Research in Obsessive-Compulsive Disorder’s (OCD) neurobiology showed dysfunction in frontostriatal circuits, and from other brain areas like parietal cortex, which plays a main role in the process of OCD genesis. These neurobiological specificities leads to impaired neuropsychological functioning in some domains. The aim of this review is to understand better the nature of neuropsychological deficits in OCD and their link to neurobiology, in order to use these knowledge to prognosticate or predict the efficacity of OCD treatment such as behaviour therapy or anti-depressant treatment.

First of all, the main cognitive functions known to be impaired in OCD are executive function, processing speed, sustained attention and non-verbal memory. Focusing on executive functions, the main domains showing deficits are inhibition, planning and decision-making. About intelligence, studies showed controversial results : some studies suggested that patients with OCD have a higher intelligence, but several studies showed a lower IQ in this population, but this latter result needs to be taking with caution because of the role of the impaired processing speed in the IQ performance calculation. Also, there seem to be an interdependency between cognitive domains leading to secondary impairments explained by a primary impairment of another cognitive function. For instance, impairment in nonverbal memory could be secondary to an encoding strategy inefficiency.

Relation between neuropsychological deficits and symptoms severity has also been investigated in several studies, who showed the absence of association between symptoms and neuropsychological test performance. On the other hand, findings also showed that if some neuropsychological deficits remain stable during time of illness, other may fluctuate with symptom severity, such as visuospatial memory or verbal memory. About the relationship between neuropsychological deficits and symptom dimensions (ordering, contamination, checking…), studied showed that symptoms dimensions are linked with specific neuroanatomical regions, correlated with differences of neuropsychological deficits according to symptoms dimension. For example, individuals experiencing OCD with checking symptoms performed lower on pattern recognition, planning, problem-solving and response inhibition compared to individuals experiencing OCD with washing symptoms dimension.

Furthermore, the role of insight in OCD symptoms on the neuropsychological performance isn’t neglectable : correlations were found between insight and response inhibition, verbal memory, categorical fluency and intelligence. But, as insight to illness is willing to change over the course of the pathology and might be more associated with certain symptom dimensions, future studies need to further investigate the relationship between insight and neuropsychological performances.

About the link between neuropsychological deficits and treatment response, some studies showed for example that lower verbal fluency is associated with lower response to behaviour therapy, while higher verbal intelligence, verbal memory and better performance on Stroop test led to a better response to cognitive behaviour therapy as well as fluoxetine treatment.

This review also focused on the specificity of neuropsychological deficits in OCD. Considering the shared risk factors (genetic and environmental) and neurobiology across psychiatric pathologies, a neuropsychological overlap is expected. But some studies showed that orbitofrontal cortex involvement was more specific in OCD. Therefore, response inhibition and alternation may be a specificity of OCD.

Finally, the authors investigated the possibility of neuropsychological deficits as an endophenotype in OCD. Endophenotypes are defined as characteristics that are not really visible to the naked eye and considered to lie between the genotype and disease phenotype. The reference criterias to state if a characteristic can be considered as endophenotype are : high heritability, consistent association with illness of interest, co-segregate in a family irrespective of expression of the illness, state independent of trait nature and expression in unaffected family members. In fact, studies showed that neuropsychological deficits such as poorer cognitive flexibility, motor inhibition, decision-making, planning and working memory were present in unaffected first-degree relatives of patients with OCD. Also, impairments in set-shifting ability, alternation, response inhibition and non-verbal memory are seen in patients even after they recovered from OCD, which suggest a trait nature of neuropsychological deficits. These studies are in favour of the consideration of neuropsychological deficits in OCD as endophenotypes, even if further studies are needed especially to investigate the genetic field in this area.

To conclude, these findings suggest significant deficits in neurocognitive domains in OCD, especially in executive functions and nonverbal memory. These impairments remain present after recovery, which support the idea of the trait nature of these deficits. On the other hand, symptom severity, comorbid psychiatric disorder and anti-depressant treatments seem to have minimal effect on neuropsychological functions. Studies also show a similar but less important deficits in unaffected family members of patients with OCD, emphasising the possibility of neuropsychological deficits to be endophenotype markers of OCD. Further studies remain necessary, especially longitudinal ones, to examine the relation between clinical symptoms and neuropsychological deficits over the course of the pathology.  

Vocabulary learned :

  • Sustained = soutenu
  • Hence = par conséquent
  • set-shifting = is an executive function that involves the ability to unconsciously shift attention between one task and another

Bibliography : Suhas, S., & Rao, N. P. (2019). Neurocognitive deficits in obsessive-compulsive disorder: A selective review. Indian journal of psychiatry, 61(Suppl 1), S30–S36. https://doi.org/10.4103/psychiatry.IndianJPsychiatry_517_18

Author : MERCIER Alice

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