Etienne Mondesert
email: etiennemondesert@e-mondesert@chu-montpellier.fr

Céline Eiden

Hélène Peyriere

Aude Formoso

Lucas Corti

Jean-Paul Cristol

Stéphanie

Stéphanie Badiou

Functional vitamin 8,2 deficiency is a consistent feature in hospital admissions for neurological disorders due to the use of nitrous oxide

Keywords: Nitrous oxide, homocysteine, methylmalonic acid, vitamin

des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.

Introduction

Inhalation of nitrous oxide is a known aetiology of vitamin B 12 deficiency, observed typically ln patients who received high doses of nitrous oxide for analgesic purposes [START_REF] Baum | When nîtrous oxide is no laughing matter: nitrous oxide and pediatric anesthesia[END_REF]. Nitrous oxide oxidizes the cobalt Co(l) form of vitamin B 12 to Co(III) [2}, thus blocking the cobalamin intracellular process. Cobalamin acts as a cofactor for two key enzymes: cytoplasmic methionine synthase (responsible for the formation of methionine and S-adenosylmethionine) and mitochondrial methylmalonyl Co-A mutase. Because reduced Co(l) form is needed for cobalamin-dependent enzyme activities, nitrous oxide-induced oxidation of cobalt compromise these pathways (Figure 1), as demonstrated for methionine synthase [3~4].

Physiologically, the reduction of Co (lll) and Co (ll) to Co (l) is ensured by reductases in the cytoplasm [5] but does not appear to be effective in counteracting nitrous oxide induced oxidation.

The nitrous oxide-induced decrease of methionine synthase could, therefore, impair Sadenosylmethionine formation. Some authors hypothesize that this could lead to a defect in myelination [START_REF] Sanders | Biologic effects of nitrous oxide: a mechanistic and toxicological review[END_REF], but S-adenosylmethionine concentrations have never been measured in humans with nitrous oxide intoxication. The mechanism of demyelination is unclear, as an animal study by Dorris [6] showed that the decrease in S-adenosylmethionine was not important during nitrous oxide exposure. Interestingly, methionine concentrations and the ratio of methionine to homocysteine were recently reported to be related to clinical severity [START_REF] Gemez | Plasma methionine and clinical severity in nitrous oxide consumption[END_REF]. Two main neurological pathologies are observed in cases of nitrous oxide-induced vitamin Bi2 functional deficiency: subacute combined degeneration of the spinal cord and peripheral neuropathy [START_REF] Garakani | psychiatric, and other medical manife5tations of nitrou5 oxide abuse: a systematic review of the case literature[END_REF]. Symptoms of subacute combined degeneration of the spinal cord and peripheral neuropathy are overlapping and include general limb numbness and weakness, mainly affecting the lower limbs. Subacute combined degeneration of the spinal cord associated with nitrous oxide abuse mainly involves the cervical posterior spinal cord, sparing the lateral spinal cord. Axonal and/or demyelinating abnormalities can be present in electromyoneurography [START_REF] Yu | Analysis of clinical charactëristics and prognostic factors in 110 patients with nitrous oxide abuse[END_REF]. Nevertheless, neurological deficits due to nitrous oxide use are probably not only related to vitamin B 12 functional deficiency, as nitrous oxide toxicity could be mediated through other pathways such as N-methyl-D-aspartate (NMDA) receptor overstimulation [START_REF] Brunt | Mechanisms involved in the neurotoxicity and abuse liability of nitrous oxide: a narrative review[END_REF]. Indeed, homocysteine and nitrous oxide itself are NMDA receptor ligands.

Vodovar et al. [START_REF] Vodovar | Vitamin 812 inactivation may not be the only cause of acquired peripheral neuropathy in chronic nitrous oxide users[END_REF] have also postulated that recurrent hypoxia induced by the use of pure oxygen-free nitrous oxide is another important mechanism in neurological impairments.

