Adaptive Deep Brain Stimulation

Artificial neural networks (ANNs), as core components of modern deep learning (DL) systems, lack the adaptive flexibility and long-term stability exhibited by biological systems. This limitation largely stems from the fact that conventional ANNs rely on uniform, local, and gradient-based parameter updates, while neglecting internal learning principles that are biological mechanisms such as neurotransmitters signalling or neuroplasticity. Consequently, many existing approaches focus on architectural expansion or mathematical fine-tuning techniques such as regularisation or parameter isolation. Inspired by the superior adaptability and plasticity of mammalian brains, we posit that neuromodulation with neurotransmitters constitutes a third axis of learning, complementary to neural activity and synaptic plasticity, and should be explicitly modelled in artificial neural networks. In this positional paper, we argue that incorporating neuromodulatory principles into ANN design represents a promising and underexplored research direction, and we advocate for greater attention to this perspective in the development of adaptive and continual learning systems.

Continual learning (CL) requires models to learn tasks sequentially, yet deep neural networks often suffer from plasticity loss and poor knowledge transfer, which can impede their long-term adaptability. Drawing high-level inspiration from global neuromodulatory mechanisms in the brain, we introduce Neuromodulation and Synchronization (NeuMoSync), a novel architecture that integrates dynamic, neuron-specific modulation into deep neural networks to enhance their adaptability and plasticity. NeuMoSync extends standard neural network architectures with learnable feature vectors for each neuron that track network-wide historical context and with a module operating at a higher level of abstraction. This module synthesizes neuron-specific signals, conditioned on both current inputs and the network's evolving state, to adaptively regulate activation dynamics and synaptic plasticity. Evaluated on diverse CL benchmarks, including memorization (Random Label CIFAR-10 and Random Label MNIST), concept drift (Shuffle CIFAR-10 and Shuffle Mini-ImageNet), class-incremental learning (Class Split ImageNet and Class Split CIFAR-100), and domain-incremental learning (Permuted MNIST), NeuMoSync demonstrates strong performance in retaining plasticity and achieves improvements in both forward and backward adaptation compared with existing methods. Ablation studies validate the necessity of each component, while analysis of the learned modulatory signals reveals interpretable coordination patterns across tasks. Our work underscores the potential of integrating global coordination mechanisms into deep learning systems to advance robust, adaptive continual learning. The code is publicly available at https://github.com/RoozbehRazavi/NeuMoSync.

Parkinson's disease (PD) affects millions worldwide and causes severe motor symptoms. Adaptive deep brain stimulation (aDBS) delivers physiologically informed stimulation that can track fluctuations in PD motor symptoms, enabling more intelligent DBS control. However, most existing aDBS approaches are primarily algorithm- and software-driven, with limited efforts toward circuit realization, particularly low-power and implantable integrated circuits. This paper presents the Silicon Leaky Integrate-and-Fire Deep Brain Stimulation (SiLIF-DBS) controller, a neuromorphic silicon neuron stimulator implemented with metal-oxide-semiconductor (CMOS) technology. For system-level evaluation, a simplified computational model of the SiLIF-DBS controller is derived and embedded within a Parkinsonian cortico-basal ganglia framework for closed-loop validation. The system is driven by beta-band subthalamic nucleus local field potentials (STN-LFPs), with their average rectified value (Beta ARV) used as the control biomarker. Our SiLIF-DBS controller for aDBS suppresses pathological beta activity while consuming only 25% of the power required by open-loop stimulation and achieving a suppression efficiency of $5.85\%$/$μ$W. Overall, our SiLIF-DBS controller achieves strong beta suppression at substantially reduced power, delivering high suppression efficiency that demonstrates it is a viable foundation for low-power implantable aDBS.

Neuromorphic and edge computing research has focused on reducing the inference cost of neural network controllers, yet in physical closed-loop systems the actuator can rival or exceed an efficient controller in energy. An efficient controller is therefore necessary but not sufficient, because the actuator becomes the cost worth reducing once inference no longer dominates it. Here, we introduce energy-aware learning, an approach that incorporates actuator energy directly into the reinforcement learning reward, and demonstrate it in closed-loop deep brain stimulation (DBS) for Parkinson's disease. A deep spiking Q-network, trained in a biophysical cortico-basal ganglia-thalamic circuit model, learns to suppress pathological alpha-beta oscillations by 45.2% while reducing stimulation charge by 80.0% relative to continuous DBS. Sparsity-constrained knowledge distillation compresses the policy onto the SynSense XyloAudio 3 neuromorphic processor at 0.52 mW inference power, yielding 28.1x lower energy per inference than an equivalent artificial neural network on conventional edge hardware. By co-optimizing stimulation energy and inference efficiency, the framework addresses both major power demands in implantable neuromodulation.

