The impact of task context on predicting finger movements in a brain-machine interface
Abstract
A key factor in the clinical translation of brain-machine interfaces (BMIs) for restoring hand motor function will be their robustness to changes in a task. With functional electrical stimulation (FES) for example, the patient's own hand will be used to produce a wide range of forces in otherwise similar movements. To investigate the impact of task changes on BMI performance, we trained two rhesus macaques to control a virtual hand with their physical hand while we added springs to each finger group (index or middle-ring-small) or altered their wrist posture. Using simultaneously recorded intracortical neural activity, finger positions, and electromyography, we found that decoders trained in one context did not generalize well to other contexts, leading to significant increases in prediction error, especially for muscle activations. However, with respect to online BMI control of the virtual hand, changing either the decoder training task context or the hand's physical context during online control had little effect on online performance. We explain this dichotomy by showing that the structure of neural population activity remained similar in new contexts, which could allow for fast adjustment online. Additionally, we found that neural activity shifted trajectories proportional to the required muscle activation in new contexts. This shift in neural activity possibly explains biases to off-context kinematic predictions and suggests a feature that could help predict different magnitude muscle activations while producing similar kinematics.
Data availability
Neural, behavioral, EMG, and online BMI performance data has been deposited in the Dryad repository (https://doi.org/10.5061/dryad.p2ngf1vtn).
-
Data from: The impact of task context on predicting finger movements in a brain-machine interfaceDryad Digital Repository, doi:10.5061/dryad.p2ngf1vtn.
Article and author information
Author details
Funding
National Science Foundation (Grant Number 1926576)
- Matthew J Mender
- Hisham Temmar
- Parag Patil
- Cynthia A Chestek
National Institute of General Medical Sciences (Grant Number R01GM111293)
- Parag Patil
- Cynthia A Chestek
National Science Foundation (Graduate Research Fellowship Program)
- Joseph T Costello
Eunice Kennedy Shriver National Institute of Child Health and Human Development (Grant Number F31HD098804)
- Samuel R Nason-Tomaszewski
National Institute of Neurological Disorders and Stroke (Grant Number T32NS007222)
- Matthew S Willsey
National Institute of Neurological Disorders and Stroke (Grant Number R01NS105132)
- Nishant Ganesh Kumar
- Theodore A Kung
The D. Dan and Betty Kahn Foundation (Grant AWD011321)
- Dylan M Wallace
University of Michigan Robotics Institute (Graduate student fellowship)
- Dylan M Wallace
A. Alfred Taubman Medical Research Institute
- Parag Patil
Craig H. Neilsen Foundation (Project 315108)
- Cynthia A Chestek
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Animal experimentation: All protocols were in accord with the National Institutes of Health guidelines and approved by the University of Michigan Institutional Animal Care and Use Committee (protocol numbers PRO00010076 and PRO00008138).
Copyright
© 2023, Mender et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 677
- views
-
- 116
- downloads
-
- 4
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Further reading
-
- Neuroscience
Detecting causal relations structures our perception of events in the world. Here, we determined for visual interactions whether generalized (i.e. feature-invariant) or specialized (i.e. feature-selective) visual routines underlie the perception of causality. To this end, we applied a visual adaptation protocol to assess the adaptability of specific features in classical launching events of simple geometric shapes. We asked observers to report whether they observed a launch or a pass in ambiguous test events (i.e. the overlap between two discs varied from trial to trial). After prolonged exposure to causal launch events (the adaptor) defined by a particular set of features (i.e. a particular motion direction, motion speed, or feature conjunction), observers were less likely to see causal launches in subsequent ambiguous test events than before adaptation. Crucially, adaptation was contingent on the causal impression in launches as demonstrated by a lack of adaptation in non-causal control events. We assessed whether this negative aftereffect transfers to test events with a new set of feature values that were not presented during adaptation. Processing in specialized (as opposed to generalized) visual routines predicts that the transfer of visual adaptation depends on the feature similarity of the adaptor and the test event. We show that the negative aftereffects do not transfer to unadapted launch directions but do transfer to launch events of different speeds. Finally, we used colored discs to assign distinct feature-based identities to the launching and the launched stimulus. We found that the adaptation transferred across colors if the test event had the same motion direction as the adaptor. In summary, visual adaptation allowed us to carve out a visual feature space underlying the perception of causality and revealed specialized visual routines that are tuned to a launch’s motion direction.
-
- Neuroscience
The classical diagnosis of Parkinsonism is based on motor symptoms that are the consequence of nigrostriatal pathway dysfunction and reduced dopaminergic output. However, a decade prior to the emergence of motor issues, patients frequently experience non-motor symptoms, such as a reduced sense of smell (hyposmia). The cellular and molecular bases for these early defects remain enigmatic. To explore this, we developed a new collection of five fruit fly models of familial Parkinsonism and conducted single-cell RNA sequencing on young brains of these models. Interestingly, cholinergic projection neurons are the most vulnerable cells, and genes associated with presynaptic function are the most deregulated. Additional single nucleus sequencing of three specific brain regions of Parkinson’s disease patients confirms these findings. Indeed, the disturbances lead to early synaptic dysfunction, notably affecting cholinergic olfactory projection neurons crucial for olfactory function in flies. Correcting these defects specifically in olfactory cholinergic interneurons in flies or inducing cholinergic signaling in Parkinson mutant human induced dopaminergic neurons in vitro using nicotine, both rescue age-dependent dopaminergic neuron decline. Hence, our research uncovers that one of the earliest indicators of disease in five different models of familial Parkinsonism is synaptic dysfunction in higher-order cholinergic projection neurons and this contributes to the development of hyposmia. Furthermore, the shared pathways of synaptic failure in these cholinergic neurons ultimately contribute to dopaminergic dysfunction later in life.