Functional motor disorders (FMDs) are distinguished by signs that lack congruence with recognised patterns of organic disease and show inconsistency over time. Their pathophysiology is poorly understood, but there is evidence that irregularities in perceptual and cognitive processing lie at the heart of these conditions. Here, we draw on a predictive coding account of functional neurological disorders to study perceptual decision-making in three groups: 20 patients with FMDs (14 with functional movements and 6 with functional weakness), 20 with phenotypically-matched organic motor disorders, and 20 age-matched healthy controls. We examine four cognitive domains with putative roles in FMD pathogenesis: attention, expectations, sensory processing (perceptual sensitivity), and metacognition (introspective evaluation of performance). We augmented a dual-task paradigm, manipulating the visual contrast required for target detection to examine these domains in one design. With sensory input (stimulus contrast) psychometrically adjusted to staircase target detection at a fixed level for all groups, the FMD group exhibited statistically equivalent attentional, expectational and metacognitive processing to healthy controls. However, we demonstrate Bayesian evidence and a frequentist trend that FMD patients require higher visual contrast than controls to maintain the same detection sensitivity (BF = 8.1, p = .066). This was statistically equivalent to the visual contrast required by the organic group, and unlikely to be accounted for by medication use or comorbid psychopathology. The organic group showed differences in processing of attention and expectations for target detection that were not observed in either healthy controls or the functional group. The distinctive behavioural profile of FMDs may arise from abnormalities in basic sensory processing, while higher attentional, expectational and metacognitive mechanisms remain intact. Conceptualising functional neurological disorders under a predictive coding account may consolidate and refine existing pathophysiological theories about them.
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http://dx.doi.org/10.1016/j.cortex.2019.12.009 | DOI Listing |
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