Neuromuscular Research Laboratory

“The Neuromuscular Research Laboratory conducts research focused on the functional limitations and neuromechanical adaptations that occur as a result of joint injury and disease. Traumatic joint injury increases the risk for early onset post-traumatic osteoarthritis. Our work aims to minimize this by identifying novel rehabilitation approaches targeting muscle weakness, biomechanical asymmetries, and functional limitations that result from joint injury. Benefits include reduced risk for re-injury and osteoarthritis, prolonged quality of life, and improved functional ability.”
Dr. Riann Palmieri-Smith, Director and Associate Professor of Athletic Training

Neuromuscular Research Laboratory

Contact

Address: 
CCRB 1213
401 Washtenaw Ave.
Ann Arbor, MI 48109-2214
(734) 647-0284
(734) 936-1925

Director

Projects

Dynamic Ankle Restraint in Patients with Functional Ankle Instability

Functional ankle instability (FAI) may be prevalent in as many as 40% of patients following an acute sprain of the lateral ligament complex. Damage to mechanoreceptors within the lateral ligaments has been hypothesized to interrupt neurological feedback mechanisms resulting in FAI. Altered afferent output from joint mechanoreceptors following injury or effusion is known to result in weakness of surrounding joint musculature, a phenomenon referred to as arthrogenic muscle response (AMR). AMR may be the underlying cause of FAI promoting a cyclic inhibition of the ankle joint musculature.

The overall goal of this investigation is to examine role of the dynamic ankle stabilizers in resisting sudden ankle inversion while walking in patients classified as functionally unstable. We hypothesize that the peroneal musculature will be inhibited hindering the dynamic control about the ankle in patients who suffer from FAI.

The Effects of Knee Injury on Muscle Activation

Knee ligament injury results in weakness of the musculature acting about the knee joint complex. This phenomenon has been termed arthrogenic muscle inhibition (AMI) and is defined as an ongoing reflex inhibition of musculature surrounding a joint following distension or damage to structures of that joint. AMI is the body’s innate response intended to protect the joint from further damage by discouraging its use. This protective mechanism comes at a high cost, as it restricts full muscle activation and therefore prevents restoration of strength possibly placing patients at greater risk for re-injury and potentially predisposing them to chronic degenerative joint conditions. Literature is available suggesting AMI is present following ACL injury and reconstruction, yet minimal data are available examining what factors impact the magnitude of the ensuing AMI following knee injury. In hopes of better understanding the factors that may result in persistent AMI, we plan to conduct an investigation to examine the impact of ACL graft type and the presence or absence of meniscal damage on the magnitude of quadriceps inhibition.

The Effect of Geographic Bone Bruises on Biological Markers and MRI Findings of Osteoarthritis After Anterior Cruciate Ligament Injury (funded by Nfl Charities)

Clinical evidence and epidemiological investigations show that anterior cruciate ligament (ACL) injury increases the risk for progressive joint degeneration, ultimately resulting in post-traumatic osteoarthritis (OA). Although clinicians and scientists are aware that ACL injury leads to degenerative joint disease, very little is known about its onset following the initial trauma and the mechanisms responsible for the loss of normal articular cartilage. Often by the time post-traumatic OA is diagnosed, excruciating pain and irreversible damage to joint surfaces has taken place leaving patients with few options to maintain quality of life. Subchondral bone injuries (“bone bruises”) accompany 80% of ACL ruptures and are thought to be the hallmark of subsequent osteoarthritis. These injuries may result in acute changes to overlying articular cartilage and subsequent degradation of both bone and cartilage. The role that subchondral bone contusions play in the development of post-traumatic osteoarthritis remains elusive and needs to be addressed so that preventive measures can be implemented. The proposed investigation will use a prospective study design with a relatively homogenous group of subjects who have sustained an acute ACL rupture and are scheduled to undergo reconstructive surgery. We plan to measure the serum concentration of selected biomarkers suggestive of inflammation and cartilage matrix turnover. Further, we will also examine magnetic resonance (MR) images using a validated pulse sequence and quantitative T2 mapping to prospectively assess changes in cartilage morphology as well as alterations in extracellular matrix components. These measurements will be made both in patients with an ACL rupture and a geographic bone bruise as well as in teammate and acquaintance control subjects with normal knees. Measurements will be gathered upon enrollment and at 12 months post-reconstruction. These data will be used to test our hypotheses that biomarkers of articular cartilage degradation are elevated in those with subchondral bone lesions and that bone bruises result in cartilage injury and loss of matrix integrity, as detected by MRI.