Electrophysiology of facilitation priming in obsessive–compulsive and panic disorders

Thomas, Susan J.; Gonsalvez, Craig J.; Johnstone, Stuart J.

doi:10.1016/j.clinph.2015.05.026

Cited by 4 publications

(2 citation statements)

References 117 publications

(117 reference statements)

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“…This raises questions on the relationships among variations in response inhibition, threat-induced state anxiety and clinical levels of anxiety. Although data in children find some evidence of associations between response inhibition and clinical anxiety (Daugherty et al 1993; Oosterlaan and Sergeant, 1996; Kooijmans et al 2000), little is known about this link in adults (Beutel et al 2010; Thomas et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Clinical anxiety promotes excessive response inhibition

et al. 2016

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Background. Laboratory tasks to delineate anxiety disorder features are used to refine classification and inform our understanding of etiological mechanisms. The present study examines laboratory measures of response inhibition, specifically the inhibition of a pre-potent motor response, in clinical anxiety. Data on associations between anxiety and response inhibition remain inconsistent, perhaps because of dissociable effects of clinical anxiety and experimentally manipulated state anxiety. Few studies directly assess the independent and interacting effects of these two anxiety types (state v. disorder) on response inhibition. The current study accomplished this goal, by manipulating state anxiety in healthy and clinically anxious individuals while they complete a response inhibition task. Method. The study employs the threat-of-shock paradigm, one of the best-established manipulations for robustly increasing state anxiety. Participants included 82 adults (41 healthy; 41 patients with an anxiety disorder). A go/nogo task with highly frequent go trials was administered during alternating periods of safety and shock threat. Signal detection theory was used to quantify response bias and signal-detection sensitivity. Results. There were independent effects of anxiety and clinical anxiety on response inhibition. In both groups, heightened anxiety facilitated response inhibition, leading to reduced nogo commission errors. Compared with the healthy group, clinical anxiety was associated with excessive response inhibition and increased go omission errors in both the safe and threat conditions. Conclusions. Response inhibition and its impact on go omission errors appear to be a promising behavioral marker of clinical anxiety. These results have implications for a dimensional view of clinical anxiety.

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Section: Introductionmentioning

confidence: 99%

Clinical anxiety promotes excessive response inhibition

et al. 2016

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“…11 studies described a sensory over-responsivity in OCD patients [71][72][73][74][75][76][77][78][79][80][81], for example, in terms of enhanced startle reaction or impaired sensory gating, and in multiple sensory domains, such as tactile and acoustic.…”

Section: Resultsmentioning

confidence: 99%

Neurodevelopmental Antecedents and Sensory Phenomena in Obsessive Compulsive Disorder: A Systematic Review Supporting a Phenomenological-Developmental Model

et al. 2022

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Background: The majority of models on obsessive compulsive disorder (OCD) endorse a top-down perspective on the cognitive mechanisms underlying OCD functioning and maintenance, whereas a bottom-up perspective is rarely pursued. Objectives: The aim of the study was to review the empirical literature on sensory phenomena (SP) and neurodevelopmental antecedents of OCD, which could support the conceptualization of an alternative, bottom-up perspective integrating neurodevelopmental and phenomenological levels of analysis on OCD. Methods: A systematic review according to PRISMA guidelines was performed in PubMed/MEDLINE, PsycInfo, the Cochrane Library, and Excerpta Medica Database (EMBASE) and focused on SP and “neurodevelopmental antecedents” (operationalized in early risk factors, neuroimaging signs, neurological soft signs, and sensory responsivity). The time interval was from inception up to March 31, 2022. Results: From the search in electronic databases, 48 studies were retained and reviewed. SP are highly prevalent in OCD patients and overrepresented in comparison with healthy controls. Similarly, OCD patients also present a higher prevalence of early environmental adversities and sensorimotor alterations in terms of neurological soft signs and sensory over-responsivity in the tactile and acoustic domains; additional findings included hypogyrification signs at neuroimaging. Both sensorimotor alterations and SP are associated with tic-related manifestations and poorer insight in OCD patients. Conclusions: On the ground of established common subjective experience of SP and premorbid neurodevelopmental features, we hypothesized an explanatory model for OCD, which considers the possible pathophysiological role for altered corollary discharge and enhanced error detection in the neurodevelopment of SP and obsessions. SP may represent the subjective experiential resonance of an individual history of persistently inaccurate sensory predictions, whereas accompanying manifestations, such as the obsessive need for order and symmetry, may represent a compensatory attempt to mitigate SP. This neurodevelopmental-phenomenological bottom-up model, describing a dimensional gradient of sensorimotor alterations and related subjective experiences, may contribute to explain the dimensional affinity between OCD and schizophrenia spectrum disorders. Furthermore, this model could be useful for the early detection of subjects at higher risk of OCD.

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