resilience in Mental Disorders in South Africa.

Three key themes were identified namely, (1) realisation of OCD, (2) disruptions to daily life and (3) managing the disruptions to daily life. Participants recounted their earliest recollections of OCD, the instances when they recognised something was wrong and ways in which they came to terms with their OCD. Disruptions to daily life included poor sleep quality, inability to enjoy leisure activities which impacted on socialisation and impairment in school/work performance. Perceived social support from family members, friends and colleagues were invaluable to helping participants manage these disruptions. Further, strategies such as self-talk, diary-keeping and humour helped them cope.

While some individuals with OCD have found ways to cope with and accept having OCD, all participants perceived their QOL to be significantly reduced and their functioning impaired due to the condition, on multiple levels. The importance of acceptance in OCD ties in with research on the potential value of Acceptance and Commitment Therapy, which could form an adjunct to more conventional techniques such as Cognitive-Behavioural Therapy. The themes emanating from this study can be used to help clinicians better understand what treatment works best for patients with OCD—and whether this treatment be focused on the individual or together with close members of their microsystem, such as spouses/partners. Further these findings may potentially help to improve access, affordability and the quality of life of South Africans living with OCD from various income backgrounds.

Obsessive–compulsive disorder (OCD), a highly prevalent psychiatric condition, is recognised as one of the 10 most disabling conditions given its impact on functioning and quality of life (QOL) [ 1 , 2 ]. OCD is characterized by recurrent and intrusive thoughts and images (obsessions) and/or repetitive behaviours (known as compulsions) [ 3 ].

There is a substantial body of quantitative evidence to suggest that OCD has a large negative influence on the daily activities and QOL of individuals living with the disorder [ 4 , 5 , 6 , 7 , 8 , 9 ]. However, there are some discrepancies in findings on the ways OCD affects life. For example, amongst an Indian OCD sample, the psychological and social domains of QOL were more affected than other domains [ 6 ]. In contrast, evidence from a South African sample of OCD patients suggested impairment in family functioning but not in other domains [ 8 ].

Qualitative studies offer a way in which these discrepancies may potentially be addressed, providing additional insights into how individuals experience disruptions in the various domains of functioning due to OCD. Improvements in understanding may ultimately lead to better management of these patients [ 10 , 11 , 12 , 13 , 14 , 15 , 16 ]. For example, some insights into the experiences of OCD are seen in a qualitative study from India [ 17 ]. In this study participants articulated that their obsessions and compulsions often made it difficult to maintain a connection with others which limited their access to emotional support and often lead to feelings of hopelessness and powerlessness, and impacted on self-esteem [ 10 , 11 , 13 , 14 , 17 ]. Findings such as these begin to provide deeper insights into individuals’ experiences of the impact of OCD on their lives.

At the time of this writing, no publications on qualitative studies on OCD amongst South African individuals were available. Locally, studies on OCD that are available have mainly focused on the functional impairment aspects of OCD, quantitatively [ 8 , 18 , 19 , 20 ]. The OCD symptom profile may look similar amongst individuals living with the disorder globally; however, it may be that the broader social, political and economic factors influence and shape the perceived experience of the condition differently amongst those living in resource-limited and thus vulnerable settings like South Africa. Accordingly, in this study, we used qualitative methods to explore the experiences of and ways in which OCD influences the daily life and functioning of South African adults living with OCD.

Theoretical framework

Globally, mental health researchers increasingly value the importance of exploring mental health holistically, through biological, psychological and sociocultural perspectives [ 21 ]. Much mental health research has been orientated towards understanding the individual, often through a biomedical lens, with little focus on the influences of the broader context within which the individual lives and how this may impact on functioning [ 21 ]. For example, various individual models exists to understand OCD [ 12 , 22 , 23 , 24 ]. More recent models of OCD—which go beyond the better known cognitive models of OCD [ 25 , 26 ], is the inference-based approach (IBA) and the autogenous-reactive model (AR). The IBA is a cognitive model of OCD [ 22 , 23 ] which posits that an individual’s fear of the self is core to various obsessions experienced. Further, the AR model of OCD [ 24 ] posits that an individual’s obsessions are triggered either internally (within the individual—e.g. through memories) or externally (i.e. triggered by external stimuli—e.g. accidents/fires) [ 12 ].

In this study, we were interested in going beyond individual factors associated with OCD and exploring the ways in which OCD impacts various life domains where interpersonal relationships are key. To this end, we used concepts associated with Ecological Systems Theory (EST), as laid out by Bronfenbrenner [ 27 , 28 ] to guide explanations of the influence of OCD on daily functioning. In keeping with EST, the individual functions within a system of nested environments, and each of these environments is connected to one another in a bi-directional way. As such, these systems function together to affect an individual’s development such as their relationships, emotions, behaviour, and general functioning. In EST these systems include (1) the microsystem—i.e. the relationship between the individual and those within their immediate environments such as members of their family and work colleagues; (2) the mesosystem—which refers to the interrelations between two or more microsystems surrounding the individual such as the relationship between the individual’s family and workplace, and family and peers; (3) the exo system—i.e. the link between two or more systems with whom the individual has indirect interaction with, but has an effect on the individual such as workplace policies; (4) the macro system—i.e. the social factors that affect the individual’s life, such as the individual’s ideology, and (5) the chronosystem—which takes into account the changes in an individual’s life over time [ 27 , 29 ]. Our study is predominantly concerned with the microsystem of the individual’s life. As such, we present findings on the impact of OCD on the individual and his/her immediate interpersonal relationships in multiple settings.

We used an exploratory qualitative research design and gathered data from individuals with a primary diagnosis of OCD using both qualitative and quantitative data collection methods. OCD was diagnosed using the Structured Clinical Interview for DSM disorders—SCID-I/P [ 30 ].

The present study was conducted at the Medical Research Council’s (MRC) Unit on Risk and Resilience in Mental Disorders. This is a cross-university research unit located at the Department of Psychiatry at Stellenbosch University (SU) and the Department of Psychiatry and Mental Health at the University of Cape Town (UCT), South Africa. This unit follows in the footsteps of the MRC Unit on Anxiety and Stress Disorders that was initiated at SU in 1997. Both are known for work on psychiatric genetics, psychiatric brain imaging, basic neuroscience, and mental health promotion. Foci include work on animal models, on clinical research, and on public health aspects. This study was embedded in a larger quantitative study focused on the phenomenology as well as the pharmacological, neurological and genetic underpinnings of OCD that was initiated to better understand the cognitive-affective processes in adult OCD patients [ 31 , 32 ]. The aims of the larger study (still ongoing) are to collect neuroimaging data (via structural and functional MRI), clinical data (via self-report and clinician administered questionnaires), and genetic data (obtained via blood samples), to enable South African researchers to make contributions to international OCD research consortia and stimulate the growth of disciplines and interdisciplinarity. In addition, it is aimed that this larger project renders new knowledge on genotype-interaction effects on key brain structures in OCD. Findings related to these aspects of the larger study are reported elsewhere [ 33 , 34 , 35 ]. The present study sought to expand on the quantitative data collected as part of the larger study by including patient perspectives on the impact of OCD in their everyday lives.

Participants and procedure

A subset of participants from the larger study were consecutively selected to receive an invitation via e-mail to be interviewed. Eligible participants were 18 years or older, with a primary diagnosis of OCD. Given that participants were recruited consecutively from the database of the larger study, no specific attempts were made to purposively recruit for gender or socioeconomic status. Recruitment of participants continued until no more new information emerged from the interviews, that is until we reached data saturation [ 36 ]. The primary diagnosis of OCD was confirmed using DSM-IV criteria. Participants were interviewed face-to face if they responded to an email invitation confirming an interest in taking part. Interviews were conducted in either English or Afrikaans, in the participants’ first language, and guided by a semi-structured interview schedule that contained a series of open-ended questions. Interviews generally lasted between 30 and 60 min. These interviews were the first contact that the interviewer (KK) had with the participants. The themes covered in the interview were (1) his/her earliest recollection of OCD symptoms, (2) his/her daily activity experiences, and (3) the coping strategies that were used over time.

Participants completed a demographic questionnaire and the Florida Obsessive–Compulsive Inventory (FOCI) [ 37 ] to measure OCD symptom severity before the start of the interview. Score categories included, mild, moderate, severe, and extreme. Additionally, a clinician-administered scale, the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) [ 38 ], was also used to assess OCD severity. Score categories also included, mild, moderate, severe, and extreme. These two severity scales (FOCI and Y-BOCS) were included to provide a better understanding of the illness profile of the participants. Trustworthiness of the qualitative data was ensured by clarifying participant responses for meaning using paraphrasing techniques.

Ethics approval

This study received approval as an amendment to the larger study by the Health Research Ethics Committee (HREC) at Stellenbosch University (M07/05/019). All participants gave written informed consent. Prior to signing the consent forms, participants were informed that participation in the present study was a once-off semi-structured interview. Participants were also informed that their participation was entirely voluntary and that they were free to withdraw from the study at any point without consequence. Further, participants were informed that they could refuse to answer any questions. Further, participants were assured that their information would be kept strictly confidential and only accessible to the student (KK), and her two supervisors (BJC & CL). Participants were informed that their data would be completely anonymized in any publications emanating from this work, and that the data will be stored securely on the password-protected computers of the student and her supervisors. Participants each received a travel voucher to reimburse them for the costs of their journey to and from the research unit.

Data analysis

Interviews were digitally recorded (with permission from the participants) and transcribed verbatim. The transcripts were thematically analysed (TA) using ATLAS.ti version 7, a computer supported qualitative data analysis software. Analysis of the transcripts followed a six stage approach to data analysis, i.e.: (1) familiarisation with the data, (2) coding relevant extracts of the data and generating an initial code list, (3) refining the codes and generating themes, (4) reviewing each theme generated in step 3, (5) refining, describing, and allocating descriptive labels to each theme, and (6) presenting the results of the data analysis [ 39 ]. In qualitative research, themes can be generated either inductively (from the data alone), deductively (informed by theory), or via a combination of the two [ 40 ]. In this study, we used a combination of the two methods. As such, EST provided a useful lens through which to interpret the inductively generated themes across the various systems in which the individual functions [ 41 ]. Pseudonyms have been used to protect participants’ identities.

Participants’ characteristics

As depicted in Table  1 , we interviewed 20 adults (mean age 45.65) with a primary diagnosis of OCD, the majority of whom were female (75%). A large proportion of participants were married (60%), and living with other adults and/or children (40%). Half of our participants (50%) graduated from university/college and most (60%) were employed either full-time or part-time. A large proportion of participants (70%) reported earning R15,000 (~ $105USD) or more per month. Illness severity (Y-BOCS- and FOCI-) scores ranged from 8 to 34 (M = 22.4 and SD = 6.62) and 5–18 (M = 10.85 and SD = 4.11), respectively, suggesting moderate severity of OCD on average over the past 7 days.

Overview of themes and sub-themes

Table  2 below provides an overview of the themes and sub-themes that were identified following thematic analysis of the data. The main themes centred on participants’ realisations of having OCD, the disruptions caused and the ways in which these were perceived and addressed.

Theme 1: Realisation of OCD

The theme ‘Realisation of OCD’ portrays participants’ journey with OCD, from their earliest recollections of their symptoms typical of the disorder, to some of the difficulties associated with coming to terms with OCD across their lifetime. Overall, this theme portrays the impact of OCD on the self.

Subtheme 1.1. Feeling more alike than different

Participants recounted their early experiences of their obsessive–compulsive symptomatology and explained that ‘back then’ they did not recognise their symptoms as irrational or excessive or as indicative of having a psychiatric condition. Rather, participants considered their thoughts and behaviours to be similar to those of other people, and a natural part of their personality. One participant reported:

I thought that it was normal to be this way because I have been this way since I was little (Sally, 62 - year - old female).

Another participant recounted:

My earliest memory was when I was bout eleven or twelve years old, I was in standard three. I only realised this later on in life but if I look back, my mother used to come into my room and say to me, why have you got so much homework, why are you spending so much time in your room? Meanwhile what I was doing was busy organising my stationery and my books and rearranging them, and packing them neatly, just, you know, doing these things over and over and over again and telling my mother I was busy with my homework. Meanwhile I wasn’t actually achieving much but that’s the first time I realised, well I didn’t realise at that age I had OCD but looking back I think that was the earliest time that I can remember having OCD (Angela, a 40 - year - old female).

Subtheme 1.2. Recognising something’s wrong

Both Sally and Angela recognized the pathological nature of their symptoms only later in life. Their externalised behaviours (compulsions) alerted members in their microsystem [e.g. parents (in childhood) and children and spouses (in adulthood)] that they needed help. One participant recounted:

I think my mom recognized ‘oh goodness, there is something wrong with this child!’ Yes, she took me to various doctors… and I got diagnosed quite quickly (Rezaan, a 23 - year - old female ).

Another participant stated:

My children told me that it’s not nice to come and visit me. I could not sit still, I still cannot sit still! […]. And worst of all, I did not realise that it was abnormal (Lucia, a 55 - year - old female).

Subtheme 1.3. Coming to terms with OCD

Participants shared mixed emotions about having OCD; some continued to be angry, sad and resentful whereas others proved more accepting towards the diagnosis. One participant stated:

… I’ve had enough of it, like I’ve been dealing with it since junior school and I hate my thoughts, I hate my little tics, so some days maybe a teensy bit satisfied but overall I’m not satisfied, no (Kelsey, a 31 - year - old female).

Similarly Stuart reported:

I’m angry, I’m disappointed and I’m sad that I had to have gone through it but what can one do. One can’t go back in time, one can’t …but yes it is sad. It’s sad that I can’t have happy memories of overseas trips, it’s sad that I can’t have happy memories of school, it’s sad that I can’t have happy memories of varsity, it’s sad that I can’t have happy memories of my first working life (Stuart, a 47 - year - old male).

Both Kelsey and Stuart described a resentment towards their OC symptoms and the intrusive nature of their OCD over time. This persistent intrusiveness lead to irritability, anger, sadness, discomfort, disgust and embarrassment. However, unlike Kelsey and Stuart, Derrick explained that he was able to accept OCD as part of his life and developed ways to improve his self-image, despite having OCD:

I’ve learned to accept myself and I’ve learned to focus on the things on my, you know my…positive things, the good things. So and I started dressing in a way that I feel more comfortable and in developing a style that I like (Derrick, a 58 - year - old male).

Also claiming acceptance of her condition, another participant stated:

So it’s definitely gotten a lot better I just don’t think it will ever go away you know, and I think I’ve accepted that (Sasha, a 37 - year - old female).

Theme 2: Disruptions to daily life

The theme ‘Disruptions to daily life’ provides an account of the important disruptions that took place in participants’ lives due to OCD. These include the impact of OCD on activities of daily living such as sleep, work and leisure, as well as the ability to establish and maintain interpersonal relationships with key members of the individual’s microsystem.

Subtheme 2.1. Disruption to sleep and rest

Participants reported that the persistent nature of their intrusive thoughts (obsessions) and the resulting anxiety lead to difficulties sleeping and resting. Participants’ lack of sleep meant that they were tired often, and not emotionally or physically available for active engagement with their family and friends.

One participant stated,

I couldn’t switch off, I would go a whole night worrying about the same thing and tomorrow morning wake up if I slept. Some nights I wouldn’t sleep and not worry about the same thing (Rheinart, a 55 - year - old male).

I missed a lot of sleep, because my ritual before going to bed was obviously in the bathroom, and I would be in the bathroom doing my ritual over and over and over until I was sobbing on the floor in tiredness (Wendy, a 26 - year - old female).

Subtheme 2.2. Disruption to leisure activities and hobbies

Participants also reported avoiding activities they enjoyed as many of these triggered symptoms of OCD. These included reading, watching TV, going on holiday, exercising, and participating in sport and hobbies. Not only did the OCD affect participation in these activities, it also impacted on participants’ ability to engage socially. As one participant stated:

…myself and a friend of mine last year we went and did a trip up to the Northern Cape and down the West Coast just taking photos of cemeteries, and he would’ve wanted to go for probably maybe 2   weeks, and I said no 4   days. I can’t be away from my house longer than 4   days. So he had to change that trip to 4   days because that was already the limit of me being away from the house… that the house is not being checked (Marcy, a 59 - year - old female).

Similarly the following participant explained:

It’s hard for me to relax, my mind doesn’t stop, my mind is in constant worry, in anticipation of bad things. Obviously yes, there are times when I can go out with some friends and my mind will be there, but a lot of the time it interferes with me trying to relax. Always on the edge of worrying about saying something wrong, or obsessing about something or whatever (Wendy, a 26 - year - old female).

Subtheme 2.3. Disruptions to productivity

Participants reported both positive and negative aspects of the influence of their OCD on productivity. On the one hand, there were those who experienced a decline in school and work performance and attendance, resulting in poor productivity. One participant reported:

There are days that I’ve spent 8   hours at work and not been able to do a single stitch of work because of the routines that I’ve had to do with OCD, and get to work and you’ve gotta check your e - mails. Then all the e - mails have to be in bold and then you, and then some of them are unbolded and then no okay it must all be unbolded then you unbold them and they’ve gotta be colour - coded. Then they’ve gotta be this then they’ve gotta be that […] and so there’ve been days that I haven’t been able to do any work (Kelsey, a 31 - year - old female).

Similarly, one participant recounted the negative impact of OCD on academic performance:

At varsity I couldn’t function at all, because the only way it would make any sense for me is if I took down every single word including “a’s” and “the “s’s” and whatever that that lecturer said, and I took it down neatly that I could be proud of my notes and they were neatly and whatever. That was impossible at Varsity, so I just stopped going to lectures and I used to bum notes off my other people and whatever (Rezaan, a 23 - year - old female).

On the other hand, there were those who reported that OCD did not impact much on their academic or work performance and sometimes even improved their occupational performance:

I think I did better than I would otherwise have done, because I pushed myself so much, I was my own biggest competition. It made me perform better (Judy, a 33 - year - old female).

Theme 3: Managing the disruptions to daily life

The theme ‘Managing the disruptions to daily life’ provides an account of the sources of support and the coping strategies that were implemented to deal with the impact of OCD.

Subtheme 3.1. Coping strategies

Over time participants found personal ways of adjusting to, coping with and accepting their condition. Strategies included (1) self-talk, (2) keeping a diary of events and situations that may trigger OCD, (3) using humour and other ways of distraction (such as working, taking part in sport, talking to others or using an elastic band), and (4) comfort eating or drinking alcohol. For example one participant explained:

I’m good now at telling myself to just stop, just put it down just stop because this is not fun anymore uhm (Sasha, a 37 - year - old female).

Another participant articulated:

So I learned a lot of methods to write it down and it also works to read it to yourself over and over and over and over and over again until you realize how irrational it is (Judy, a 33 - year - old female).

Judy went on state that:

…And I put a rubber band on my arm/wrist and I shoot myself with dizziness if I get this stuff in my head… (Judy).

Subtheme 3.2. Perceived social support

Participants were ambivalent about the support that they received. Some were positive believing that their significant others assisted in improving their QOL whereas others were critical about the ways in which they were treated. For example, some participants spoke of various individuals in their lives who provided solid support to them, and who were invaluable to managing the impact of OCD on their lives. They considered family members as important sources of support, as they provided physical (e.g. taking part in rituals), emotional (e.g. providing constant reassurance), and financial support to participants. One participant stated:

…when I was diagnosed with OCD they were very supportive, very very supportive. In terms of financially supporting my therapy, financially supporting my education, and emotionally supporting me etc . (Stuart).

