Nejvíce citovaný článek - PubMed ID 23701862
Standardized low-resolution electromagnetic tomography in obsessive-compulsive disorder--a replication study
Introduction: Deficits in neurocognitive mechanisms such as inhibition control and cognitive flexibility have been suggested to mediate the symptoms in obsessive-compulsive disorder (OCD). These mechanisms are proposedly controlled by the "affective" and "executive" orbitofronto-striato-thalamo-cortical (CSTC) circuits with well-documented morphological and functional alterations in OCD that are associated with OCD symptoms. The precuneus region has been suggested in OCD as another key structure associated with the mechanism of "thought-action fusion." Our study aimed to elucidate the association of the altered functional coupling of the CSTC nodes (and precuneus), the OCD symptoms, and interference control/cognitive flexibility. Methods: In a group of 36 (17 medicated and 19 drug-free) OCD patients and matched healthy volunteers, we tested functional connectivity (FC) within the constituents of the dorsolateral prefrontal cortex "executive" CSTC, the orbitofrontal cortex/anterior cingulate "affective" CSTC, and precuneus. The functional connections showing the strongest effects were subsequently entered as explanatory variables to multiple regression analyses to identify possible associations between observed alterations of functional coupling and cognitive (Stroop test) and clinical measures (obsessions, compulsions, and anxiety level). Results: We observed increased FC (FWE p < 0.05 corr.) between CSTC seeds and regions of the parieto-occipital cortex, and between the precuneus and the angular gyrus and dorsolateral prefrontal cortex. Decreased FC was observed within the CSTC loop (caudate nucleus and thalamus) and between the anterior cingulate cortex and the limbic lobe. Linear regression identified a relationship between the altered functional coupling of thalamus with the right somatomotor parietal cortex and the Stroop color-word score. Similar association of thalamus FC has been identified also for obsessions severity. No association was observed for compulsions and anxiety. Conclusions: Our findings demonstrate altered FC in OCD patients with a prevailing increase in FC originating in CSTC regions toward other cortical areas, and a decrease in FC within the constituents of CSTC loops. Moreover, our results support the role of precuneus in OCD. The association of the cognitive and clinical symptoms with the FC between the thalamus and somatomotor cortex indicates that cognitive flexibility and inhibitory control are strongly linked and both mechanisms might contribute to the symptomatology of OCD.
- Klíčová slova
- Stroop test, anxiety, functional connectivity, inhibitory/interference control, obsessions and compulsions, obsessive–compulsive disorder, resting state,
- Publikační typ
- časopisecké články MeSH
BACKGROUND: The underlying symptomatology of obsessive-compulsive disorder (OCD) can be viewed as an impairment in both cognitive and behavioral inhibition, regarding difficult inhibition of obsessions and behavioral compulsions. Converging results from neuroimaging and electroencephalographic (EEG) studies have identified changes in activities throughout the medial frontal and orbital cortex and subcortical structures supporting the cortico-striato-thalamo-cortical circuit model of OCD. This study aimed to elucidate the electrophysiological changes induced by autobiographical and general anxiety scenarios in patients with OCD. METHODS: Resting-state eyes-closed EEG data were recorded in 19 OCD patients and 15 healthy controls. Cortical EEG sources were estimated by standardized low-resolution electromagnetic tomography (sLORETA). The changes in the emotional state were induced by two different scenarios: the autobiographical script related to patient's OCD symptoms and the script triggering general anxiety. RESULTS: During the resting state, we proved increased delta activity in the frontal, limbic and temporal lobe and the sub-lobar area in OCD patients. In a comparison of neural activities during general anxiety in OCD patients and the control group, we proved an increase in delta (parietal, temporal, occipital, frontal and limbic lobes, and sub-lobal area), theta (temporal, parietal and occipital lobes) and alpha-1 activities (parietal lobe). Finally, we explored the neural activity of OCD patients during exposure to the autobiographic scenario. We proved an increase in beta-3 activity (left frontal lobe). CONCLUSION: Our study proved differences in neural activation in OCD patients and healthy controls during imagination of general anxiety. Exposure to the autobiographic OCD scenario leads to activation of left frontal brain areas. The results show the possibility of using specific scenarios in OCD therapy.
- Klíčová slova
- anxiety, autobiographical script, cognitive-behavior therapy, electroencephalography, obsessive–compulsive disorder,
- Publikační typ
- časopisecké články MeSH
Obsessive-compulsive disorder (OCD) is a neuropsychiatric disorder with 1-3% prevalence. OCD is characterized by recurrent thoughts (obsessions) and repetitive behaviors (compulsions). The pathophysiology of OCD remains unclear, stressing the importance of pre-clinical studies. The aim of this article is to critically review a proposed animal model of OCD that is characterized by the induction of compulsive checking and behavioral sensitization to the D2/D3 dopamine agonist quinpirole. Changes in this model have been reported at the level of brain structures, neurotransmitter systems and other neurophysiological aspects. In this review, we consider these alterations in relation to the clinical manifestations in OCD, with the aim to discuss and evaluate axes of validity of this model. Our analysis shows that some axes of validity of quinpirole sensitization model (QSM) are strongly supported by clinical findings, such as behavioral phenomenology or roles of brain structures. Evidence on predictive validity is contradictory and ambiguous. It is concluded that this model is useful in the context of searching for the underlying pathophysiological basis of the disorder because of the relatively strong biological similarities with OCD.
- Klíčová slova
- OCD, animal model, brain circuits, human, quinpirole, rat,
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
BACKGROUND: Obsessive-compulsive disorder (OCD) is associated with cognitive dysfunction. Although there are several studies focused on the neurobiology of OCD, little is known about the biological correlates of the cognitive deficit linked to this disorder. The aim of our study was to examine the association between cognitive impairment and current source density markers in patients with OCD. METHODS: Resting-state eyes-closed electroencephalography (EEG) data were recorded in 20 patients with OCD and 15 healthy controls who were involved in the study. Cortical EEG sources were estimated by standardized low-resolution electromagnetic tomography in seven frequency bands: delta (1.5-6 Hz), theta (6.5-8 Hz), alpha-1 (8.5-10 Hz), alpha-2 (10.5-12 Hz), beta-1 (12.5-18 Hz), beta-2 (18.5-21 Hz), and beta-3 (21.5-30 Hz). Cognitive performance was measured by the Trail-Making Test (versions A and B), Stroop CW Test, and D2 Test. RESULTS: Frontal delta and theta EEG sources showed significantly higher activity in the whole group of patients with OCD (N=20) than in control subjects (N=15). Subsequent analysis revealed that this excess of low-frequency activity was present only in the subgroup of eleven patients with cognitive impairment (based on the performance in the Trail-Making Test - A). The subgroup of patients with normal cognitive functions (N=9) did not differ in cortical EEG sources from healthy controls. CONCLUSION: The present results suggest that frontal low-frequency cortical sources of resting-state EEG rhythms can distinguish groups of cognitively impaired and cognitively intact patients with OCD. Based on our results, future studies should consider whether the present methodological approach provides clinically useful information for the revelation of cognitive impairment in patients with OCD.