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REVIEW ARTICLE  
Year : 2019  |  Volume : 61  |  Issue : 7  |  Page : 30-36
Neurocognitive deficits in obsessive–compulsive disorder: A selective review


Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India

Click here for correspondence address and email

Date of Web Publication9-Jan-2019
 

   Abstract 


Obsessive–compulsive disorder (OCD) is a debilitating mental illness characterized by an early onset and chronic course. Evidence from several lines of research suggests significant neuropsychological deficits in patients with OCD; executive dysfunction and nonverbal memory deficits have been reported consistently in OCD. These deficits persist despite controlling potential confounders such as comorbidity, severity of illness, and medications. Neuropsychological impairments are independent of illness severity, thus suggesting that the neuropsychological deficits are trait markers of the disease. In addition, these deficits are seen in first-degree relatives of individuals with OCD. These reports suggest that neuropsychological deficits are potential endophenotype markers in OCD. Neuropsychological studies in pediatric OCD are limited; they show impairments of small effect size across multiple domains but with doubtful clinical significance. Preliminary evidence shows that different symptom dimensions of OCD may have unique neuropsychological deficits suggestive of discrete but overlapping neuroanatomical regions for individual symptom dimensions. Overall, neuropsychological deficits further support the role of frontostriatal circuits in the neurobiology of OCD. In addition, emerging literature also suggests the important role of other areas, in particular parietal cortex. Preliminary evidence suggests the possible role of neuropsychological deficits to be markers of treatment response but needs to be examined in future. Longitudinal studies with examination of patients at different time points and examination of their potential utility as predictors of treatment response are needed in future.

Keywords: Endophenotype, executive functions, memory, neurocognition, obsessive–compulsive disorder

How to cite this article:
Suhas S, Rao NP. Neurocognitive deficits in obsessive–compulsive disorder: A selective review. Indian J Psychiatry 2019;61, Suppl S1:30-6

How to cite this URL:
Suhas S, Rao NP. Neurocognitive deficits in obsessive–compulsive disorder: A selective review. Indian J Psychiatry [serial online] 2019 [cited 2019 Mar 26];61, Suppl S1:30-6. Available from: http://www.indianjpsychiatry.org/text.asp?2019/61/7/30/249682





   Introduction Top


Obsessive–compulsive disorder (OCD) is a common mental illness characterized by an early onset and chronic course.[1] Although there are limited epidemiological studies focusing on OCD, the lifetime prevalence of OCD in India has been reported to be around 0.6%[2] and the point prevalence has been reported to be around 3.3%.[3] Research from the past three decades has resulted in increased understanding of course, outcome, and pathophysiology of OCD and related disorders. OCD and related disorders stand unique, independent of anxiety disorders, in the recent diagnostic and classificatory systems.[4]

Evidence from several lines of research into the neurobiology of OCD suggests abnormalities in frontostriatal circuits, with contribution from other brain areas like parietal cortex to play critical role in the pathogenesis of OCD.[5],[6] Neuroimaging and neuropsychological tests have received considerable scientific attention to further elucidate the nature of abnormalities in these brain circuits. In addition to understanding the functional abnormalities in these circuits, neuropsychological deficits have also been studied as potential endophenotype, predictor of response to treatment, and prognostic marker of OCD as well.[7],[8],[9] While the neurocognitive domains involved in OCD are reasonably well established, the existing literature about their clinical utility as marker for treatment response or prognostication is still preliminary and often unclear.

This review aims to summarize nature of neuropsychological deficits in OCD and their contribution toward understanding neurobiology as well as potential application to prognosticate/predict treatment response. This selective review does not aim to systematically examine all available literature but focus on key findings and in particular on relation between clinical features, subgroups, and neuropsychological deficits seen in OCD.