Another participant explained how his children’s involvement in his rituals provided reassurance:

I would ask my children…, they all drive - they (are) all big and I would ask them to ride to a specific corner and go and check if there is not a cyclist going there. In the end I think they might have done it once or twice (Rheinart, a 55 - year - old male).

Participants also spoke of the strong support they received from their close friends, their healthcare providers, colleagues at work and support group members. Humour, in particular, was perceived as a supportive gesture and helped some participants to function and feel accepted—socially and at work—despite OCD. One participant mentioned how her and her friends would humour her situation,

…For example, a story like Dr. Monk, who is obsessive – compulsive, then I always said to them, “I’m Mr. Monk, “then they laugh, then they click and say,” Yes, yes, now we know exactly why you were like that… (Sandra, a 39 - year - old female).

In contrast, others perceived little emotional and social support from their loved ones. Participants perceived this lack of support to be as a consequence of family members’ limited understanding of their disorder. One participant recalled:

You know I’ve explained to him […]I don’t think he understands why I get so anxious or why I, if I just cry, what it, he doesn’t see what’s going on in my head. Sometimes what’s going on in my head is so so much, that when you tell someone, that’s not much, you know but in your head it’s too big, so it’s very difficult to explain. […] I’m just saying that the level is different and yes he doesn’t always understand but he’s still there. Yes, he’s still there (Wendy, a 26 - year - old female ).

In this study we qualitatively explored the ways in which OCD influences the daily life and functioning of South African adults living with OCD. We used EST as a broad theoretical lens through which to identify the composition of participant’s ecological systems. Our findings provide a closer look at participants’ microsystems, that is—the impact of OCD on the individual over time, on everyday living and relationships with family, peers and colleagues. Further, our findings also provide an account of the strategies participants used to cope with OCD, and the sources of support that were available to them.

Our study is part of a growing body of qualitative literature on OCD using exploratory approaches to better understand the perspectives of individuals living with OCD [ 11 , 12 , 13 , 15 , 17 ]. In her paper, Knapton [ 11 ] argues that the majority of studies on OCD are quantitative in nature and that our understanding of OCD, “has largely come from participants’ judgments of pre-defined and inflexible statements rather than from extended and unrestricted descriptions”, and that this approach limits, “intra-participant variation” (p. 2). In the current study, the findings provide instances of consistent and contrasting accounts of the experience of OCD—highlighting the heterogeneity of the disorder, and the importance of exploring individual perspectives.

Our findings provided an account of participant’s realisation of having OCD. Our findings demonstrated that, initially (often reflecting back to childhood), individuals with OCD perceived their symptoms as normal , that they were similar to other people, and that their behaviours and thoughts were part of their personality . It was only when symptoms began to markedly disrupt daily life and functioning, in addition to causing major distress, that they realised that these were pathological or indicative of having a psychiatric problem, warranting a visit to the clinic. Notably, research suggests that individuals with OCD sometimes lack such insight into the excessiveness of their symptoms [ 42 ]. Given that some individuals without OCD also experience OC - like symptoms, the behaviour is often interpreted as normal [ 43 ] or minimalized as “just a bad habit” that can easily be addressed. Family members and spouses in particular were key to helping participants recognise their symptoms as excessive. As shown in other research, participants’ compulsions i.e. externalised behaviour such as checking or washing, were key to recognition of the disorder [ 42 ]. However, it has been shown that family members themselves often experience marked distress when observing compulsions associated with OCD [ 16 ]. Interactions with significant others in the context of OCD was not necessarily perceived as positive though. For example, in their study of individuals living with OCD and their partners in Norway, Walseth et al. found that patients often reported feeling monitored and surveillanced by their partners [ 16 ]. This seems to be an important area for therapeutic focus, to eliminate potentially persecutory actions by family members towards those with OCD, and to also help mitigate the frustration and disconnect individuals with OCD feel with family members who seemingly do not understand them or their OCD [ 17 ]. Failure to address this may lead to avoidance of interaction by those with OCD and their partners and lead to performing behaviours in secrecy, and increasing what Walseth et al. [ 16 ] refer to as a ‘mental distance’.

Our findings also showcased the disruptions to daily life due to OCD. Similar to other studies [ 44 , 45 ], our findings demonstrated OCD’s deep impact on sleep quality, leisure activities, and participants’ interpersonal relationships with friends and family. Participants in our study experienced difficulty preparing for sleep as thoughts and rituals had to be performed continuously. Evidence for sleep disruption due OCD is not consistent across studies, with some demonstrating difficulty sleeping and resulting exhaustion [ 46 , 47 ], and others not [ 48 ]. The findings that do suggest sleep disturbance also included references to difficulties in daily functioning, overall physical and mental health [ 49 ]. For our participants, a lack of sleep and the associated consequences exacerbated their perceptions of their illness severity, ultimately affecting their ability to function daily [ 50 ]. Leisure activities are found to benefit and assist mental illness in the process of recovery [ 51 ]. However, consistent with other studies, participants found it difficult to engage in activities they enjoy, as many of these activities triggered symptoms of OCD. Moreover, engaging in leisure activities provide opportunities for socialisation. As such, withdrawal from these activities may ultimately also lead to isolation [ 45 , 52 ].

Consistent with some quantitative [ 53 , 54 ] and qualitative work [ 11 , 13 , 17 ], several participants commented on the impact of their OCD on attendance and performance at school/university, and/or work. In their study with nine British individuals living with OCD, the authors identified the theme of ‘Failing at life’ and described this as the overwhelming impact of the disorder on education and careers [ 13 ]. Similar to participants in our study, these participants spoke of their goals and expectations being delayed or thwarted as a consequence of this disorder [ 13 ]. Consequently, individuals with OCD may feel hopeless and powerless, because they cannot live up to particular expectations or potential, which impacts on their self-esteem [ 17 ]. On the other hand, there is not much evidence for the positive impact that OCD may have on school and work as found in this study, despite two qualitative studies making slight mention of it [ 10 , 13 ]. For example, echoing the words of one of our participants, the one study [ 10 ] reported how OCD enabled one of their participants to be thorough and good with detail.

Our findings also showcased the ways in which participants managed the disruptions due to OCD in their lives. Participants identified physical, emotional and financial support from significant others as crucial in managing and coping with their OCD. This finding is consistent with studies that have shown the positive impact of perceived social support on individuals’ ability to cope with the difficulties of OCD [ 55 , 56 ]. Similar to our findings, some studies show that most family members of individuals living with OCD accommodate them in most respects—e.g. actively assisting the OC individual by participating in their rituals or doing chores for them in order to save time or reduce frustration [ 16 , 57 ]. However, there also is strong evidence to suggest that family support and involvement may exacerbate dysfunctional behaviours [ 58 , 59 ]. Whereas participants in our study explicitly stated an appreciation of this type of accommodation, and perceived it as a means of social support—studies show that this type of accommodation seems to interfere with a positive response to treatment [ 16 , 60 ]. Furthermore, while participants were mostly positive about the support they received from their significant others, there were concerns about their illness as being burdensome and traumatic for the families [ 61 , 62 ]. Arguably, these concerns may lead to avoidance of sharing and ultimately, to feeling isolated. This hypothesis is consistent with findings from a recent qualitative study where participants reported feeling disconnected from family and friends [ 17 ]. As such, emotional responses towards family and friends may range from positive and appreciative to fears of being burdensome and withdrawal—highlighting that it is an important avenue for further research. Indeed, some literature suggests that involving family in treatment (e.g. partners, in couple-based therapy) may not be suitable for everyone [ 16 ]. Furthermore, other studies have also demonstrated that familial responses to OCD vary, and in some instances may become a source of conflict that can contribute to even poorer relationship functioning, marital discord, and divorce [ 63 , 64 , 65 ]. The inability to maintain a meaningful connection with others limits patients’ access to emotional support and is likely to perpetuate feelings of hopelessness and helplessness [ 10 , 11 , 13 , 14 , 17 ].

Participants in the current study experienced OCD as disturbing, destructive, and debilitating, causing strong emotional reactions such as anxiety, irritation, anger, sadness, discomfort, and disgust. This ties in with diagnostic nomenclatures such as the DSM [ 3 ] and the ICD [ 66 ], which describes OCD as a condition characterised by intrusive thoughts and compulsions associated with significant distress. Feelings of anger, dissatisfaction, and hopelessness are also typical of patients with mental health problems such as OCD [ 13 , 17 , 67 ]. Our participants reported various ways of coping and adjusting to, and being flexible about the demands of their condition and its sequelae. Participants reported shifting from first attempting to solve OCD itself (problem-focused coping) to attempting to solve the emotions associated with their OCD (emotion-focused coping) [ 68 ]. As participants shift from problem-focused coping to emotion-focused coping, they change their thoughts and the way they view their disorder and therefore move towards feelings of acceptance, i.e. accepting their condition and wanting to be accepted by others. This relative acceptance of an OCD diagnosis resonates with Relational Frame Theory (RFT) which forms the basis of Acceptance and Commitment Therapy (ACT) [ 69 ]. ACT is an empirically-based psychological intervention that uses acceptance strategies mixed with commitment and behavior-change strategies, to increase psychological flexibility. There is a fair amount of research on ACT as a model and a treatment for OCD spectrum disorders [ 70 ]. The acceptance/commitment concept leads us back to the present study’s first theme labelled “realisation of OCD”. As noted previously, whether participants accepted the diagnosis and its chronic nature or not, its impact on their daily lives is unmistakeable, and influences relationships significantly. It may be argued that if patients with OCD can learn to stop avoiding and denying their OC symptoms and accept the existence and the need for treatment thereof, they may be able to move forward in their lives. With this understanding, individuals may begin to accept their diagnosis and its sequelae, and commit to making the necessary changes in their behavior, regardless of what is going on in their lives.

Limitations and recommendations

This study has a few limitations. First, the sample size is relatively small but nevertheless comparable to other qualitative work. Second, interviews were once-off, thus providing little opportunity for rapport building between the interviewer and the interviewee. Follow-up interviews may have provided an opportunity for participants to feel sufficiently more comfortable to provide more in-depth information. Finally, we acknowledge that interviews with family members, friends and work colleagues may have afforded a more in-depth account of the bi-directionality of the impact of OCD on members of participant’s microsystem. Interviews with these key role players in participants’ lives will be an important avenue for further research to go beyond just identifying individual level factors to target in interventions.

In conclusion, this qualitative study of the lived experiences of adults with OCD identified 3 three main themes, centring on participants’ realisations of having OCD, the disruptions caused and the ways in which these were perceived and addressed. Our findings were consistent with those from quantitative studies, but provides added depth that may assist in the care of these patients. For example, in the current study the findings provide instances of consistent and contrasting accounts of the experience of OCD—highlighting the heterogeneity of the disorder, and the importance of exploring individual perspectives. The involvement of the family and significant others in the patient’s symptoms and treatment was also addressed; the findings here have emphasized that these relationships are dynamic and may not necessarily be constructive, warranting special attention and adjustment during therapy. A discussion of management and coping with OCD emphasized the importance of acceptance. This ties in with recent work on the potential value of ACT, either as monotherapy or as an adjunct to conventional techniques such as Cognitive Behavioural Therapy (CBT). Many caveats in our knowledge remain. For example, whether the South African experiences of living with OCD are significantly different from other contexts, is not yet known. Also, how local challenges—e.g. limited accessibility, affordability and specialization—shape experiences of South Africans with OCD, is another potential research avenue to be explored.

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Authors’ contributions

KCK: Conceptualisation of idea, data collection and analysis, preparation of full first draft of manuscript. These data were collected as part of Ms. Kohlers master’s thesis in research at Stellenbosch University, under the supervision of BC and CL. BC: Conceptualisation of research question, assisting with data analysis, contributing to writing of manuscript. CL: Conceptualisation of research question, assisting with recruitment and data collection, assisting with data analysis, contributing to writing of manuscript. All authors read and approved the final manuscript.

Acknowledgements

We are grateful for the contributions and time of the individuals with OCD who agreed to participate and share their stories. We would like to acknowledge those who assisted with data collection, transcription and translation.

Competing interests

The authors declare that they have no competing interests.

Availability of data and materials

Due to ethical concerns and participant’s links to a larger ongoing study, the data are not openly available.

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All participants provided written informed consent for publication.

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This study received approval from the Health Research Ethics Committee (HREC) at Stellenbosch University (M07/05/019). All participants provided written informed consent.

Ms. Kirsten Kohler received funding from the National Research Foundation (SFH160609169643). Opinions expressed and conclusions arrived at, are those of the authors and are not necessarily to be attributed to the NRF.

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Kirsten Celeste Kohler & Bronwynè Jo’sean Coetzee

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Christine Lochner

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Kohler, K.C., Coetzee, B.J. & Lochner, C. Living with obsessive-compulsive disorder (OCD): a South African narrative. Int J Ment Health Syst 12 , 73 (2018). https://doi.org/10.1186/s13033-018-0253-8

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DOI : https://doi.org/10.1186/s13033-018-0253-8

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• Obsessive–compulsive disorder
• Daily functioning
• Quality of life
• Qualitative
• Thematic analysis

International Journal of Mental Health Systems

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Cognitive Dysfunction in Obsessive-Compulsive Disorder

• Anxiety Disorders (A Pelissolo, Section Editor)
• Published: 16 July 2016
• Volume 18 , article number  80 , ( 2016 )

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• Karim N’Diaye 1 &
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Obsessive-compulsive disorder (OCD) is a mental disorder featuring obsessions (intrusive thoughts) and compulsions (repetitive behaviors performed in the context of rigid rituals). There is strong evidence for a neurobiological basis of this disorder, involving limbic cortical regions and related basal ganglion areas. However, more research is needed to lift the veil on the precise nature of that involvement and the way it drives the clinical expression of OCD. Altered cognitive functions may underlie the symptoms and thus draw a link between the clinical expression of the disorder and its neurobiological etiology. Our extensive review demonstrates that OCD patients do present a broad range of neuropsychological dysfunctions across all cognitive domains (memory, attention, flexibility, inhibition, verbal fluency, planning, decision-making), but some methodological issues temper this observation. Thus, future research should have a more integrative approach to cognitive functioning, gathering contributions of both experimental psychology and more fundamental neurosciences.

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Benzina, N., Mallet, L., Burguière, E. et al. Cognitive Dysfunction in Obsessive-Compulsive Disorder. Curr Psychiatry Rep 18 , 80 (2016). https://doi.org/10.1007/s11920-016-0720-3

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Clinical advances in obsessive-compulsive disorder: a position statement by the International College of Obsessive-Compulsive Spectrum Disorders

Fineberg, Naomi A. a,,b,,c ; Hollander, Eric d ; Pallanti, Stefano e,,f ; Walitza, Susanne g,,h,,i ; Grünblatt, Edna g,,h,,i ; Dell’Osso, Bernardo Maria j,,k,,l,,m ; Albert, Umberto n ; Geller, Daniel A. o ; Brakoulias, Vlasios p,,q ; Janardhan Reddy, Y.C. r ; Arumugham, Shyam Sundar r ; Shavitt, Roseli G. s ; Drummond, Lynne t ; Grancini, Benedetta b,,j ; De Carlo, Vera b,,j ; Cinosi, Eduardo a,,b ; Chamberlain, Samuel R. u,,v ; Ioannidis, Konstantinos u,,v ; Rodriguez, Carolyn I. k,,w ; Garg, Kabir b ; Castle, David x ; Van Ameringen, Michael y,,z ; Stein, Dan J. aa ; Carmi, Lior bb,,cc ; Zohar, Joseph bb,,dd ; Menchon, Jose M. ee

a University of Hertfordshire, Hatfield

b Hertfordshire Partnership University NHS Foundation Trust, Welwyn Garden City, Hertfordshire

c University of Cambridge School of Clinical Medicine, Cambridge, UK

d Department of Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, New York, USA

e Istituto di Neuroscienze, University of Florence, Firenze, Italy

f Albert Einstein College of Medicine, Bronx, New York, USA

g Department of Child and Adolescent Psychiatry and Psychotherapy, University Hospital of Psychiatry Zurich, University of Zurich

h Neuroscience Center Zurich, University of Zurich and ETH Zurich

i Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland

j University of Milan, Department of Biomedical and Clinical Sciences Luigi Sacco, Ospedale Sacco-Polo Universitario, ASST Fatebenefratelli-Sacco, Milan, Italy

k Department of Psychiatry and Behavioural Sciences, Stanford University, California, USA

l CRC ‘Aldo Ravelli’ for Neurotechnology and Experimental Brain Therapeutics, University of Milan, Milan

m Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford

n Department of Medicine, Surgery and Health Sciences, UCO Clinica Psichiatrica, University of Trieste, Trieste, Italy

o Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA

p Western Sydney Obsessive-Compulsive and Related Disorders Service, Western Sydney Local Health District, Blacktown Hospital, Blacktown, New South Wales

q Translational Research Health Institute (THRI), Clinical and Health Psychology Research Initiative (CaHPRI) and School of Medicine, Western Sydney University, Sydney, Australia

r OCD Clinic, Department of Psychiatry, National Institute of Mental Health and Neuro Sciences (NIMHANS), Bengaluru, India

s OCD Spectrum Disorders Program, Institute and Department of Psychiatry, Hospital das Clinicas da Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo-SP, Brazil

t Consultant Psychiatrist, SW London and St George’s NHS Trust and St George’s, University of London, London

u Department of Psychiatry, University of Cambridge, Cambridge

v Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK

w Veterans Affairs Palo Alto Health Care System, Palo Alto, California, USA

x St. Vincent’s Hospital Melbourne and The University of Melbourne, Melbourne, Australia

y Department of Psychiatry and Behavioural Neurosciences, McMaster University

z Hamilton Health Sciences, Hamilton, Ontario, Canada

aa SA MRC Unit on Risk and Resilience in Mental Disorders, Department of Psychiatry and Neuroscience Institute, University of Cape Town, Cape Town, South Africa

bb The Post Trauma Center, Chaim Sheba Medical Center, Ramat Gan

cc The Data Science Institution, The Interdisciplinary Center, Herzliya

dd Tel Aviv University, Tel Aviv-Yafo, Israel

ee Department of Psychiatry, Bellvitge University Hospital-IDIBELL, University of Barcelona, Cibersam, Barcelona, Spain

Received 27 January 2020 Accepted 16 March 2020

Correspondence to Kabir Garg, Hertfordshire Partnership University NHS Foundation Trust, Welwyn Garden City, Hertfordshire, UK, E-mail: [email protected]

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CC-BY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

In this position statement, developed by The International College of Obsessive-Compulsive Spectrum Disorders, a group of international experts responds to recent developments in the evidence-based management of obsessive-compulsive disorder (OCD). The article presents those selected therapeutic advances judged to be of utmost relevance to the treatment of OCD, based on new and emerging evidence from clinical and translational science. Areas covered include refinement in the methods of clinical assessment, the importance of early intervention based on new staging models and the need to provide sustained well-being involving effective relapse prevention. The relative benefits of psychological, pharmacological and somatic treatments are reviewed and novel treatment strategies for difficult to treat OCD, including neurostimulation, as well as new areas for research such as problematic internet use, novel digital interventions, immunological therapies, pharmacogenetics and novel forms of psychotherapy are discussed.

