About

Julius P. A. Dewald is a Professor of Physical Therapy and Human Movement Sciences, as well as a Professor of Physical Medicine & Rehabilitation and Biomedical Engineering at Northwestern University. His educational background includes a BS in Physical Therapy and Rehabilitation Medicine and an MS in Neurophysiology and Rehabilitation Medicine from Vrije Universiteit Brussel, Belgium, and a PhD in Neurophysiology & Biophysics from Loma Linda University. His research focuses on the quantification of motor impairments following brain injury due to stroke or cerebral palsy, and the development of neuroscientific models to understand these impairments. Dewald's work integrates neurophysiology, neuropharmacology, imaging, signal analysis, rehabilitation robotics, and clinical insights to advance understanding of movement disorders caused by central nervous system lesions. He leads the Neuroimaging and Motor Control Laboratories at Northwestern, which are dedicated to understanding motor recovery post-stroke, brain plasticity, and developing therapeutic training techniques to improve arm function. His research involves investigating cortical reorganization using techniques such as EEG, MRI, TMS, and Diffusion Tensor Imaging, aiming to illustrate differences in brain organization between normal and injured brains. Dewald's team is also developing neural-machine interfaces and neuroprostheses to restore hand function in stroke patients, especially those with severe impairments. Additionally, his work includes impairment quantification to elucidate neural constraints in movement coordination, and the development of robotic devices for assessment and intervention. His research is largely funded by NIH, the Department of Education, and the American Heart Association, and it aims to translate basic science findings into effective clinical interventions for individuals with stroke and cerebral palsy.

Research topics

• Physical medicine and rehabilitation
• Medicine
• Psychology
• Anatomy
• Neuroscience
• Physical therapy
• Surgery
• Computer Science
• Physics
• Cardiology
• Internal medicine
• Radiology

Selected publications

• Disentangling acute motor deficits and adaptive responses evoked by the loss of cerebellar output

  eLife · 2025-01-29

  preprintOpen access

  Abstract Cerebellar patients exhibit various motor impairments, but the sequence of primary and compensatory processes leading to these deficits remains unclear. To investigate this, we reversibly blocked cerebellar outflow in monkeys performing planar reaching. The block caused a spatially tuned reduction in hand velocity due to decreased muscle torque, especially in movements with high coupling torques. Examining repeated movements to the same target revealed that during multi-joint reaching movements, the reduced velocity was driven by an acute deficit superimposed on a gradually emergent strategic slowing aimed at minimizing passive inter-joint interactions. However, the reduced velocity did not explain the decomposed and variable trajectories observed during the cerebellar block. Our findings suggest that loss of cerebellar signals leads to motor impairments through insufficient muscle torques and an altered control strategy to compensate for the impaired control of limb dynamics. However, impaired feedforward control also increases motor noise, which cannot be strategically eliminated.

  PublisherDOI

• Enhancing Hip Extension Moments During Gait Initiation for Studying Abnormal Hip Extension - Adduction Coupling in Stroke

  Biosystems & biorobotics · 2025-01-01

  book-chapter
  PublisherDOI

• Author response: Disentangling acute motor deficits and adaptive responses evoked by the loss of cerebellar output

  2025-06-06

  peer-reviewOpen access

  Patients with cerebellar damage experience various motor impairments, but the specific sequence of primary and compensatory processes that contribute to these deficits remains unclear. To clarify this, we reversibly blocked cerebellar outflow in monkeys engaged in planar reaching tasks. This intervention led to a spatially selective reduction in hand velocity, primarily due to decreased muscle torque, especially in movements requiring high inter-joint torque coupling. When examining repeated reaches to the same target, we found that the reduced velocity resulted from both an immediate deficit and a gradually developing compensatory slowing to reduce passive inter-joint interactions. However, the slowed hand velocity did not account for the fragmented and variable movement trajectories observed during the cerebellar block. Our findings indicate that cerebellar impairment results in motor deficits due to both inadequate muscle torque and an altered motor control strategy for managing impaired limb dynamics. Additionally, impaired motor control elevates noise, which cannot be entirely mitigated through compensatory strategies.

  PublisherDOI

• Effects of asymmetrical postural demands on sternocleidomastoid reflex in the startReact paradigm

