Year : 2019  |  Volume : 61  |  Issue : 7  |  Page : 30--36

Neurocognitive deficits in obsessive–compulsive disorder: A selective review

Satish Suhas, Naren P Rao 
 Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India

Correspondence Address:
Dr. Naren P Rao
Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka


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.

How to cite this article:
Suhas S, Rao NP. Neurocognitive deficits in obsessive–compulsive disorder: A selective review.Indian J Psychiatry 2019;61:30-36

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Suhas S, Rao NP. Neurocognitive deficits in obsessive–compulsive disorder: A selective review. Indian J Psychiatry [serial online] 2019 [cited 2019 Jan 16 ];61:30-36
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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

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}

Some of the more specific neuropsychological tests used in OCD with the possible neuroanatomical correlates are summarized in [Table 2].{Table 2}

 Neuropsychological Deficits in Obsessive–Compulsive Disorder

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

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}

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.


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.

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Conflicts of interest

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1Abramowitz JS, Taylor S, McKay D. Obsessive-compulsive disorder. Lancet 2009;374:491-9.
2Reddy YC, Rao NP, Khanna S. An overview of Indian research in obsessive compulsive disorder. Indian J Psychiatry 2010;52:S200-9.
3Jaisoorya TS, Janardhan Reddy YC, Nair BS, Rani A, Menon PG, Revamma M, et al. Prevalence and correlates of obsessive-compulsive disorder and subthreshold obsessive-compulsive disorder among college students in Kerala, India. Indian J Psychiatry 2017;59:56-62.
4American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. American Psychiatric Association; 2013. Available from: [Last accessed on 2018 Jul 15].
5Maia TV, Cooney RE, Peterson BS. The neural bases of obsessive-compulsive disorder in children and adults. Dev Psychopathol 2008;20:1251-83.
6Saxena S, Rauch SL. Functional neuroimaging and the neuroanatomy of obsessive-compulsive disorder. Psychiatr Clin North Am 2000;23:563-86.
7Chamberlain SR, Blackwell AD, Fineberg NA, Robbins TW, Sahakian BJ. The neuropsychology of obsessive compulsive disorder: The importance of failures in cognitive and behavioural inhibition as candidate endophenotypic markers. Neurosci Biobehav Rev 2005;29:399-419.
8Rao NP, Reddy YC, Kumar KJ, Kandavel T, Chandrashekar CR. Are neuropsychological deficits trait markers in OCD? Prog Neuropsychopharmacol Biol Psychiatry 2008;32:1574-9.
9Viswanath B, Janardhan Reddy YC, Kumar KJ, Kandavel T, Chandrashekar CR. Cognitive endophenotypes in OCD: A study of unaffected siblings of probands with familial OCD. Prog Neuropsychopharmacol Biol Psychiatry 2009;33:610-5.
10Saxena S, Brody AL, Schwartz JM, Baxter LR. Neuroimaging and frontal-subcortical circuitry in obsessive-compulsive disorder. Br J Psychiatry Suppl 1998;(35):26-37.
11Wechsler D. The measurement and appraisal of adult intelligence. Acad Med 1958;33:706.
12McCrimmon AW, Smith AD. Review of the Wechsler abbreviated scale of intelligence, second edition (WASI-II). J Psychol Educ Assess 2013;31:337-41.
13Schrank FA. Woodcock-Johnson III tests of cognitive abilities. In: Contemporary Intellectual Assessment: Theories, Tests, and Issues. New York, US: Guilford Press; 2005. p. 371-401.
14Terman LM, Merrill MA. Stanford-Binet Intelligence Scale: Manual for the Third Revision, Form L-M. Oxford, England: Houghton Mifflin; 1960.
15Krikorian R, Bartok J, Gay N. Tower of London procedure: A standard method and developmental data. J Clin Exp Neuropsychol 1994;16:840-50.