Introduction

Once a neglected illness, obsessive-compulsive disorder (OCD) is now recognized as a common, highly disabling and potentially treatable early-onset brain disorder. Clinical and translational research in OCD grows apace, and over the past 10 years has contributed to substantial advances in understanding of the phenomenology, brain-based biology and treatment response, leading to innovations in nosological conceptualizations, therapeutic interventions and services. Recent changes in the DSM-5 ( American Psychiatric Association, 2013 ) and ICD-11 ( WHO, 2018 ) diagnostic classification systems have set OCD at the head of a new family of obsessive-compulsive spectrum disorders [otherwise known as Obsessive-Compulsive or Related Disorders, or, Obsessive-Compulsive and Related Disorders (OCRDs)], including body dysmorphic, hoarding, hair-pulling, skin picking and olfactory reference disorders and hypochondriasis, all sharing compulsive behaviour as a cardinal characteristic. Serotonin reuptake inhibitors [selective serotonin reuptake inhibitors (SSRIs), clomipramine] or cognitive behavioural therapy (CBT) involving exposure and response prevention (ERP), represent the mainstay of contemporary treatment for OCD, with emerging evidence suggesting that early intervention produces better outcomes ( Fineberg et al., 2019 ). However, a substantial minority of patients still fail to respond either in any meaningful way, or in terms of residual symptoms. Treatment-resistant OCD has become a fruitful research focus for clinical treatment and specialist services development, worldwide.

A number of evidence-based clinical guidelines for managing OCD have been published ( Bandelow et al., 2012 ; Baldwin et al., 2014 ; Sookman et al., 2015 ). However, recent feedback from topic experts and stakeholders (National Institute for Health and Care Excellence, 2019) has identified the need for an update, highlighting that clinical practice has progressed in many areas. This includes evidence of efficacy for new pharmacological interventions and augmentation therapies among treatment-resistant groups, advances in invasive and noninvasive neurostimulation technology as well as rapid advances in information technology and telecommunications and the introduction of technology-enhanced interventions. Yet, in many parts of the world, access to recommended treatments and specialist care services, in particular for children, remains limited.

The International College of Obsessive-Compulsive Spectrum Disorders (ICOCS; www.ICOCS.org ) is a global network of expert clinicians, researchers and ‘experts by experience of OCD’, whose principal objective is to support and stimulate the study and treatment of obsessive-compulsive spectrum disorders. In recognition of the need for updated clinical guidance on the treatment of OCD, the ICOCS has developed this position statement, based on expert consensus and including a balanced representation of genders, child versus adult psychiatrists and early career scientists, with global and ethnic diversity. Agreement was reached on the key issues to be covered at a series of meetings, and the authors of each section were chosen based on their expertise in that area. An initial draft was prepared, based on a literature review, and circulated first among the authors and then to all ICOCS members and iterative edits were incorporated. In sum, we have selected those recent therapeutic advances judged by a range of experts to be of most relevance to the treatment of OCD, including products that are not licensed or labelled for treatment of OCD by the US Food and Drug Administration (FDA) ( Table 1 ), which are marked with an asterisk (*) throughout the article, based on new and emerging evidence from clinical and translational science

Global assessment of obsessive-compulsive disorder

A comprehensive assessment of OCD requires trained clinicians who perform direct interviews with the patient and, whenever possible, with family members, so that an accurate diagnosis can be determined and individualized treatment can be tailored. The hallmarks of OCD are obsessions (recurrent, intrusive, unwanted thoughts, images or impulses and compulsions (repititive behaviours or mental acts that the individual feels compelled to perform), these can present together or separately.The most common symptom dimensions of OCD are contamination/washing, aggression/checking, symmetry/ordering/arranging, sexual/religious (also known as ‘taboo thoughts’) and hoarding ( Rosario-Campos et al., 2006 ). Importantly, according to DSM-5, a diagnosis of Hoarding Disorder should be assigned when symptoms pertain to this single dimension ( American Psychiatric Association, 2013 ). The presence and severity of symptoms can be measured by validated instruments ( Goodman et al., 1989 ; Rosario-Campos et al., 2006 ; Storch et al., 2010 ), which is relevant to tailoring the behavioural treatment and monitoring treatment response objectively. For the OCD diagnosis, while free-form interviews by clinicians are commonly used, structured interviews offer advantages in terms of objectivity and psychometric properties ( Rapp et al., 2016 ). Suitable interviews for the diagnosis of OCD in adulthood include the Structured Clinical Interview for DSM-5 Disorders ( First et al., 2016 ), or the Mini International Neuropsychiatric Interview ( Sheehan et al., 1998 ). The Yale–Brown Obsessive-Compulsive Scale (Y-BOCS) is the gold-standard for assessing symptom severity in diagnosed adult patients, and incorporates a detailed checklist for individual symptoms ( Goodman et al., 1989 ). For initial screening, six brief questions can be used. These include as follows: (1) Do you wash or clean a lot? (2) Do you check things a lot? (3) Is there any thought that keeps bothering you that you would like to get rid of but can’t? (4) Do your daily activities take a long time to finish? (5) Are you concerned about orderliness or symmetry? (6) Do these problems trouble you? Positive response to one or more statements would indicate a need for more detailed assessment ( Fineberg et al., 2008 ).

Obsessions and compulsions tend to occur concomitantly in the vast majority of people with OCD ( Shavitt et al., 2014 ). In addition, compulsions are commonly preceded not only by obsessions but also by subjective experiences of incompleteness, or ‘not feeling just-right’, or so-called sensory phenomena (perceptual experiences that precede or accompany compulsions) ( Shavitt et al., 2014 ). We could expect these phenomena to be targeted by cognitive-behavioural techniques in a way similar to the premonitory urges in the behavioural treatment of tic disorders ( McGuire et al., 2015 ).

Another relevant clinical feature that merits attention when assessing subjects with OCD is the degree of insight, meaning the extent to which the person recognizes that his/her beliefs are not true ( Eisen et al., 1998 ). Insight (good or fair insight, poor insight, absent insight/delusional beliefs) is a diagnostic specifier for OCD, body dysmorphic disorder (BDD) and hoarding disorder in the DSM-5 ( American Psychiatric Association, 2013 ). In general, subjects with OCD have at least good insight, with only a minority presenting poor insight or delusional OCD ( Shavitt et al., 2014 ). The presence of tic symptomatology represents another clinically relevant diagnostic specifier in the DSM-5, as tic may predict a more favourable response to dopamine antagonist agents ( Bloch et al., 2006 ). Finally, the clinician must obtain information regarding avoidance behaviours, which commonly occurs as a means to handle the distress evoked by the obsessions and constitutes one of the main targets of the cognitive-behavioural treatment for this disorder ( Drummond, 2014 ). Functional impairment varies in OCD. It is an important domain that reflects clinical severity and constitutes an indirect measure of improvement during treatment. Impairment can be measured indirectly with OCD severity scales or with specific measures [e.g., the WHO Disability Assessment Schedule 2.0 ( Üstün et al., 2010 ) or the Cognitive Assessment Instrument of Obsessions and Compulsions ( Dittrich et al., 2011 )].

Comorbidity is almost always present with OCD and is often ‘phase-specific’ ( Pallanti and Grassi, 2014 ). Assessment of specific comorbidities, like tic disorders, anxiety and depressive disorders, disruptive disorders, eating disorders, autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and schizophrenia ( Zohar, 1997 ), is essential in guiding the formulation of an effective treatment strategy. Comorbidity has also been a focus of emerging genetic studies of OCD. For example, a recent study in 4645 OCD patients found different genotypes to be associated with different OCD comorbidities. Thus, OCD comorbid with bipolar disorders was associated with COMT , OPRM1 and GRIK1 genotypes; OCD and depressive disorders were associated with OPRM1 and CYP3A4/5 genotypes; OCD comorbid with ADD/ADHD was associated with 5HT2C genotypes; and OCD comorbid with anxiety was associated with CYP3A4/5 genotypes ( Nezgovorova et al., 2018 ). However, these findings should be viewed with caution, as the ‘candidate gene’ approach, in which specific genes are tested for association with specific disorders, chosen for the biological plausibility of their relationship, using relatively small samples of affected subjects and healthy controls, has been criticized for overestimating statistical associations. Attempts to replicate the findings have tended to produce disappointing results. Therefore, more unbiased forms of the association study, such as genome-wide association studies (GWAS), which test the association between a disease and multiple genetic variants across the whole genome, are to be preferred ( Gordon, 2018 ; National Advisory Mental Health Council Workgroup on Genomics, 2019 ). A recent meta-analysis of GWAS of eight psychiatric disorders identified a common genetic factor linking OCD, anorexia nervosa and Tourette’s syndrome (Lee et al ., 2019b).

Interestingly, comorbid disorders that start before the onset of OCD symptoms seem to influence the occurrence of additional comorbidities over time. In a cohort of 1001 patients with OCD, separation anxiety disorder preceded OCD in 17.5% of individuals and was associated with a higher lifetime frequency of posttraumatic stress disorder; ADHD preceded OCD in 5.0% of subjects, and was associated with higher lifetime frequencies of substance abuse and dependence; tic disorders preceded OCD in 4.4% of subjects and were associated with higher lifetime frequencies of OCD spectrum disorders ( de Mathis et al., 2013 ). In children and adolescents, in addition to the considerations for the adult subjects, a history of paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) should be taken, as this could also have treatment implications ( Wilbur et al., 2019 ). Taken together, these findings emphasize the importance of identifying comorbid disorders, as they may serve as markers of different biological or clinical substrates of potential relevance for treatment planning (see section Future directions for research).

OCD needs to be differentiated from: anxiety disorders presenting with recurrent fears (as in the phobias) and excessive worry (as in generalized anxiety disorder); ruminations accompanying depressive mood in depressive disorders; OCD-related disorders like BDD (where there are specific concerns with one’s appearance), hair-pulling disorder (the only compulsion); tic disorders; eating disorders (concerns focussed on weight and shape and food); psychotic disorders (especially in poor-insight OCD and so-called schizo-obsessive disorder) and obsessive-compulsive personality disorder (with the hallmarks of enduring rigidity and perfectionism over the lifetime) ( American Psychiatric Association, 2013 ).

Along with the identification of the most bothersome symptoms, the clinician should investigate the age of onset of symptoms and the age when a diagnosis of OCD has been determined, because these data can help to predict the prognosis ( Fineberg et al., 2019 ). OCD frequently emerges in childhood, in which group accurate diagnosis is essential for care planning. Paediatric clinicians can ask simple screening questions such as ‘do you ever have unwanted thoughts or worries that won’t go away? Are there things you have to do over and over again, even though you don’t want to or that don’t make sense?’ The formal diagnosis should be made with a structured interview and the nationwide translated versions of the standardized Children’s Y-BOCS (CY-BOCS), which has good reliability ( López-Pina et al., 2015a , b ).

Awareness of other conditions associated with the onset and course of OCD symptoms can also be of help in treatment planning, because OCD frequently follows a chronic course, with most patients reporting residual symptoms, or present an episodic course with long symptom-free periods (Skoog and Skoog, 1999 ). For example, a cross-cultural study has shown an association between reproductive cycle events and the onset (mostly menarche) or exacerbation of OCD during the premenstruum, pregnancy, postpartum and menopause ( Guglielmi et al., 2014 ). Relevant to prevention strategies, exacerbation during or after first pregnancy posed a significant risk to exacerbation in or after a subsequent pregnancy. The underlying factors responsible for triggering exacerbation remain to be understood, especially the role of oestrogen and oxytocin ( Guglielmi et al., 2014 ).

Information on the family history of OCD, tics and other psychiatric disorders and the understanding of OCD among family members and family accommodation are also relevant to treatment-planning and adherence. Evidence shows that successful treatment depends on the reduction of the participation of the family members in the patient’s compulsive behaviours (i.e., reduction of accommodation) ( Gomes et al., 2017 ). Moreover, a recent analysis suggested that children with a family history of OCD have a six times lower response to CBT ( Garcia et al., 2010 ).

Suicidality should be included when assessing people with OCD ( Dell’Osso et al., 2018 ). A recent meta-analysis ( Angelakis et al., 2015 ) found that OCD patients showed relatively increased risk of ‘suicidality’, when compared with healthy controls. In terms of absolute risk, estimates vary. Among 582 patients with OCD, 36% reported lifetime suicidal thoughts, 20% had made suicidal plans, 11% had already attempted suicide and 10% presented with current suicidal thoughts ( Torres et al., 2011 ). In another study of 425 outpatients, recruited by the ICOCS network, 14.6% of the sample reported at least one suicide attempt during their lifetime ( Dell’Osso et al., 2018 ). In the study by Torres et al. (2011 ), comorbid depressive disorder and posttraumatic stress disorder were associated with a range of suicidal behaviours. Sexual/religious symptoms and comorbid substance use disorders were associated with suicidal thoughts and plans, while impulse control disorders were associated with current suicidal thoughts, suicide plans and attempts. In the study of Dell’Osso et al. (2018 ), comorbid tic disorders as well as medical disorders and a previous history of hospitalization were also associated with increased suicidality.

Neuropsychological assessment of patients with OCD suggests that there are deficits across a broad range of domains (Fineberg et al ., 2018a). For example, a recent meta-analysis found that patients with symptoms related to symmetry and orderliness were more likely to have poor performance on memory, visuospatial ability, verbal working memory and cognitive flexibility tests, whereas patients with doubting and checking were more likely to perform poorly on memory and verbal memory tasks ( Bragdon et al., 2018 ). Other meta-analyses have found cognitive flexibility and response inhibition to be impaired in OCD in general (all literature pooled), with medium–large effect sizes ( Lipszyc and Schachar, 2010 ; Chamberlain et al., 2019 ). It must be considered that comorbid neurodevelopmental disorders, such as ASD ( Postorino et al., 2017 ), or ADHD are expected to influence performance on distinct tests, especially but not exclusively in youth.

Behavioural analysis of OCD involves obtaining a history to ascertain the specific situations that provoke obsessions, anxious thoughts or uncomfortable feelings and then separating out the compulsions or anxiolytic behaviours. This is important, as during therapy the patient needs to face up to the anxiety-provoking thoughts or uncomfortable feelings while resisting the urge to ‘put this right’ using compulsive thoughts, behaviours or avoidance. Full descriptions of behavioural analysis are given elsewhere ( Drummond, 2014 ). From a cognitive perspective, there have been several theories about the underlying beliefs that may trigger OCD, such as the failure to challenge underlying beliefs sufficiently ( Emmelkamp et al., 1988 ), inflated responsibility and guilt if compulsions were not acted upon and negative consequences occurred ( Salkovskis, 1985 , 1999 ), or an overinflated idea of danger ( Jones and Menzies, 1998 ) (see section Novel forms of psychotherapy below).

Early intervention in obsessive-compulsive disorder

OCD frequently has an onset early in life ( Fineberg et al., 2019 ). Childhood or adolescent onset accounted for more than 50% of the sample in a recent international multisite report ( Dell’Osso et al., 2016 ). Unfortunately, early onset is all too often not associated with early help-seeking and recognition of the illness. OCD has been consistently associated with a long duration of untreated illness (DUI) – around 7 years on average ( Dell’ Osso et al. , 2019 ) – with this period accounting, in many cases, for more than half of the overall duration of illness ( Albert et al., 2019 ; Dell’ Osso et al. , 2019 ). Longer DUI implies late interventions and poor therapy response, particularly in relation to pharmacological treatment ( Dell’Osso et al., 2010 ; Albert et al., 2019 ). The need for service investment in early intervention for OCD is further highlighted by studies indicating that OCD is among the top 10 most disabling of all disorders, accounting for 2.2% of all years lost to disability ( Ayuso-Mateos, 2006 ), with economic costs to society including those associated with lost productivity, which are long-lasting and profound. It has been estimated that in the USA, over $10 billion dollars per year are spent on treatments for OCD alone ( Hollander et al., 2016 ).

OCD has been traditionally viewed as a secretive illness with some phenotypes (e.g., with sexual, religious or aggressive content) being particularly associated with reluctance to seek help ( Dell’Osso et al., 2015 ). There may also be difficulty detecting the disorder in childhood ( Storch et al., 2014 ). Nonetheless, a greater effort needs to be made at multiple levels (e.g., education, service development and screening of ‘at risk’ individuals) to implement effective strategies for prevention, early diagnosis and intervention. For instance, there have been reports indicating that the earliest symptoms shown by OCD patients belong to the symmetry and ordering dimension ( Kichuk et al., 2013 ) and these may represent a red flag for early detection of subthreshold/early symptoms.

Children of individuals with OCD represent another high-risk group deserving attention and potentially needing preventive interventions. The presence of tic, paediatric acute-onset neuropsychiatric syndrome, obsessive-compulsive personality disorder and impulse control disorders may be indicators of comorbid OCD or herald the subsequent development of OCD ( Fineberg et al., 2019 ). Staging models may also be useful ( Fineberg et al., 2019 ; Fontenelle and Yücel, 2019 ), with four major stages proposed (from stage 0 ‘increased risk, asymptomatic’ to stage 4 ‘severe illness’). However, their clinical utility and applicability remain to be investigated. Interventions such as psychoeducation and reduction of family accommodation represent promising areas for prevention and early intervention when OCD is at its early stages in high-risk groups ( Brakoulias et al., 2018 ). One Australian health service ( Brakoulias, 2018 ) has recently begun using existing early intervention services for psychosis to provide early intervention to patients with OCD ( Brakoulias, 2018 ) (Western Sydney Obsessive-Compulsive and Related Disorders Service).

Cognitive behavioural therapy, selective serotonin reuptake inhibitor or their combination as a first-line treatment for adults with obsessive-compulsive disorder

Pharmacological therapies (SSRIs and the tricyclic clomipramine) ( Zohar et al., 1996 ; Fineberg et al., 2012 ) and psychological therapies (ERP, CBT) ( Abramowitz, 2006 ) are often efficacious in treating OCD in adults. As SSRIs and CBT have been thought to have broadly similar efficacy in acute treatment, current guidelines recommend taking account of patients’ clinical features, needs and preference as well as service availability when choosing a first-line treatment ( Baldwin et al., 2014 ). Monotherapy with CBT involving ERP is particularly recommended as an initial treatment in those with mild–to-moderate OCD, in the absence of severe depression, in those who do not prefer medications and where this form of treatment is accessible, available and preferred by patients (National Institute for Health and Clinical Excellence, 2005a; Koran et al., 2007 ; Katzman et al., 2014 ; Janardhan Reddy et al., 2017 ). In contrast, SSRIs are particularly recommended as a first-line treatment option in more severe OCD, in those who have comorbid depression, in those with previous history of good response to SSRIs, in those who are uncooperative with CBT or in situations where ERP/CBT is not available, accessible or preferred by patients. A combination of CBT involving ERP and SSRIs is often recommended in severe OCD, in the presence comorbid depression and in poor responders to CBT or SSRIs alone (National Institute for Health and Clinical Excellence, 2005b; Skapinakis et al., 2016b ; Hirschtritt et al., 2017 ; Janardhan Reddy et al., 2017 ). In essence, most guidelines recognize SSRIs and CBT involving ERP as first-line monotherapies, but prefer CBT involving ERP over SSRIs.

Several meta-analyses and systematic reviews have demonstrated SSRIs and clomipramine ( Ackerman and Greenland, 2002 ; Soomro et al., 2008 ; Skapinakis et al., 2016b ) and CBT involving ERP to be more effective than placebo (frequently waiting list in CBT trials) in the treatment of OCD ( Gava et al., 2007 ; Rosa-Alcázar et al., 2008 ). Although an earlier meta-analysis suggested superiority of clomipramine over SSRIs ( Ackerman and Greenland, 2002 ), a recent network meta-analysis failed to demonstrate the superiority of clomipramine over SSRIs ( Skapinakis et al., 2016b ). Direct head-to-head comparisons of various medications are few and there seems to be no individual differences in efficacy among SSRIs ( Skapinakis et al., 2016b ), although, of course, they may differ in side effect profiles.

