Abstract
Previous research showed that dysfunctions of fronto-striatal neural networks are implicated in the pathophysiology of obsessive–compulsive disorder (OCD). Accordingly, patients with OCD showed altered performances during decision-making tasks. As P300, evoked by oddball paradigms, is suggested to be related to attentional and cognitive processes and generated in the medial temporal lobe and orbitofrontal and cingulate cortices, it is of special interest in OCD research. Therefore, this study aimed to investigate P300 in OCD and its associations with brain activity during decision-making: P300, evoked by an auditory oddball paradigm, was analysed in 19 OCD patients and 19 healthy controls regarding peak latency, amplitude and source density power in parietal cortex areas by sLORETA. Afterwards, using a fMRI paradigm, Blood–oxygen-level-dependent (BOLD) contrast imaging was conducted during a delay-discounting paradigm. We hypothesised differences between groups regarding P300 characteristics and associations with frontal activity during delay-discounting. The P300 did not differ between groups, however, the P300 latency over the P4 electrode correlated negatively with the NEO-FFI score openness to experience in patients with OCD. In healthy controls, P300 source density power correlated with activity in frontal regions when processing rewards, a finding which was absent in OCD patients. To conclude, associations of P300 with frontal brain activation during delay-discounting were found, suggesting a contribution of attentional or context updating processes. Since this association was absent in patients with OCD, the findings could be interpreted as being indeed related to dysfunctions of fronto-striatal neural networks in patients with OCD.
Highlights
Obsessive–compulsive disorder (OCD) is a psychiatric condition that involves neurobiological dysfunctions of frontostriatal neural networks
In a recently published study, using the same dataset as the present investigation, the results indicated that activation of dorsolateral and medial prefrontal cortex (PFC) as well as ventral striatum activation differed between OCD patients and healthy volunteers during the delay-discounting paradigm [37]
No differences between groups were observed for the BIS-11 total score, distinct differences emerged for the BIS-11 subscales, with OCD patients reaching lower scores in attentional impulsiveness (OCD: M = 12.58, standard deviations (SD) = 3.08; control: M = 17.63, SD = 4.0; U = 42.5, Z = − 4.05, p < 0.001) and higher scores in motor impulsiveness compared to the control group (OCD: M = 21.47, SD = 2.59; control: M = 19.32, SD = 3.13; U = 104.0, Z = − 2.25, p = 0.025)
Summary
Obsessive–compulsive disorder (OCD) is a psychiatric condition that involves neurobiological dysfunctions of frontostriatal neural networks. It has been suggested that OCD is caused by abnormal activity in the cortico-striato-thalamo-cortical (CSTC) circuits, including the orbitofrontal cortex (OFC), the striatum within basal ganglia and the thalamus [5, 6], which is summarised as the neuroanatomical hypothesis. European Archives of Psychiatry and Clinical Neuroscience of diminished inhibitory effects of the striatum (especially the globus pallidus internus) on the thalamus. This hypothesis suggests that OCD could be associated with dysfunctional cognitive and metacognitive processing. In order to investigate the proposed OFC hyperactivity in OCD patients, the P300 component of auditory event-related potentials (ERPs) could be a suitable tool, as it is proposed that P300 is generated in the medial temporal lobe, OFC and cingulate cortex [7]. The P300 occurs with a latency of approximately 300–500 ms after the occurrence of rare or task-related stimuli or after a target stimulus (compared to non-target stimuli) and was measured over frontalto-temporal and parietal electrodes
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