Compulsive behavior is a core symptom of both obsessive compulsive disorder (OCD) and cocaine addiction (CA). Across both pathologies, one can identify a priori goal-directed actions (purportedly anxiolytic checking or washing in OCD and pleasure-seeking drug use in addiction) that turn into rigid, ritualized and repetitive behaviors over which the patient loose control. One possible psychopathological mechanism underlying compulsivity is behavioral inflexibility, namely a deficit in the aptitude to dynamically adapt to novel contexts and changing reward rules. The probabilistic reversal learning paradigm allows to objectively assess behavioral flexibility by challenging participants with a task where they have to learn through trials-and-errors which of two stimuli is the most-often rewarded one, while adjusting to sudden inconspicuous contingency reversals. We therefore hypothesized that both OCD and CA would be associated with impaired cognitive flexibility, as measured through perseverative response rate following contingency reversals in this task. Interestingly, impulsivity may also be assessed within this task via the tendency of participants to switch from one stimulus to the other following probabilistic errors. To investigate cognitive inflexibility in relation to CA and OCD respectively, we first compared the performance in a probabilistic reversal learning task of cocaine users, ex cocaine users (abstinent for 2 months or more), and controls, as well as that of participants from the general population whose obsessive-compulsive traits were assessed using the OCI-R, a well-validated self-questionnaire. Our task yielded results similar to those found in the literature: cocaine addicts changed their responses more often, and learned less effectively. Ex-cocaine addicts performed better than addicts but worse than controls, suggesting that addicts’ poor results may be in part explained by reversible cognitive consequences of addiction. Addicts with less cognitive impairments may also be less likely to relapse. Regarding the relationship of flexibility to subclinical OCD traits, we found no link between OCI-R score and perseveration, or between impulsiveness and excessive switching.

Objectives: The current study aimed to determine whether reversal learning impairments and feedback-related negativity (FRN), reflecting reward prediction error signals generated by negative feedback during the reversal learning tasks, were associated with social disinhibition in a group of participants with traumatic brain injury (TBI). Methods: Number of reversal errors on a social and a non-social reversal learning task and FRN were examined for 21 participants with TBI and 21 control participants matched for age. Participants with TBI were also divided into low and high disinhibition groups based on rated videotaped interviews. Results: Participants with TBI made more reversal errors and produced smaller amplitude FRNs than controls. Furthermore, participants with TBI high on social disinhibition made more reversal errors on the social reversal learning task than did those low on social disinhibition. FRN amplitude was not related to disinhibition. Conclusions: These results suggest that impairment in the ability to update behavior when social reinforcement contingencies change plays a role in social disinhibition after TBI. Furthermore, the social reversal learning task used in this study may be a useful neuropsychological tool for detecting susceptibility to acquired social disinhibition following TBI. Finally, that the FRN amplitude was not associated with social disinhibition suggests that reward prediction error signals are not critical for behavioral adaptation in the social domain. (JINS, 2016, 21, 303–313)

The aim of this study was to explore the cerebral correlates of functional deficits that occur in behavioral variant frontotemporal dementia (bvFTD). A specific neuropsychological battery, the Social cognition & Emotional Assessment (SEA; Funkiewiez et al., 2012), was used to assess impaired social and emotional functions in 20 bvFTD patients who also underwent structural MRI scanning. The SEA subscores of theory of mind, reversal-learning tests, facial emotion identification, and apathy evaluation were entered as covariates in a voxel-based morphometry analysis. The results revealed that the gray matter volume in the rostral part of the medial prefrontal cortex [mPFC, Brodmann area (BA) 10] was associated with scores on the theory of mind subtest, while gray matter volume within the orbitofrontal (OFC) and ventral mPFC (BA 11 and 47) was related to the scores observed in the reversal-learning subtest. Gray matter volume within BA 9 in the mPFC was correlated with scores on the emotion recognition subtest, and the severity of apathetic symptoms in the Apathy scale covaried with gray matter volume in the lateral PFC (BA 44/45). Among these regions, the mPFC and OFC cortices have been shown to be atrophied in the early stages of bvFTD. In addition, SEA and its abbreviated version (mini-SEA) have been demonstrated to be sensitive to early impairments in bvFTD (Bertoux et al., 2012). Taken together, these results suggest a differential involvement of orbital and medial prefrontal subregions in SEA subscores and support the use of the SEA to evaluate the integrity of these regions in the early stages of bvFTD. (JINS, 2012, 18, 972–985)

Previous lesion studies of color-reversal learning in pigeons show that an impairment results when (1) the tectofugal visual pathway is damaged at either the thalamic level (nucleus rotundus) or the telencephalic level (ectostriatum), or (2) the thalamofugal visual pathway is damaged at the telencephalic level (the visual Wulst). An impairment does not result, however, when the thalamic source of thalamofugal input (n. opticus principalis thalami or OPT) to the visual Wulst is damaged. These results suggest that the visual Wulst plays a role in color-reversal learning as a consequence of visual information routed from the tectofugal pathway via other visual areas in the telencephalon. One such area is the hyperstriatum ventrale (HV). In the present study, after ablation of the medial and lateral regions of HV, pigeons were trained postoperatively to discriminate between two colors presented simultaneously. After reaching criterion, the pigeons were required to perform a series of discrimination reversals in which the positive and negative stimuli were interchanged. Lesions of medial HV resulted in impaired performance of a color-discrimination task (i.e. original learning), but did not affect discrimination reversal. An impairment in color-reversal learning resulted from combined damage to lateral HV and the fronto-thalamic tract (FT), which carries ascending visual input from OPT to the visual Wulst. No deficits were observed when either lateral HV or FT were damaged alone. These findings suggest that both the thalamofugal and tectofugal pathways provide the visual Wulst with visual input relevant to color-reversal learning.

The performance of pigeons on a color-reversal learning task was assessed after thalamic lesions disrupting the thalamofugal and tectofugal visual pathways. Successful performance of a simultaneous color discrimination was accomplished after surgery, and a series of reversals of the original discrimination followed during which the positive and negative consequences associated with the stimuli were interchanged. Shimizu and Hodos (1989) had reported that lesions of two laminae in the visual wulst (IHA and HD), both targets of the avian thalamofugal pathway, resulted in increased errors in a color-reversal learning task in pigeons. This finding suggested that the thalamofugal pathway might play a role in visual discrimination involving stimulus context changes. In the present study, lesions of the OPT complex (the thalamic source of afferents to IHA and HD) were found to have no effect on color-reversal learning performance. Instead, we found that damage to nucleus rotundus (the thalamic component of the tectofugal pathway) resulted in deficits that were far in excess of those that had been obtained after IHA and HD lesions. We suggest that the color-reversal learning deficits after Wulst lesions are not due to the Wulst's connections with the thalamofugal pathway, but rather to its connections with the tectofugal pathway.