Electroencephalogram (EEG) analysis remains the clinical gold standard for epilepsy diagnosis and seizure detection. While Deep Learning (DL) has significantly advanced automated EEG interpretation, its transition from controlled experimental settings to routine clinical deployment is severely bottlenecked by fundamental architectural flaws. Standard DL models operate as opaque black-boxes lacking clinical interpretability, demand massive amounts of balanced annotated data, and incur steep computational costs incompatible with resource-constrained wearable or implantable neuromodulation devices. This paper presents a comprehensive review of these prevailing limitations and explores Kolmogorov-Arnold Networks (KANs) as a emerging paradigm for EEG-based seizure detection. By replacing the fixed activation functions of traditional neurons with flexible, learnable functions along the network's connections, KANs bridge the critical gap between predictive accuracy and mathematical transparency. We systematically analyze how KAN architectures resolve the shortcomings of traditional DL-based models by offering exceptional parameter efficiency, inherent interpretability for physician trust, and robust performance under data scarcity. Ultimately, this review establishes KANs not merely as an incremental algorithmic update, but as a fundamental paradigm shift necessary to actualize next-generation, patient-specific, and thoroughly transparent clinical EEG monitoring systems.

Computational models of epilepsy promise patient-specific treatment design, but most optimization workflows still search for parameters that perform well on average. In neuromodulation, this is a weak target: a protocol that improves the mean response can still fail in the patient whose network is least tolerant to stimulation. We present a literature-guided minimax pipeline that couples PubMed-scale hypothesis extraction, The Virtual Brain (TVB) Epileptor simulations, and large-language-model-guided black-box optimization. The optimizer proposes either intrinsic model-control parameters or clinically interpretable external-stimulation protocols; TVB evaluates each proposal across sampled virtual patients; and the objective maximizes worst-case reward, defined as the negative variance of simulated seizure activity. In the intrinsic model-control experiment, the best archived parameter set improved worst-case reward from -0.5285 to -0.3182, a 39.8% gain over baseline. The clinical-style external-stimulation search produced a much smaller worst-case improvement (1.7%), and a 20-patient virtual cohort showed no aggregate benefit (p=0.9019), despite a 55% responder rate and a positive temporal-lobe subgroup signal. The study should be read as an in silico proof of concept for robust, literature-aware neurostimulation design, not as clinical evidence.

Cognitive science remains split between cognitivism - which accounts for recursion and language but cannot ground formal symbols in meaning - and 4E approaches - which ground cognition in the body but rarely specify the body's architecture in enough detail to support generativity. We argue the impasse stems from an incomplete account of the embodied agent's architecture, and propose one: the Sensation Modulating Network (SMN), the cognitive agent conceived as the whole body, organized at every anatomical scale by opponent dynamics, built from Sensation Modulators that sense and act through one substrate, paired into Coordinated Action Zones routed by a body-wide broadcast network. Three commitments give the SMN its purchase. Haltability - the recruitment of antagonistic affordance into co-activated equilibrium - provides the architectural locus that object-directed phenomenology, in Husserl's sense, requires: opponency enables co-activation, co-activation enables halt, halt enables attention, attention enables intentional directedness, with no module added on top. The dual-signal property of self-modulatable action patterns (SMAPs) makes the self/world distinction a structural feature of the wiring rather than a category the agent applies. And a four-level action-pattern hierarchy - Basal, Haltable, Negotiable, Transactional - gives a single trajectory from autonomic regularity to public conventionalization, locating the conditions for grammar-grounded generativity as architectural transitions. The SMN reconciles the cognitivism-4E debate: recursion lives in the modifiable dynamics of Negotiable Action Patterns, embodiment in the opponent substrate that supports them. A tentative formalism and eight predicted registers (seven testable, one hypothetical), with reference simulations, are given in an appendix.