Most studies of CBT involving ERP included symptomatic patients stabilized on antidepressants ( Skapinakis et al., 2016b ). Although the observed effect size of CBT was larger than the SSRIs and clomipramine, this superiority could well be attributed to the additive or synergistic effects of two effective treatment modalities. Therefore, it is not clear whether the efficacy data attributed to CBT with ERP can be generalized to patients who are not taking medication for OCD. The efficacy of CBT as monotherapy still needs to be established clearly in drug-naïve or drug-free patient population for it to be recommended as initial monotherapy in this population.

Some studies suggest that a combination of CBT and an SSRI may be superior to SSRI monotherapy ( Foa et al., 2005 ; Liu et al., 2005 ; Franklin et al., 2011 ; Romanelli et al., 2014 ; Meng et al., 2019 ), exposure monotherapy ( Cottraux et al., 1990 , Fineberg et al., 2018a ) or multimodal CBT ( Hohagen et al., 1998 ). However, it is uncertain whether combining ab-initio CBT and an SSRI is advantageous compared to either treatment used alone ( Albert et al., 2012 ). Confidence in the superiority of the combination of medications and psychotherapy partly stems from the fact that, as described above, most psychotherapy trials are considered variants of combination trials because most patients in these studies were stabilized on SSRI or clomipramine ( Skapinakis et al., 2016b ). Most guidelines and literature recommend a combination of SSRIs and CBT involving ERP in severe OCD, but the recommendation is based on evidence of its efficacy as an augmenting strategy in patients who have clinically significant symptoms despite treatment with medications and not necessarily in severe OCD ( Simpson et al., 2008 , 2013 ). A recent randomized feasibility study that included patients treated in primary care found that although combined treatment with SSRI and ERP was associated with the largest improvement after 16 weeks, SSRI monotherapy was the most efficacious and cost effective treatment after 52 weeks ( Fineberg et al., 2018b ). If replicated, this finding would carry major implications for health services planning, especially where resources are limited, such as lower and middle income countries.

The critical importance of adequate treatment of obsessive-compulsive disorder in children and young people

For children and young people, CBT should always be the first-line approach ( Sánchez-Meca et al., 2014 ; Skapinakis et al., 2016a ), with ERP as core elements ( Lewin et al., 2014 ). ERP is both highly effective and also an acceptable intervention for youth ages 3–8 years with OCD ( Lewin et al., 2014 ). Children with a strong family history of OCD are reported to respond less well to conventional CBT ( Garcia et al., 2010 ), possibly owing to family accommodation of their symptoms. Key adaptations for younger children include extensive parental involvement targeting family accommodation and frequent family meetings while delivering a full course of ERP. According to the study of Sánchez-Meca et al. (2014 ), effect sizes were large for CBT ( d + = 1.742) and combined (medication plus CBT) interventions ( d + = 1.710) and moderate for pharmacological only treatments ( d + = 0.746). Family-based CBT ( Piacentini et al., 2011 ; Freeman et al., 2014 ) is also effective for children and adolescents with OCD, especially when there is a high degree of accommodation. The extant literature also supports CBT when delivered in group settings. More recently, the use of technical devices (smart phones and tablets) using App-delivered CBT seems promising.

Medication is, however, indicated for children and young people when symptoms are more severe, CBT has failed, skilled CBT is unavailable, and there is a comorbid disorder (e.g., depression) that may respond to medication, or when, in the judgement of the parent or clinician, earlier introduction of medicines is clinically indicated. SSRIs have been shown in randomized controlled trials to be well tolerated and effective in youth ( Geller et al., 2004 ; Skarphedinsson et al., 2015 ). Sertraline and fluvoxamine have been approved for children from 6 to 8 years of age. Dosing schedules should include low starting doses, slow titration schedules and maximum recommended doses. Following adequate response and stabilization, treatment should be reviewed after 6–12 months.

In the case of nonresponse or inadequate response, another SSRI should be tried ( Geller et al., 2004 , 2012 ; Locher et al., 2017 ). Treatment with SSRIS in CBT-resistant patients may improve OCD symptoms. Although clomipramine may be effective, it is not recommended as a first-line treatment because of its potential side effects. However, if there are no cardiac contraindications, clomipramine* is also an option in youth but requires electrocardiogram monitoring. In the case of insufficient efficacy of drug treatment with several SSRIs and clomipramine, or in the presence of tic disorder, augmentation with antipsychotics, for example, aripiprazole* or risperidone* in low dosage may be used. Minimal duration on antipsychotics (these medications are not approved or indicated for paediatric use) is encouraged and close monitoring is required.

Relapse prevention

Relapse prevention strategies play an essential role for the optimal clinical management of OCD, considering its frequently chronic course and relapsing nature. Recovery occurs in only about one-fifth of adult cases, while for children, the mean persistence rates for full or subthreshold OCD have been estimated at around 60% ( Maina et al., 2001 ; Stewart et al., 2004 ). Earlier age of OCD onset, increased illness duration, inpatient status, the presence of comorbidities and a positive family history seem to predict greater rates of persistence ( Geller et al., 2003 ; Stewart et al., 2004 ). Furthermore, relapses in OCD are associated not only with considerable distress, significant functional impairment and impairment of quality of life ( Hollander et al., 2010 ) but also with a decreased response to a previous efficacious treatment ( Maina et al., 2001 ).

To date, relapse prevention studies in OCD have mainly investigated SSRIs and clomipramine as the maintenance treatment, with the duration of treatment under placebo-controlled conditions extending up to 12 months. Studies with a longer follow-up period or investigating relapse following CBT are relatively scarce. In the case of adults, the majority of relapse prevention studies have shown an overall superiority of SSRI compared with placebo in preventing relapse ( Fineberg et al., 2007 ) and that discontinuation of maintenance treatment, even after a period of prolonged well-being under SSRI, is associated with a heightened relapse risk. Relapse was particularly prominent in patients with comorbidities, which is the rule rather than the exception in children with OCD. As childhood and adolescence are critical periods for achievement of social, educational and occupational milestones, relapse prevention is particularly relevant for the younger patient population ( Fineberg et al., 2019 ). There has been one randomized controlled relapse prevention study in paediatric OCD, which showed an advantage for paroxetine* over placebo ( Geller et al., 2004 ). As there is no available evidence suggesting a duration of treatment beyond which treatment can be discontinued safely, more recent guidelines emphasized the importance of maintaining medication for at least 12 months to reduce relapse risk ( Baldwin et al., 2014 ).

The clinician’s role in enabling an informed choice about whether or not to discontinue medication at any particular time is challenging, considering the limitations of the available relapse prevention studies. Strategies for safely managing emerging relapse, such as reinstating either ‘booster’ CBT or medication at the first sign of symptoms, do not have established evidence of efficacy. Nevertheless, it is advisable to establish a relapse-management plan, in cooperation with patients and their families based on vigilance for emergent symptoms and rapid access to treatment previously known to be effective. If medication is to be discontinued, this should be done gradually, after a careful explanation of the potential consequences, such as withdrawal symptoms and relapse risk. SSRI tapering over a period of months, rather than weeks, may reduce the risk of withdrawal symptoms ( Horowitz and Taylor, 2019 ).

Treatment-resistant obsessive-compulsive disorder – novel pharmacotherapies tested in adults

After well supported first- and second-line treatments and strategies have been exhausted, some patients will continue to experience impairing OCD symptoms. Next-step treatment strategies may include continuing with the chosen SRI for an extended period of time, switching to another SRI, augmenting the SRI with a second-generation antipsychotic agent* or raising the dose of SRI to the highest tolerated level* ( Fineberg and Craig, 2007 ; Bandelow et al., 2008 ; Fineberg et al., 2012 ; Stein et al., 2012 ).

Although switching to another SRI often is recommended, there is little evidence to support this approach in OCD. When a partial or moderate response has been achieved following the adequate first-line treatment, there is randomized controlled trial (RCT) and meta-analytic evidence to support augmentation with an second-generation antipsychotic ( Brakoulias and Stockings, 2019 ; Dold et al., 2015 ; Stein et al., 2012 ; Zhou et al., 2019 ); however, the use of these agents would be considered off-label. Of these agents, risperidone* is supported by the greatest number of studies, which have generally been positive ( Brakoulias and Stockings, 2019 ). Two RCTs ( Muscatello et al., 2011 ; Sayyah et al., 2012 ), several open-label studies (Connor et al ., 2005; Pessina et al ., 2009; Ak et al ., 2011), and multiple case reports have demonstrated the efficacy in OCD of aripiprazole* as an augmentation agent (Matsunaga et al ., 2011; Higuma et al ., 2012; Hou and Lai, 2014; Ercan et al ., 2015; Akça and Yilmaz, 2016; Patra, 2016; Brakoulias and Stockings, 2019 ). One meta-analysis also found a larger effect size for aripiprazole than for risperidone: Cohen’s d = 1.11 (aripiprazole) versus d = 0.53 (risperidone) (Veale et al ., 2014). Quetiapine* has also been examined as an augmentation agent in OCD, but the evidence is conflicting. Despite several positive studies (Atmaca et al ., 2002; Denys et al ., 2004; Vulink et al ., 2010; Diniz et al ., 2011), negative results have been found in many placebo-controlled trials (Carey et al ., 2005; Kordon et al ., 2008; Fineberg et al ., 2013).

Contrary to the depression literature, a meta-analysis of SSRIs in OCD found that high doses (high end of recommended dosage, not higher than recommended doses) were more effective than medium or low doses in the first-line treatment of OCD ( Bloch et al., 2010 ). Response was more robust for patients with comorbid tics and in individuals who had received more than 12 weeks of maximal SSRI monotherapy ( Bloch et al., 2008 ). However, tolerability is a significant issue as compared with lower doses so that this strategy requires caution in primary care settings ( Stein et al., 2012 ). The Food and Drug Administration in the USA raised a safety warning in 2011 against citalopram doses higher than 40 mg/day due to a modest but probable risk of arrhythmias ( US Food and Drug Administration, 2012 ). However, a more recent meta-analysis identified only 18 cases where electrocardiogram QTc prolongation or torsades de pointes was associated with citalopram at doses between 20 and 60 mg/day. The authors concluded that these cardiac adverse events were infrequent ( Tampi et al., 2015 ).

When an inadequate treatment response persists, less well supported treatment strategies (lacking multiple randomized, controlled trials or meta-analyses) may be considered ( Koran et al., 2007 ; Koran and Simpson, 2013 ), including use of glutamate modulators*, d-amphetamine* or oral morphine sulfate*.

Glutamate modulators such as memantine*, riluzole*, topiramate*, lamotrigine*, N-acetylcysteine* and ketamine* have varying levels of support ( Koran et al., 2007 ; Pittenger et al., 2011 ; Koran and Simpson, 2013 ; Pittenger, 2015 ). Memantine augmentation showed benefit in case studies and open-label trials ( Poyurovsky et al., 2005 ; Pasquini and Biondi, 2006 ; Aboujaoude et al., 2009 ; Feusner et al., 2009 ; Stewart et al., 2010 ; Bakhla et al., 2013 ). In addition, two RCTs of memantine showed exceptionally high response rates (100% in one study), inconsistent with the literature ( Ghaleiha et al., 2013 ; Haghighi et al., 2013 ). Riluzole augmentation showed promise in a case series and open-label trial ( Coric et al., 2003 , 2005 ). Subsequent small controlled studies have been mixed ( Pittenger et al., 2008 ; Emamzadehfard et al., 2016 ). While topiramate augmentation showed promise in case studies and open-label trials ( Rubio et al., 2006 ; Van Ameringen et al., 2006 ; Van Ameringen and Patterson, 2015 ), small RCTs have also produced mixed results ( Mowla et al., 2010 ; Berlin et al., 2011 ; Afshar et al., 2014 ). Lamotrigine augmentation showed mixed results in case reports ( Kumar and Khanna, 2000 ; Uzun, 2010 ; Arrojo-Romero et al., 2013 ; Hussain et al., 2015 ) and benefits in two small RCTs ( Bruno et al., 2012 ; Khalkhali et al., 2016 ). Limited data suggest that N-acetylcysteine is of benefit in some cases of refractory OCD ( Lafleur et al., 2006 ), with mixed data in four RCTs ( Afshar et al., 2012 ; Sarris et al., 2015 ; Paydary et al., 2016 ; Costa et al., 2017 ). N-acetylcysteine is generally well tolerated. A single intravenous dose of ketamine has been reported to be of rapid (in hours) and robust benefit in unmedicated adults with OCD in case report and open-label studies ( Rodriguez et al., 2011 , 2016 ) and a randomized controlled cross-over study ( Rodriguez et al., 2013 ). In an open-label trial of medicated OCD adults with multiple comorbidities, depression improved on ketamine but improvement in OCD symptoms was minimal, and two patients developed new-onset irritability and suicidal ideation ( Bloch et al., 2012 ; Niciu et al., 2013 ). Experience with intranasal ketamine in OCD is very limited ( Adams et al., 2017 ; Rodriguez et al., 2017 ). Ketamine should only be administered at sites with expertise in this approach, with appropriate precautions including monitoring for side effects and screening individuals who have a current or past substance abuse problem ( Sanacora et al., 2017 ).

In two double-blind, placebo-controlled studies, d-amphetamine was superior to placebo in unmedicated OCD adults ( Insel et al., 1983 ; Joffe et al., 1991 ). A subsequent double-blind comparison of SSRI augmentation with d-amphetamine versus high-dose caffeine showed benefit of both drugs ( Koran et al., 2009 ). Oral morphine showed benefit in a case series ( Warneke, 1997 ) and in a double-blind crossover study ( Koran et al., 2005 ) in adults with OCD. Precautions should be taken in the case of both d-amphetamine and morphine to screen out individuals who have current or past substance abuse ( Koran et al., 2007 ).

Other drugs, such as pindolol*, clonazepam*, buspirone*, or lithium*, have been tested, but the results have been mixed and some of the placebo-controlled trials have not found positive results. Some promising results have been found with the 5HT3 antagonist ondansetron* ( Serata et al., 2015 ) and a clinical trial is currently underway ( ClinicalTrials.gov, 2017 ) though a double-blind placebo-controlled trial of low daily dosages of odansetron* (0.5 and 0.75 mg) in a relatively large sample was negative ( ClinicalTrials.gov, 2015 ).

Treatment-resistant obsessive-compulsive disorder – noninvasive neurostimulation

Noninvasive neuromodulatory interventions targeting the corticostriatothalamocortical (CSTC) circuits hold promise as augmenting intervention for treatment-resistant OCD ( Lusicic et al., 2018 ). Repetitive transcranial magnetic stimulation (rTMS)* is the best studied noninvasive modulatory intervention in OCD. rTMS delivered at low-frequency rTMS (≤1 Hz) (LF-rTMS) is thought to inhibit the activity of underlying cortical regions, while high-frequency rTMS, provided at ≥5 Hz, is thought to enhance cortical activity ( Lefaucheur et al., 2014 ). Conventional rTMS, provided through the figure-8 coil, is relatively focal, modulating superficial cortical regions over a depth of around 2 cm ( Lefaucheur et al., 2014 ). LF-rTMS* protocols targeting the supplementary motor area (SMA) have been found to be helpful for OCD in multiple RCTs and meta-analyses ( Mantovani et al., 2010 ; Gomes et al., 2012 ; Hawken et al., 2016 ; Zhou et al., 2017 ; Rehn et al., 2018 ). This effect has been found to last up to 3 months ( Gomes et al., 2012 ). A recent trial demonstrated superior efficacy of this protocol over antipsychotic augmentation in treatment-resistant OCD subjects ( Pallanti et al., 2016 ). However, given recent inconsistent reports on inhibitory rTMS protocols targeting the SMA ( Arumugham et al., 2018 ; Harika-Germaneau et al., 2019 ; Pelissolo et al., 2016 ), there is a need for large multicentre trials to confirm its efficacy at this location.

LF-rTMS targeting the orbitofrontal cortex (OFC)* has also shown promise in small RCTs ( Ruffini et al., 2009 ; Nauczyciel et al., 2014 ). There is a need for larger trials targeting the OFC to confirm its efficacy and tolerability. RCTs targeting the dorsolateral prefrontal cortex have, in contrast – and unlike in major depressive disorder – shown highly inconsistent findings in OCD ( Lusicic et al., 2018 ). A multisite randomized sham-controlled trial found high-frequency deep rTMS, using an H7 coil, over the dorsomedial prefrontal cortex/anterior cingulate cortex to be efficacious and well tolerated in a treatment resistant OCD population ( Carmi et al., 2019 ). This FDA approval and CE (Conformité Européene) certification device for the treatment of resistant OCD. However, considering the cost of this device, there is a need for replication studies confirming the efficacy of the above protocol, which included personalized symptom provocation as an interventional component. Less-expensive deep coils, which have shown promise in targeting the dorsomedial prefrontal cortex in open-label trials on OCD ( Modirrousta et al., 2015 ; Dunlop et al., 2016 ), are yet to be evaluated under controlled conditions.

Transcranial direct current stimulation (tDCS)* involves administration of low-amplitude (1–2 mA) electric current to the brain between a cathode and anode. Anodal tDCS is thought to enhance cortical excitability and cathodal tDCS to have an inhibitory effect ( Rachid, 2019 ). The SMA and OFC are key targets. A randomized sham-controlled trial ( n = 24 treatment-resistant OCD subjects) demonstrated efficacy for anodal tDCS administered over bilateral pre-SMA and cathodal tDCS over right supraorbital regions ( Gowda et al., 2019 ). However, another randomized crossover trial ( n = 12) found clinical improvement with cathodal tDCS over pre-SMA, while anodal tDCS was ineffective ( D’urso et al., 2016 ). Thus, replication studies are needed to determine the optimal stimulation protocol for tDCS over SMA in OCD*. Another randomized sham-controlled trial ( n = 21 treatment-resistant OCD patients) showed efficacy for cathodal tDCS delivered over the OFC and the anode over the right cerebellum, but the effect was not sustained at follow-up ( Bation et al., 2019 ). Other promising results in treatment-resistant OCD for protocols targeting OFC and other cortical regions, such as dorsolateral prefrontal cortex and dorsomedial prefrontal cortex, are found in case reports and small uncontrolled studies and have to be confirmed in well designed trials ( Brunelin et al., 2018 ; Rachid, 2019 ). Furthermore, studies present significant heterogeneity and methodological differences in sample selection criteria, concomitant treatment and tDCS stimulation protocols ( da Silva et al., 2019 ; Rachid, 2019 ). Some authors suggest that overall cathodal tDCS may be better than anodal in treating OCD ( Rapinesi et al., 2019 ).

Currently, there are no RCTs to support the efficacy of electroconvulsive therapy* (ECT) in OCD ( Fontenelle et al., 2015 ). Hence, ECT may be recommended only for acute treatment of comorbid conditions such as depression or psychosis*.

To summarize, LF-rTMS delivered over the SMA (with figure-8 coil) and HF-deep-rTMS over the dorsomedial prefrontal cortex/anterior cingulate cortex (with H7 coil) appear promising interventions in treatment-resistant OCD. There is a pressing need for large replication studies and evaluation of long-term effects/maintenance protocols. The evidence for tDCS is highly preliminary and further exploratory studies are encouraged.

