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Friday, March 31, 2017
9:00 AM, Nord 400
Speaker: Max Freeberg
Mentor: Prof. Triolo
Friday, March 24, 2017
9:00 AM, Nord 400
Speaker: David Cunningham, Ph.D.
Human Performance and Engineering Laboratory
Kessler Foundation Research Center
Title: Tailoring brain stimulation to the nature of rehabilitative therapies and their unique mechanisms of neuroplasticity
Over the past decade there has been growing interest in combining non-invasive brain stimulation with rehabilitation in order to accelerate rehabilitative outcomes in patients with chronic stroke. The primary application of non-invasive brain stimulation has involved augmenting mechanisms of neuroplasticity which are unique to intensively training the paretic limb and restraining or otherwise discouraging movement of the non-paretic limb. However, several groups have discussed the importance of bilateral therapies, involving the paretic and non-paretic limb simultaneously, as they may provide a more feasible alternative, especially for patients with a greater disability. Still, because there is limited understanding of what neurophysiologic mechanisms underlie bilateral therapies there has been a lack of discussion on how to pair non-invasive brain stimulation in order to complement bilateral task practice. Further, the pairing of non-invasive brain stimulation with therapy has also failed to consider mechanisms of neuromuscular fatigue which occurs over the duration of a therapeutic session. This talk presents two experiments which investigates the mechanisms of bilateral therapy and neuromuscular fatigue and discusses tailoring non-invasive brain stimulation based on their unique mechanisms of neuroplasticity.
Friday, March 17, 2017
Note Time and Location Changes
12:00PM, Wickenden 321
Speaker: Frank Willett
Mentor: A. Bolu Ajiboye, Ph.D.
Title: (Dissertation Defense) "Intracortical Brain-Computer Interfaces: Modeling the Feedback Control Loop, Improving Decoder Performance, and Restoring Upper Limb Function with Muscle Stimulation"
Intracortical brain-computer interfaces (iBCIs) can help to restore movement and communication to people with chronic tetraplegia by recording neural activity from the motor cortex and translating it into the motion of an external device (typically a computer cursor or robotic arm). In this work, we focus on three avenues for advancement: (1) better understanding the feedback control loop created by the interaction between the user and the iBCI, (2) leveraging that understanding to improve the performance of decoding algorithms that translate neural activity into movement, and (3) restoring control over a person's own arm and hand by using a combined iBCI and muscle stimulation system.
In Chapters 2-3, we develop a deeper understanding of how linear decoders operate in closed-loop. Using data from the BrainGate2 pilot clinical trial, we develop a feedback control model that describes how users modulate their neural activity to move towards their target, stop accurately, and correct for movement errors. We use the model to characterize the errors made by linear decoders and find that they are signal-independent (i.e. they do not scale with the size of the user's motor command). As a consequence, we show that linear decoders only work well within a narrow range of movement scales and perform poorly when both precise and gross movements are required, in contrast to able-bodied movements that achieve success over a wide range of scales.
In Chapters 4-6, we explore three avenues for improving decoder performance based on the above results. First, we improve the linear decoder's ability to enable movements of different scales by adding a separate decoding pathway that can extract non-linear movement scale information from the neural activity. We show that this new pathway improves the user's ability to stop precisely on the target without sacrificing movement speed. Second, we show that our feedback control model can be used to optimize decoder performance by predicting, via simulation, which parameters will lead to the best closed-loop performance. Third, we test whether the feedback control model can improve decoder calibration by more accurately estimating the user's intended movements. Contrary to expectation, we found that all intention estimation methods we tested performed equivalently, despite differing significantly in their ability to accurately describe user intent.
In Chapters 7-8, we make progress towards a combined iBCI and functional electrical stimulation (FES) system that can restore motion to a person's own arm and hand. In a non-human primate model, we develop and test a new decoding method that enables direct cortical control over muscle stimulation and that can be calibrated automatically (without the need for expert design of muscle stimulation patterns). Finally, we demonstrate, for the first time, a person in the BrainGate2 pilot clinical trial using a combined FES + iBCI system to make continuously controlled, multi-joint reaching and grasping movements to match target postures and to complete functional tasks (eating mashed potatoes and drinking from a cup of coffee).
Friday, March 10, 2017
8:30 AM, Wolstein Research Building, Room 1413
Speaker: Benjamin D. Greenberg, MD PhD
Center for Neurorestoration and Neurotechnology
Providence VA Medical Center
Title: Brain Circuit-Based Treatments for Obsessive-Compulsive Disorder: A model for Neuropsychiatry
Friday, February 24, 2017
Nord 400, 9:00 AM
Speaker: Cale Crowder
Advisor: Dr. Robert Kirsch
Title: System Identification of the Human Motor Cortex
Abstract: Cervical spinal cord injury (SCI) can result in paralysis of all four limbs - a condition known as tetraplegia. Recently, our research group demonstrated an intramuscular functional electrical stimulation (FES) system controlled by an intracortical brain computer interface (BCI) implanted in the human motor cortex. The combined FES-BCI system was able to restore limited movement to a study participant's paralyzed arm. While the participant was able to perform simple tasks, such as self-feeding, self-drinking, and self-bathing, the FES-BCI system was inconsistent in its behavior. The purpose of the present study is to simplify the FES-BCI system controller in order to achieve better performance. Our objective is to extract additional information from the motor cortex in order to decrease the mental energy exerted by our participant in controlling the FES-BCI system. To extract additional information from the motor cortex, we are utilizing so-called "system identification," which uses established methods to build a model of a physiological system. During this seminar, we will describe the challenges of using a FES-BCI system, provide an introduction to system identification, and demonstrate, via modeling, how system identification can be used to extract information from the human motor cortex.