   Neuropsychological Tests Commonly Used in Obsessive–Compulsive Disorder Top


Considering the involvement of frontostriatal circuits in the pathogenesis of OCD,[6],[10] majority of the neuropsychological studies have focused on these circuits. Some studies have examined other brain circuits as well. Commonly used neuropsychological tests in patients with OCD are summarized in [Table 1].
Table 1: Commonly examined neurocognitive domains and neuropsychological tests used in obsessive-compulsive disorder

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Some of the more specific neuropsychological tests used in OCD with the possible neuroanatomical correlates are summarized in [Table 2].
Table 2: Neuroanatomical correlates of commonly used neuropsychological tests in obsessive-compulsive disorder

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   Neuropsychological Deficits in Obsessive–Compulsive Disorder Top


Studies in symptomatic OCD suggest impairment in executive function, processing speed, sustained attention, and nonverbal memory.[41],[43],[44],[45],[46],[47] Subdomains of executive function that have shown deficits include response inhibition, planning, decision-making, and encoding of nonverbal memory. These findings remain significant even after controlling the effects of age, gender, and education.[48] Although earlier accounts presumed OCD patients to have higher intelligence,[49] several studies have shown that persons with OCD have lower full-scale IQ and performance IQ as compared to controls.[50] However, one cannot rule out the confounding effect of impaired processing speed in performance IQ tests.[50]

Interdependency between cognitive domains

Several authors have hypothesized that impairments in all these domains may not be primary and possibly secondary to deficits in other cognitive domains. For example, impairments in decision-making could be secondary to impairments in divided attention, action restrain, and action cancellation.[21] Similarly, impairments in nonverbal memory could be mediated by deficient encoding strategies[51] or due to impairments in meta-memory, one's knowledge about one's own memory.[52] They argue that this “doubt about one's memory” may be associated with checking compulsions, therefore leading to poorer performance on formal neuropsychological testing. This is further supported by evidence that those with checking compulsions are less confident of their memory.[53] Others have argued that there may be a memory bias toward threat-related stimulus in environment thus leading to relative deficits on nonthreat-related memory performance;[54],[55] but, this is not completely accepted.[56],[57] As majority of the neuropsychological tests are dependent on performance speed,[58] some authors have argued that personality traits of perfectionism and response slowing linked to depressive symptoms[59],[60] may artificially result in impaired performance on formal testing.


   Relation between Clinical Features, Subgroups, and Neuropsychological Deficits Top


Relation with symptom severity

Several studies have suggested significant association between the severity of symptoms and neuropsychological deficits in OCD.[61],[62],[63],[64] However, other studies have reported the absence of association between symptoms and neuropsychological test performance.[65],[66] Some have suggested performance to be independent of symptom severity but dependent on the duration of the illness.[67] A few studies have also reported the presence of significant neuropsychological deficits in the premorbid phase, in symptomatic recovery, as well as in patients who have recovered from OCD, further supporting the absence of relation between symptom severity and neuropsychological performance.[8],[68],[69] However, one cannot rule out the possibility that some neuropsychological deficits may remain stable throughout the course of the illness but others (composite performance, visuospatial memory, and verbal memory) may fluctuate with symptom severity.[63],[70],[71] Future studies with longitudinal designs need to examine the relation between obsessive–compulsive symptoms' severity and neuropsychological deficits.

Relation with age at onset of obsessive–compulsive disorder

Pediatric-onset OCD is considered as a unique subtype of OCD by several investigators with differences in sex ratio,[72] its association with different comorbidities (with higher prevalence of tics and attention deficit hyperactivity disorder),[73] and presence of less obsessional triggers for compulsions[74] compared to adult-onset OCD. Few authors have also proposed differences in neurobiology[75],[76] as well as differential genetic susceptibility.[77] These differences are also reflected in differences in neuropsychological performance between adult-onset and pediatric OCD. Overall, children with OCD seem to have no clinically significant impairments in neuropsychological performance as compared to healthy controls.[78],[79] Studies looking into the comparison of the neuropsychological profiles of adult OCD and pediatric-onset OCD have revealed more impairment in set shifting, nonverbal memory, and processing speed in adults with OCD but not in children suffering from OCD.[45],[78] This suggests that some forms of childhood-onset OCD could be different from others who persist into adulthood, thus suggesting a neurodevelopmental subtype of OCD.

