scholarly journals Set-shifting-related basal ganglia deformation as a novel familial marker of obsessive–compulsive disorder

2021 ◽  
pp. 1-4
Author(s):  
Masanori Isobe ◽  
Matilde Vaghi ◽  
Naomi A. Fineberg ◽  
Annemieke M. Apergis-Schoute ◽  
Edward T. Bullmore ◽  
...  

The symptoms of obsessive–compulsive disorder (OCD) are suggestive of cognitive rigidity, and previous work identified impaired flexible responding on set-shifting tasks in such patients. The basal ganglia are central to habit learning and are thought to be abnormal in OCD, contributing to inflexible, rigid habitual patterns of behaviour. Here, we demonstrate that increased cognitive inflexibility, indexed by poor performance on the set-shifting task, correlated with putamen morphology, and that patients and their asymptomatic relatives had common curvature abnormalities within this same structure. The association between the structure of the putamen and the extradimensional errors was found to be significantly familial in OCD proband–relative pairs. The data implicate changes in basal ganglia structure linked to cognitive inflexibility as a familial marker of OCD. This may reflect a predisposing heightened propensity toward habitual response patterns and deficits in goal-directed planning.

2001 ◽  
Vol 59 (3A) ◽  
pp. 587-589 ◽  
Author(s):  
Débora Palmini Maia ◽  
Francisco Cardoso

Tourette syndrome (TS) is a neuropsychiatric disorder characterized by a combination of multiple motor tics and at least one phonic tic. TS patients often have associated behavioral abnormalities such as obsessive compulsive disorder, attention deficit and hyperactive disorder. Coprolalia, defined as emission of obscenities or swearing, is one type of complex vocal tic, present in 8% to 26% of patients. The pathophysiology of coprolalia and other complex phonic tics remains ill-defined. We report a patient whose complex phonic tic was characterized by repetitively saying "breast cancer" on seeing the son of aunt who suffered from this condition. The patient was unable to suppress the tic and did not meet criteria for obsessive compulsive disorder. The phenomenology herein described supports the theory that complex phonic tics result from disinhibition of the loop connecting the basal ganglia with the limbic cortex.


2013 ◽  
Vol 28 (S2) ◽  
pp. 17-17
Author(s):  
E. Burguière

It has been shown these last years that optogenetic tool, that uses a combination of optics and genetics technics to control neuronal activity with light on behaving animals, allows to establish causal relationship between brain activity and normal or pathological behaviors [3]. In combination with animal model of neuropsychiatric disorder, optogenetic could help to identify deficient circuitry in numerous pathologies by exploring functional connectivity, with a specificity never reached before, while observing behavioral and/or physiological correlates. To illustrate the promising potential of these tools for the understanding of psychiatric diseases, we will present our recent study where we used optogenetic to block abnormal repetitive behavior in a mutant mouse model of obsessive-compulsive disorder [1]. Using a delay-conditioning task we showed that these mutant mouse model had a deficit in response inhibition that lead to repetitive behaviour. With optogenetic, we could stimulate a specific circuitry in the brain that connect the orbitofrontal cortex with the basal ganglia; a circuitry that has been shown to be dysfunctional in compulsive behaviors. We observed that these optogenetic stimulations, through their effect on inhibitory neurons of the basal ganglia, could restore the behavioral response inhibition and alleviate the compulsive behavior. These findings raise promising potential for the design of targeted deep brain stimulation therapy for disorders involving excessive repetitive behavior and/or for the optimization of already existing stimulation protocol [2].


1998 ◽  
Vol 10 (1) ◽  
pp. 116-117 ◽  
Author(s):  
Philip R. Saba ◽  
Khurshed Dastur ◽  
M. Reza Raji ◽  
Matcheri S. Keshavan ◽  
M. Ammar Katerji

1996 ◽  
Vol 26 (6) ◽  
pp. 1261-1269 ◽  
Author(s):  
D. M. Veale ◽  
B. J. Sahakian ◽  
A. M. Owen ◽  
I. M. Marks

SynopsisForty patients with obsessive–compulsive disorder (OCD) were compared to matched healthy controls on neuropsychological tests which are sensitive to frontal lobe dysfunction. On a computerized version of the Tower of London test of planning, the patients were no different from healthy controls in the accuracy of their solutions. However, when they made a mistake, they spent more time than the controls in generating alternative solutions or checking that the next move would be correct. The results suggest that OCD patients have a selective deficit in generating alternative strategies when they make a mistake. In a separate attentional set-shifting task, OCD patients were impaired in a simple discrimination learning task and showed a continuous cumulative increase in the number who failed at each stage of the task, including the crucial extra-dimensional set shifting stage. This suggests that OCD patients show deficits in both acquiring and maintaining cognitive sets.The cognitive deficits in OCD may be summarized as: (i) being easily distracted by other competing stimuli; (ii) excessive monitoring and checking of the response to ensure a mistake does not occur; and (iii) when a mistake does occur, being more rigid at setting aside the main goal and planning the necessary subgoals. Both studies support the evidence of fronto-striatal dysfunction in OCD and the results are discussed in terms of an impaired Supervisory Attentional System.


2009 ◽  
Vol 4 (1) ◽  
pp. 35-45 ◽  
Author(s):  
Stephen Correia ◽  
Emily Hubbard ◽  
Jason Hassenstab ◽  
Agustin Yip ◽  
Josef Vymazal ◽  
...  

1998 ◽  
Vol 173 (S35) ◽  
pp. 38-44 ◽  
Author(s):  
Jeffrey M. Schwartz

Background Recent research has demonstrated that cognitive-behavioural therapy (CBT) for obsessive-compulsive disorder (OCD) can systematically modify cerebral metabolic activity in a manner which is significantly related to clinical outcome.Method A substantial body of research is reviewed which supports an involvement of neural circuitry connecting the orbitofrontal cortex, cingulate gyrus and basal ganglia in the expression of the symptoms of OCD.Results Data are presented which expand upon previous work demonstrating effects of CBTon functional interactions between limbic cortex and the basal ganglia.Conclusions The relevance of these effects of CBTon brain function is discussed in the context of recent advances in our knowledge of cortical–basal ganglia physiology. The clinical importance of these data is best appreciated when they are seen to reflect the interactive nature of the relationships between cognitive choice, behavioural output and brain activity.


1997 ◽  
Vol 10 (2-3) ◽  
pp. 101-103 ◽  
Author(s):  
Faustino Lopez-Rodriguez ◽  
Ibrahim Gunay ◽  
Nancy Glaser

This report presents a syndrome resembling obsessive convulsive disorder (OCD) secondary to a stroke in the left basal ganglia. The patient's syndrome is virtually identical to those that have been described in bilateral damage of the basal ganglia. However, the stroke described in this case report is located unilaterally in the left basal ganglia. In addition, experience in treating a patient with OCD induced by structural damage of basal ganglia is presented.


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