  Frontiers in Human Neuroscience · 2025-09-23 · 4 citations

  articleOpen access

  Introduction: startReact, the rapid release of a planned movement following a startling acoustic stimulus (usually >100 dB), is widely used to assess reticulospinal tract (RST) involvement in motor control. The sternocleidomastoid (SCM) reflex within 120 ms often identifies true startle responses, i.e., responses facilitated by RSTs in the absence of cortical control. However, as the SCM is a postural muscle, its reflexive activation may be influenced by inhibitory anticipatory postural adjustments (APAs), particularly during tasks with greater head/neck postural demands. Methods: We compared SCM activation during unilateral shoulder abduction (SABD) versus hand opening (OPEN) tasks. Due to the increased asymmetrical head/neck postural demands in SABD, we hypothesized an APA-induced delay in SCM activation during SABD compared to the OPEN task, with a contralateral bias due to contralateral cortical circuits triggering APAs. Results: Our results revealed significantly longer SCM latency-exceeding the 120 ms cutoff-during SABD relative to OPEN. This suggested that APAs during postural tasks, resulting from unilateral SABD, altered the expression of the startReact response. To confirm this finding, we implemented an innovative, data-driven method to determine the appropriate SCM cutoff based on the physiological difference between startle-induced SCM reflexes and task-induced SCM activation. Using this method, we observed reduced contralateral SCM reflexive activation compared to ipsilateral, during SABD but not in OPEN. Discussion: This provides evidence for the first time that SCM reflexive activation in startReact is posture-dependent. Our novel classification method offers a robust framework for identifying true startle responses across different tasks, offering broader applicability for studies investigating RST involvement in motor control.

  PublisherOA PDFDOI

• A novel protocol to investigate the monoaminergic relationship between descending nociceptive and motor unit neuromodulation

  2025-07-14

  articleOpen accessSenior author

  Chronic pain is a multifaceted condition involving complex interactions between sensory and motor systems, in part modulated by monoaminergic neurotransmitters such as serotonin (5-HT) and norepinephrine (NE). Diffuse noxious inhibitory control (DNIC) and motor unit (MU) facilitation are critical processes that reflect descending nociceptive inhibition [1] and motor neuromodulation, respectively. This study presents a novel protocol combining pain-related evoked potentials (PREP) recorded via electroencephalography (EEG) and high-density surface electromyography (HDsEMG) to assess the effects of an experimental painful stimulus-the cold pressor test (CPT)-on both nociceptive and MU neuromodulation. Healthy, young participants completed pre-and post-CPT assessments, with PREP and HDsEMG data collected in three experimental components. Although the sample size was small, promising trends in post-CPT responses for both nociceptive and MU parameters suggest the feasibility of this approach. The findings support the hypothesis that the CPT induces enhanced nociceptive inhibition and MU facilitation in healthy controls, likely mediated by increased widespread monoaminergic drive. Future studies with larger sample sizes and diverse participant populations, including those with chronic pain conditions, will be necessary to validate these results and explore the protocol's ability to capture both nociceptive inhibition and facilitation.Clinical Relevance-This provides the first step towards furthering our understanding of the interplay between nociceptive processing and motor impairments, two of the hallmark signs across chronic pain conditions.

  PublisherOA PDFDOI

• Quantifying structural properties of forearm flexor muscles in individuals with hemiparetic cerebral palsy using diffusion tensor imaging

  Physiological Reports · 2025-06-01 · 1 citations

  articleOpen access

  This study investigated diffusion tensor imaging (DTI) derived macro- and micro-structural musculoskeletal adaptations in forearm flexor muscles in individuals with hemiparetic cerebral palsy (HCP) and typically developing (TD) individuals, and their relationship to reduced grip strength. In 14 individuals with HCP and 16 TD individuals, T1-weighted and diffusion-weighted magnetic resonance images of both forearms were acquired, and maximum grip strength was measured. In two forearm flexors, muscle volume, DTI-based diffusivity metrics, and probabilistic tractography derived fascicle architecture was estimated. Linear mixed-effects models evaluated interlimb differences in structural parameters and their impact on grip strength. In the HCP group, paretic muscles showed significant reductions in volume, diffusivity values, fascicle lengths, and physiological cross-sectional area as compared to nonparetic forearm and TD participants. Furthermore, reduced muscle volume and diffusivity together explained 62% of the grip strength deficit. These findings demonstrate that decreased muscle volume and altered microstructure, as indicated by reduced diffusivity, contribute significantly to functional impairments in HCP. DTI-based diffusivity metrics non-invasively reveal crucial insights into pathophysiological changes in muscle tissue, such as muscle atrophy and fibrosis. Future therapies should focus on both muscle macro- and micro-structural adaptations as targets to improve motor function in HCP.

  PublisherOA PDFDOI

• Early Development of Selective Motor Control in Preterm Infants With and Without Cerebral Palsy

  medRxiv · 2025-05-11 · 2 citations

  preprintOpen accessSenior author

  Abstract Objectives To characterize early developmental trajectories of selective motor control (SMC) in very preterm infants and examine associations with later cerebral palsy (CP) diagnosis and gross motor function. Methods Very preterm infants (<32 weeks’ gestation) were recorded every 2–4 weeks until 5 months post-term age (PTA). SMC was scored from 352 videos (n=47 infants; 12 with CP) using BabyOSCAR, a validated observational tool. Linear mixed models examined SMC trajectories by CP diagnosis and Gross Motor Function Classification System (GMFCS) level. ROC curves tested the ability of early SMC change (40–45 weeks) to predict CP. Results SMC scores increased over time, but infants with CP showed slower gains. Between 41–63 weeks, group differences emerged and widened (p<0.001). Change in BabyOSCAR score from 40–45 weeks predicted CP with 92% sensitivity and 100% specificity (AUC=0.98). GMFCS groups showed distinct trajectories, with children classified as GMFCS III–V changing scores less. Infants with unilateral CP showed increasing asymmetry from 42 weeks PTA. Conclusions SMC develops rapidly after term age but is altered in infants with CP, particularly among those later classified as GMFCS III–V. Early trajectories may reflect emerging corticospinal connectivity and offer a clinically useful marker of functional motor outcomes.

