scholarly journals Abnormal brain functional network dynamics in obsessive–compulsive disorder patients and their unaffected first‐degree relatives

2021 ◽  
Author(s):  
Ziwen Peng ◽  
Ya Guo ◽  
Xiangshu Wu ◽  
Qiong Yang ◽  
Zhen Wei ◽  
...  
1989 ◽  
Vol 155 (S8) ◽  
pp. 15-24 ◽  
Author(s):  
D. L. Murphy ◽  
J. Zohar ◽  
C. Benkelfat ◽  
M. T. Pato ◽  
T. A. Pigott ◽  
...  

Involvement of the brain serotonin (5-HT) neurotransmitter system in obsessive-compulsive disorder (OCD) was originally suggested on the basis of therapeutic effects found with the semi-selective serotonin uptake inhibitor, clomipramine. More recent studies directly comparing clomipramine with non-selective or norepinephrine-selective uptake inhibitors, such as desipramine or nortriptyline, as well as studies with new, more selective serotonin uptake inhibitors, including fluvoxamine and fluoxetine, have supported that hypothesis. Clomipramine's antiobsessional effect has been augmented with the serotonin precursor, L-tryptophan, or with lithium, which has prominent serotonergic effects. Patients whose OCD symptoms improved on clomipramine worsened when the drug was discontinued (regardless of duration of therapy) and improved when clomipramine was reinstituted. OCD symptoms also worsened when metergoline, a 5-HT antagonist, was given to patients who had improved with clomipramine. Metergoline given alone had no effect. Administration of m-chlorophenylpiperazine (m-CPP), a 5-HT receptor agonist, to untreated OCD patients increased their anxiety, depression, and dysphoria, and exacerbated their OC symptoms. After 4 months of clomipramine therapy, m-CPP failed to produce the same behavioural effects, suggesting an alteration of a 5-HT subsystem (possibly downregulation of some 5-HT receptors). The data reviewed suggest an important role for an abnormal brain 5-HT subsystem in patients with OCD.


2020 ◽  
Vol 237 (10) ◽  
pp. 3117-3123
Author(s):  
Christine Lochner ◽  
Samuel R. Chamberlain ◽  
Martin Kidd ◽  
Lian Taljaard ◽  
Naomi A. Fineberg ◽  
...  

2007 ◽  
Vol 164 (2) ◽  
pp. 335-338 ◽  
Author(s):  
Samuel R. Chamberlain ◽  
Naomi A. Fineberg ◽  
Lara A. Menzies ◽  
Andrew D. Blackwell ◽  
Edward T. Bullmore ◽  
...  

2018 ◽  
Vol 57 ◽  
pp. 24-30 ◽  
Author(s):  
Katharina Bey ◽  
Christian Kaufmann ◽  
Leonhard Lennertz ◽  
Anja Riesel ◽  
Julia Klawohn ◽  
...  

2019 ◽  
Vol 50 (9) ◽  
pp. 1490-1500 ◽  
Author(s):  
Chenjie Dong ◽  
Qiong Yang ◽  
Jingjing Liang ◽  
Carol A. Seger ◽  
Hongying Han ◽  
...  

AbstractBackgroundCompulsive behaviors in obsessive-compulsive disorder (OCD) have been related to impairment within the associative cortical-striatal system connecting the caudate and prefrontal cortex that underlies consciously-controlled goal-directed learning and behavior. However, little is known whether this impairment may serve as a biomarker for vulnerability to OCD.MethodsUsing resting-state functional magnetic resonance imaging (fMRI), we employed Granger causality analysis (GCA) to measure effective connectivity (EC) in previously validated striatal sub-regions, including the caudate, putamen, and the nucleus accumbens, in 35 OCD patients, 35 unaffected first-degree relatives and 35 matched healthy controls.ResultsBoth OCD patients and their first-degree relatives showed greater EC than controls between the left caudate and the orbital frontal cortex (OFC). Both OCD patients and their first-degree relatives showed lower EC than controls between the left caudate and lateral prefrontal cortex. These results are consistent with findings from task-related fMRI studies which found impairment in the goal-directed system in OCD patients.ConclusionsThe same changes in EC were present in both OCD patients and their unaffected first-degree relatives suggest that impairment in the goal-directed learning system may be a biomarker for OCD.


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