16Veale DM, Sahakian BJ, Owen AM, Marks IM. Specific cognitive deficits in tests sensitive to frontal lobe dysfunction in obsessive-compulsive disorder. Psychol Med 1996;26:1261-9.
17Buelow MT, Suhr JA. Construct validity of the Iowa gambling task. Neuropsychol Rev 2009;19:102-14.
18Berch DB, Krikorian R, Huha EM. The corsi block-tapping task: Methodological and theoretical considerations. Brain Cogn 1998;38:317-38.
19Rabinovici GD, Stephens ML, Possin KL. Executive dysfunction. Continuum (Minneap Minn) 2015;21:646-59.
20Jensen AR, Rohwer WD Jr. The stroop color-word test: A review. Acta Psychol (Amst) 1966;25:36-93.
21Eagle DM, Bari A, Robbins TW. The neuropsychopharmacology of action inhibition: Cross-species translation of the stop-signal and go/no-go tasks. Psychopharmacology (Berl) 2008;199:439-56.
22Lipszyc J, Schachar R. Inhibitory control and psychopathology: A meta-analysis of studies using the stop signal task. J Int Neuropsychol Soc 2010;16:1064-76.
23Henry JD. A meta-analytic review of wisconsin card sorting test and verbal fluency performance in obsessive-compulsive disorder. Cogn Neuropsychiatry 2006;11:156-76.
24Purcell R, Maruff P, Kyrios M, Pantelis C. Neuropsychological deficits in obsessive-compulsive disorder: A comparison with unipolar depression, panic disorder, and normal controls. Arch Gen Psychiatry 1998;55:415-23.
25Maj M, Satz P, Janssen R, Zaudig M, Starace F, D'Elia L, et al. WHO neuropsychiatric AIDS study, cross-sectional phase II. Neuropsychological and neurological findings. Arch Gen Psychiatry 1994;51:51-61.
26Blackburn HL, Benton AL. Revised administration and scoring of the digit span test. J Consult Psychol 1957;21:139-43.
27Tombaugh TN. Trail making test A and B: Normative data stratified by age and education. Arch Clin Neuropsychol 2004;19:203-14.
28Evans AS, Preston AS. Test of everyday attention. In: Kreutzer JS, DeLuca J, Caplan B, editors. Encyclopedia of Clinical Neuropsychology. New York: Springer New York; 2011. p. 2491-2. Available from: [Last accessed on 2018 Oct 12].
29Poreh A. Rey auditory verbal learning test. In: The Corsini Encyclopedia of Psychology. American Cancer Society; 2010. p. 1. Available from: [Last accessed on 2018 Oct 12].
30Deckersbach T, Savage CR, Henin A, Mataix-Cols D, Otto MW, Wilhelm S, et al. Reliability and validity of a scoring system for measuring organizational approach in the complex figure test. J Clin Exp Neuropsychol 2000;22:640-8.
31Benton AL. A visual retention test for clinical use. Arch Neurol Psychiatry 1945;54:212-6.
32Borod JC, Goodglass H, Kaplan E. Normative data on the Boston diagnostic aphasia examination, parietal lobe battery, and the Boston naming test. J Clin Neuropsychol 1980;2:209-15.
33de Renzi E, Vignolo LA. The token test: A sensitive test to detect receptive disturbances in aphasics. Brain 1962;85:665-78.
34Patterson J. Multilingual aphasia examination. In: Kreutzer JS, DeLuca J, Caplan B, editors. Encyclopedia of Clinical Neuropsychology. New York: Springer New York; 2011. p. 1674-6. Available from: [Last accessed on 2018 Oct 12].
35Shulman KI. Clock-drawing: Is it the ideal cognitive screening test? Int J Geriatr Psychiatry 2000;15:548-61.
36Tamkin AS, Jacobsen R. Age-related norms for the Hooper visual organization test. J Clin Psychol 1984;40:1459-63.
37Benton AL, Varney NR, Hamsher KD. Visuospatial judgment. A clinical test. Arch Neurol 1978;35:364-7.
38Gross-Isseroff R, Sasson Y, Voet H, Hendler T, Luca-Haimovici K, Kandel-Sussman H, et al. Alternation learning in obsessive-compulsive disorder. Biol Psychiatry 1996;39:733-8.
39Lawrence NS, Wooderson S, Mataix-Cols D, David R, Speckens A, Phillips ML, et al. Decision making and set shifting impairments are associated with distinct symptom dimensions in obsessive-compulsive disorder. Neuropsychology 2006;20:409-19.