Language models are instruction-tuned to refuse harmful requests, but the mechanisms underlying this behavior remain poorly understood. Popular steering methods operate on the residual stream and degrade output coherence at high intervention strengths, limiting their practical use. We introduce contrastive neuron attribution (CNA), which identifies the 0.1% of MLP neurons whose activations most distinguish harmful from benign prompts, requiring only forward passes with no gradients or auxiliary training. In instruct models, ablating the discovered circuit reduces refusal rates by over 50% on a standard jailbreak benchmark while preserving fluency and non-degeneracy across all steering strengths. Applying CNA to matched base and instruct models across Llama and Qwen architectures (from 1B to 72B parameters), we find that base models contain similar late-layer discrimination structures but steering these neurons produces only content shifts, not behavioral change. These results demonstrate that neuron-level intervention enables reliable behavioral steering without the quality tradeoffs of residual-stream methods. More broadly, our findings suggest that alignment fine-tuning transforms pre-existing discrimination structure into a sparse, targetable refusal gate.

This research addresses a validated TMS EEG cleaning pipeline and a corresponding benchmark dataset. It evaluates two widely used artifact removal pipelines. A reference dataset of carefully preprocessed EEG signals was established to support future algorithm development and enable systematic comparison of automated artifact removal strategies, despite the absence of a true physiological ground truth. The study evaluates the effectiveness of two widely used source based artifact removal approaches and examines their impact on signal quality improvement and preservation of TMS-evoked potentials. The results support the robustness of the proposed preprocessing workflow and demonstrate its potential for improving data reliability in both research and clinical applications. A key goal is integrating TMS EEG and embedding it within a larger BCI framework. Ultimately, these efforts aim to enhance understanding of cortical dynamics and expand the clinical and research applications of TMS EEG.

Neuroscience and Artificial Intelligence (AI) have made impressive progress in recent years but remain only loosely interconnected. Based on a workshop convened by the National Science Foundation in August 2025, we identify three fundamental capability gaps in current AI: the inability to interact with the physical world, inadequate learning that produces brittle systems, and unsustainable energy and data inefficiency. We describe the neuroscience principles that address each: co-design of body and controller, prediction through interaction, multi-scale learning with neuromodulatory control, hierarchical distributed architectures, and sparse event-driven computation. We present a research roadmap organized around these principles at near, mid, and long-term horizons. We argue that realizing this program requires a new generation of researchers trained across the boundary between neuroscience and engineering, and describe the institutional conditions: interdisciplinary training, hardware access, community standards, and ethics, needed to support them. We conclude that NeuroAI, neuroscience-informed artificial intelligence, has the potential to overcome limitations of current AI while deepening our understanding of biological neural computation.

Continuous adaptive learning, the ability to adapt to the environment and keep improving performance, is a hallmark of natural intelligence. Biological organisms excel in acquiring, transferring, and retaining knowledge while adapting to volatile environments, making them a source of inspiration for artificial neural networks (ANNs). This study explores how neuromodulation, a building block of learning in biological systems, can help address catastrophic forgetting and enhance the robustness of ANNs in continual learning. Driven by neuromodulators including dopamine (DA), acetylcholine (ACh), serotonin (5-HT) and noradrenaline (NA), neuromodulatory processes in the brain operate at multiple scales, facilitating dynamic responses to environmental changes through mechanisms ranging from local synaptic plasticity to global network-wide adaptability. Importantly, the relationship between neuromodulators and their interplay in modulating sensory and cognitive processes is more complex than previously expected, demonstrating a "many-to-many" neuromodulator-to-task mapping. To inspire neuromodulation-aware learning rules, we highlight (i) how multi-neuromodulatory interactions enrich single-neuromodulator-driven learning, (ii) the impact of neuromodulators across multiple spatio-temporal scales, and correspondingly, (iii) strategies for approximating and integrating neuromodulated learning processes in ANNs, and (iv) an architectural-general formulation of multi-neuromodulatory dynamics. We also present a conceptual study to showcase how neuromodulation-inspired mechanisms, such as DA-driven reward processing and NA-based cognitive flexibility, can enhance ANN performance in a Go/No-Go task. Though multi-scale neuromodulation, we aim to bridge the gap between biological and artificial learning, paving the way for ANNs with greater flexibility, robustness, and adaptability.