Treatment-resistant obsessive-compulsive disorder – deep brain stimulation and ablative neurosurgery

A significant number (10–40%) of patients do not respond to any available therapy and suffer from severe, enduring symptoms and dysfunction ( Fineberg and Gale, 2005 ; Denys, 2006 ; Gupta et al., 2019 ). For this highly refractory patient group, ablative neurosurgery* and deep brain stimulation* (DBS) remain modalities to be considered. These procedures are usually delivered as an adjunct to existing pharmacological treatments, and CBT is frequently also administered, either during the acute treatment phase or follow-up. DBS is considered an experimental treatment, but has an FDA ‘humanitarian device exemption’ for severe refractory OCD ( US Food and Drug Administration, 2009 ).

Stereotactic neurosurgical procedures for intractable OCD have been available for >50 years ( Miguel et al., 2019 ). The procedures include dorsal anterior cingulotomy and anterior capsulotomy and are reserved for the most severe, treatment nonresponsive patients. A systematic review involving 10 studies and 193 participants suggested both procedures were efficacious ( Brown et al., 2016 ). The authors reported a mean Y-BOCS reduction of 37% for cingulotomy and 57% for capsulotomy. The rates of serious or permanent adverse events were 5.2% in the cingulotomy studies and 21.4% in the capsulotomy studies. Another recent review of publications on anterior capsulotomy spanning over five decades ( Pepper et al., 2019 ) reported ‘significant clinical response’ in 73–90% of patients and ‘remission’ in 24–39% of patients with treatment-resistant OCD.

DBS was investigated as a partially reversible alternative to surgical ablation ( Nuttin et al., 1999 ). The original stimulation target was similar to the site of anterior capsulotomy, that is, ventral capsule/ventral striatum (VC/VS). Three reasonably sized studies have provided evidence in favour of the acute efficacy of DBS in the VC/VS. The first involved 24 patients who were followed up to four years and reported a 37% median improvement in baseline Y-BOCS scores ( Luyten et al., 2016 ). ‘ON’ phases of stimulation were compared with ‘OFF’ phases (no stimulation), demonstrating that improvements were unlikely to represent ‘placebo’ effects. The second study investigated 16 patients, initially as open label, reporting a 46% reduction in baseline Y-BOCS at 8 months as well as a significant difference (25%) in Y-BOCS scores when compared with sham stimulation in a subsequent month-long double-blind phase ( Denys et al., 2010 ). A recent 12-month multicentre study of 30 patients given VC/VS DBS ( Menchón et al., 2019 ) reported a mean reduction of baseline Y-BOCS of 42%. Sixty percent of patients were responded (reduction in baseline Y-BOCS > 40%).

The long-term benefits of VC/VS DBS are less certain. An open-label follow up study of 10 patients ( Greenberg et al., 2006 ) reported a reduction in mean Y-BOCS from 34.67 at baseline (severe) to 22.37 (moderate) at 36 months. In addition, significant improvements in global functioning, depression and anxiety persisted.

The anteromedial subthalamic nucleus (amSTN) has been identified as another promising target for DBS in OCD. Sixteen patients were randomized according to a crossover design to either 3 months active or sham treatment, resulting in a significantly greater reduction in mean Y-BOCS in the stimulation versus sham group (endpoint 19 ± 8 versus 28 ± 7) ( Mallet et al., 2008 ). It remains unclear whether VC/VS holds any advantage over amSTN DBS. A recent ‘mechanism of effect’ study of six OCD patients, in which electrodes were implanted in both these sites, found differential improvements in mood (VC/VS) and cognitive flexibility (amSTN), suggesting that DBS exerts therapeutic effects at these targets via different brain networks ( Tyagi et al., 2019 ).

There have been no head-to-head trials comparing ablative neurosurgery with DBS. A recent review ( Pepper et al., 2015 ) retrospectively evaluated 20 studies of varying methodological quality involving 62 patients who underwent DBS of the VC/VS or the nucleus accumbens and 108 patients who underwent anterior capsulotomy. The capsulotomy group showed a significantly higher (51%) mean reduction in Y-BOCS than the DBS group (40%). No difference in surgical complication rates was observed. Adverse events across both modalities included intracranial haemorrhage (2–5%), persisting postoperative side effects (5–7%), cognitive and personality changes (7–13%) and suicide (1–2%). Weight gain (defined by an increase >10%) was significantly higher in the capsulotomy group (29 versus 3%). In other studies ( Mallet et al., 2008 ; Menchón et al., 2019 ), hypomania after electrode implantation is commonly (6%) reported.

In summary, studies of both DBS and ablative neurosurgery have shown these techniques are clinically effective for this highly refractory and extremely chronically disabled patient group. However, there is as yet insufficient evidence to determine which technique to choose at an individual patient level. Further clarification of the differential effects of ablation and stimulation across the different candidate neural targets, as well as better understanding of the interaction between somatic, pharmacological and psychological interventions, have the potential to advance the field towards a personalized approach. Agreement over standardized patient selection and treatment protocols that would allow clinical outcomes data to be collected and compared across treatment centres, represents an achievable milestone towards this goal ( Menchón et al., 2019 ). Meanwhile, technological innovations, for example, MRI-guided focussed ultrasound, laser interstitial thermal therapy ( Miguel et al., 2019 ), offer potential for safer and more cost-effective surgical approaches.

Future directions for research

Problematic usage of the internet.

Problematic use of the internet (PUI) is an umbrella term for a range of repetitive functionally impairing compulsive behaviours including gambling, gaming, sexual behaviour, shopping, video-streaming or social media use. While advances have been made in defining diagnostic criteria and developing rating scales for some forms of PUI (e.g., Gaming Disorder) ( Király et al., 2015 ), a considerable amount of research is needed to understand better the broad range of PUI phenomena and translate the known behavioural phenotypes into valid and reliable diagnostic criteria and assessment tools, to facilitate the systematic investigation of aetiological factors and brain-based mechanisms, as a platform for the development of preventive and therapeutic interventions ( Fineberg et al., 2018c ).

Significant cross-sectional associations between PUI and OCD symptoms have been found ( Carli et al., 2013 ). For example, in a two-site international online survey, ADHD and social anxiety disorder were associated with high PUI scores in young participants, whereas OCD and generalized anxiety disorder were associated with high PUI scores in older participants ( Ioannidis et al., 2018 ).

Novel digital interventions in obsessive-compulsive disorder

Digital technology offers new opportunities for monitoring and interventions. The extensive use of smartphones and the vast amounts of information they contain has positioned them as a proxy for behavioural and social interactions ( WHO, 2016 ). Harnessing smartphone technology along with smart wearables (e.g., smart watches) is expected to be a valuable source of continuous, objective and reliable data for clinical characterization, behavioural monitoring and treatment support ( Marzano et al., 2015 ). This is true for several disorders, but especially true for obsessive-compulsive problems such as PUI, as the digital media that is directly linked to the disorder is the same one that can accurately monitor the behaviour ( Ferreri et al., 2019 ).

Accordingly, using digital technology along with big data analyses may enable the potential to characterize the ‘digital phenotype’ of the disorder ( Ferreri et al., 2019 ) and to identify those individuals most at risk (e.g., by monitoring online internet usage in comparison with changes in diurnal variation, lack of human contact, lack of geographical movement, restricted circles of friends, etc.). A research avenue in this direction is to use (real time) big data analysis, alongside machine learning algorithms, to establish identifiable OCRD-specific illness patterns and use those real-time results to create an immediate feedback loop with the patient, which could then be used therapeutically by providing direct feedback on their behaviour and progress.

Other forms of active online intervention have become increasingly available for OCRD ( Whiteside et al., 2013 ) and may potentially enhance and facilitate treatment adherence ( Andersson et al., 2014 ; Marzano et al., 2015 ). For example, WhatsApp group interventions, in which the patient reports to their clinician, in real time, their difficulties, daily achievement and progress, enable continual communication, real-time reporting, prompt responses and rapid intervention when needed. In addition, the digital intervention may serve as a platform for continuous monitoring of tasks delivered in face-to-face meetings. Another example of existing digital interventions is the proactive use of webcams and smartphone cameras. Using this domain and with patient’s consent, the clinician has the opportunity to monitor patients in their natural environment. As the digital platform bridges the elapsed time between therapeutic sessions, it overcomes geographical distances and enables therapeutic practice in the patient’s natural environment ( WHO, 2016 ), where symptoms are manifested daily. In addition to enriching the clinical picture by direct observation of symptoms, it confers the general assertive outreach benefits of telemedicine, which can be critical for otherwise difficult to treat socially isolated patients who cannot access help otherwise.

In practice, this approach breaks down the traditional terminology of ‘outpatient’, ‘in-patient’ and ‘day hospitalization’, by allowing real time, objective and continuous monitoring ( WHO, 2016 ). The combination of digital monitoring and online communication produces a form of ‘virtual hospitalization’, enabling comprehensive and intensive treatment by offering continued monitoring and delivery of therapy in the patient’s natural environment, where the OCD usually occurs, and not within the artificial setting of the clinic. While such approaches are still under development, digital tools seem to bear great potential and may change the landscape of treatment in OCRDs, providing potentially cost-effective alternatives to hospitalization or outpatient clinics.

Immunological therapies

Inflammation and release of inflammatory cytokines affect brain circuitry involving both reward and threat-sensitivity, producing potentially adaptive and beneficial behavioural responses ( Raison and Miller, 2013 ). There is growing evidence of dysfunctional immunological function in the pathogenesis of a significant subset of OCD patients. Elevated levels of basal ganglia antibodies have been detected in adult OCD patients’ plasma compared with psychiatric control groups ( Nicholson et al., 2012 ). In addition, significantly increased levels of CSF autoantibodies directed against basal ganglia and thalamus were found among drug-naive OCD patients, and were associated with increased levels of CSF glutamate and glycine, indicating underpinning abnormalities in excitatory neurotransmission and correlating with hyperactivity in the ventral cognitive circuit ( Bhattacharyya et al., 2009 ). Translocator protein distribution volume, a marker of the microglial component of neuroinflammation, was found to be significantly elevated in the CSTC circuit of OCD subjects compared with healthy controls, demonstrating inflammation within the neurocircuitry extending beyond the basal ganglia, and affecting the adult population rather than solely childhood OCD ( Attwells et al., 2017 ).

A common genetic link may explain an excess of some autoimmune comorbidities. For example, in the acute paediatric onset subset of children (PANDAS), there is immunological cross-reactivity with epitopes associated with streptococcal infection expressed on the surface of basal ganglia neurons. About 20% of the mothers of children fulfilling criteria for PANDAS ( Chang et al., 2015 ) had at least one autoimmune disease. Multigenerational studies also show that OCD patients’ relatives are more likely to have an autoimmune disease such as Sjögren’s syndrome, coeliac disease, Guillian Barrè, Crohn’s disease, Hashimotos Thyroiditis, type I diabetes mellitus, ulcerative colitis, multiple sclerosis and psoriasis vulgaris ( Mataix-Cols et al., 2018 ). A subset of patients with PANDAS with motor symptoms demonstrated antineural antibodies against dopamine (D1) receptors as well as elevated antibodies against tubulin, lysoganglioside and higher activation of calmodulin-dependent protein kinase II (Cox et al ., 2015).

Immunomodulatory therapy represents a new field of investigation in OCD. While treatment with antimicrobials has delivered inconsistent results ( Burchi and Pallanti, 2018 ), other immunological modulators, such as celecoxib* ( Shalbafan et al., 2015 ) and nonspecific nonsteroidal anti-inflammatory drugs ( Spartz et al., 2017 ), have produced some positive findings, the latter only in a subset of young people. Thus, evidence of the usefulness of this approach in OCD remains insufficient. Nevertheless, researchers and clinicians should consider genetic and immunological profile differences in the search for precise individualized therapy for OCD.

Novel forms of psychotherapy

Although it may seem logical to try to tackle OCD using cognitive therapy, little evidence suggests that it offers any advantage to graded exposure and self-imposed response prevention ( Tyagi et al., 2010 ; Ougrin, 2011). Poorly applied cognitive therapy, such as that expecting patients to re-evaluate actual dangers, may make some patients with OCD worse. This is because the process of looking for evidence to confirm or refute the obsessions can become incorporated into rituals. Cognitive therapy may also turn out to be less cost-efficient, as it requires more training and supervision for the therapist and usually takes more time in therapy. It is therefore probably best used in situations where there is OCD refractory to ERP therapy ( Drummond and Edwards, 2018 ).

Rational emotive therapy, on the other hand, has been shown to have some possible beneficial effects in OCD ( Emmelkamp et al., 1988 ). Australian researchers have developed danger ideation reduction therapy (DIRT), using rational emotive therapy but with instructions not to undergo exposure for patients with contamination fears; good outcomes in case reports and some small controlled trials have been found ( Jones and Menzies, 1998 ; Krochmalik et al., 2001 ; Maqbool et al., 2017 ). The techniques used in DIRT include cognitive restructuring using rational emotive therapy ( Ellis, 1962 ); filmed interviews with people who work in feared situations; corrective information about the real risks of ‘contamination’ as opposed to the deleterious effects of overzealous hand-washing and attentional focussing whereby patients are taught to focus the mind away from the danger-related intrusive thoughts.

In recent years, the so-called Third Wave Therapies have been used in a number of psychiatric conditions ( Pérez Álvarez, 2012 ). The therapy of this type most commonly used in OCD is mindfulness, which teaches an individual to focus on the world around them rather than their internal dialogue. A recent study demonstrated that both cognitive restructuring and also mindfulness led to a small improvement in Y-BOCS score when compared with waiting list controls. However, the strength of efficacy for both treatments appeared to be less than that generally found with ERP ( Rupp et al., 2019 ). Despite promising results for metacognitive therapy in patients with OCD in case series, a full controlled trial has yet to be performed ( Melchior et al., 2019 ).

Many OCD patients describe their compulsions as habitual, that is, fixed ‘stimulus-response ’acts that, through habit learning, occur automatically in response to a specific environmental trigger. Habit reversal therapy (HRT) ( Azrin and Nunn, 1973 ) is a long-established form of therapy that helps patients alter habitual performance through a variety of behavioural methods. HRT is reported to be efficacious for the treatment of Tourette syndrome and Tic Disorders and has more recently been applied with success in OCRDs such as trichotillomania and skin picking behaviours. However, there remains a scarcity of evidence from controlled trials to support the efficacy of HRT in OCRDs in general and OCD in particular (Lee et al ., 2019a). Emerging neurosciences evidence identifying faulty habit learning in OCD (Fineberg et al ., 2018a) suggests further study of HRT in OCD would be worthwhile.

Pharmacogenetics

Pharmacogenetics or pharmacogenomics define genetic variants that influence either drug metabolism, delivery, affinity to receptors or transporters may contribute to the prediction of drug efficacy or toxicity, promoting precision medicine (Hess et al ., 2015). Because approximately one-quarter of OCD patients do not respond to treatment with either SSRIs or CBT alone, or their combination ( Hirschtritt et al., 2017 ), it has been suggested that pharmacogenetics may contribute to better drug-response prediction and side effect tolerance ( Zai et al., 2014 ).

Currently, several pharmacogenetic approaches using hypothesis-free GWAS have been conducted into the association between candidate genes and drug response in OCD patients ( Di Bella et al., 2002 ; Denys et al., 2007 ; Van Nieuwerburgh et al., 2009 ; Miguita et al., 2011 ; Grünblatt et al., 2014 ; Zai et al., 2014 ; Umehara et al., 2015 ; Mas et al., 2016 ; Qin et al., 2016 ; Umehara et al., 2016 ; Taj et al ., 2018; Lisoway et al., 2018 ; Sina et al., 2018 ; Abdolhosseinzadeh et al., 2019a , b ; Alizadeh et al., 2019 ). The candidate genes investigated belong to: (1) pharmacokinetic regulating genes, such as the CYP450 liver enzymes such as CYP2D6 and CYP2C19; (2) serotonergic systems, such as SLC6A4 and its promoter, HTTLPR, HTR2A, HTR2C, HTR1B and TPH2; (3) glutamatergic systems, such as SLC1A1, DLGAP2, DLGAP2, GRIN2B, GRIK2, SLIT, SLITRK5; (4) dopaminergic systems, such as COMT, MAOA, DRD2 and DRD4 and (5) other systems, such as BDNF, NTRK3, MOG, OLIG2 and DISP1.

Currently, no consensus with sufficiently robust results exists in the pharmacogenetics of OCD, due to the fact that many studies used naturalistic approaches, did not employ double blinded designs or crossed over with the tested drug, used a variety of drugs and doses, as well as used various cutoffs and measures determining response. Although there is still a need systematically to assess the pharmacogenetic link between treatment response (to SSRIs, tricyclics, antipsychotics, clomipramine, etc.) and certain genes, some data are already available, though very limited, on the Internet (e.g., https://www.pharmgkb.org ; Whirl-Carrillo et al., 2012 ) summarizing some findings on pharmacogenetics of some drugs and giving some recommendations aligning with those of the FDA, European Medicine Agency, Pharmaceutical and Medical Devices Agency, Japan and Health Canada (Sante Canada).

Until just 40 years ago, OCD was considered rare, of psychological origin and without effective treatment. Now, all have changed; the finding in the 1970s and 1980s that serotonergic medication (clomipramine, followed by SSRIs) was effective ( Montgomery, 1980 ; Zohar et al., 1987 ; Zohar and Insel, 1987 ) opened the door to great interest in OCD ( Zohar, 2012 ). This led to the development of specific forms of psychological intervention (ERP) which replaced the dynamic approach and to a focus on the serotonergic system in the treatment and pathophysiology of OCD. As a result of neuroscience insights including endophenotype-based approaches (reviewed in Fineberg et al., 2018a ), OCD has been removed from the anxiety disorder grouping in the DSM-5 ( American Psychiatric Association, 2013 ) and ICD-11 ( WHO, 2018 ) and now stands at the head of a new family of OCRDs.

The realization that OCRDs as a group are different from other anxiety disorders has led to significant changes in understanding their impact (the prevalence of OCRD in the population is more than 9%) ( Carmi et al., 2019 , in submission) and to refinement of the treatment approach (e.g., focussing on the urge to perform compulsions and the need for higher doses of serotonergic medication).

This position statement highlights the major changes that have been taking place in the last few years in the field of OCD, in terms of conceptualization, diagnosis, assessment, intervention (with focus on early intervention), strategies for optimizing the efficacy of specific pharmacological intervention (SRI) with specific psychological intervention (ERP), the critical role of treatment of children and young adults and the importance of maintenance of well-being.

As new neuroscience insights are revealed, new therapeutic interventions are being explored (e.g., glutamatergic agents, dopaminergic modulators, etc.). This position statement also covers invasive and noninvasive neuromodulation as experimental interventions, including deep TMS (achieving FDA indication for OCD in 2018) ( US Food and Drug Administration, 2018 ).

Looking to the future, other exciting avenues for investigation include the use of digital tools to monitor (and eventually to diagnose OCRDs), better understanding of links between excessive Internet use and OCRDs, advanced genetic methods and new pharmacological domains (e.g., immunological systems). Indeed, it seems that the future was never so bright for OCRD patients. We trust that this position statement has managed to capture, describe, explain and shed light on many of these developments, including those in the front line of understanding and treatment of OCRD in the future.

Acknowledgements

The authors wish to acknowledge the members of the International College of Obsessive-Compulsive Disorders ( www.ICOCS.org ), who have contributed to the development of this article. With particular thanks for critically reviewing the statement and editing the manuscript, to Rajshekhar Bipeta, Julius Burkauskas, Artemisa Dores, Giacomo Grassi, Donatella Marazziti, Pedro Morgado and Humberto Nicolini. We grateful to the European College of Neuropsychopharmacology (ECNP) Obsessive-Compulsive and Related Disorders Research Network (OCRN) for providing monetary support for the open access article processing charges for this article. We are also grateful to the ECNP OCRN, American College of Neuropsychopharmacology and the World Psychiatric Association Scientific Section for Anxiety and Obsessive-Compulsive and Related Disorders, for providing networking support.

