|Year : 2014 | Volume
| Issue : 2 | Page : 78-82
Neurocognitive deficits in obsessive compulsive disorder: A state or trait phenomenon?
Sachin Sharma1, Supriya Vaish1, JK Trivedi2, PK Dalal2
1 Department of Psychiatry, Subharti Medical College, Meerut, India
2 Department of Psychiatry, King George Medical College, Lucknow, Uttar Pradesh, India
|Date of Web Publication||20-Mar-2015|
134, Ram Sadan, Baghpat Road, Meerut, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Background: Studies have shown that in obsessive-compulsive disorder (OCD), there is impairment of neurocognitive functioning during the symptomatic phase. However, studies that explore the "state or trait" dependent nature of these neurocognitive deficits are largely lacking. By comparing the neuropsychological functions of the clinical and subclinical group of OCD patients and healthy controls; we tried to establish whether neuropsychological deficits in OCD were "state" dependent or independent. Materials and Methods: Twenty "mild to moderate" OCD patients, 15 subclinical (remitted) OCD patients, and 20 matched healthy controls were compared and assessed on computerized battery of neuropsychological tests including Wisconsin card sorting test, continuous performance test, and spatial working memory test. The observations were statistically analyzed. Results: Executive functions in both the subclinical and clinical groups performed poorly when compared to healthy controls. The patient groups made significantly more wrong responses, more missed responses and took more time to respond. On the test of spatial working memory, the mild to moderate OCD patients showed significant impairment, but not the subclinical patients group. Conclusion: Thus, we conclude that cognitive dysfunctions are core and enduring deficits of OCD, they seem to continue into the subclinical- well state. Certain cognitive deficits, depending on their presence or absence in subclinical cases, may be identified as "state" or "trait" markers of OCD.
Keywords: Neurocognitive functions, obsessive compulsive disorder, state marker, trait marker
|How to cite this article:|
Sharma S, Vaish S, Trivedi J K, Dalal P K. Neurocognitive deficits in obsessive compulsive disorder: A state or trait phenomenon?. J Mental Health Hum Behav 2014;19:78-82
|How to cite this URL:|
Sharma S, Vaish S, Trivedi J K, Dalal P K. Neurocognitive deficits in obsessive compulsive disorder: A state or trait phenomenon?. J Mental Health Hum Behav [serial online] 2014 [cited 2020 Apr 9];19:78-82. Available from: http://www.jmhhb.org/text.asp?2014/19/2/78/153715
| Introduction|| |
Obsessive-compulsive disorder (OCD) has high lifetime prevalence of 2-3% in many parts of the world; furthermore, it is among one of the most disabling conditions (World Health Organization Report in 2009).  There is now enhanced awareness that like schizophrenia, mood disorders and neurological disorders, OCD may be associated with a distinct pattern of neuropsychological deficits. These deficits in OCD consist primarily of executive deficits  involving frontal striatal system dysfunction,  impairment in visuospatial abilities,  and nonverbal memory. , Some studies also report deficit in attention set shifting abilities, response inhibition and trial and error learning. ,,, However, results of the neuropsychological studies have been inconsistent.
Ascertaining whether the cognitive impairment is a function of the present disease "state" or a long-term, stable "trait" has both heuristic and clinical implication. Cognitive deficits could be functioning as an intermediate variable between neurobiological abnormalities and OCD symptoms.
The studies in the field of cognitive dysfunctions in OCD patients have been done primarily in the west. , The literature in this regard strikingly lacks in the developing nations like India,  thus, an interesting area to be explored, as the Indian settings are quite different from the west in terms of culture and family dynamics. Objective of the present study was to throw light on the state and trait characteristics of neuropsychological deficits in OCD.
| Materials and Methods|| |
To evaluate whether the neuropsychological variables in OCD patients are a "state" or a "trait" phenomenon, a single point comparative noninvasive study of three groups including-15 subclinical (Group A) (Yale Brown's obsessive compulsive scale score [Y-BOCS] scores 0-7) and 20 clinical cases (Group B) (Y-BOCS scores 8-23) of OCD and well-matched control group of 20 subjects (Group C) was done. The study was carried out over a period of 1-year.
