The Executive Function Of OCD Patients And Medication Effect: An ERP Reaserch

Obsessive-compulsive disorder (OCD) is the fourth most prevalent psychiatric disorder, with a lifetime prevalence of2～3%in United States. The core symptoms of OCD are Obsession and Compulsion (OC). In order to find out the pathogeny of these symtoms to develop more effective therapeutic method, numerous researchers have discussed this question from various principles, such as Psychopathology, Neuroscience, Molecular Biology and so on. The debate has not reached an agreement till now.In1992, Otto et al. proposed that the basis of Obsessions is the defect of the "Executive Function"(EF). EF is a fundamental concept including a wide range of cognitive processes and behavioral competencies. Some neuroscientists proposed that the OC symptoms reflect the cortico-strialtal-thalamic-cortical dysfunction. Based on this neuropsychological hypothesis, lots of researchers discussed the EF of OCD patients from different aspects, such as planning,, inhibitory control, working memory, etc. But most of these researches failed to get consistent results. In1997, Schwartz et al. put forward the hypothesis that the excessive neural activity, in part,"hyperactive error signals", involved in OCD symptomatology represents. And in2000, Gehring et al. used Error-Related Negtivity (ERN), one of the components of the Event-Related Brain Potentials (ERP), to exame the "hyperactive error signals" hypothesis and then proposed an "Action-Monitoring Dysfunction" hypothesis. Since then, a large number of researches used ERN as an index to reflect the EF of OCD (especially Action-Monitoring function and Error-Monitoring function) and tried to test the "Action-Monitoring Dysfunction" hypothesis. Some of these researches, which support this hypothesis, figured out that OCD patients showed significant larger ERN amplitude than Health Control participants (HC group) when they committed error reponses. But some other studies did not find the significant difference of the ERN amplitude between OCD patients and HC group.By overviewing the previous studies, we propose that there are two possible reasons for the inconsistent results in preious studies. The first, Benzodiazepine drugs may influence the action-monitoring system of the patients. The second, the tasks used by previous studies almost focused on the "cold" EF. While many studies showed that the damage of "hot" EF may be more related to the core symptoms of OCD. Therefore, the present study controlled the use of Benzodiazepine drugs and used both Go/Nogo task (reflecting "cold" EF) and Gambling task (reflecting "hot" EF) to exame our opinion and try to explore the pathogenesis of OCD.Three matched groups of participants: umOCD (OCD patients who did not take Benzodiazepine drugs), mOCD (OCD patients who took Benzodiazepine drugs), and HC (Health controls) took part in2experiments. Experiment1used Go/Nogo task to evoke Go/Nogo-ERN. It turned out that the amplitude of Go/Nogo-ERN in mOCD group was significant smaller than umOCD group. This verified that Benzodiazepine drugs could reduce the Action-Monitoring function and Error-Monitoring function. There was no significant difference in Go/Nogo-ERN amplitude between umOCD and HC group, which suggested that the "Action-Monitoring Dysfunction" hypothesis for OCD was not reliable. Experiment2made use of Gambling task to evoke Gamb-ERN. The Gamb-ERN in umOCD group was significantly larger than that in HC group. It means that when the patients conducting on-line evaluation of the riskiness of options and decisions, the umOCD's ACC area was more activated than HC's. Combining the results from Experiments1and2we draw an important conclusion that the Gamb-ERN, reflecting "hyperactive riskiness on-line evaluation", a kind of "hot" EF dysfunction, measured from the umOCD patients more reliably reflects the pathogenesis of OCD, relative to tradisional ERN which reflects "cold" EF dysfunction.