Response to: ‘Hyperbinding’ in functional movement disorders: role of supplementary motor area efferent signalling

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We thank Dr Dutta for his thoughtful critique of our paper, ‘Increased beta synchronization underlies perception-action hyperbinding in functional movement disorders’.^1^ The letter raises important points about the role of the supplementary motor area (SMA) in sensory suppression during voluntary movements and its potential relevance to understanding the neural dysfunctions in functional movement disorders (FMD).^2^ Specifically, the SMA is thought to send efferent signals to modulate sensory feedback, that is, the perception of action effects, and reduce sensory input from this feedback during voluntary action.^3^ This mechanism may be particularly relevant to FMD, where patients often struggle to differentiate volitional from non-volitional movements.^4^

In our study, we did not investigate response–effect bindings or sensory suppression. Instead, we focused on stimulus–response (S–R) bindings and demonstrated that beta event-related synchronization over the SMA predicts behavioural S–R binding effects, which were significantly stronger in FMD patients compared to healthy controls. The SMA is increasingly recognized as a key brain region for integrating perception and action.^5^ This applies to both the integration of externally perceived stimuli with responses (as in S–R bindings) and the integration of responses with perceived effects or sensory effect anticipation (as in response–effect bindings). In fact, these dual functions align with ideomotor principles, where the anticipation of effects drives motor behaviour.^6^ Thereby, it has been suggested that SMA (and pre-SMA) activations are directly linked to the complexity of perception–action associations.^5^

Following this suggestion, increased SMA beta synchronization may reflect a more complex perception–action association network in FMD patients compared to healthy controls, which may in turn arise from the fact that FMD patients not only bind relevant stimulus information to responses but also irrelevant stimuli or stimulus features. In our study, for example, task-irrelevant features such as the colour and position of stimuli (note that only the orientation of stimuli was task relevant) may have been more likely to be bound into S–R associations in FMD patients than in healthy controls. This propensity to bind irrelevant features likely contributes to difficulties in shielding intentions from competing goals, potentially leading to disorganized or inefficient responses.^7^

Thus, a significant open question is whether patients with FMD exhibit a general tendency towards ‘hyperbinding’ or if this tendency is particularly pronounced when irrelevant stimuli are involved. Future studies, especially those employing tasks like the distractor–response binding task^8,9^ should explore whether the inclination to integrate irrelevant stimuli plays a key role in the disorder—both behaviourally and in electrophysiological data, particularly regarding post-movement beta event-related synchronization.

Dr Dutta’s point about reduced sensory suppression fits well with the complexity argument regarding the processing of S–R and response–effect bindings in the SMA. Less effective sensory suppression could contribute to increased complexity in perception–action association networks, as irrelevant stimuli and features become more likely to influence response selection. We agree that this interplay warrants further investigation to advance the pathophysiological understanding of FMD and other movement disorders, such as Parkinson’s disease.^10^