- Informed consent.
- Age group: 18-55 years
- Confirmed diagnosis of OCD according to Diagnostic and Statistical Manual for Mental disorder-IV (DSM IV) (APA, 1994) criteria
- Yale Brown's obsessive compulsive scale score to be <24
- The subject should have passed at least class 10 th
- History suggestive of other significant physical or neuropsychiatric disorder which can cause cognitive impairment
- History of psychoactive substance dependence or abuse
- Those patients receiving the medications associated with cognitive effects like tricyclic antidepressants, antipsychotics, lithium, and benzodiazepines were excluded.
Subjects satisfying the selection criteria (inclusion and exclusion criteria) were included in the study. After ensuring that the patients were free of benzodiazepine medication (if being taken, on the day of evaluation excluded), were then administered a semi-structured proforma including Y-BOCS symptoms checklist. They were assessed on the computer-based neurocognitive tests-including Wisconsin card sorting test (WCST) by Revonsuo and Portin (1995) where the stimulus cards reflect three stimulus parameters-color, form, and number. The response cards display figures of varying forms (crosses, circles, triangles, or stars), colors (red, blue, yellow, or green) and number of figures (one, two, three, or four). These cards are numbered from 1 to 64 on the lower left corner of the reverse side of ensuring a standard order of presentation. It can be applied on the subject in the age group of 6 ½ to 89 years.
With the exception of learning to learn the score (t = 0.658), which is one of the parameters of WCST, interscorer reliability coefficients range from 0.895 to 1.000. Intrascorer reliability coefficients range from 0.828 to 1.0. Continuous performance test (CPT) by Conner (1994), the test requires a participant to respond to a specified target when it is presented spontaneously within a stream of interfering visual stimuli. The task involves monitoring a random series of geometrical figures.
Attention/vigilance involves maintaining readings to respond to a particular target stimulus and inhibiting responses to nontargets over a period of time. It requires one to distinguish targets from nontargets an ability known as sensitivity. The results obtained are in terms of correct responses, wrong responses, missed responses and the reaction or response time. In the test, target stimulus is rare in frequency and presentation latency is brief. A total of 328 stimuli are presented, of which 28 are for practice. Stimulus duration and interstimulus latency are 50 ms and 1000 ms, respectively. Spatial working memory test (SWMT) by Revonsue and Portin (1995) the test of memory for spatial locations, the subject views a brief presentation of black circle on computer screen and then asked to point the location of circle after a delay of "0" s and 20 s, randomly. During the 20 s delay, the subject is engaged in a distraction task by asking to repeat continuously a three digits number, appearing on the screen, in severe order. The result in SWMT is obtained as the number of correct responses and number of nonadjacent errors at 0 s and 20 s delay, respectively.
For control group
The subjects satisfying the selection criteria, along with the usage of semi-structured proforma and general health questionnaire (Goldberg, 1972), were evaluated on the same computer based neurocognitive tests. The timings for administering the computer-based tests were between 12.00 noon and 4.00 pm.
| Results|| |
Maximum number of patients were in the age group of 18-26 years (65% in the clinical group and 60% in the subclinical group), predominantly males (60%). The mean duration of illness in the subclinical group was 5 + 1.534 years and in the clinical group was 4.65 + 2.06 years [Table 1]. On the WCST, both the subclinical and clinical groups performed significantly poor when compared with healthy controls. The patients (clinical and subclinical) used significantly more number of trials to complete the test (P < 0.001 for the clinical group and P < 0.01 for a subclinical group). They made more number of errors which implies that they had more difficulty in understanding the concept of the test (Percentage errors - P < 0.001 for both patient groups) in comparison to the healthy control. Patients made significantly more number of nonperseveration errors (P < 0.001 for both patient groups) which implies that either they were not interpreting the feedback properly, or they were matching the cards without any concept in mind. The patients also made more number of perseveration errors (P < 0.001 for both patient groups) indicative that they had difficulty in shifting between categories, although they were receiving the feedback to do so. The patients made significantly less number of conceptual responses (P < 0.001 for both groups) further supporting the notion that their understanding of the test was poorer than the controls. Trials to complete the first category were also statistically significantly taken more in the patient group indicating that the patient-initially had more problem in understanding the test than the controls. A parameter - "learning to learn scale" could not be obtained for all subjects. It requires that the subject should complete at least two and attempt at least three categories, which was not possible in all cases [Table 2], [Table 3] and [Table 4].