40van den Heuvel OA, Veltman DJ, Groenewegen HJ, Cath DC, van Balkom AJ, van Hartskamp J, et al. Frontal-striatal dysfunction during planning in obsessive-compulsive disorder. Arch Gen Psychiatry 2005;62:301-9.
41Savage CR, Baer L, Keuthen NJ, Brown HD, Rauch SL, Jenike MA, et al. Organizational strategies mediate nonverbal memory impairment in obsessive-compulsive disorder. Biol Psychiatry 1999;45:905-16.
42Kuelz AK, Hohagen F, Voderholzer U. Neuropsychological performance in obsessive-compulsive disorder: A critical review. Biol Psychol 2004;65:185-236.
43Olley A, Malhi G, Sachdev P. Memory and executive functioning in obsessive-compulsive disorder: A selective review. J Affect Disord 2007;104:15-23.
44Mataix-Cols D, Alonso P, Hernández R, Deckersbach T, Savage CR, Manuel Menchón J, et al. Relation of neurological soft signs to nonverbal memory performance in obsessive-compulsive disorder. J Clin Exp Neuropsychol 2003;25:842-51.
45Abramovitch A, Abramowitz JS, Mittelman A. The neuropsychology of adult obsessive-compulsive disorder: A meta-analysis. Clin Psychol Rev 2013;33:1163-71.
46Cox CS. Neuropsychological abnormalities in obsessive-compulsive disorder and their assessments. Int Rev Psychiatry 1997;9:45-60.
47Tallis F. The neuropsychology of obsessive-compulsive disorder: A review and consideration of clinical implications. Br J Clin Psychol 1997;36(Pt 1):3-20.
48Kashyap H, Kumar JK, Kandavel T, Reddy YC. Neuropsychological functioning in obsessive-compulsive disorder: Are executive functions the key deficit? Compr Psychiatry 2013;54:533-40.
49Stein DJ, Stone MH. Essential papers on obsessive-compulsive disorder. New York: New York University Press; 1997. p. 413.
50Abramovitch A, Anholt G, Raveh-Gottfried S, Hamo N, Abramowitz JS. Meta-analysis of intelligence quotient (IQ) in obsessive-compulsive disorder. Neuropsychol Rev 2018;28:111-20.
51Konishi M, Shishikura K, Nakaaki S, Komatsu S, Mimura M. Remembering and forgetting: Directed forgetting effect in obsessive-compulsive disorder. Neuropsychiatr Dis Treat 2011;7:365-72.
52Flavell JH, Wellman HM. Metamemory. 1975. Available from: [Last accessed on 2018 Jul 10].
53Tolin DF, Abramowitz JS, Brigidi BD, Amir N, Street GP, Foa EB, et al. Memory and memory confidence in obsessive-compulsive disorder. Behav Res Ther 2001;39:913-27.
54Radomsky AS, Rachman S, Hammond D. Memory bias, confidence and responsibility in compulsive checking. Behav Res Ther 2001;39:813-22.
55Coles ME, Heimberg RG. Memory biases in the anxiety disorders: Current status. Clin Psychol Rev 2002;22:587-627.
56Foa EB, Amir N, Gershuny B, Molnar C, Kozak MJ. Implicit and explicit memory in obsessive-compulsive disorder. J Anxiety Disord 1997;11:119-29.
57Ceschi G, Van der Linden M, Dunker D, Perroud A, Brédart S. Further exploration memory bias in compulsive washers. Behav Res Ther 2003;41:737-48.
58Spreen O, Strauss E. A Compendium of Neuropsychological Tests: Administration, Norms, and Commentary. 2nd ed. New York, US: Oxford University Press; 1998.
59Moritz S, Ruhe C, Jelinek L, Naber D. No deficits in nonverbal memory, metamemory and internal as well as external source memory in obsessive-compulsive disorder (OCD). Behav Res Ther 2009;47:308-15.
60Aycicegi A, Dinn WM, Harris CL, Erkmen H. Neuropsychological function in obsessive-compulsive disorder: Effects of comorbid conditions on task performance. Eur Psychiatry 2003;18:241-8.
61Abramovitch A, Dar R, Schweiger A, Hermesh H. Neuropsychological impairments and their association with obsessive-compulsive symptom severity in obsessive-compulsive disorder. Arch Clin Neuropsychol 2011;26:364-76.
62Lacerda AL, Dalgalarrondo P, Caetano D, Haas GL, Camargo EE, Keshavan MS, et al. Neuropsychological performance and regional cerebral blood flow in obsessive-compulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2003;27:657-65.