This article refers to studies funded by the National Institute for Health Research (NIHR) RFPB (Grant Reference Number PB-PG-0712-28044, NIHR RfPB PB-PG-1216-20005). The views expressed are those of the authors and not necessarily those of the NIHR or the Department of Health and Social Care.

N.A.F. was supported by a COST Action Grant (CA16207; European Network for Problematic Usage of the Internet; European Cooperation in Science and Technology; www.cost.eu .) and a NIHR grant [NIHR RfPB PB-PG-1216-20005; FEasibility and Acceptability of Transcranial Stimulation in Obsessive-Compulsive Symptoms (FEATSOCS)]. S.R.C. was supported by a Wellcome Trust Clinical Fellowship. E.H. was funded by DOD, and OPD-FDA. E.G. was funded by the University of Zurich.

All authors were involved in drafting the manuscript and agreed to its publication. All authors read and approved their sections of the final version of the manuscript.

Conflicts of interest

N.A.F. declares that in the past 3 years, she had held research or networking grants from the ECNP, UK NIHR, EU H2020, MRC, University of Hertfordshire. In the past 3 years, she had either accepted travel or hospitality expenses or both from the BAP, ECNP, RCPsych, CINP, International Forum of Mood and Anxiety Disorders, World Psychiatric Association and Indian Association for Biological Psychiatry. In the past 3 years, she had received payment from Taylor and Francis and Elsevier for editorial duties. In the past 3 years, she had accepted a paid speaking engagement in a webinar sponsored by Abbott. Previously, she had accepted paid speaking engagements in various industry supported symposia and have recruited patients for various industry-sponsored studies in the field of OCD treatment. She leads an NHS treatment service for OCD. She holds Board membership for various registered charities linked to OCD. She gives expert advice on psychopharmacology to the UK MHRA and NICE. S.W. has received royalties from Thieme, Hogrefe, Kohlhammer, Springer, Beltz in the last 5 years. Her work was supported by the Swiss National Science Foundation (SNF), diff. EU FP7s, HSM Hochspezialisierte Medizin of the Kanton Zurich, Switzerland, Bfarm Germany, ZInEP, Hartmann Müller Stiftung, Olga Mayenfisch, Gertrud Thalmann and Vontobel Fonds in the last 5 years. She received no honoraria from pharmaceutical or other industrial companies in the last 36 months. Outside professional activities and interests are declared under the link of the University of Zurich, https://www.uzh.ch/prof/ssl-dir/interessenbindungen/client/web . V.B. has received lecture honoraria from Lundbeck and Otsuka. V.B. is a clinical investigator in a clinical trial funded by Boeringher Ingelheim and has obtained competitive grant funding from a Pfizer Neuroscience Grant, the Nepean Medical Research Foundation, the University of Sydney, Western Sydney University, Western Sydney Local Health District and the Better Foundation. C.I.R. has served as a consultant for Allergan, BlackThorn Therapeutics, Rugen Therapeutics and Epiodyne, receives research grant support from Biohaven Inc. and a stipend from APA Publishing for her role as Deputy Editor at The American Journal of Psychiatry . J.M.M. has received honoraria and travel grants from Exeltis, Janssen, Servier, AbBiotics and Medtronic in the last 36 months. B.M.D. has received lecture honoraria from Lundbeck, Angelini, Janssen, Neuraxpharma, Arcapharma and Livanova. Y.C.J.R. has received grants from the Department of Biotechnology (DBT) and the Indian Council of Medical Research (ICMR) of the Government of India and is currently involved in a study funded by the National Institute of Mental Health (NIMH), USA. Y.C.J.R. is the lead author of the Indian Psychiatric Society (IPS) Clinical Practice Guidelines for Obsessive-Compulsive Disorder and is also the lead author of the Clinical Practice Guidelines for Cognitive Behaviour Therapies in Anxiety Disorders and Obsessive-Compulsive Related Disorders (in press). D.J.S. has received either research grants or consultancy honoraria from Lundbeck and Sun or both. S.P. declares funding from the National Institute of Mental Health, USA; R21 NCTID NCT03669315. J.Z. received grants and research support from Lundbeck, Servier, Brainsway, Pfizer and the DOD, honoraria and consultation fees from Lundbeck, Roche, Lilly, Servier, Pfizer. S.R.C. consults for Promentis and Ieso Digital Health. S.S.A. has received research funding grant from the Wellcome Trust-DBT India alliance and Indian Council of Medical Research. M.V.A. reports being on the Advisory Boards of Allergan, Almatica, Brainsway, Janssen, Lundbeck, Myriad Neuroscience, Otsuka and Purdue Pharma (Canada); M.V.A. is on the Speaker’s Bureau for Allergan, Lundbeck, Otsuka, Pfizer, Purdue Pharma (Canada) and Takeda; and has received research support from Janssen, Purdue Pharma (Canada), the Canadian Foundation for Innovation and Hamilton Academic Health Sciences Organization (HAHSO). D.A.M.D.G. has received grant or research support from the Eunice Kennedy Shriver National Institute of Child Health and Human Development subcontract with Duke Clinical Research Center Pediatric Trials Network, Biohaven Pharmaceuticals, Neurocrine Biosciences, Nuvelution Pharma, Peace of Mind Foundation, Syneos Health and Teva Pharmaceutical Industries. He has served as a consultant to the Arlington Youth Counseling Center. He has served on the editorial board of Annals of Clinical Psychiatry . He has received honoraria from the Massachusetts Psychiatry Academy and the American Academy of Child and Adolescent Psychiatry. He has held stock options/ownership in Assurex Health and Revolutionary Road. R.G.G.S. receives a productivity grant from the National Council for Scientific and Technological Development, Brazilian Federal Government (CNPq). L.D. declares that she holds small investments in pharmaceutical and biotechnology firms, including AstraZeneca, Bioventic, Hikma Pharmaceutical, International Biotech Trust, Reneuron, Syncona and Yourgene. U.A. has received lecture honoraria from Lundbeck, Angelini, Janssen, Neuraxpharma and Innova Pharma. There are no conflicts of interest for the remaining authors.

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Advances in the diagnosis and treatment of obsessive-compulsive disorder (OCD) and OCD related disorders

Obsessive-compulsive disorder, commonly referred to as OCD, is a chronic condition characterised by recurrent persistent thoughts which usually co-occur with repetitive compulsive behaviour. Individuals with OCD or OCD related disorders (e.g. body dysmorphic disorder, hoarding disorder, trichotillomania, excoriation, hypochondria, and olfactory reference syndrome) typically show distress, which often affects their daily functioning and well-being. Even though several treatments for OCD are available, the presence of several psychiatric comorbidities in this population makes its diagnosis and management particularly challenging.

This Collection welcomes original research articles investigating recent advances in the diagnosis and treatment of OCD and OCD related disorders. Intervention studies are also welcome.

Ioannis Angelakis BSc, MSc, PgDip, PhD, BCBA, FHEA

University of Liverpool, UK

Pedro Morgado, PhD

University of Minho, Portugal

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Obsessive-Compulsive Disorder : Advances in Diagnosis and Treatment

• 1 Department of Psychiatry, University of California, San Francisco
• 2 Department of Psychiatry and Yale Child Study Center, Yale University School of Medicine, New Haven, Connecticut
• 3 Department of Psychiatry and University of Florida Genetics Institute, Gainesville
• Comment & Response Deep Brain Stimulation for Obsessive-Compulsive Disorder Sina Kohl, PhD; Jens Kuhn, MD JAMA
• Comment & Response Deep Brain Stimulation for Obsessive-Compulsive Disorder—Reply Matthew E. Hirschtritt, MD, MPH; Michael H. Bloch, MD, MS; Carol A. Mathews, MD JAMA

Question   What advances in screening, diagnosis, and management of adult obsessive-compulsive disorder (OCD) have been introduced in the past 5 years?

Findings   In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition , OCD is now defined separately from anxiety disorders and there is an increased emphasis on the role of or relationships to comorbid tics, hoarding, and poor insight. There is growing support for novel dissemination methods for behavioral interventions (eg, online-based therapy), pharmacologic approaches (eg, neuroleptic augmentation of antidepressants), and neuromodulation (eg, deep-brain stimulation).

Meaning   More accurate screening, precise diagnosis and formulation, and empirically supported treatments may lead to improved prognosis for adults with OCD.

Importance   Obsessive-compulsive disorder (OCD) is a neuropsychiatric disorder associated with significant impairment and a lifetime prevalence of 1% to 3%; however, it is often missed in primary care settings and frequently undertreated.

Objective   To review the most current data regarding screening, diagnosis, and treatment options for OCD.

Evidence Review   We searched PubMed, EMBASE, and PsycINFO to identify randomized controlled trials (RCTs), meta-analyses, and systematic reviews that addressed screening and diagnostic and treatment approaches for OCD among adults (≥18 years), published between January 1, 2011, and September 30, 2016. We subsequently searched references of retrieved articles for additional reports. Meta-analyses and systematic reviews were prioritized; case series and reports were included only for interventions for which RCTs were not available.

Findings   Among 792 unique articles identified, 27 (11 RCTs, 11 systematic reviews or meta-analyses, and 5 reviews/guidelines) were selected for this review. The diagnosis of OCD was revised for the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition , which addresses OCD separately from anxiety disorders and contains specifiers to delineate the presence of tics and degree of insight. Treatment advances include increasing evidence to support the efficacy of online-based dissemination of cognitive behavioral therapies, which have demonstrated clinically significant decreases in OCD symptoms when conducted by trained therapists. Current evidence continues to support the use of selective serotonin reuptake inhibitors as first-line pharmacologic interventions for OCD; however, more recent data support the adjunctive use of neuroleptics, deep-brain stimulation, and neurosurgical ablation for treatment-resistant OCD. Preliminary data suggest safety of other agents (eg, riluzole, ketamine, memantine, N -acetylcysteine, lamotrigine, celecoxib, ondansetron) either in combination with selective serotonin reuptake inhibitors or as monotherapy in the treatment of OCD, although their efficacy has not yet been established.

Conclusions and Relevance   The dissemination of computer-based cognitive behavioral therapy and improved evidence supporting it represent a major advancement in treatment of OCD. Although cognitive behavioral therapy with or without selective serotonin reuptake inhibitors remains a preferred initial treatment strategy, increasing evidence that supports the safety and efficacy of neuroleptics and neuromodulatory approaches in treatment-resistant cases provides alternatives for patients whose condition does not respond to first-line interventions.

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Hirschtritt ME , Bloch MH , Mathews CA. Obsessive-Compulsive Disorder : Advances in Diagnosis and Treatment . JAMA. 2017;317(13):1358–1367. doi:10.1001/jama.2017.2200

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My OCD Story: Chapter 6 & Conclusion

Posted April 13, 2021

PLEASE NOTE: The following blog post contains discussion of topics that may be upsetting, including suicide. Please take care of yourself as you read this article. If you are in crisis, know that help is only a call or click away at 1-800-273-8255 or  suicidepreventionlifeline.org .

Chapter 6: Life after treatment 

Several years after extensive treatment, here I am about to graduate college. I was able to take acting classes and improve myself as an actor. I was in many plays and musicals during my time in college. I made connections with my peers and with my professors. I was able to study abroad for a summer in Barcelona. I tried new foods and explored Europe. I now live on my own in an apartment with my friends. I cook meals for myself every day. I have the most wonderful friends who are supportive and kind. I work at a toy store down the street from my apartment. I love to do art and my bedroom is covered with my imperfect paintings and drawings. I love to write stories and plays and I share them with my teachers and with my friends. I can finally say that I am living a happy life. These are all things I never thought I would ever be able to do because of how OCD had taken over my life. 

Of course, I still have challenges in regards to my OCD. Occasionally my OCD will slip into my school work. I often have to challenge myself to do things imperfectly instead of striving for perfection that will never be. I still have a hard time eating from time to time. Trying new food is hard, though I can usually get myself to do it. Washing dishes in my apartment can sometimes be a challenge. I sometimes will feel insecure in my friendships and will compulsively ask for reassurance that everything is still okay. 

Despite these challenges, I can gladly say that OCD does not impede on my ability to function. I now consider myself to have mild OCD, where at one point it was considered to be extremely severe. I never thought I would be in a place in my life where OCD wasn’t always on the forefront of my mind, but these days it doesn’t come up much at all. 

Before treatment, I was always secretive about my struggles with mental health. I felt ashamed and never wanted anyone to know what I was dealing with. When it was time for me to go back to school, I knew that people would have questions about where I had been for the past few months. My therapists at the program told me that I should have an answer prepared for these questions. They told me it was completely up to me how much I wanted to tell people or if I even wanted to tell people at all. I spent a long time thinking about what I wanted to tell people. I practiced answering the questions in the mirror before bed. I ultimately decided that the telling the truth would be the easiest route. I didn’t want to hide what I was going through anymore. After going through treatment, I didn’t have nearly as much shame surrounding my OCD. I knew that it didn’t define me. I also knew that the lack of education available about OCD was the reason why there were so many misconceptions about it. I decided that I was going to be an advocate for myself and for the other people in the OCD community by being open and honest about my experiences. 

The first person I ended up telling was a girl in my tutoring group. She asked me one day why I was there. I hesitated at first. My instinct was to brush her off. I took a deep breath and I told her that I was getting tutoring because I had missed school for a few months to do intensive treatment for my OCD. She asked me questions about what it was like and I answered honestly. I told her that it was long and difficult but that it ultimately was the thing that saved my life. She told me that she was asking so many questions because she had just been diagnosed with OCD and she was looking for treatment options. We talked for a long time about what treatment options are available and commiserated about the things that OCD had taken away from us. 

To this day, I try to be open and honest about my experiences with OCD. I aim to educate the people around me about what OCD is and how misunderstood it can be. For the past few years, I have led a team for the IOCDF 1 Million Steps for OCD Walk. Together with my team, I have been able to raise money for this organization that means so much to me and my family. Every year at the Walk, I get to see some of my old therapists who are also walking. They always tell me how proud they are of me. I can’t help but agree with them. I couldn’t be prouder of how far I have come. 

Conclusion: Looking Back 

I have a memory of being in a heap on the floor in front of my parents’ bedroom door. I was probably about five or six. I remember banging my tiny fists on their closed door and screaming for them to hear me. I banged on the door until my hands were bruised and I screamed until I lost my voice. I eventually gave up and wept right there on the floor. I felt alone and scared. Did they not hear me? Or did they just not want to listen? After a while I brought myself back to my bed and stared at the ceiling until I fell asleep. 

I look back at that tiny heap on the floor and I see that all she wanted was to be heard. She was scared and didn’t know how to express that to the people she loved the most. She yelled and screamed at them and pushed them away. I look back and see I was doing the best I could with what I was given. Struggling with something didn’t make me a bad kid. 

I still am working on not viewing myself as someone who was a bad or angry kid. I also look back at my parents and know that they were also doing the best they could. We were all fighting OCD even though it might have seemed like we were fighting each other at the time. This is why educating people about OCD is so important. The more people know about it, the easier it will be for families to spot when their child is struggling. 

Since my diagnosis in 2015, my dad has made education his mission. The hospital where I did my program was participating in a walk for OCD. My dad asked to join their team even though no one else in my family was able to go with him to the walk. At the walk he met some other 50 people who had had similar experiences as our family. They encouraged him to get involved with the International OCD Foundation. 

After hearing about the foundation he decided he wanted to be involved. In the summer of 2017, I went to San Francisco with my dad for the Annual OCD Conference. While at the Conference I went to seminars and met other people who also had OCD. I learned so much about OCD and how to be an advocate for people with OCD. 

I know that I am incredibly lucky to be able to tell my story. I am thankful that I was fortunate enough to have access to the treatment that got me to where I am today. Not everyone who has OCD is so fortunate. Many people cannot afford treatment. Others live far away from any sort of program for OCD. 

A lot of these people who are struggling go their whole lives without receiving any treatment, simply because of a lack of accessibility of treatment. Many will not even receive a diagnosis due to lack of understanding of this disorder. Without any sort of treatment, I don’t know what my life would have looked like. It is likely that I would not have lived long enough to be where I am now. OCD disrupted my life for over 17 years and I will not allow it to disrupt my life moving forward. That being said, I know that it is a privilege to be able to say that. 

OCD can be complicated and hard to understand. It can be difficult to recognize in both children and adults. However, there is always hope for a better life free from OCD. There is no cure, of course. I will be living with OCD for the rest of my life. It will ebb and flow and sometimes it will make my life more difficult. Having these experiences with OCD has made me strong and resilient. I am very different than I was when OCD had its hold on me. But I will always have a soft spot for that little girl crying in a heap outside her parents’ bedroom door.