Symptom dimensions of obsessive–compulsive disorder and neuropsychological deficits

Evidence from several lines of research suggests stable symptom dimensions in OCD. Although the number of dimensions is still debated, symmetry/ordering, hoarding, contamination/cleaning, aggressive/checking, and sexual/religious symptom dimensions are well accepted.[80],[81],[82] The symptom dimensions have also been linked to specific neuroanatomical regions.[83],[84],[85],[86],[87] Understandably, a few studies have also examined the relation between symptom dimensions and neuropsychological deficits. Different methods have been employed to examine neuropsychological correlates of symptom dimensions; some studies have used factor-analyzed symptom dimensions, others have used dimensional scores on specific instruments such as the Dimensional Yale-Brown Obsessive–Compulsive Scale, and a few others have compared discrete groups of patients such as checkers and washers. A summary of these findings is given in [Table 3]. While there is an overlap, there are specific and distinct neuropsychological deficits associated with unique symptom dimensions as well. Few studies have compared between subgroups of OCD based on symptom dimensions and reported poorer pattern recognition, planning, problem–solving, and response inhibition among those with checking compared to those with washing.[88],[89]
Table 3: Symptom dimensions in obsessive-compulsive disorder and neuropsychological deficits

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Insight and its relationship with neuropsychological performance

Insight into symptoms in OCD is an important predictor of treatment response. Poorer insight is associated with complex clinical presentation, greater dysfunction, and poorer prognosis.[93],[94],[95],[96],[97] However, the relationship between insight into the illness and neuropsychological performance is sparsely examined. Kashyap et al.[98] examined the neuropsychological correlates of insight and reported significant correlation between insight and response inhibition, verbal memory, category fluency, and intelligence. As insight to illness fluctuates over the course of the illness and may be more frequently associated with certain symptom dimensions,[99] future studies need to consider these additional factors in examining the relationship between insight and neuropsychological deficits.

Neuropsychological deficits and treatment response

A few studies have examined utility of neuropsychological tests to predict response to treatment, both pharmacological and psychological. In one of the first studies, lower verbal fluency was associated with poorer response to behavior therapy.[100] Another study reported that higher verbal intelligence, verbal memory, and better performance on Stroop test were associated with better response to cognitive behavior therapy or fluoxetine.[101] In another interesting study, poorer performance on the Iowa gambling task was associated with poor response to selective serotonin reuptake inhibitors (SSRIs) alone but better response to augmentation with an antipsychotic drug.[102]

SSRIs which form the mainstay of treatment in OCD have been reported to confound the performance, especially on tests of planning.[42] However, other authors have argued for the absence of significant effect of medications.[103] A study with large number of drug-naïve OCD patients reported significant impairment in tower of London, further supporting the primary nature of deficits and absence of significant effect of medications.[104] On the contrary, few studies have suggested improvement in neuropsychological test performance after treatment with SSRIs.[70],[71],[105] Overall, these reports suggest that neuropsychological deficits seen in OCD are primary and not secondary to SSRIs. On the other hand, one cannot rule out the effect of antipsychotics commonly used for augmentation of SSRI treatment[106],[107] and associated use of anticholinergic medications.

Effect of other moderating variables

Several researchers have suggested that comorbid depression, medication/s, and personality styles such as inflated sense of responsibility could significantly influence neuropsychological impairments seen in OCD.[59],[60],[108],[109],[110] Symptoms of depression such as decreased psychomotor activity, loss of energy, and amotivation may affect the performance of individual.[111] Only a few studies have specifically examined the effect of depressive symptoms on neuropsychological performance in OCD; one study compared patients with OCD and those with unipolar depression and reported greater cognitive deficits in OCD compared to unipolar depression.[24] Abramovitch et al.[45] examined the relationship between severity of depression and neuropsychological performance. This meta-analysis did not suggest significant relation between depressive symptoms and neuropsychological performance in OCD. Further, evidence for persisting neuropsychological deficits in recovered OCD patients in the absence of depression or anxiety[8] provides further support to the view that these deficits are primary to OCD and not secondary to depression.

