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Colon, A.

Publications and source records attributed to Colon, A..

3 recordsLinked to original sources

Insular error network enables self-correcting intracranial brain-computer interface

Error recognition is fundamental to adaptive behavior, enabling rapid compensatory action when outcomes deviate from expectations. Central to this function are neural circuits for performance monitoring, encoding cognitive signals that could support more reliable neural interfaces. Here, we recorded intracranial electroencephalography (iEEG) in epilepsy patients to enable a motor brain-computer interface (BCI) while sampling error-related activity across a distributed network. Our work reveals high-frequency population dynamics emerging in the anterior insula and propagating to the prefrontal cortex as the interface fails to follow the users intention. We identify spatially organized insular responses to error processing and movement feedback, highlighting it as a heterogeneous hub linking action and outcome. Real-time integration of error responses enables a self-correcting neural interface that enhances usability by reducing the need for manual user intervention. Together, our work demonstrates a human intracranial BCI harnessing insular brain activity, integrating cognitive processes directly into device control.

neuroscience↗

Executed and imagined grasping movements can be decoded from lower dimensional representation of distributed non-motor brain areas.

Using brain activity directly as input for assistive tool control can circumvent muscular dysfunction and increase functional independence for physically impaired people. Most invasive motor decoding studies focus on decoding neural signals from the primary motor cortex, which provides a rich but superficial and spatially local signal. Initial non-primary motor cortex decoding endeavors have used distributed recordings to demonstrate decoding of motor activity by grouping electrodes in mesoscale brain regions. While these studies show that there is relevant and decodable movement related information outside the primary motor cortex, these methods are still exclusionary to other mesoscale areas, and do not capture the full informational content of the motor system. In this work, we recorded intracranial EEG of 8 epilepsy patients, including all electrode contacts except those contacts in or adjacent to the central sulcus. We show that executed and imagined movements can be decoded from non-motor areas; combining all non-motor contacts into a lower dimensional representation provides enough information for a Riemannian decoder to reach an area under the curve of 0.83 {+/-} 0.11. Additionally, by training our decoder on executed and testing on imagined movements, we demonstrate that between these two conditions there exists shared distributed information in the beta frequency range. By combining relevant information from all areas into a lower dimensional representation, the decoder was able to achieve high decoding results without information from the primary motor cortex. This representation makes the decoder more robust to perturbations, signal non-stationarities and neural tissue degradation. Our results indicate to look beyond the motor cortex and open up the way towards more robust and more versatile brain-computer interfaces.

neuroscience↗

Novelty Processing Depends on Medial Temporal Lobe Structures

ObjectivesThe goal of the present study was to identify the role of the medial temporal lobe (MTL) in the detection and later processing of novelty stimuli. MethodsTwenty-one epilepsy patients with unilateral MTL resection (10 left-sided; 11 right-sided) performed an adapted visual novelty oddball task. In this task two streams of stimuli were presented on the left and right of fixation while the patients electroencephalogram was measured. Patients responded to infrequent target stimuli, while ignoring frequent standard, and infrequent novel stimuli that could appear either contra- or ipsilateral to the resected side. ResultsNovelty detection, as indexed by the N2 ERP component elicited by novels, was not affected by the MTL resections. Later processing of novels, however, as indexed by the novelty P3 ERP component, was reduced for novels presented contra-versus ipsilateral to the resected side. Target processing, as indexed by the P3b, was unaffected. ConclusionsThe current results suggest that MTL structures play a role in novelty processing, but that the novelty signal may originate from a distinct neural source.

neuroscience↗