Comparing the subclinical (in "remission") patients were compared with the clinical group, statistically significant decline, in the parameters of percentage of total number of errors (P < 0.01), percentage perseveration errors (P < 0.01), percentage nonperseveration errors (P < 0.05), and percentage conceptual level response (P < 0.01) was seen more in the clinical group. Though on the parameters of trial administered, categories completed and trials to complete first category, the clinical group performed relatively poor yet were not statistically significantly impaired- hence, it is possible that these three parameters are "state" markers rather than "trait" markers.
| Discussion|| |
The poor performance shown by the patients on various parameters of WCST meant that they had poor executive function, deficits in set shifting, inhibition control, attention, and trial and error learning. The findings of the study are consistent with the deficits in the areas of set shifting ability, perseveration errors, response inhibition, and trial and error learning as seen in a number of earlier studies. ,,,,,, Some other studies have, however, failed to replicate these findings. ,,,
On the test for attention, vigilance and concentration abilities - CPT, the patient groups made significantly more wrong responses, that is, the errors of commission (P < 0.01 for both the clinical and subclinical group) and more missed response, that is, errors of omission (P < 0.05 for the subclinical comparison and P < 0.001 for the clinical comparison). These two parameters, the "vigilance," the subjects, are presented with a series of briefly presented stimuli and instructed to respond only to selected target stimuli and ignore all others. Similar findings of deficits in inhibition control and response inhibition have been seen in many earlier studies. ,,,,,,, When the subclinical and the clinical group were compared, statistically significant difference was seen only in the domain of "missed responses" that is errors of omission (P < 0.01) thus suggesting a possibility of these parameters being a "state" marker, and others being "trait" markers.
The patient group also took more time to respond than the control group and the differences were statistically significant (P < 0.001 each). When the clinical group was compared to the subclinical group, though the clinical group took more time to respond, yet statistical significance was not seen (P = 0.362).
The patients with mild to moderate OCD performed significantly worse than the control group on SWMT involving visual memory for prior actions. This makes sense when considering that certain OC behaviors involve doubting and checking behaviors that one might associate with visual memory for action, though the study does not differentiate among subtypes or quality of symptom expression. The findings are consistent with earlier studies.  Nevertheless, a link between OC behavior and working memory deficits has not been clearly demonstrated,  thus inviting future studies.
The subclinical OCD patient group did not show poor performance than the control group on SWMT. These findings do not provide evidence for a deficit in SWMT proper. This view is held by other studies.  A study suggested the deficits in SWMT in patients of OCD was significantly only for a region covering the anterior cingulate cortex hence suggesting that the abnormal performance pattern may be secondary to another aspect of executive dysfunction of OCD.  The patients performed significantly poor the pattern recognition test as compared to control subjects at 0 s delay. Significant deficits related to the ability to recognize the spatial locations of a set of stimuli reported after a delay of 20 s. Several studies have reported visual memory deficits on task requiring recall at 10 s or more. ,
The findings match most of the previous studies that have shown impairment visual reproduction and delayed recognition of figures, encoding, and retrieval. ,,,,,,,,
This immediate or working memory has been associated reliably with skill acquisition. The deficits in spatial working memory in OCD as suggested by the study, point toward the involvement of dorsal and ventral streams of neural connections originating at posterior regions, parietal region for spatial stimuli, and feeding forward to the prefrontal cortex. 
