Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2013
How specific are inhibitory deficits to obsessive-compulsive disorder? A neurophysiological comparison with panic disorder.
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Thomas Susan J, Gonsalvez Craig J, Johnstone Stuart J
Аннотация
OBJECTIVE: Impaired inhibition may perpetuate repetitive symptoms in obsessive-compulsive disorder (OCD), however OCD-specific deficits have yet to be established. We investigated neural correlates of inhibition in OCD vs. healthy and anxious controls.
METHODS: ERPs and reaction times (RTs) were compared between participants with OCD (n=20), panic disorder (PD; n=20) and healthy controls (HCs; n=20) during an adapted Go/NoGo task, which manipulated inhibitory difficulty.
RESULTS: A classic P3 NoGo anteriorisation effect occurred across groups. Both clinical groups showed RT impairment, and similar topographical anomalies of several (P2, N2 and P3) ERP components. Notably, both clinical groups lacked the strong frontally maximal N2 component topography seen in the HCs, across stimuli. Additionally, with increasing inhibitory difficulty, N2 latency increased in HCs but not in the clinical groups.
CONCLUSIONS: Unexpectedly, ERP and behavioural anomalies during inhibition in OCD were not qualitatively different to those in PD, but were generally more severe. Common general and inhibitory deficits may underlie intrusive mental phenomena in both conditions.
SIGNIFICANCE: This first ERP response inhibition study in OCD to include anxious controls disconfirmed hypotheses regarding OCD-specific inhibitory deficits, indicating the importance of comparing OCD to other conditions, to evaluate neurobiological models.
METHODS: ERPs and reaction times (RTs) were compared between participants with OCD (n=20), panic disorder (PD; n=20) and healthy controls (HCs; n=20) during an adapted Go/NoGo task, which manipulated inhibitory difficulty.
RESULTS: A classic P3 NoGo anteriorisation effect occurred across groups. Both clinical groups showed RT impairment, and similar topographical anomalies of several (P2, N2 and P3) ERP components. Notably, both clinical groups lacked the strong frontally maximal N2 component topography seen in the HCs, across stimuli. Additionally, with increasing inhibitory difficulty, N2 latency increased in HCs but not in the clinical groups.
CONCLUSIONS: Unexpectedly, ERP and behavioural anomalies during inhibition in OCD were not qualitatively different to those in PD, but were generally more severe. Common general and inhibitory deficits may underlie intrusive mental phenomena in both conditions.
SIGNIFICANCE: This first ERP response inhibition study in OCD to include anxious controls disconfirmed hypotheses regarding OCD-specific inhibitory deficits, indicating the importance of comparing OCD to other conditions, to evaluate neurobiological models.