Nitrous oxide use has been reported to the French Addictovigilance Network and also at a European level and worldwide [12][START_REF] Van Aerts | Recreational use of nitrous oxide: a growing concern for Europe[END_REF][START_REF] Van Aerts | Recreational use of nitrous oxide: a growing concern for Europe[END_REF][15][START_REF] Redmond | Nitrous oxide-induced neurological disorders: an increasing public health concern[END_REF][START_REF] Micallef | Waming on Increased serious health complications related to non-medical use of nitrous oxide[END_REF]. Vitamin B 12 functional deficiency occurs after substantial nitrous oxide use, such as the chronic inhalation of hundreds of ''whippits" (approximately s g of nitrous oxide) or several containers (cylinders or tanks of nitrous oxide 600g or 2,000g) of nitrous oxide per day [18|. ln some cases, vitamin 8" functional deficiency occurs ln the presence of other risk factors or after acute consumption [START_REF] Chen | An unusual case of subacute combined degeneration due to nitrous oxide abuse, which relapsed after bafiatric surgery: a case report[END_REF][START_REF] Alt | Severe myeloneuropathy from aciite highlose nitrous oxide (N20) abuse[END_REF].

Blood nitrous oxide measurement is feasible [START_REF] Saloojee | Estimation of nitrous oxide in blood. Gas chromatographic analysis of trace or analgesic levels[END_REF] but is of very little interest due to its very short half-life. Interestingly, plasma vitamin B 12 concentrations are not always decreased in patients with nitrous oxide intoxication, whereas plasma homocysteine and methylmalonic acid concentrations, which reflect vitamin B 12 functional deficiency, appear to be more reliably elevated [START_REF] Oussalah | Global burden related to nitrous oxide exposure in medical and recreational settings: a systematic review and individual patient data meta-analysis[END_REF][START_REF] Grzych | Comparison of biomarker for diagnosis of nitrous oxide abuse: challenge of cobalamin metabolic parameters, a retrospective study[END_REF].

Oral or intramuscular supplementation of vitamin B 12 is used to treat these patients, together with .cessation of nitrous oxide use and physiotherapy. Although correction of vitamin B 12 deficiency and reversibility of symptoms can be achieved, some patients have long-term sequelae such as residual limb numbness |13,24].

To investigate biological markers in the diagnosi5 of nitrous oxide intoxications, we conducted a single-centre retrospective survey of hospitalized patients presenting with nitrous oxide-induced neurological disorders.

Material and methods

Patients

Data from patients aged 17 or more admitted to our university hospital (emergency unit or neurology department) for nitrous oxide-induced neurological disorders between 1 January 2020 and 31 0ctober 2022 were collected retrospectively. To be included, patients had to have at least one concentration of vitamin B 12 , homocysteine, or methylmalonic acid measured. Patients with known inherited metabolic diseases were excluded. Clinical, biological, neuroimaging and sociodemographic data were analyzed. Nitrous oxide inhalation was reported according to the patient's self-declaration and was considered chronic when used more than twice per week for at least two months. Associated self-reported toxic substance use, including alcohol, cannabis, cocaine, ketamine, and opioids, were recorded. Diagnoses of subacute combined degeneration of the spinal cord and peripheral neuropathy were recorded from the medical records. This study was approved by the local institutional review board and declared under the number 202201305.

Laboratory measurements

Biological data were collected from laboratory assessments performed as routine at the beginning of hospitalization. Concentrations of vitamin B 12 , homocysteine, methylmalonic acid and folate were measured in plasma collected in a lithium heparin tube after centrifugation 10min at 2000 times gravity speed. Electro chemiluminescence assays using a Cobas 8000® (Roche Diagnostics, Meylan, France) were employed to measure folate and vitamin 8" concentrations based on competition with intrinsic factors for vitamin 8,2. Plasma homocysteine and methylmalonic acid concentrations were measured by liquid chromatography coupled with tandem mass spectrometry (Waters, Milford, USA) and gas chromatography coupled mass spectrometry Thermo-scientific, Hennigsdorf, Germany), respectively. The manufacturer's reference range for folate was 8.8-60.8nmol/L, and for vitamin B 12 was 145-569pmol/L. The reference range for homocysteine was <15 mol/L, and for methylmalonic acid was <0.5 mol/L.

Other parameters, haemoglobin, mean corpuscular volume and estimated glomerular filtration (eGFR) were also collected.