Friday, February 24, 2017
11am, Cleveland Clinic Lerner Research Institute, in room NE1-205
Dr. Peter Adamczyk will be presenting "Semi-Active Foot Prostheses for Low-Power Gait Restoration" in the APT Center Distinguished Lecture Series. Dr. Adamczyk directs the UW Biomechatronics, Assistive Devices, Gait Engineering and Rehabilitation Laboratory (UW BADGER Lab), at the University of Wisconsin-Madison, which aims to enhance physical and functional recovery from orthopedic and neurological injury through advanced robotic devices. Dr. Adamczyk will discuss his group's work on the mechanisms by which these injuries impair normal motion and coordination, and target interventions to encourage recovery and/or provide biomechanical assistance.
Dr. Adamczyk's presentation information is attached, as well as a map and parking directions.
Lab Website: http://uwbadgerlab.engr.wisc.edu/
Call for individual meetings
If you would like to meet with Dr. Adamczyk, please email Andrew Shoffstall (firstname.lastname@example.org) by Friday, February 17th, with your availability for the following times and locations:
Cleveland Clinic: Friday, February 24th, from 8am - 11am
Case Western Reserve University: Friday, February 24th, from 2pm - 5pm
Map and Parking directions | Adamczyk Talk Info
Friday, February 17, 2017
Nord 400, 9:00 AM
Speaker: Daniel Young
Advisor: Dr. Bolu Ajiboye
Title: Artifact Reduction Techniques Enable Neural Control of FES Actuated Movements
Hundreds of thousands of people live with loss of motor function due to spinal cord injury (SCI) and have indicated strong interest in neuroprosthetics that restore arm movements. Functional Electrical Stimulation has restored independence to people with spinal cord injuries, enabling activities such as eating, writing, and grooming. Intracortical brain computer interfaces (iBCI's) have been explored as potential command interfaces for neuroprosthetics because they can record neural activity related to complex reaching kinematics (10+ degrees of freedom) in humans with paralysis. In order to restore thought-controlled arm and hand movements after paralysis, our group implanted one participant with two recording intracortical microelectrodes in the left primary motor cortex and 24 stimulating intramuscular electrodes in the right limb.
However, iBCI's utilize precise recordings of microvolt sized signals while FES generates relatively larger electric fields in the paralyzed limbs. Electrical artifacts during stimulation can interfere with extracting accurate movement intentions and may limit the usefulness of iBCIs for control of FES prostheses. This work characterizes the stimulation artifacts we recorded on the intracortical microelectrodes and demonstrates their effect on our system performance. We implemented three cleaning methods for reducing the artifacts and present results comparing their effectiveness. The best cleaning method reduced artifact sizes by 2+ orders of magnitude and fully recovered neural information during stimulation periods. This method can be easily implemented in real time, enabling closed-loop brain control of both intramuscular and surface FES prosthetics.
Friday, February 10, 2017
8:30 AM, Wolstein 1413
Speaker: Andre Machado, M.D.
Friday, February 3, 2017
Friday, January 27, 2017
Nord 400, 9:00 AM
Speaker: Kubinar Gunalan
Advisor: Prof. Cameron McIntyre
Title: Methods to predict axonal activation in patient-specific models of deep brain stimulation
Abstract: Deep brain stimulation (DBS) of the subthalamic region is an established clinical therapy for the treatment of Parkinson's disease. Most computational models of DBS predict the generation of action potentials in axons surrounding the stimulating electrode and clinical software tools employing axon stimulation models are now commonly used to estimate the volume of tissue activated. However, the simplifying assumptions used in various DBS models can have a substantial impact on the stimulation predictions. I will review a range of different computational models for predicting axonal activation, including McNeal-type, Warman-type, and Butson-type models, and evaluate their accuracy in the context of clinical subthalamic DBS. In general, the results demonstrate that simplified models perform poorly when compared to detailed McNeal-type models.
Friday, January 20, 2017
Neural Prosthesis Seminar
Wolstein Auditorium, 8:30 AM
Speaker: Stephen B. McMahon
Div. Neuroscience, Kings College London
Title: Chronic pain mechanisms and how they may be affected by spinal cord stimulation
Friday, January 13, 2017
Nord 400, 9:00 AM
Speaker: Rajat Shivacharan
Advisor: Prof. Dominique Durand
Title: Can neural activity propagate via electric fields?
Abstract: Although electric fields are frequently overlooked due to more prominent neuron to neuron communication such as synaptic transmission, current studies on epileptiform behavior strongly suggest electric field transmission can play an important role in neural propagation. Experiments conducted in our lab have shown that propagation of epileptiform behavior in rodent hippocampi propagates at a unique speed of 0.1 m/s and can take place in the absence of synaptic transmission, leaving electric field as the logical mode of transmission. However, none of these studies show that the spontaneous bursting activity is solely generated from electric fields. Using in vitro experiments, we test the hypothesis that spontaneous epileptiform activity in the hippocampus can propagate via electric fields.