63Rao NP, Arasappa R, Reddy NN, Venkatasubramanian G, Reddy YC. Emotional interference in obsessive-compulsive disorder: A neuropsychological study using optimized emotional stroop test. Psychiatry Res 2010;180:99-104.
64Segalàs C, Alonso P, Labad J, Jaurrieta N, Real E, Jiménez S, et al. Verbal and nonverbal memory processing in patients with obsessive-compulsive disorder: Its relationship to clinical variables. Neuropsychology 2008;22:262-72.
65Bédard MJ, Joyal CC, Godbout L, Chantal S. Executive functions and the obsessive-compulsive disorder: On the importance of subclinical symptoms and other concomitant factors. Arch Clin Neuropsychol 2009;24:585-98.
66Bucci P, Galderisi S, Catapano F, Di Benedetto R, Piegari G, Mucci A, et al. Neurocognitive indices of executive hypercontrol in obsessive-compulsive disorder. Acta Psychiatr Scand 2007;115:380-7.
67Okasha A, Rafaat M, Mahallawy N, El Nahas G, El Dawla AS, Sayed M, et al. Cognitive dysfunction in obsessive-compulsive disorder. Acta Psychiatr Scand 2000;101:281-5.
68Bannon S, Gonsalvez CJ, Croft RJ, Boyce PM. Executive functions in obsessive-compulsive disorder: State or trait deficits? Aust N Z J Psychiatry 2006;40:1031-8.
69Grisham JR, Anderson TM, Poulton R, Moffitt TE, Andrews G. Childhood neuropsychological deficits associated with adult obsessive-compulsive disorder. Br J Psychiatry 2009;195:138-41.
70van der Wee NJ, Ramsey NF, van Megen HJ, Denys D, Westenberg HG, Kahn RS, et al. Spatial working memory in obsessive-compulsive disorder improves with clinical response: A functional MRI study. Eur Neuropsychopharmacol 2007;17:16-23.
71Kim MS, Park SJ, Shin MS, Kwon JS. Neuropsychological profile in patients with obsessive-compulsive disorder over a period of 4-month treatment. J Psychiatr Res 2002;36:257-65.
72Castle DJ, Deale A, Marks IM. Gender differences in obsessive compulsive disorder. Aust N Z J Psychiatry 1995;29:114-7.
73Mancebo MC, Garcia AM, Pinto A, Freeman JB, Przeworski A, Stout R, et al. Juvenile-onset OCD: Clinical features in children, adolescents and adults. Acta Psychiatr Scand 2008;118:149-59.
74Kalra SK, Swedo SE. Children with obsessive-compulsive disorder: Are they just “little adults”? J Clin Invest 2009;119:737-46.
75Geller E, Faerber EN, Legido A, Melvin JJ, Hunter JV, Wang Z, et al. Rasmussen encephalitis: Complementary role of multitechnique neuroimaging. AJNR Am J Neuroradiol 1998;19:445-9.
76Trifiletti RR, Packard AM. Immune mechanisms in pediatric neuropsychiatric disorders. Tourette's syndrome, OCD, and PANDAS. Child Adolesc Psychiatr Clin N Am 1999;8:767-75.
77Pauls DL, Alsobrook JP 2nd, Goodman W, Rasmussen S, Leckman JF. A family study of obsessive-compulsive disorder. Am J Psychiatry 1995;152:76-84.
78Abramovitch A, Abramowitz JS, Mittelman A, Stark A, Ramsey K, Geller DA, et al. Research review: Neuropsychological test performance in pediatric obsessive-compulsive disorder – A meta-analysis. J Child Psychol Psychiatry 2015;56:837-47.
79Beers SR, Rosenberg DR, Dick EL, Williams T, O'Hearn KM, Birmaher B, et al. Neuropsychological study of frontal lobe function in psychotropic-naive children with obsessive-compulsive disorder. Am J Psychiatry 1999;156:777-9.
80Leckman JF, Grice DE, Boardman J, Zhang H, Vitale A, Bondi C, et al. Symptoms of obsessive-compulsive disorder. Am J Psychiatry 1997;154:911-7.
81Mataix-Cols D, Rauch SL, Manzo PA, Jenike MA, Baer L. Use of factor-analyzed symptom dimensions to predict outcome with serotonin reuptake inhibitors and placebo in the treatment of obsessive-compulsive disorder. Am J Psychiatry 1999;156:1409-16.
82Baer L. Factor analysis of symptom subtypes of obsessive compulsive disorder and their relation to personality and tic disorders. J Clin Psychiatry 1994;55 Suppl:18-23.
83Koch K, Wagner G, Schachtzabel C, Schultz CC, Straube T, Güllmar D, et al. White matter structure and symptom dimensions in obsessive-compulsive disorder. J Psychiatr Res 2012;46:264-70.