Results

Population and clinical features

Among the 31 included patients, the majority were men (79%) with a median age of 23.7years (range 17.4 -41.2 years). Clinical manifestations included inferior and/or superior limb numbness (51.6%), unsteady gait (35.5%), balance disorders (32.2%) and vesical dysfunction (6.4%). Nineteen of 25 (76%) patients had sensory and/or motor nerve abnormalities on electromyoneurography and were diagnosed with peripheral neuropathy, 14 of 29 (48.3%) patients had cervical and/or thoracic spinal cord lesions on medullar magnetic resonance imaging and were diagnosed with myelopathy, and one patient was diagnosed with a psychotic episode. Guillain-Barre syndrome was suspected in five patients, and two were treated with polyclonal immunoglobulins. Most (81%) patients reported massive chronic inhalation of nitrous oxide, which ranged from 200 small cartridges (8g) per month to 10 cylinders (600g) per day. The duration of nitrous oxide consumption was less than one month in six cases, with vitamin B 12 deficiency present in two of them. The first was a 25-year-old woman with a recent decrease in food intake and a weight loss of 14.5 kg over six months who had been diagnosed with peripheral neuropathy and who had a reported consumption of thirty cartridges of nitrous oxide a few days before symptoms onset. Her vitamin B 12 concentration was 97.3 pmol/L. The second was a 38-yearold woman with a history of sleeve surgery one year before her hospitalization who presented with subacute combined degeneration of the spinal cord after substantial intake of nitrous oxide during the three weekends preceding hospitalization. Her vitamin 8,2 concentration was 132.8 pmol/L. Twenty-four (77.4%) patients were hospitalized for an average of 10days, and 25.8% of them were admitted for follow-up care to a rehabilitation centre after hospitalization. Seven patients were discharged from the hospital within 24h. All patients received oral or intramuscular vitamin 8,2 supplementation during hospitalization and after discharge (1 mg per day for ten days, then 1 mg per week for one to three months). All were advised to discontinue nitrous oxide completely, and eight received physiotherapy re-education.

Clinical outcome

Two patients were readmitted to the emergency unit within a month for clinical worsening of their gait disorders, which had led to falls. Twelve cases were re-evaluated within six months but without available biological data since a part of their follow-up was performed outside the hospital. Two had a normal clinical examination, six had clinically significant improvement, two were stable, and two exhibited clinical worsening. Nineteen cases were without follow-up or did not present to the follow-up visit.

Biological findings

Biological findings on admission are summarized in Figure 2. The median plasma vitamin B 12 concentration in 31 patients was 134.6 pmol/L including 17 cases (54.8%) with a concentration below the lower limit of the reference range (145pmovL). ln three patients, vitamin B 12 concentrations were above the upper limit of the normal range (569 pmol/L); these patients had supplemented themselves with vitamin B 12 shortly before being hospitalized. No other cases of self-supplementation were identified. These three vitamin B 12 outliers were excluded from descriptive statistics shown in Figure 2. Plasma homocysteine concentrations were assessed in 23 of 31 (74%) patients, and methylmalonic acid concentrations were available in 18 of 31 (58%) patients. The median homocysteine concentration was 87.7 mol/L, and the median methyl-malonic acid concentration was 3.8 mol/L. these concentrations were, in all cases, above the normal ranges. Minor elevation of the plasma methylmalonic acid concentration (0.51 mol/L and O.74 mol/L) was observed in two patients; both had elevated homocysteine concentrations (86.6 mol/L and 141.6mol/L). The median plasma folate concentration in 87% of patients was 20.1 nmol/L, with values < 8,8nmol/L in only four patients. Kidney function was normal with a median eGFR of 126.6 ml/min/1.73m 2 , and no patient had an eGFR <60mL/min/1.73m 2 . Macrocytic anaemia occurred in two male patients; the haemoglobin concentration in the first was 119g/L with a mean corpuscular volume of 109 fl, and in the second, the haemoglobin concentration was 119g/L with a mean corpuscular volume of 101 fl. Four patients had normocytic anaemia: a woman with a haemoglobin concentration of 113 g/L and mean corpuscular volume of 94 fl, three men with haemoglobin concentrations between 107 g/L and 126g/L and mean corpuscular volumes between 82 and 88 fl. The median mean corpuscular volume for all patients was close to the upper limit (96fl), and six patients had a mean corpu5cular volume greater than 100 fl with a normal haemoglobin concentration.