Sources 

Adams, Gail B., et al. “Obsessive Compulsive Disorder in Children and Adolescents: The Role of the School Psychologist in Identification, Assessment, and Treatment.” School Psychology Quarterly , vol. 9, no. 4, Win 1994, pp. 274–94. 1995-33363-001, EBSCOhost , doi:10.1037/h0088290. Beyond Fear: Incompleteness and Disgust in Pediatric Obsessive-Compulsive Disorder . Lund University, Faculty of Medicine, 2019. Children with OCD. [Electronic Resource] . New York, N.Y. : Films Media Group, [2013], c1997., 1997. Chilvers, Rebecca. Different for Dads? : The Association between Paternal OCD, Parenting and Child Functioning . 2013. Dacey, John S., et al. Your Anxious Child: How Parents and Teachers Can Relieve Anxiety in Children . John Wiley & Sons, Incorporated, 2016. ProQuest Ebook Central , http://ebookcentral.proquest.com/lib/emerson/detail.action?docID=4457837 . Gold-Steinberg, Sharon, and Deirdre Logan. “Integrating Play Therapy in the Treatment of Children with Obsessive-Compulsive Disorder.” American Journal of Orthopsychiatry , vol. 69, no. 4, Oct. 1999, pp. 495–503. 1999-01577-007, EBSCOhost , doi:10.1037/h0080 Hershfield, J., & Bell, J. (2016). When a family member has Ocd: mindfulness & cognitive behavioral skills to help families affected by obsessive-compulsive disorder . Sydney: Read How You Want. 53 “International OCD Foundation | What Is OCD?” International OCD Foundation , https://iocdf.org/about-ocd/. Accessed 4 Sept. 2019. “International OCD Foundation | Have We Forgotten the Children Who Have a Parent with OCD?: Accommodation and Early Intervention.” International OCD Foundation , “International OCD Foundation | My Parents Don’t Believe I Have OCD.” International OCD Foundation , https://iocdf.org/expert-opinions/my-parents-dont-believe-i-have-ocd/. Accessed 4 Sept. 2019. Ivarsson, Tord, and Robert Valderhaug. “Symptom Patterns in Children and Adolescents with Obsessive–compulsive Disorder (OCD).” Behaviour Research and Therapy , vol. 44, no. 8, Aug. 2006, pp. 1105–16. ScienceDirect , doi:10.1016/j.brat.2005.08.008. Kelly, K. (2018, December 7). ‘Glee’ Jayma Mays has OCD like character Emma. Retrieved from https://www.digitalspy.com/tv/ustv/a331994/glee-jayma-mays-has-ocd-like-character-emma/ Kenyon, Katherine M., and Warren O. Eaton. “Age at Child Obsessive-Compulsive Disorder Onset and Its Relation to Gender, Symptom Severity, and Family Functioning.” Archives of Scientific Psychology , vol. 3, no. 1, Nov. 2015, pp. 150–58. 2015-51690-001, EBSCOhost , doi:10.1037/arc0000022. Kohler, Kirsten Celeste, et al. “Living with Obsessive-Compulsive Disorder (OCD): A South African Narrative.” International Journal of Mental Health Systems , vol. 12, no. 1, Dec. 2018, p. 73. Springer Link , doi:10.1186/s13033-018-0253-8. Landsman, K. J., Rupertus, K. M., & Pedrick, C. (2006). Loving someone with Ocd: help for you and your family . Oakland, CA: New Harbinger Publications. 54 Leonard, Henrietta L., et al. “A 2- to 7-Year Follow-up Study of 54 Obsessive-Compulsive Children and Adolescents.” Archives of General Psychiatry , vol. 50, no. 6, June 1993, pp. 429–39. jamanetwork.com , doi:10.1001/archpsyc.1993.01820180023003. Myrick, Amie C., and Eric J. Green. “Incorporating Play Therapy into Evidence-Based Treatment with Children Affected by Obsessive Compulsive Disorder.” International Journal of Play Therapy , vol. 21, no. 2, Apr. 2012, pp. 74–86. 2012-10037-001, EBSCOhost , doi:10.1037/a0027603. Newhouse-Oisten, Mindy K., et al. “An Evaluation of Modified Exposure Therapy for a Child Diagnosed with Obsessive Compulsive Disorder and Pervasive Developmental Disorder–not Otherwise Specified.” Behavior Analysis: Research and Practice , vol. 16, no. 3, Aug. 2016, pp. 147–55. 2016-31966-001, EBSCOhost , doi:10.1037/bar0000048. Reid, Keshia M. “The Relationship Between Parents’ Poor Emotional Health Status and Childhood Mood and Anxiety Disorder in Florida Children, National Survey of Children’s Health, 2011–2012.” Maternal and Child Health Journal , vol. 19, no. 5, May 2015, pp. 1071–77. Springer Link , doi:10.1007/s10995-014-1607-8. Stearns, Peter N. Anxious Parents : A History of Modern Childrearing in America . NYU Press, 2003. Viol, Kathrin, et al. “Erroneously Disgusted: fMRI Study Supports Disgust-Related Neural Reuse in Obsessive-Compulsive Disorder (OCD).” Frontiers in Behavioral Neuroscience , vol. 13, 2019. Frontiers , doi:10.3389/fnbeh.2019.00081. Weg, Allen Howard. OCD Treatment through Storytelling : A Strategy for Successful Therapy . New York : Oxford University Press, 2011., 2011. 55 Wu, Monica S., et al. “Comparing OCD-Affected Youth with and without Religious Symptoms: Clinical Profiles and Treatment Response.” Comprehensive Psychiatry , vol. 86, Oct. 2018, pp. 47–53. ScienceDirect , doi:10.1016/j.comppsych.2018.07.009.

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• v.52(Suppl1); 2010 Jan

An overview of Indian research in obsessive compulsive disorder

Y. c. janardhan reddy.

Department of Psychiatry, National Institute of Mental Health and Neurosciences (NIMHANS), Hosur Road, Bangalore - 560 029, Karnataka, India

Naren P. Rao

Sumant khanna.

Obsessive-compulsive disorder (OCD) was considered a relatively rare disorder until about two decades ago. Since then, considerable advance has been made in understanding the various aspects of OCD that include epidemiology, clinical features, comorbidity, biology and treatment. In the last one decade, there has also been interest in a group of related disorders called obsessive-compulsive spectrum disorders. There is substantial research from India on various aspects of OCD, particularly from the National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore. We attempt to review all the relevant Indian data on OCD.

ADULT OBSESSIVE-COMPULSIVE DISORDER

Epidemiology.

There is only one epidemiological study from India.[ 1 ] The study found lifetime prevalence of 0.6%. This rate is considerably lower compared to the 2-3% rate reported in the European and North American studies.[ 2 , 3 ] However, similar low rate ranging from 0.5-0.9% was observed in a study from Taiwan.[ 4 ] It is not clear why lifetime prevalence rate of OCD is lower in some countries although the rates are not very low compared to the conservative estimate of 1% rate of OCD.[ 5 ] However, further research is needed into the epidemiological aspects of OCD in India since the data available is limited.

Phenomenology of obsessive-compulsive disorder in adults

Phenomenology has been an important area of research in the field of OCD that has attracted the attention of Indian researchers. The earliest such study was by Dutta Ray in 1964[ 6 ] followed by a series of articles by Akhtar et al . on phenomenology and socio-cultural determinants of symptoms in OCD,[ 7 – 9 ] Chakraborty and Banerji, in a study that compared 200 “obsessionals” with 200 controls reported a high rate of family history of obsessional illness (26%) and premorbid obsessional personality (26%).[ 10 ] Two other studies also reported high rates of obsessive personality.[ 11 , 12 ]

Khanna et al . in an exploratory study examined whether a reactive-endogenous dichotomy exists.[ 13 ] Acute onset and fluctuating course was significantly commoner in the reactive subgroup. In an attempt to clarify the nosological status of OCD, Gojer et al . compared 53 cases of OCD with an equal number of subjects with depression and anxiety neurosis.[ 14 ] There were more similarities in the OCD and anxiety neurosis group than the depressive group.

Khanna and Channabasavanna developed a classificatory system for obsessions and compulsions based on form and content.[ 15 , 16 ] Obsessions were categorized into six categories of form and twelve categories of content and compulsions in to four categories of form and eight categories of content. In the same sample of patients, phenomenology was analyzed using cluster analysis.[ 17 ] Four reliable clusters were derived using variables present in 10-90% of the subjects: Washing, checking, thoughts of past and embarrassing behavior. Depression occurred as a unique cluster. Subtypes of OCD were also examined in the same sample.[ 18 ] The study showed that washers and checkers are valid subtypes of OCD.

In another study,[ 19 ] 222 consecutive subjects were evaluated using the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) symptom checklist[ 20 ] and the Scale for Assessment of Form and Content (SFC).[ 21 ] The data was subjected to factor analysis with varimax rotation. The main factors that emerged were washers, checkers, hoarding and two pure obsession factors. The obsession groups had a preponderance of sexual and religious themes. The findings are largely in concordance with those of studies from other parts of the world suggesting similarity across cultures.[ 22 , 23 ] The study, however, supports separating obsessions from compulsions because two pure obsession factors emerged, which is in keeping with the findings of the two previous studies.[ 24 , 25 ] Three recent studies of OCD in adults have also used the Y-BOCS to measure obsessive-compulsive symptoms.[ 19 , 26 – 28 ] The phenomenology of OCD in these studies is similar to that described in the western population.[ 29 ]

Jaisoorya et al . examined gender differences in OCD.[ 30 ] Males had an early onset of OCD, and had a higher prevalence of symmetry/religious obsessions, miscellaneous compulsions, and comorbid attention deficit hyperactivity disorder (ADHD). Females had higher prevalence of cleaning compulsions and comorbid trichotillomania.

Kamath et al . examined suicidal behavior in 100 consecutive DSM-IV OCD patients;[ 28 ] 59% had ‘worst ever’ (lifetime) suicidal ideation and 28% had current suicidal ideation. History of suicidal attempt was reported in 27% of the subjects. Major depression, unmarried status and hopelessness were the major risk factors for suicidal behavior.

Gururaj et al . assessed the family burden, quality of life and disability in OCD patients and compared them with patients with schizophrenia of comparable severity.[ 31 ] Patients with schizophrenia had higher family burden but were comparable to OCD patients with respect to quality of life and disability. The study showed that OCD patients were associated with significant disability, poor quality of life and high family burden comparable to schizophrenia.

Insight into obsessive-compulsive disorder

Traditionally, OCD is described as a condition in which patients have good insight into their symptoms. The DSM-IV field trial demonstrated a broad range of insight with 30% having poor insight.[ 32 ] Subsequent studies have also reported poor insight in 15-36% of patients with OCD.[ 33 – 36 ] The DSM-IV has added a new OCD specifier: “With poor insight” which involves a lack of recognition that the symptoms are unreasonable or excessive.[ 37 ]

There is paucity of data regarding the clinical correlates and treatment response of poor insight in OCD. A significant limitation of most of the studies is that they did not use validated measure of insight. Only one study[ 33 ] used the Brown Assessment of Beliefs Scale (BABS) developed specifically to assess insight.[ 38 ] In a recent Indian study, demographic and clinical correlates of poor insight OCD, and the association between response to specific serotonin reuptake inhibitors (SSRIs) and baseline insight was examined in a sample of 100 DSM-IV OCD subjects by using the BABS as a measure of insight.[ 27 ] The sample had 25 subjects with poor insight and the remaining 75 had good insight. Those with poor insight had earlier age-at-onset, more severe illness, higher comorbidity rate particularly major depression, over representation of miscellaneous obsessions and hoarding and poorer treatment response. The study suggests that OCD with poor insight could be a distinct subtype. That a significant proportion of OCD patients have poor insight has important treatment implications. Patients with poor insight could easily get misdiagnosed as psychotic and treated accordingly. The study suggests that drug treatment response is poor in those with poor insight. The finding is in sharp contrast to the findings of a previous study that reported that degree of insight at baseline did not predict response to sertraline.[ 33 ] It is clinically pertinent to examine if poor insight patients do better with addition of neuroleptics. There is, however, no evidence as yet to suggest that those with poor insight respond better to augmentation with antipsychotics. On the other hand, a few studies have shown that insight improves after treatment with SSRIs.[ 35 , 36 ]

Comorbidity

Studies of comorbidity are varied and have examined a broad range of topics including spectrum disorders, comorbidity with schizophrenia and bipolar disorder and even prevalence of OCD in Parkinson’s disease.

Obsessive-compulsive (OC) spectrum disorders have over the past few years emerged as a unique and fascinating category of related conditions.[ 39 ] Jaisoorya et al . examined the prevalence of putative OC spectrum disorders in a large sample of OCD subjects (n = 231) in comparison with relatives of neurologically ill patients (n = 200).[ 26 ] Prevalence of tic disorders (39% vs. 12%), hypochondriasis (13% vs. 0), BDD (3% vs. 0) and trichotillomania (3% vs. 0) were significantly greater in OCD subjects compared to controls. However, the prevalence of sexual compulsions, pathological gambling, eating disorders, and depersonalization disorder was not greater in the OCD subjects compared to controls. The findings of this study suggest that tic disorders, hypochondriasis, BDD, and trichotillomania are perhaps part of the OC spectrum disorders. The evidence for exclusion of other disorders from the hypothesized OC spectrum is not conclusive because of the rarity of the occurrence of some of these disorders in the study sample. The findings are somewhat similar to those of a study that reported high rates of BDD, hypochondriasis and low rate of eating disorders and most impulse control disorders other than pathological skin picking.[ 40 ] Only one patient in the sample had an eating disorder. The finding is in sharp contrast to a previous study that reported high rates of eating disorders among OCD patients.[ 41 ]

This divergence should be viewed in the light of the rare reporting of eating disorders in Asian countries[ 42 , 43 ] but could well be a correlate of cultural beliefs and attitudes that have been identified as significant contributing factors in the development of eating disorders.[ 43 ] Jaisoorya et al . examined the differences between tic related and non tic related OCD with respect to sociodemographics, symptom profile, and comorbidity.[ 44 ] Tic related OCD had an early age at onset, over representation of males, aggressive obsessions, cleaning compulsions and comorbid trichotillomania.

In a chart review of comorbidity in 218 OCD subjects, 17% had major depression, 6% dysthymia, and 7% any anxiety disorder.[ 45 ] Comorbidity rates were low and there were not many differences between those with and without comorbidity except that female subjects were more likely to have depression. Kalra et al . compared OCD with and without comorbid Axis I disorders in a sample of 54 subjects and found that those with comorbidity had higher scores on depression and OCD severity scales.[ 46 ] The study findings were in tune with earlier literature from rest of the world. Gupta et al . examined level of comorbid depression in patients with OCD, psychotic depression and chronic medical illness.[ 47 ] All three groups had moderate to high levels of depression, with OCD group intermediary between psychotic depression and physical illness. However, the OCD group had more life events than depression or physical illness.

Rajkumar et al .[ 48 ] studied the clinical profile of schizophrenic patients with and without comorbid OCD (50 in each group). Schizo-obsessive patients had higher rates of paranoid symptoms and first-rank symptoms of schizophrenia. They had lower anergia, higher depression scores, more comorbid personality disorders, and disability. Significant correlations were observed between OCD severity scores and schizophrenia symptom dimension scores. Authors concluded that “schizo-obsessive” schizophrenia may be a distinct subtype with unique clinical characteristics.

A retrospective chart analysis of 15 cases OCD with psychosis found that obsessive doubts, washing and checking compulsions were the most common OC symptoms.[ 49 ] Twelve cases had a diagnosis of schizophrenia, while three had atypical psychosis. About half the patients had First Rank symptoms of schizophrenia. Nearly three-fourth of the sample showed significant improvement on treatment with a combination of antipsychotic and antiobsessional drugs.

Zutshi et al .[ 50 ] examined differences between bipolar OCD and non-bipolar OCD. Bipolar OCD was associated with episodic course, a higher family loading for mood disorders, and higher rates of comorbid depression, social phobia and generalized anxiety disorder. In majority of the patients, OCD predated bipolar disorder and OCD worsened during depression and improved during mania. Authors concluded that OCD in those with bipolar disorder may be pathophysiologically related to bipolar disorder.

Harbishettar et al .[ 51 ] systematically assessed OC symptoms and OCD in 69 Parkinson’s disease patients and matched medically ill controls. There was no difference between the groups with respect to OC symptoms, OCD both clinical and subclinical and tics. Also, there was no relationship between severity of Parkinson’s disease and OC symptoms. Authors speculated that different circuitry may be involved in the pathophysiology of OCD and Parkinson’s disease although basal ganglia involvement may be common to both the disorders.

Course and outcome

There is limited literature on the long-term course and outcome of OCD. In an 11-13 year follow-up study of 75 subjects with OCD, Reddy et al .[ 52 ] reported a favorable outcome in majority of the subjects: 43% had no OCD, 33% had subclinical OCD and only 24% had clinical OCD. Median time to reach ‘no OCD’ and ‘subclinical’ status was 42 months and 84 months respectively. Interestingly, 37% were in true remission (‘no OCD’ and not on any treatment) for a median period of 132 months. Those who had ‘mixed’ OCD and Axis I comorbidity had poorer outcome. Age of onset and duration of illness had no effect on outcome. Optimistic outcome reported in this study is somewhat different from the findings of studies from other parts of the world which have reported lower rates of remission. Previous studies included samples that were severe and chronically ill with high rates of comorbidity. The subjects in the study by Reddy et al . were largely self-referred, moderately ill, and did not have history of treatment resistance. The findings of this study, therefore, could be generalized for patients routinely seen in the outpatient consultation at clinics and secondary-care hospitals in India.

Math et al .[ 53 ] in another follow-up study explored if the long term outcome of ‘predominantly obsessive’ subjects differs from that of ‘mixed’ OCD. They studied the five to six-year course and outcome of 54 patients with ‘predominantly obsessions’ and 54 with ‘mixed’ subtype of OCD. The course of the illness was similar in both and a majority (72%) did not have clinical OCD at follow up.

In another study, Shetti et al .[ 54 ] examined the differences between SSRI responders and non responders. They assessed 67 SRI responders and 55 non responders. Base line severity of illness, comorbid major depression, sexual obsessions, washing and miscellaneous compulsions, early age at onset, ‘mixed’ OCD and poor insight were associated with poor response to SRIs.

NEUROBIOLOGY

Neurotransmitters in obsessive-compulsive disorder.

A serotonergic hypothesis of OCD was suggested originally by the observed differential efficacy of SRIs in alleviating OCD symptoms.[ 55 ] Since then, numerous studies of peripheral receptor binding in the blood or concentrations of serotonin metabolites in cerebrospinal fluid have been performed but have yielded inconsistent results.[ 56 ] Pharmacological challenge studies provide another indirect approach. By administering serotonergic agents and measuring endocrine and behavioral responses, investigators have attempted to study the central serotonergic functioning in OCD. It is observed that OCD patients become significantly more anxious and dysphoric after administration of meta-chlorphenyl-piperazine (mCPP), a 5-HT receptor agonist.[ 55 ] In addition, obsessive-compulsive symptoms worsen. However, there appears to be blunted cortisol and prolactin response in response to mCPP. In an attempt to replicate these findings, mCPP was administered orally in a randomized double-blind design to 34 OCD patients who were either drug-naïve or drug-free for a minimum of four weeks.[ 57 ] The cortisol and prolactin responses were contrasted with those of 18 drug-free healthy subjects. The OCD patients showed significantly blunted cortisol and prolactin responses to mCPP challenge as compared to normal subjects. However, mCPP did not produce any significant exacerbation of obsessive-compulsive symptoms in the patients. These findings are suggestive of a serotonin (5-HT) receptor hyporesponsivity in the HPA axis. Even though previous studies indicate a hyperresponsivity of the 5-HT receptor system as shown by significant symptom worsening following serotonergic challenge,[ 58 , 59 ] the Indian study failed to replicate those results.[ 58 ] It was postulated that the 5-HT receptor hyporesponsivity in the HPA axis may be a biological “trait marker” of OCD, and may not be directly involved in the mediation of symptomatology of the disorder. It could also be inferred that the discrepancy among studies regarding the behavioural responses to mCPP challenge may in part be due to differences in the basic environmental conditions across various studies.[ 60 ] In a previous study by the same group, an endocrinological blunting in the absence of a behavioural increase in obsessive-compulsive symptoms was documented after oral administration of mCPP; however, when exposure was incorporated into the paradigm, with oral mCPP, exacerbation of obsessive-compulsive symptoms was noted.[ 61 ]

A normal endocrinological response after treatment with clomipramine was also independently documented.[ 62 ] It is a matter of conjecture whether stimulation of noradrenergic system by the α2 adrenergic antagonistic action of mCPP, or behavioral exposure conditions during the challenge procedure are also partly responsible for the symptom exacerbation as noted in previous studies.[ 57 ]

In summary, pharmacological challenge studies and other studies that have explored serotonergic hypothesis in OCD, have very limited evidence to support a primary serotonergic dysfunction in OCD.[ 63 ] However, a modulation of serotonergic system clearly plays a role in effective pharmacotherapy of at least a significant proportion of OCD patients.

In a study by Khanna et al . there was a blunted growth hormone, cortisol and ACTH response to clonidine in OCD.[ 64 ] On qualitative analysis three possible responses of growth hormone were obtained: Accentuation (>10 ng/ ml), normal (5-10 ng/ml) and attenuation (<10 ng/ml). Most patients with an accentuated response were patients with compulsions, pure obsessions were significantly more likely to have blunted responses. The study findings suggest noradrenergic dysfunction in OCD and also imply noradrenergic heterogeneity in the observation that pure obsessions tend to have a more down regulated noradrenergic system as compared to the compulsives. Based on their work, Khanna et al . concluded that serotonergic hypothesis may not explain all the abnormalities seen in OCD and that complex interactions between various neurotransmitters as well as the environmental conditions may be necessary to cause OCD.[ 57 ]

Soft neurological signs

Thirty-seven drug free non-depressed OCD subjects and 20 normal healthy volunteers were screened for SNS.[ 65 ] The OCD subjects had significantly more total SNS as compared to normals. These findings were most marked in the frontal lobe functions. There was a trend towards significance in temporal lobe functions, while other test findings were not impaired. If individual items were studied the problems were predominantly in complex motor tasks. There was no significant laterality effect.