84Mataix-Cols D, Wooderson S, Lawrence N, Brammer MJ, Speckens A, Phillips ML, et al. Distinct neural correlates of washing, checking, and hoarding symptom dimensions in obsessive-compulsive disorder. Arch Gen Psychiatry 2004;61:564-76.
85Harrison BJ, Pujol J, Cardoner N, Deus J, Alonso P, López-Solà M, et al. Brain corticostriatal systems and the major clinical symptom dimensions of obsessive-compulsive disorder. Biol Psychiatry 2013;73:321-8.
86van den Heuvel OA, Remijnse PL, Mataix-Cols D, Vrenken H, Groenewegen HJ, Uylings HB, et al. The major symptom dimensions of obsessive-compulsive disorder are mediated by partially distinct neural systems. Brain 2009;132:853-68.
87Pujol J, Soriano-Mas C, Alonso P, Cardoner N, Menchón JM, Deus J, et al. Mapping structural brain alterations in obsessive-compulsive disorder. Arch Gen Psychiatry 2004;61:720-30.
88Leopold R, Backenstrass M. Neuropsychological differences between obsessive-compulsive washers and checkers: A systematic review and meta-analysis. J Anxiety Disord 2015;30:48-58.
89Nedeljkovic M, Kyrios M, Moulding R, Doron G, Wainwright K, Pantelis C, et al. Differences in neuropsychological performance between subtypes of obsessive-compulsive disorder. Aust N Z J Psychiatry 2009;43:216-26.
90Kashyap H, Kumar JK, Kandavel T, Reddy YC. Relationships between neuropsychological variables and factor-analysed symptom dimensions in obsessive compulsive disorder. Psychiatry Res 2017;249:58-64.
91Hashimoto N, Nakaaki S, Omori IM, Fujioi J, Noguchi Y, Murata Y, et al. Distinct neuropsychological profiles of three major symptom dimensions in obsessive-compulsive disorder. Psychiatry Res 2011;187:166-73.
92Omori IM, Murata Y, Yamanishi T, Nakaaki S, Akechi T, Mikuni M, et al. The differential impact of executive attention dysfunction on episodic memory in obsessive-compulsive disorder patients with checking symptoms vs. those with washing symptoms. J Psychiatr Res 2007;41:776-84.
93Erzegovesi S, Cavallini MC, Cavedini P, Diaferia G, Locatelli M, Bellodi L, et al. Clinical predictors of drug response in obsessive-compulsive disorder. J Clin Psychopharmacol 2001;21:488-92.
94Ravi Kishore V, Samar R, Janardhan Reddy YC, Chandrasekhar CR, Thennarasu K. Clinical characteristics and treatment response in poor and good insight obsessive-compulsive disorder. Eur Psychiatry 2004;19:202-8.
95Catapano F, Perris F, Fabrazzo M, Cioffi V, Giacco D, De Santis V, et al. Obsessive-compulsive disorder with poor insight: A three-year prospective study. Prog Neuropsychopharmacol Biol Psychiatry 2010;34:323-30.
96Matsunaga H, Kiriike N, Matsui T, Oya K, Iwasaki Y, Koshimune K, et al. Obsessive-compulsive disorder with poor insight. Compr Psychiatry 2002;43:150-7.
97Catapano F, Sperandeo R, Perris F, Lanzaro M, Maj M. Insight and resistance in patients with obsessive-compulsive disorder. Psychopathology 2001;34:62-8.
98Kashyap H, Kumar JK, Kandavel T, Reddy YC. Neuropsychological correlates of insight in obsessive-compulsive disorder. Acta Psychiatr Scand 2012;126:106-14.
99Cherian AV, Narayanaswamy JC, Srinivasaraju R, Viswanath B, Math SB, Kandavel T, et al. Does insight have specific correlation with symptom dimensions in OCD? J Affect Disord 2012;138:352-9.
100Sieg J, Leplow B, Hand I. Neuropsychological Deficits and Treatment Response in Obsessive-Compulsive Disorder. Verhaltenstherapie 1999;9:7-14.
101D'Alcante CC, Diniz JB, Fossaluza V, Batistuzzo MC, Lopes AC, Shavitt RG, et al. Neuropsychological predictors of response to randomized treatment in obsessive-compulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2012;39:310-7.
102BCavedini P, Bassi T, Zorzi C, Bellodi L. The advantages of choosing antiobsessive therapy according to decision-making functioning. J Clin Psychopharmacol 2004;24:628-31.
103Mataix-Cols D, Alonso P, Pifarré J, Menchón JM, Vallejo J. Neuropsychological performance in medicated vs. unmedicated patients with obsessive-compulsive disorder. Psychiatry Res 2002;109:255-64.