Only four patients had biological data available within six months after admission. Their homocysteine concentrations were between 34.7mol/L and 156.5 mol/L and their methylmalonic acid concentrations were from O.63mol/L to 1.55 mol/L. Their vitamin B 12 concentrations ranged from 186 pmol/L to 504 pmol/L.

Discussion

We report a French case series of nitrous oxide-induced neurological disorders. The number of patients, 31 in 34 months, confirms the epidemiological reports of growing nitrous oxide use in France, especially among young patients in the past three years [START_REF] Van Aerts | Recreational use of nitrous oxide: a growing concern for Europe[END_REF][START_REF] Van Aerts | Recreational use of nitrous oxide: a growing concern for Europe[END_REF][START_REF] Einsiedlei | A rise in cases of nitrous oxide abuse: neurological complications and biological findings[END_REF]. The diagnosis of neurological complications induced by nitrous oxide is not easy; patients do not always admit their consumption, and quantification can be inaccurate. Another difficulty is the differential diagnosjs with other types of neuropathies, notably with Guillain-Barré syndrome, as occurred in five patients in our cohort, resulting in potentially unnecessary polyclonal immunoglobulin treatments.

Although absolute vitamin B 12 deficiency was observed only in 54.8% of patients, 100% had a biological profile corresponding to a functional 8,2 deficiency characterized by elevation of homocysteine and methylmalonic acid concentrations. A difficulty in interpreting plasma vitamin B 12 concentrations is the definition of the cut-off. Manufacturers of analytical equipment use a cut-off for vitamin B 12 concentration of 145pmol/L, whereas we advocate that a grey zone should be considered between 150 pmol/L and 220 pmol/L [START_REF] Rothen | Identification of patients with cobalamin deficiency crucially depends on the diagnostic strategy[END_REF], corresponding to 29% of patients in the present study. Nevertheless, the biological profile of functional B 12 deficiency was consistent with that observed in other large case series [START_REF] Gemez | Plasma methionine and clinical severity in nitrous oxide consumption[END_REF][START_REF] Yu | Analysis of clinical charactëristics and prognostic factors in 110 patients with nitrous oxide abuse[END_REF][START_REF] Grzych | Comparison of biomarker for diagnosis of nitrous oxide abuse: challenge of cobalamin metabolic parameters, a retrospective study[END_REF][START_REF] Berling | Nitrous oxide-induced predominantly motor neuropathies: a follow-up study[END_REF][START_REF] Zheng | The sharp rise of neurological disorders associated with recreational nitrous oxide use in China: a single center experience and a brief review of Chinese literature[END_REF]. It is essential that clinicians are aware that normal or elevated B 12 concentrations might not exclude exposure to nitrous oxide and may indicate selfsupplementation [START_REF] Temple | Nitrous oxide abuse induced subacute combined degeneration despite patient initiated B 12 supplementation[END_REF]. An explanation for normal plasma vitamin B 12 concentrations is that the oxidized vitamin Bi2 molecule still interacts with the recombinant intrinsic factor used in the electro-chemiluminescence assay.

Clinicians should also recognize that in complex cases, homocysteine and methylmalonic acid concentrations have an important role in detecting functional vitamin B 12 deficiency. Plasma homocysteine concentrations may increase to greater than 15 mol/L, reaching 180 mol/L, due to disturbance of the remethylation pathway. In parallel, an increase of plasma methylmalonic acid concentrations may be observed ranging from 0.51 mol/L to 28 mol/L Of note the two lowest increases in the concentration of methylmalonic acid (0.51 mol/l and O.74 mol/L) were associated with very high homocysteine concentrations (86.6 mol/L and 141.6 mol/L), in agreement with literature data showing that methionine synthase is more sensitive to nitrous oxide exposure than methylmalonyl Co-A mutase, ln addition, methylmalonic acid could be normalized with prolonged self-supplementation, while homocysteine concentrations appear not to normalize until discontinuation of nitrous oxide use [START_REF] Waclawik | Myeloneuropathy from nitrous oxide abuse: unusually high methylmalonic acid and homocysteine levels[END_REF]. Although an increase in homocysteine concentrations is not a specific biomarker of vitamin B 12 deficiency, it appears as a sensitive biomarker for nitrous oxide use. However, for a correct interpretation of homocysteine elevation, other factors should be evaluated, such as chronic kidney insufficiency, folate deficiency, iatrogenic interaction, and inherited disorders of one carbon metabolism [START_REF] Desouza | Drugs affecting homocysteine metabolism: impact on cardiovascular risk[END_REF][START_REF] Gerrard | Homocystinuria diagnosis and management: it is not all classical[END_REF].

