For a better experience, click the Compatibility Mode icon above to turn off Compatibility Mode, which is only for viewing older websites.

Multiscale Neuromuscular Biomechanics Laboratory

man sits looking into a microscope while image of muscle tissue and tweezers is projected on computer screen

Benjamin Binder-Markey, DPT, PhD, directs the Multiscale Neuromuscular Biomechanics Laboratory at Drexel University. The lab integrates physical therapy, basic science, and engineering principles through the use of experimental and computational modeling methods to better understand how changes in muscle properties following injury or disease affect physical function. This work aims to develop new technologies and interventions that significantly improve patient care and outcomes. Our work focuses on understanding how skeletal muscle adapts following injury or disease and optimizing skeletal muscle recovery. One focus of our work explores how peripheral or central nervous system injuries combined with muscle adaptation affect physical function. Another focus strives to understand the time course and causes of skeletal muscle wasting due to cancer-driven cachexia and its effect on function and morbidity. NIH, Hartwell Foundation, The Foundation for Physical Therapy Research, American Heart Association, The Brinson Foundation and Shirley Ryan AbilityLab Catalyst Fund have funded this work.

Principal Investigator

Ben Binder-Markey, PT, DPT, PhD

Benjamin Binder-Markey, PT, DPT, PhD
Assistant Professor - Physical Therapy and Rehabilitation Sciences

Lebow Engineering Center, Room 437
Market St. and 31st St., Philadelphia, PA 19104



Research Gate | PubMed | Google Scholar

Quantify biomechanical changes within muscle following stroke and botulinum toxin (BTX) use.

Botulinum toxin (BTX) is the go-to treatment for hyperactive muscles following a stroke to decrease the resistance to movement this hyperactivity causes. However, our initial results have led to an unexpected finding that chronic stroke survivors who received BTX injections demonstrate marked increases in their passive muscle properties, absent in equally impaired chronic stroke survivors who never received BTX injections. It appears that these BTX injections have the opposite of the desired effect and potentially cause long-term increases in passive torques and decreases in passive range of motion. These findings were most surprising and have important clinical implications for the future use of BTX.

This project seeks to quantify how muscle structures change post-stroke and BTX use. We are currently using pre-clinical and computational modeling to determine the structural adaptations and sources within muscles that result in these passive stiffness changes following BTX injection. With the knowledge of interventional targets, we are testing novel interventions aimed at preventing these changes.

This work is funded by an NIH K12 career development grant and a Foundation for Physical Therapy Research Grant.

Identification of Biological Targets to Reduce Muscle Stiffness and Optimize Function Following Long-Term Botulinum Neurotoxin Therapy in Cerebral Palsy.

Cerebral Palsy (CP) is the most common cause of childhood physical and movement disability in the United States with 1 out of every 345 children identified as having CP. CP is a non-progressive neurological injury that occurs at or around birth, yet as the child develops, their muscles do not grow properly. Thus, their muscles become relatively smaller and stiffer, exacerbating impaired movement due to muscle weakness and hyperactivity from the initial neurological injury. As the child develops, muscle hyperactivity and increasingly stiff muscles often result in fixed muscle contractures with joints that are exceedingly hard to move, requiring surgery. Botulinum neurotoxin (BoNT) injections have become the standard of care to delay these invasive surgeries. BoNT induces local muscle paralysis reducing muscle hyperactivity and the associated muscle stiffness. Unfortunately, almost all children receiving BoNT injections eventually need surgery. However, it is unknown how BoNT affects growing muscle, especially that of children with CP. Impairments following BoNT could have detrimental consequences by increasing muscle stiffness and further impairing muscle growth, decreasing the muscle’s function, and potentially speeding up time to surgery. Thus, it is critical to ensure that potential long-term detrimental side-effects following BoNT injections do not outweigh short-term benefits. The long-term goal of this work is to optimize muscle function in children with CP allowing them to achieve their highest quality of life. Thus the goal of this project is to identify the structural and biologic targets for alternative or adjunct interventions to use with BoNT that optimize muscle function in children with CP and subsequently improve their quality of life.

This work is funded by the Hartwell Foundation’s Independent Biomedical Researcher Award.

Develop rehabilitation tailored pre-clinical models of cancer-associated cachexia to characterize physical and functional decline mediators in cancer.

The primary objective of this project seeks to determine the impact of cachexia on physical activity and function by developing a pre-clinical animal model of cancer that is optimized to study rehabilitation interventions. Given the multifactorial nature of functional change in cancer patients, animal studies permit the investigation of specific mechanisms linking cachexia and function. However, most cancer animal models are optimized for primary tumor pathology instead of longitudinal sequelae; as a result, the few current models of cachexia use rare tumor phenotypes and rapidly succumb to primary tumor burden. Additionally, prior studies of these models of cachexia have not examined function with translationally significant depth or precision. Thus, the longitudinal sequence of pathophysiologic and functional changes linked to cachexia are undefined. This project seeks to determine this relationship by using a new approach that utilizes a cachexia model optimized for longitudinal observations and measures of function innovative to cancer biology.

Determining sources of passive biomechanical stiffness within muscle.

This project seeks to determine how muscle structure contributes to passive mechanical properties of muscle. Collagen content is often used as a surrogate for connective tissue quantity to infer muscle stiffness and load-bearing capacity. However, prior attempts to correlate passive mechanical properties with collagen content have not been successful. We found that this is likely due to not accounting for the high variability in intramuscular connective tissue, which causes collagen content to vary greatly between and within muscles. This collagen variability is driven primarily by dense connective tissue structures (i.e., internal tendon and fascial sheets) within the muscle. A consequence of these findings indicates that a single collagen content measurement, as often taken, does not accurately represent the muscle’s complex distribution of connective tissue and likely does not accurately reflect a muscle's load-bearing capacity. To further complicate the passive mechanics story, passive mechanical properties do not accurately scale from the sarcomere to the whole muscle level, as is the case with active length-tension properties.

Using computational modeling, we have set out to identify sources that could contribute to the non-linear scaling of passive fascicle mechanics to whole muscle mechanics. Thus far, we have found that to model muscle passive mechanical properties accurately, the model must reflect the complexity of the muscle. To a first approximation, architectural normalization helps, but additional terms including surrogate parameters for connective tissue content and muscle shear are needed to provide high-resolution properties. However, the precise structures representing these surrogate mathematical terms are not currently clear and are the subject of ongoing investigations.

Doctoral Students

tim mcginley in blue collared shirt with white lab coat

  • Tim McGinley, BMES PhD Student


  • Simrit Rajan, Biology Undergraduate Researcher
  • Jared Featherston, Biology Undergraduate Researcher


  • Dheer Varsani, Mech Eng. Co-op student 2022 (Drexel Undergraduate Student)
  • Antonio Hernandez-Cortes, Biomed Eng. Co-op student 2022 (Drexel Undergraduate Student)
  • Skylar Verrone, Mech Eng. Co-Op student 2021 (Drexel Undergraduate Student)

Internal Collaborators

  • Simon Giszter, PhD College of Medicine, Department of Neurobiology and Anatomy MORE INFO
  • Kara Spiller, PhD, School of Biomedical Engineering, Science and Health Systems MORE INFO
  • Lin Han, PhD, School of Biomedical Engineering, Science and Health Systems MORE INFO

External Collaborators

  • Ishan Roy, MD, PhD – Shirley Ryan Abilitylab MORE INFO
  • Richard Lieber, PhD – Shirley Ryan Abilitylab MORE INFO
  • Julius PA Dewald, PT, PhD – Northwestern University MORE INFO
  • Wendy Murray, PhD – Northwestern University MORE INFO