Electrophysiological studies

Most electrophysiological studies in OCD have either tried to localize the site of the disorder at a structural or functional substrate, or have been based on the associated increased autonomic arousal. Khanna concluded that in most cases there was no obvious EEG abnormality in OCD; when it was present it was likely to be a non-specific disturbance in the temporal and frontotemporal regions.[ 66 ]

In OCD there was a decreased power in the nondominant frontomedial and posterior temporal regions in the computerized EEG analysis. There were no significant differences in the coherence observed from these sites.[ 67 ] The study suggested nondominant frontomedial hypofunctioning to be associated with OCD.

In a study of resting middle latency auditory and visual evoked potentials in 50 OCD subjects and 40 normal controls, there were no significant differences between the two groups for amplitude and latency or left-right ratios.[ 68 ] The study did not support any laterality deficit in OCD and was inconsistent with the hypothesis of left frontal lobe dysfunction in OCD.[ 69 ] A more prolonged post imperative negativity and a higher amplitude of the late component of the Contingent Negative Variation (CNV) has been repeatedly recorded.[ 66 ] OCD patients exhibited higher amplitude of the ‘late’ component of the CNV. The role of the mesencephalic reticular formation with modulation by the frontal granular cortex in the genesis of these potentials has been stressed.

Bereitschafts potential has been found absent or to have a decreased onset latency in 44 subjects with OCD.[ 70 ] A deficit of the complex motor programming circuit similar to those observed in Gilles de la Tourette syndrome has been put forth on the basis of this observation.[ 70 ] Based on the evidence from electrophysiological, neuropsychological, scan, lesion, and psychosurgical studies, Khanna also proposed an integrated model of possible frontal dysfunction in OCD with associated dysfunction in other areas of the brain such as cingulum and basal ganglia.[ 66 ]

Immunological factors

Khanna et al . documented increased levels of serum immunoglobulins in OCD subjects as compared to normal controls, with specific reference to IgG.[ 71 ] The IgG levels were high even after clinical improvement. The authors speculated that the immunological abnormality could be a marker of vulnerability to OCD. They also discussed the possibility that the immunological dysfunction could be due to an unidentified infectious agent or an autoimmune process. As an extension of the hypothesis, viral antibodies were measured in the blood[ 72 ] and cerebrospinal fluid (CSF) of OCD subjects.[ 73 ] IgG viral antibodies for herpes simplex virus-1 (HSV-1), varicella zoster, cytomegalo virus, measles and mumps were studied in 76 subjects with OCD and compared with 55 normal healthy volunteers. There was a significantly higher titer for HSV-1 antibodies in both serum and CSF. The sera: CSF ratios were suggestive of intrathecal synthesis. The study on viral antibodies in CSF suggests a role for HSV-1 in OCD. However, caution needs to be exercised in interpreting the finding because of certain methodological issues raised in the paper by the authors.

Exploration of the contribution of immunological mechanisms in the manifestation of OCD continued in a recent study by Bhattacharya et al . that investigated the presence of auto antibodies directed against the basal ganglia or thalamus in the serum as well as CSF of 23 OCD patients compared with 23 matched psychiatrically normal controls using western blot.[ 74 ] They further investigated CSF amino acid (glutamate, GABA, taurine, and glycine) levels and examined the extent to which these levels were related to the presence of auto - antiibodies. There was evidence of significantly more binding of CSF auto - antiibodies to homogenate of basal ganglia as well as to homogenate of thalamus among OCD patients compared to controls. There was no significant difference in the pattern of binding between patients and controls using serum. CSF glutamate and glycine levels were also significantly higher in OCD patients compared with controls, and CSF glycine levels were also significantly higher in those OCD patients who had auto - antiibodies compared to those without. The study implicates autoimmune mechanisms in the pathogenesis of OCD and also provides preliminary evidence that auto antobodies against basal ganglia and thalamus may cause OCD by modulating excitatory neurotransmission.

In support of the possible immunological mechanisms in the causation of at least some forms of OCD, a few clinical studies have examined the association between infections and OCD. A study reported OCD in some cases of Herpes Simplex encephalitis.[ 75 ] In a study of 20 subjects with rheumatic chorea, four subjects (20%) had OCD.[ 76 ] The relationship between OCD and rheumatic chorea and Pediatric, Autoimmune, Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS) is well known.[ 77 ] Considering the association between rheumatic fever and OCD, and possible long term neuropsychiatric sequelae in those with history of rheumatic fever because of possible autoimmune insult to basal ganglia, a study recently examined the prevalence of OCD in adults with Rheumatic Heart Disease (RHD).[ 78 ] Of the 100 subjects with RHD, 10 had clinical OCD. This rate is at least five-fold higher than the reported global general population rate of OCD[ 5 ] and over 15-fold higher than the 0.6% rate of OCD in India.[ 1 ] The finding lends support to the hypothesis that OCD could be a long term complication of autoimmune basal ganglia insult in childhood just as RHD is a long term sequel of autoimmune damage to the heart. The results of this study need to be replicated in a controlled study.

Chakrabarty et al . investigated glutamatergic dysfunction linked to immune pathogenesis in 21 OCD patients and 18 healthy controls by collecting CSF.[ 79 ] They estimated glutamate levels and found that OCD patients had higher glutamate levels. Age, gender, duration of illness, severity of illness did not have any effect on glutamate levels.

NEUROPSYCHOLOGY

Neuropsychological studies have provided important clues in understanding the neurobiological basis of OCD. As neuropsychological deficits are potential endophenotype markers, studies have examined patients in symptomatic phase, recovered phase and also in unaffected first degree relatives.

Trivedi et al .[ 80 ] examined executive functions, vigilance and spatial working memory in 30 OCD patients and 30 age and education matched control subjects. OCD patients had significant deficits in all the cognitive domains. There was a positive correlation between severity of illness and attention deficits but there was no correlation between duration of illness and cognitive dysfunction. A study by Tarafder et al .[ 81 ] examined neuropsychological disposition and executive functions in 20 OCD patients and 20 matched normal healthy controls. Subcortical-cerebellar-spinal domain was found to be associated with cognitive style and executive functions, affirming the neurobiological basis of the disorder.

Rao et al . examined neuropsychological deficits in 30 recovered OCD patients in comparison with 30 matched healthy controls.[ 81 ] They were assessed on tasks for attention, executive function, memory and intelligence. Patients had significant deficits in tests of set shifting ability, alternation, response inhibition and non verbal memory. There was no correlation between illness related variables neuropsychological deficits. The study findings suggest neuropsychological deficits are possibly state independent.

In a recent study by Viswanath et al . 25 unaffected siblings of probands with familial OCD in comparison with 25 matched healthy controls had significant deficits in tests of decision making and behavioral reversal but not in other tests of attention, executive function, intelligence and memory.[ 82 ] The deficits are consistent with the proposed neurobiological model of OCD involving the orbitofrontal cortex and suggest that the deficits could be potential endophenotypes in OCD.

Family studies

Methodologically sound studies in the last decade have reported higher morbid risk for OCD among first-degree relatives of OCD probands[ 83 , 84 ] but Indian studies have reported either no increase in morbid risk[ 85 ] or much less than what was previously reported.[ 86 ] The rate of OCD in 135 first-degree relatives of 33 adult OCD probands was comparable to the rate in 148 adults from the general population in the study by Guruswamy et al .[ 85 ]

In the family study of juvenile OCD, that examined first-degree relatives of 35 juvenile OCD probands and 34 matched normal controls,[ 86 ] the morbid risk for OCD among relatives of OCD probands was 5%, while none of the relatives of controls had OCD. In addition, none of the relatives had Tourette syndrome and only one relative of OCD proband had chronic tics. The study concluded that most juvenile cases of OCD were nonfamilial and unrelated to tic disorders, while only a few were familial.

Sagnik et al . examined familiality of washers and checkers by interviewing first-degree relatives of 25 checkers, 30 washers and 40 psychiatrically normal control probands.[ 87 ] The morbid risk of OCD was significantly higher among relatives of checker probands (19.4%) than in the relatives of washer (8.7%) or control probands (5.4%), while the morbid risk for relatives of washer and control probands was not significantly different. In all, 67% of the checker relatives with OCD were checkers, while 54% of the washer relatives with OCD were washers. The study provided preliminary evidence of familiality of the checker subtype of OCD.

Miscellaneous

Chakraborty et al . examined the role of oxidative stress in pathogenesis of OCD.[ 88 ] They estimated serum Thiobarbituric Acid Reacting Substances (TBARS) formed as a result of free radical lipid peroxidation in 39 newly diagnosed drug free OCD patients and 33 disease free control subjects. Patients had significantly higher TBARS than controls. In addition, there was a strong positive correlation between TBARS and the disease severity. The study suggests that oxidative stress induced increased free radical are generated in OCD patients.

OCD IN CHILDREN AND ADOLESCENTS

Demographics.

In all the studies of OCD in children and adolescents reported from India, males have outnumbered female subjects.[ 86 , 89 – 91 ] Male preponderance in juvenile OCD is consistent with the previous clinical studies of juvenile OCD justifying the argument that gender distribution in OCD is developmentally sensitive.[ 92 ]

Phenomenology

A study by Khanna and Srinath from India was one of the earliest studies to systematically examine the clinical profile of OCD in children in comparison with the OCD in adults.[ 93 ] In this sample, obsessions were less frequent compared to compulsions. Obsessions of harm, religion, and impersonal images were commonly reported. Washing, praying, touching, counting and spitting were the common compulsions.

Recent studies from India[ 89 , 90 ] have examined the phenomenology of OCD in children using the chilldren’s version of the Yale-Brown Obsessive-Compulsive Scale (CY-BOCS), the instrument that is widely used all over the world.[ 94 ] In a study of 58 children and adolescents, all aged 16 years and below,[ 90 ] contamination obsessions were the commonest (62%), followed by obsessions related to aggression (57%), symmetry (34%), sex (22%), religion (22%), somatic (12%), and hoarding (7%). Regarding compulsions, cleaning and washing was the commonest (69%) followed by repeating (52%), checking (47%), ordering (29%), counting (15%), and hoarding (7%). The miscellaneous obsessions and compulsions were present in 65% and 47% of the subjects respectively. The phenomenology of OCD in these studies is similar to that reported in a group of 70 young patients at the National Institute of Mental Health (NIMH) in USA.[ 95 ]

In one study,[ 91 ] the phenomenology in juvenile OCD was compared with that of adult-onset OCD and juvenile-onset adult OCD, in view of the previously reported findings that juvenile OCD could be phenotypically different from adult OCD[ 96 , 97 ] and juvenile-onset adult OCD.[ 98 ] Obsessions related to contamination and compulsions related to checking and miscellaneous types were common in juvenile OCD. In addition, the mean Y-BOCS score was greater in the juvenile OCD and juvenile-onset adult OCD subjects compared to the adult-onset OCD subjects suggesting greater severity of OCD in the juvenile groups. The variations in the clinical manifestations support developmental variability in the expression of OCD. However, they are not consistent with specific variations reported in previous studies.[ 97 , 98 ] For example, OCD in juveniles was associated with a higher frequency of aggression/catastrophic obsessions, hoarding and saving compulsions.[ 97 ] Sexual obsessions were selectively more prevalent in adolescents compared with children or adults. It is possible that sexual and aggressive obsessions were underrepresented in this sample due to the fact that the subjects kept them secret because of embarrassment and possible guilt associated in revealing them. However, there could also be a true cross-cultural variation in the phenotypic manifestation of OCD.

Psychiatric comorbidity is common in adults with OCD. Similarly, studies of juvenile OCD have found high rates of comorbid major depression (10%-73%), anxiety disorders (26%-76%), and tic disorders (17%-59%).[ 89 ] Three Indian studies have systematically examined the comorbidity in juveniles with OCD.[ 89 – 91 ] Rates of comorbid major depression, dysthymia, and bipolar disorder have ranged from 14-23%, 0-2%, and 0-2% respectively. Among anxiety disorders, rates of panic disorder, social phobia, specific phobias, overanxious disorder and separation anxiety disorder ranged from 0-6%, 0-13%, 5-7%, 0-7%, and 5-7% respectively.

Of considerable interest is the comorbid relationship between tic disorders, disruptive behavior disorders and juvenile OCD. Rates of TS have varied from 11-15% and that of other tic disorders from 17-59%.[ 89 ] In the three Indian studies, rates of TS and chronic tics are in the range of 8-11% and 2-23% respectively. In the follow-up study by Leonard et al . TS was present in 15% of the sample and any tics in 59% of the sample.[ 99 ] The rate of TS in the Indian juvenile OCD samples is somewhat comparable to the rates in previous studies, but the overall rate of tic disorders and, in particular, chronic tics are somewhat lower. In a recent study, the clinical profile of OCD+ tics patients was examined in juvenile OCD, juvenile-onset adult OCD and adult-onset OCD subjects.[ 91 ] Miscellaneous compulsions such as touching, tapping, rubbing, blinking, staring etc (73% vs. 45% vs. 32%) and pathological doubts (40% vs. 13% vs. 9%) and ADHD (26% vs. 3% vs. 0) were over represented in the juvenile OCD group compared to the other two groups. The miscellaneous compulsions of the type reported in this study were also reported in previous studies of OCD patients with tics[ 100 , 101 ] but the obsessions are not similar to the ones reported in other studies that found mainly excess of aggressive, sexual, and symmetry obsessions.[ 101 , 102 ] Further, the elevated rate of ADHD in juvenile OCD with tics support the previous observations that ADHD, tics and OCD commonly co-occur in juvenile OCD[ 99 , 103 ] and are possibly interrelated sharing a common pathophysiology.[ 104 ]

Comorbid ADHD is considered by some to be a developmental marker of juvenile OCD.[ 105 ] In the study by Leonard et al .[ 106 ] the rate of ADHD was 26% and in the studies by Geller and colleagues,[ 97 , 105 , 107 ] the rate of ADHD was as high as 57%. In the three Indian studies, rates of ADHD ranged from 3 to 18%.[ 89 – 91 ] The rates of ADHD in Indian samples are considerably lower than the rates reported in previous studies. The samples in the previous studies by Geller and colleagues were recruited from a specialized pediatric OCD program, whereas the Indian samples were largely “self-referred” and this difference in the ascertainment method might possibly explain the variation in the rates across the samples. However, at least in one study,[ 91 ] the 18% rate of ADHD was higher than the 5-10% rate reported in community samples.[ 108 , 109 ] The elevated rate of ADHD in juvenile OCD in this study is consistent with the findings of previous studies[ 97 , 105 , 107 ] although the rate of ADHD is much lower than the 51-57% in children and 36-39% in adolescents reported in the studies by Geller and others.[ 97 , 107 ]

In the study by Jaisoorya et al . juvenile OCD was compared with adult-onset OCD, using multinomial logistic regression analysis.[ 91 ] There was positive association of chronic tics, ADHD, major depressive disorder, and Body Dysmorphic Disorder (BDD) with juvenile OCD. The TS showed an almost significant association with juvenile OCD. The BDD also had a positive association with juvenile-onset adult OCD. In addition regression analysis (juvenile-onset adult OCD vs. adult-onset OCD), showed positive association between social phobia, chronic tics and MDD and juvenile-onset adult OCD. These findings suggest that there are age-specific correlates of the disorder across the life cycle. Further, the findings suggest that OCD in juveniles is perhaps a developmental subtype of OCD with specific correlates such as high rate of ADHD and tic disorders.[ 96 , 97 , 107 ]

COURSE AND OUTCOME OF JUVENILE OBSESSIVE-COMPULSIVE DISORDER

Follow-up studies of OCD in children and adolescents have reported low rates of remission.[ 106 , 110 – 112 ] Similarly, studies of adult OCD have reported worse course in those with early onset of illness.[ 113 , 114 ] However, studies on long-term course and outcome of OCD in juveniles are few and many have small sample sizes. We discuss here a two to nine year follow-up study of 58 children and adolescents with DSM-III-R OCD from India.[ 90 ] The subjects were largely ‘self-referred’ (93%) and ‘drug-naïve’ (90%) at the time of consultation. None had received any form of psychotherapeutic intervention and none were treatment refractory at the time of first consultation. Most were treated with medications and only a few of them with a combination of medicines and exposure and response prevention. At the time of follow-up, only 29% were still receiving medication. The median duration without any treatment at the time of follow-up was 49 months. At follow-up, 62% of the subjects were in full remission or had ‘no OCD’ (Total Y-BOCS score = 0 to 3), 17% had subclinical OCD (Y-BOCS score, 4-15) and only 21% had clinical OCD (Y-BOCS>15). The median time to achieve full remission was 24 months and subjects were symptom free for a mean of 41 months prior to follow-up assessment. However, the most significant finding is that 28 subjects (48%) were in true remission (full remission and not on any treatment) and were not receiving treatment for a mean period of 58 months. Duration of follow-up and age-at-onset emerged as significant predictors of full remission. The odds of younger subjects having full remission or no OCD outcome were 1.5 times that of older subjects. Those who had ‘no OCD’ at follow-up had earlier age-at-onset of illness.

The high rate of ‘true remitters’ is in sharp contrast to the 6% rate in the study by Leonard and others.[ 106 ] The rate of clinical OCD (21%) at follow-up is low compared to the high rates of clinical OCD (35%-68%) reported in previous studies.[ 106 , 110 – 112 , 115 ] Favorable prognosis in this study could be due to several reasons. First, the sample was largely ‘self-referred’, ‘drug-naïve’, moderately ill, with relatively low rate of comorbidity (55%). In the classic study by Leonard et al ., the subjects were severely and chronically ill with history of treatment resistance in 75% of them and 100% comorbidity.[ 106 ] Second, a low rate of tic disorders (16%) and ADHD (3%) could have contributed to better prognosis.

The study findings suggest that juvenile OCD, at least, in self-referred, drug-naïve outpatient clinical samples has a good prognosis. The findings can be generalized to psychiatric hospital settings in India and perhaps to general psychiatric practice settings in the Western countries.

Indian research on various aspects of OCD has shown broad similarities with that of research from the other parts of the world. Clinical profile of OCD seems to be similar to what is described in the literature. Comorbid patterns also appear to be similar across cultures. Follow-up studies have shown that prognosis is favorable in the long-run. There is evidence from a large Indian study that tic disorders, hypochondriasis, BDD and trichotillomania are perhaps part of the putative OC spectrum disorders. However, eating disorders are uncommon in patients with OCD.

Biological research in OCD in India has paralleled the interest in the area in other parts of the world. There seems to be a consensus that serotonergic hypothesis may not explain all the abnormalities in OCD and that complex interactions between various neurotransmitters as well as environmental factors may be necessary to cause OCD. Although not a single case of PANDAS has been reported from India, several studies have shown the possible role of immunological factors in the causation of OCD.

Substantial research has been carried out in juveniles with OCD. The rates of ADHD and TS are somewhat lower in Indian samples compared to those from other parts of the world. There is a suggestion that juvenile OCD could be a developmental subtype of the disorder. Juvenile OCD seems to have a favorable prognosis.

There is surprisingly limited amount of data from India on treatment aspects of OCD. Currently, at NIMHANS, Bangalore there is ongoing research on various aspects of OCD such as clinical profile, course, biology and treatment.

Source of Support: Nil

Conflict of Interest: None declared