To summarize, in complex cases, cobalamin metabolism biomarkers, such as the measurement of vitamin B 12 , homocysteine, and methylmalonic acid concentrations, are helpful in making the diagnosis. Nevertheless, vitamin B 12 supplementation should be initiated prior to the receipt of biological results, as they are not available in all laboratories or 24 hours a day, seven days a week. Vitamin B 12 treatment combined with monitoring of improvement in neurological status could be an alternative strategy for centres without access to these markers.

Regarding other biomarkers, we found that a decrease in the plasma folate concentration, a low haemoglobin concentration, or an increased mean corpuscular volume had a poor diagnostic value, as previously shown by a meta-analysis [START_REF] Oussalah | Global burden related to nitrous oxide exposure in medical and recreational settings: a systematic review and individual patient data meta-analysis[END_REF]. Macrocytic anaemia was not prevalent in our case series, but macrocytosis was often present. We also observed that neurological disorders were present without macrocytic anaemia.

Inhaled nitrous oxide misuse is becoming commonplace for many reasons: it is legal (only the sale to minors is prohibited in France), easily accessible, and often considered a safe and harmless substance. This is becoming a public health burden by generating a clinically significant number of neurological and rehabilitation hospitalizations involving mainly young patients.

Patients with neurological impairment caused by nitrous oxide can suffer long-term consequences in terms of mobility restrictions, affecting dramatically their quality of life [START_REF] Yu | Analysis of clinical charactëristics and prognostic factors in 110 patients with nitrous oxide abuse[END_REF][START_REF] Berling | Nitrous oxide-induced predominantly motor neuropathies: a follow-up study[END_REF]. Follow-up of this population is a major issue, as only 12 cases attended a follow-up visit within six months in our cohort. Not all patients recovered clinically and biologically, suggesting that nitrous oxide-induced neurological impairment persists for a clinically significant period, even with Vitamin B 12 supplementation. An alternative explanation could be that not all patients completely stopped nitrous oxide consumption, even though they claimed to have done so during a follow-up visit. This explanation in accord with the high homocysteine concentrations observed in the few patients with biological follow-up. Stopping nitrous oxide is critical for recovery, and attendance at an addiction clinic must be integrated into care plans.

Surveys carried out among French students showed a high prevalence of health students abusing nitrous oxide (76.6 and 80% at least one time) [32][START_REF] Cohen | A crosssectional study: nitrous oxide abuse in Parisian medical students[END_REF]. In our case series, patients were mainly unemployed (45.2%), some had a professional activity (38.7%), and only two were students. The inhalation of nitrous oxide in France seems not to be limited to students, but data on the general population are lacking, and evaluation seems necessary.

This study has some limitations as electromyoneurography was not always undertaken, and remethylation biomarkers such as methionine or S-adenosylmethionine formation were not always assessed. In addition, nitrous oxide use was based only on self-declared patient data.

Conclusions

Neurological disorders related to nitrous oxide use are increasing in the south of France, as in the whole country. Awareness of nitrous oxide complications must be reinforced, especially in young adults that are of the most concern. in complex cases of nitrous oxide intoxication, the determination of homocysteine and methylmalonic acid concentrations to detect functional vitamin B 12 deficiency is helpful in diagnosis.

Acknowledgements

None

Funding

None to declare.

Authors contributions

Etienne Mondesert: formal analysis, original draft writing; Céline E{den: conceptualization, review and editing; Hélène Peyriere. review and editing, Aude Formoso: resources, review and editing; Lucas Corti: resources, review and editing, Jean-Paul Cristol: conceptualization, review and editing, Stéphanie Badiou: supervision, original draft writing.

Disclosure 5tatement

No potential conflict of interest was reported by the authors.