  PublisherOA PDFDOI

• Author response: Disentangling acute motor deficits and adaptive responses evoked by the loss of cerebellar output

  2025-01-29

  peer-reviewOpen access

  Cerebellar patients exhibit various motor impairments, but the sequence of primary and compensatory processes leading to these deficits remains unclear. To investigate this, we reversibly blocked cerebellar outflow in monkeys performing planar reaching. The block caused a spatially tuned reduction in hand velocity due to decreased muscle torque, especially in movements with high coupling torques. Examining repeated movements to the same target revealed that during multi-joint reaching movements, the reduced velocity was driven by an acute deficit superimposed on a gradually emergent strategic slowing aimed at minimizing passive inter-joint interactions. However, the reduced velocity did not explain the decomposed and variable trajectories observed during the cerebellar block. Our findings suggest that loss of cerebellar signals leads to motor impairments through insufficient muscle torques and an altered control strategy to compensate for the impaired control of limb dynamics. However, impaired feedforward control also increases motor noise, which cannot be strategically eliminated.

  PublisherDOI

• Contralesional recruitment and localization of EEG signal complexity in stroke: A recurrence quantification analysis of hierarchical motor tasks

  Journal of Neural Engineering · 2025-06-20

  articleOpen access

  Abstract Objective: This study quantifies EEG complexity in chronic hemiparetic stroke patients performing hierarchical motor tasks, examining the degree of contralesional motor resource recruitment in maladaptive neural responses. Approach: We applied recurrence quantification analysis (RQA) and nonlinear dynamical measures to examine spatial patterns of motor-related EEG complexity under varying shoulder abduction torque levels (20% and 40%) in both stroke survivors and healthy control participants, enabling comparative analyses of adaptive neural responses. Results: Our findings show a statistically significant increase in EEG signal complexity within the contralesional hemisphere of stroke participants, particularly under higher shoulder abduction loads. Consistent with previous studies, we observed abnormal muscle coactivation patterns between proximal and distal muscles, along with distinct shifts in EMG vector direction in stroke-impaired limbs. These shifts in coactivation patterns suggest constraints in muscle coactivation patterns resulting from losses in corticofugal projections and upregulated brainstem pathways. Significance: We introduce a novel application of RQA to quantify nonlinear EEG complexity during motor execution in chronic stroke. Unlike traditional spectral or connectivity-based EEG methods, RQA quantifies temporally evolving, nonlinear recurrence patterns that reflect maladaptive contralesional motor recruitment. Our findings demonstrate that increased EEG complexity correlates with impaired motor control and reliance on compensatory pathways, offering new insight into neural reorganization after stroke. These results position RQA as a promising, clinically meaningful, and computationally efficient tool to evaluate cortical dynamics and guide targeted neurorehabilitation strategies aimed at minimizing maladaptive plasticity.

  PublisherDOI

• Author response: Disentangling acute motor deficits and adaptive responses evoked by the loss of cerebellar output

  2025-06-25

  peer-reviewOpen access

  Reversible cerebellar disruption in non-human primates reveals an acute muscle torque deficit and an adaptive slowing strategy to manage limb dynamics, underscoring distinct primary, and compensatory mechanisms underlying motor impairment.

  PublisherDOI

Recent grants

• NIH Grant R01HD047569

  NIH · $1.1M · 2011

• NIH Grant R01HD084009

  NIH · $1.3M · 2019

• Determination of the Recruitment of Indirect Motor Pathways in Chronic Hemiparetic Stroke

  NIH · $416k · 2019–2023

• NIH Grant R03HD039804

  NIH · $145k · 2005

• Contralesional Corticobulbospinal Structural and Functional Changes Post Stroke: Biomarkers for the upper limb flexion synergy

  NIH · $2.7M · 2019–2025

Frequent coauthors

• Yuan Yang

  Northwestern University

  55 shared

• C. J. Heckman

  Shirley Ryan AbilityLab

  43 shared

• Michael D. Ellis

  40 shared

• Jun Yao

  37 shared

• Alfred C. Schouten

  Delft University of Technology

  36 shared

• Gregory E. P. Pearcey

  Northwestern University

  31 shared

• Randall F. Beer

  Northwestern University

  28 shared

• Wendy M. Murray

  28 shared