Specificity of neuropsychological deficits in obsessive–compulsive disorder

The dysfunction of frontostriatal circuits is not specific to OCD alone and has been implicated in the neurobiology of other neuropsychiatric disorders as well. There is significant overlap of neuropsychological impairment across OCD, schizophrenia, and depression. Kazhungil et al.[112] compared the neuropsychological profile of OCD and schizophrenia and reported no significant differences between the two groups and also failed to establish a unique neuropsychological profile for schizo-obsessive disorder. Considering the shared risk factors, both genetic and environmental, and shared neurobiology across psychiatric disorders, this considerable overlap in neuropsychological deficits is expected. The deficits across all three disorders are fairly consistent with predominant frontal involvement with deficits in verbal working memory, interference testing, fluency, and set shifting.[113] While there are similarities in the domains, there are differences as well in cognitive domains and severity of the deficits.[24],[68],[114] The involvement of the orbitofrontal cortex is however more specific to OCD.[115],[116] Hence, domains of response inhibition and alternation may be specific to OCD.

Neuropsychological deficits as endophenotype in obsessive–compulsive disorder: Current status

Endophenotypes are characteristics that are not readily visible to the naked eye and considered to lie between the genotype and disease phenotype. A candidate measure has to satisfy certain criteria to be considered as endophenotype. These criteria include (a) high heritability, (b) consistent association with illness of interest, (c) co-segregate in a family irrespective of expression of the illness, (d) state independent or trait nature, and (e) expression in unaffected family members.[117],[118] Several neurophysiological, biochemical, and endocrinological measures have been proposed as endophenotypes in neuropsychiatry. Similarly, neuropsychological deficits have also been proposed as endophenotype marker in OCD. Neuropsychological deficits in the form of poorer cognitive flexibility, motor inhibition,[119],[120] decision-making, behavioral reversal[9] planning, and working memory[121] are seen in unaffected first-degree relatives of patients with OCD. Impairments in set-shifting ability, alternation, response inhibition, and nonverbal memory[8] are seen in patients even after symptomatic recovery suggesting trait nature of these deficits. These studies support neuropsychological deficits in OCD as endophenotypes. However, studies need to examine the relation between the neuropsychological deficits and potential genetic correlates in future.


   Conclusions Top


Evidence from several lines of research suggests significant impairments in neurocognitive domains in OCD. Impairments in executive functions and nonverbal memory are well replicated by different studies. Impairments are seen before the onset of symptoms and persist in recovered phase as well suggesting the trait nature of the deficits. These deficits persist even after controlling potential confounding factors. Symptom severity, comorbid psychiatric conditions, and SSRIs seem to have minimal effect on neuropsychological performance. Studies also suggest similar but less severe deficits in unaffected first-degree relatives of patients with OCD, raising the possibility that these deficits are endophenotype marker of OCD. A few differences exist between subgroups, namely pediatric OCD as compared to adult OCD and different symptom dimensions suggesting possible differences in neurobiology between these subtypes.

Neuropsychological deficits have been demonstrated in patients with OCD prior to the onset of the illness[69] and even after recovery from clinical symptoms.[8] They are also present in first degree relatives of patients suffering from OCD.[9] However, longitudinal studies examining the same individuals across time points are lacking which could give definitive evidence to the relation between clinical symptoms and neuropsychological deficits over the course of the illness. Such longitudinal studies would also evaluate whether these deficits are static or progressive. Further studies need to also take into consideration the possible differences between pediatric and adult-onset OCD. Finally, there is an immediate need for uniform assessments in OCD as at present, there are no guidelines or consensus on the tests to be used. Such a consensus cognitive battery could allow cross-cultural comparison of results and could be used in future for multicentric trials for prediction of treatment response.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Correspondence Address:
Dr. Naren P Rao
Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/psychiatry.IndianJPsychiatry_517_18

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