Ali Rabiee

Sima Ghafoori

Anna Cetera

Walter Besio

Reza Abiri

Reza Abiri Decoding Reach

Decoding Reach-to-Grasp Movements: A Comparative study of TCRE and EEG for High-Performance BCI Systems

come   L'archive ouverte pluridisciplinaire

Experimental Setup & Paradigm:

• Participants observed and grasped two objects requiring distinct grips (Precision for Object A, Power for Object B) in a randomized order.

• Setup involved participants positioned 30cm from objects, with a threesecond observation followed by an audio-cued grasping action.

Preprocessing:

• High-pass filter at 1Hz applied.

• Bandpass filter (1Hz-60Hz) with a notch filter for 50Hz line noise.

• Implemented wavelet denoising using the 'db8' Daubechies wavelet.

• Z-score normalization for data standardization.

• Data segmentation: 1 second before to 1 second after movement onset.

• Independent Component Analysis (ICA) to ensure high data fidelity.

Feature Extraction and Classification:

• Time Region of Interest (tROI): [-1, 1] s (0 s = movement onset)

• Decomposed signals using Complex Morlet wavelet (cmor) into frequency bands: Delta, Theta, Alpha, Beta, and Gamma.

• Extracted statistical features from the wavelet coefficients of each band and channel: Mean, Variance, Skewness, Kurtosis (Total Features: 80)

• Machine Learning Models Employed: SVM, XGBoost, KNN, LDA, Logistic Regression

Results (Cont.) Classification Accuracies:

Translational Neurorobotics Lab

• Both EEG and tEEG demonstrate pronounced neural responses to grasping actions, but the patterns are more complex in tEEG

• tEEG recordings appear to show greater channel-to-channel variability than EEG, suggesting that tEEG may be more sensitive to different neural or artifact sources • The Tripolar (tEEG) method, through this research, establishes itself as a potentially more sensitive and accurate tool compared to traditional EEG, particularly in applications requiring higher SNR and nuanced ERP analysis.

• The enhanced classification accuracies of tEEG further solidify its prominence, making it a valuable choice for neuroscientific studies and applications seeking detailed neural insights and superior data classification.

• Plans are underway to expand the research by increasing the number of human subjects, amplifying the number of channels used, and incorporating a variety of grasp types to provide a more comprehensive analysis and further validate the findings.

ERP Comparison:

• Both EEG and tEEG demonstrate pronounced neural responses to grasping actions, but the patterns are more complex in tEEG

• tEEG recordings appear to show greater channel-to-channel variability than EEG, suggesting that tEEG may be more sensitive to different neural or artifact sources

  Introduction Decoding Reach-to-Grasp Movements: A Comparative study of TCRE and EEG for High-Performance BCI Systems Ali Rabiee, Sima Ghafoori, Anna Cetera, Walter Besio, Reza Abiri Department of Electrical, Computer, and Biomedical Engineering, University of Rhode Island, Kingston, RI Conclusions & Future works Materials and Methods Materials and Methods (Cont.) Motivation: • BCIs & Their Potential: Enhancing the lives of those with motor impairments via direct brain-to-computer communication [1].

Figure 1 :ResultsFigure 2 :Figure 3 :

 123 Figure 1: The complete experimental setup with its components

[ 1 ]

 1 Wolpaw, Jonathan R., and Dennis J. McFarland. "Control of a two-dimensional movement signal by a noninvasive brain-computer interface in humans." Proceedings of the national academy of sciences 101, no. 51 (2004): 17849-17854. [2] Grafton, Scott T. "The cognitive neuroscience of prehension: recent developments." Experimental brain research 204 (2010): 475-491. [3] Nunez, Paul L., Richard B. Silberstein, Peter J. Cadusch, Ranjith S. Wijesinghe, Andrew F. Westdorp, and Ramesh Srinivasan. "A theoretical and experimental study of high resolution EEG based on surface Laplacians and cortical imaging." Electroencephalography and clinical neurophysiology 90, no. 1 (1994): 40-57.

  • Decoding Challenge: Grasping, a complex integration of sensory perceptions, motor planning, and cognitive intentions, remains a significant decoding challenge in BCIs [2]. • EEG Limitations: Traditional EEG offers a means to decode grasping but suffers from low spatial resolution and is prone to disturbances [3]. Introducing tEEG: Exploring Tripolar EEG (tEEG) as a solution, offering enhanced spatial resolution and signal clarity. • In-Depth Comparison: Comparing tEEG with conventional EEG, focusing on SNR, ERPs, and classification accuracies. • Advanced Decoding: Leveraging wavelets and advanced machine learning to enhance the decoding accuracy of grasping intentions.