Thus, on WCST, both the subclinical and clinical groups (mild to moderate OCD) performed poorly when compared to healthy controls suggesting impaired executive functions and frontal lobe dysfunctions in OCD. Findings from of CPT, suggests impaired attention, vigilance, and concentration abilities in OCD. On the test of spatial working memory, the mild to moderate OCD patients showed significant impairment, but not the subclinical patients group. This finding does not provide evidence for a deficit in SWMT proper in OCD.
| Conclusion|| |
The results indicate that the patients with OCD shows a specific pattern of cognitive deficits related to spatial working memory, set shifting, abstract reasoning, planning ability and concentration and attentional task.
Thus, to conclude cognitive dysfunctions are core and enduring deficits of OCD, they seem to continue into the "subclinical - well state" (as per Y-BOCS tool). Certain cognitive deficits, owing to presence or absence in "subclinical" cases, may be state and/or trait markers of OCD. Deficient performance within these cognitive domains has important implications for clinical outcome measures including employability, social competency, and successful independent living.
| Limitations|| |
Due to the constraints of time bound study and stringent selection criteria, the sample size was small and hence the results are subjected to type II error. The study is a cross-sectional study, to further clarify the state-trait controversy longitudinal studies are needed.
The study had a clinic sample, most of the patients being on regular medications and follow-up, whether these findings can be generalized to other OCD patients (e.g. drug-free patients) who are not coming for follow-up is not known.
Owing to the limited time factor and resources, not many tests for neurocognitive tests could be done, for example, other studies also included tests like Block Design Subset of the Wechsler Adult Intelligence Scale, Mental Rotation Test, Moneys Road Map test.
| Future Studies|| |
Further, studies should focus on testing, whether optimizing the prophylactic pharmacological treatment and psycho-education might reduce cognitive impairment, and whether the OCD patients would benefit from neuropsychological rehabilitation in order to reduce the impact of cognitive impairment on their overall functioning.
High risk group studies, that is studies in the group of individuals with an increased genetic risk for OCD (e.g. monozygotic twins, first degree relatives) but without outright experiences of the illness, are valuable adjunct to investigation into temporal evaluation of cognitive dysfunction in OCD.
| References|| |
Kessler RC, Aguilar-Gaxiola S, Alonso J, et al
. The global burden of mental disorders: An update from the WHO World Mental Health (WMH) Surveys. Epidemiologia e psichiatria sociale 2009;18:23-33.
Lucey JV, Burness CE, Costa DC, Gacinovic S, Pilowsky LS, Ell PJ, et al.
Wisconsin Card Sorting Task (WCST) errors and cerebral blood flow in obsessive-compulsive disorder (OCD). Br J Med Psychol 1997;70 (Pt 4):403-11.
Anderson KE, Savage CR. Cognitive and neurobiological findings in obsessive-compulsive disorder. Psychiatr Clin North Am 2004;27:37-47, viii.
Hollander E, Cohen L, Richards M, Mullen L, DeCaria C, Stern Y. A pilot study of the neuropsychology of obsessive-compulsive disorder and Parkinson's disease: Basal ganglia disorders. J Neuropsychiatry Clin Neurosci 1993;5:104-7.
Christensen KJ, Kim SW, Dysken MW, Hoover KM. Neuropsychological performance in obsessive-compulsive disorder. Biol Psychiatry 1992;31:4-18.
Savage CR, Keuthen NJ, Jenike MA, Brown HD, Baer L, Kendrick AD, et al.
Recall and recognition memory in obsessive-compulsive disorder. J Neuropsychiatry Clin Neurosci 1996;8:99-103.
Behar D, Rapoport JL, Berg CJ, Denckla MB, Mann L, Cox C, et al.
Computerized tomography and neuropsychological test measures in adolescents with obsessive-compulsive disorder. Am J Psychiatry 1984;141:363-9.
Malloy P. Frontal lobe dysfunction in obsessive-compulsive disorder. In: Perecman E, editor. The Frontal Lobes Revisited. New York: The IRBN Press; 1987. p. 207-23.