104Krishna R, Udupa S, George CM, Kumar KJ, Viswanath B, Kandavel T, et al. Neuropsychological performance in OCD: A study in medication-naïve patients. Prog Neuropsychopharmacol Biol Psychiatry 2011;35:1969-76.
105Rosenblat JD, Kakar R, McIntyre RS. The cognitive effects of antidepressants in major depressive disorder: A systematic review and meta-analysis of randomized clinical trials. Int J Neuropsychopharmacol 2015;19. pii: pyv082.
106Terry AV Jr., Mahadik SP. Time-dependent cognitive deficits associated with first and second generation antipsychotics: Cholinergic dysregulation as a potential mechanism. J Pharmacol Exp Ther 2007;320:961-8.
107Keefe RS, Silva SG, Perkins DO, Lieberman JA. The effects of atypical antipsychotic drugs on neurocognitive impairment in schizophrenia: A review and meta-analysis. Schizophr Bull 1999;25:201-22.
108Moritz S, Kloss M, von Eckstaedt FV, Jelinek L. Comparable performance of patients with obsessive-compulsive disorder (OCD) and healthy controls for verbal and nonverbal memory accuracy and confidence: Time to forget the forgetfulness hypothesis of OCD? Psychiatry Res 2009;166:247-53.
109Simpson HB, Rosen W, Huppert JD, Lin SH, Foa EB, Liebowitz MR, et al. Are there reliable neuropsychological deficits in obsessive-compulsive disorder? J Psychiatr Res 2006;40:247-57.
110Abbruzzese M, Ferri S, Scarone S. Wisconsin card sorting test performance in obsessive-compulsive disorder: No evidence for involvement of dorsolateral prefrontal cortex. Psychiatry Res 1995;58:37-43.
111Basso MR, Bornstein RA, Carona F, Morton R. Depression accounts for executive function deficits in obsessive-compulsive disorder. Neuropsychiatry Neuropsychol Behav Neurol 2001;14:241-5.
112Kazhungil F, Kumar KJ, Viswanath B, Shankar RG, Kandavel T, Math SB, et al. Neuropsychological profile of schizophrenia with and without obsessive compulsive disorder. Asian J Psychiatr 2017;29:30-4.
113Moritz S, Birkner C, Kloss M, Jahn H, Hand I, Haasen C, et al. Executive functioning in obsessive-compulsive disorder, unipolar depression, and schizophrenia. Arch Clin Neuropsychol 2002;17:477-83.
114Nielen MM, Den Boer JA. Neuropsychological performance of OCD patients before and after treatment with fluoxetine: Evidence for persistent cognitive deficits. Psychol Med 2003;33:917-25.
115Huey ED, Zahn R, Krueger F, Moll J, Kapogiannis D, Wassermann EM, et al. Apsychological and neuroanatomical model of obsessive-compulsive disorder. J Neuropsychiatry Clin Neurosci 2008;20:390-408.
116Menzies L, Chamberlain SR, Laird AR, Thelen SM, Sahakian BJ, Bullmore ET, et al. Integrating evidence from neuroimaging and neuropsychological studies of obsessive-compulsive disorder: The orbitofronto-striatal model revisited. Neurosci Biobehav Rev 2008;32:525-49.
117Turetsky BI, Calkins ME, Light GA, Olincy A, Radant AD, Swerdlow NR, et al. Neurophysiological endophenotypes of schizophrenia: The viability of selected candidate measures. Schizophr Bull 2007;33:69-94.
118Gottesman II, Gould TD. The endophenotype concept in psychiatry: Etymology and strategic intentions. Am J Psychiatry 2003;160:636-45.
119Chamberlain SR, Menzies L, Hampshire A, Suckling J, Fineberg NA, del Campo N, et al. Orbitofrontal dysfunction in patients with obsessive-compulsive disorder and their unaffected relatives. Science 2008;321:421-2.
120Chamberlain SR, Fineberg NA, Menzies LA, Blackwell AD, Bullmore ET, Robbins TW, et al. Impaired cognitive flexibility and motor inhibition in unaffected first-degree relatives of patients with obsessive-compulsive disorder. Am J Psychiatry 2007;164:335-8.
121Delorme R, Goussé V, Roy I, Trandafir A, Mathieu F, Mouren-Siméoni MC, et al. Shared executive dysfunctions in unaffected relatives of patients with autism and obsessive-compulsive disorder. Eur Psychiatry 2007;22:32-8.