	Objectives:
	•

Table 1 :

 1 Classification accuracies of various models for different subjects, comparing EEG and tEEG

Acknowledgments

Research reported in this presentation was partially supported by the Rhode Island Institutional Development Award (IDeA) Network of Biomedical Research Excellence from the National Institute of General Medical Sciences of the National Institutes of Health under grant number P20GM103430.

References


Robert Beyer

Ali Rabiee

Sarah Ostadabbas

Reza Abiri

Human-Inspired Vision-Based Reaching and Grasping for Assistive Robotic Arms with Reinforcement Learning

published or not. The documents may come

Introduction

Human-Inspired Vision-Based Reaching and Grasping for Assistive Robotic Arms with Reinforcement Learning Motivation:

• Improving the lives of those with severely upper limb motor impairments via a semi-autonomous assistive robotic arm [1]. • Current assistive robotic arms require some voluntary movements to control a joystick for complex reach-to-grasp. • Human-inspired approaches and AI algorithms might offer better solutions to tackle the complexity of reach-to-grasp in assistive robotic arms [2].

Objectives:

• Adopting human-inspired approaches to explore the challenge of reach-to-grasp within vision-based robotic arms.

Simulation Pipeline & Q-Learning:

• Employed PyBullet virtual environment, OpenAI Gym, and PyTorch

• Update rule: goal is convergence to optimal Q* and therefore π*

• In classic RL solved by tabular approach

Deep RL:

• Estimate optimal Q-function with CNNs:

• Minimize loss function:

• Perform update:

• Reward functions: depends on distance to the mug and punish total steps Results (Cont.)

Translational Neurorobotics Lab

Effect of Reward Functions:

Results • Overall, the algorithm achieved better performance using the reward function R3.

Summarized results (SG: successful grasp):

• R3 outperformed in comparison to R1 and R2

• We achieved 90.03% success rate for an autonomous 3D reach-to-grasp task in an assistive robotic arm trained using deep RL. • As future steps:

• Implementing the pipeline using real physical robotic arm and exploring more daily objects through our development pipeline.

• Collecting data from human subject during performing natural 6D reach-to-grasp tasks.

• Training the vision-based robotic arm using human-inspired 6D grasp pose.

• Developing shared autonomy algorithms to enable the paralyzed patients to interact with the assistive robotic arms for performing daily manipulation tasks.

•

  Developing deep reinforcement learning (deep RL) algorithms to train an assistive robotic arm for reach-to-grasp tasks. • Optimizing the reward function for convergence of training in shorter time of training.

Figure 1 :

 1 Figure 1: Upper panel: Q-learning update rule. Down panel left: an image of real assistive robotic arm with 6 DOF. Down panel right: the simulation setup with virtual RGB-D cameras.The robotic arm attempts to reach and grasp the mug using 3D translational motions (X, Y, Z).

Figure 3 :

 3 Figure 3: Left plot: the success rate of deep RL algorithm using the three different reward functions. Right plot: corresponding steps required for training the deep RL algorithms.

Figure 4 :

 4 Figure 4: Training and success rate of the deep RL algorithm using the reward function R3.

  [1] S. Seko et al., "ECoG based BCI control of reaching and grasping with a robotic arm using stacked discrete commands," in Society for Neuroscience Annual Meeting (SfN 2021), Chicago, IL, USA, Nov. 08-11 2021.[2] S. Gu et al., "Deep reinforcement learning for robotic manipulation," arXiv preprint arXiv:1610.00633, vol. 1, 2016.

Figure 2 :

 2 Figure 2: Upper panel: CCN structure within the deep RL pipeline. Lower panel: the deep RL pipeline from the input (e.g. RGB images) to output actions to command the robotic arm

Acknowledgments

Research reported in this presentation was partially supported by the Rhode Island Institutional Development Award (IDeA) Network of Biomedical Research Excellence from the National Institute of General Medical Sciences of the National Institutes of Health under grant number P20GM103430.

References