Head D, Bolton D, Hymas N. Deficit in cognitive shifting ability in patients with obsessive-compulsive disorder. Biol Psychiatry 1989;25:929-37.
Veale 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.
Bannon 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.
Kennedy BL, Schwab JJ, Morris RL, Beldia G. Assessment of state and trait anxiety in subjects with anxiety and depressive disorders. Psychiatr Q 2001;72:263-76.
Rao NP, Reddy YC, Kumar KJ, Kandavel T, Chandrashekar CR. Are neuropsychological deficits trait markers in OCD? Prog Neuropsychopharmacol Biol Psychiatry 2008;32:1574-9.
Abbruzzese 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.
Hollander E, Schiffman E, Cohen B, Rivera-Stein MA, Rosen W, Gorman JM, et al.
Signs of central nervous system dysfunction in obsessive-compulsive disorder. Arch Gen Psychiatry 1990;47:27-32.
Hymas N, Lees A, Bolton D, Epps K, Head D. The neurology of obsessional slowness. Brain 1991;114 (Pt 5):2203-33.
Boone KB, Ananth J, Philpott L, Kaur A, Djenderedjian A: Neuropsychological characteristics of nondepressed adults with obsessive-compulsive disorder. Neuropsychiatry Neuropsychol Behav Neurol 1991;4:96-109.
Zielinski CM, Taylor MA, Juzwin KR. neuropsychological deficits in obsessive compulsive disorder. Neuropsychiatry Neuropsychol Behav Neurol 1991;4:110-26.
Abbruzzese M, Bellodi L, Ferri S, Scarone S. Frontal lobe dysfunction in schizophrenia and obsessive-compulsive disorder: A neuropsychological study. Brain Cogn 1995;27:202-12.
Boldrini M, Del Pace L, Placidi GP, Keilp J, Ellis SP, Signori S, et al.
Selective cognitive deficits in obsessive-compulsive disorder compared to panic disorder with agoraphobia. Acta Psychiatr Scand 2005;111:150-8.
Schmidtke K, Schorb A, Winkelmann G, Hohagen F. Cognitive frontal lobe dysfunction in obsessive-compulsive disorder. Biol Psychiatry 1998;43:666-73.
van der Wee NJ, Ramsey NF, Jansma JM, Denys DA, van Megen HJ, Westenberg HM, et al.
Spatial working memory deficits in obsessive compulsive disorder are associated with excessive engagement of the medial frontal cortex. Neuroimage 2003;20:2271-80.
Aronowitz BR, Hollander E, Decaria C, Cohen L, Saoud JB, Stein DJ. Neuropsychology of obsessive-compulsive disorder. Preliminary findings. Neuropsychiatry Neuropsychol Behav Neurol 1994;7:81-6.
Savage CR, Baer L, Keuthen NJ, Brown HD, Rauch SL, Jenike MA. Organizational strategies mediate nonverbal memory impairment in obsessive-compulsive disorder. Biol Psychiatry 1999;45:905-16.
Savage CR. The Role of emotion in strategic behaviour: Insights from psychopathology. In: Feldman Barrett L, Solovey P, editors. The Wisdom in Feeling: Psychological Processes in Emotional Intelligence. New York: Guilford Press; 2002.
Cohen LJ, Hollander E, DeCaria CM, Stein DJ, Simeon D, Liebowitz MR, et al.
Specificity of neuropsychological impairment in obsessive-compulsive disorder: A comparison with social phobic and normal control subjects. J Neuropsychiatry Clin Neurosci 1996;8:82-5.
Dirson S, Bouvard M, Cottraux J, Martin R. Visual memory impairment in patients with obsessive-compulsive disorder: A controlled study. Psychother Psychosom 1995;63:22-31.
Wilson FA, Scalaidhe SP, Goldman-Rakic PS. Dissociation of object and spatial processing domains in primate prefrontal cortex. Science 1993;260:1955-8.
[Table 1], [Table 2], [Table 3], [Table 4]