Katherine S. Rudolph, PT, Ph.D.

Associate Professor, Physical Therapy

Director, Motion Analysis Laboratory

Location

Proctor 206

Contact

krudolph@une.edu

(207) 221-4113

Eligible for Student Opportunities

Dr. Katherine (Katy) Rudolph is a physical therapist and researcher in the Department of Physical Therapy in the Westbrook College of Health Professions at UNE. She earned an M.S.P.T. at Boston University in 1989 and a Ph.D. in Biomechanics and Movement Science from the University of Delaware in 1998. After post-doctoral training in the Center for Biodynamics at Boston University she accepted a faculty position at UD where she remained from September 1999 through August 2011. She joined the UNE family in September 2011.

Credentials

Education

Research

Current research

Chronic Pain, Motor Output and Motor Learning in Knee Osteoarthritis

NIH 1R15AR068627 (PI: Rudolph); 04/01/2016 - 03/31/2019; $300,000 direct costs

By 2030, it is estimated that 67 million people will have osteoarthritis (OA) in the US and the majority of them will have OA in the knee that begins in middle age. Patients endure pain for many years before they have a total knee replacement. The number of years that knee OA patients endure pain takes a toll on their knee function and quality of life but it also impacts how the nervous system processes pain signals. Central sensitization of pain is a heightened
response to painful stimuli that is a protective mechanism designed to allow the body to heal.

Under normal circumstances, central sensitization subsides when tissue healing is complete. However, sometimes central sensitization persists and pain is exaggerated or no longer originates from a peripheral source. This abnormal sensory processing can lead to misdiagnosis and poor outcomes to treatments because the source of the pain is in the central nervous system not in peripheral tissues. Central sensitization of pain has been demonstrated in people
with knee OA and it is exacerbated by another anomalous pain mechanism: reduced conditioned pain modulation (CPM). CPM involves the application of a painful “conditioning stimulus” that elicits a reduction in the perception of pain. The presence of central sensitization
and reduced conditioned pain modulation can make knee OA much harder to treat, however clinicians are now augmenting traditional physical therapy interventions with treatments like cognitive behavioral therapy and mind-body treatments that can influence how the central nervous system processes the pain signals. Unfortunately, those interventions do not influence the movement patterns used by people that can hasten joint degeneration including reduced knee motion and higher muscle co-contraction combined with buckling. These movements produce greater loads and higher shear forces in the knee that are particularly detrimental to articular cartilage. Recently physical therapy interventions have been developed to address the abnormal movement and muscle activation patterns but none have been shown to be any more
effective than traditional aerobic or strengthening exercises. This may be due to deficits in the ability to learn new motor programs to stabilize the knee which is highly plausible considering that motor output and motor learning rely on accurate sensory feedback that we know is impaired in people with knee OA. This study will investigate the presence of central sensitization and reduced CPM and their influence on motor adaptation and learning in this population. The results will provide valuable insight into motor control that can be used to further develop
treatments that will improve knee function while slowing progress of the disease.

Is it exercise or its associated pain that leads to exercise-induced hypoalgesia?

The human nervous system has the innate ability to enhance or reduce the experience of pain and physical therapists can use those innate mechanisms to reduce pain in their patients in order to increase activity, participation in daily life and improve quality of life. Physical therapy patients are often familiar with transcutaneous electrical stimulation (TENS) which is the application of electrical pulses that produce a strong but comfortable tingling sensation. The strong comfortable sensation elicits mechanisms in the nervous system that reduce the perception of pain. Less known is the use of electrical stimulation to produce a painful (noxious) sensation that elicits the pain inhibitory mechanisms as well and can lead to long-term pain reduction.

Exercise is another physical therapy intervention that produces pain reduction. Studies have shown that even relatively low-level exercise such as an isometric contraction lasting 90 s, at a relatively low level of force (30% of maximum force) produces pain relief. Although many studies have demonstrated exercise-induced hypoalgesia (EIH), the muscle contractions used in such study often produce significant muscle fatigue and pain. Therefore, it is unclear whether EIH is induced by the exercise (muscle contraction) itself or the pain associated with the exercise. The purpose of this study is to determine if exercise-induced hypoalgesia is elicited by muscle contractions alone, or by the pain associated with muscle contractions. The results will provide a better understanding of the mechanisms underlying exercise-induced analgesia that will improve accurate exercise prescription to induce analgesia.

Selected publications

Book Chapters

James MA, Rudolph KS: Shoulder Pain in Paraplegia and Tetraplegia: The Weight Bearing Upper Extremity. in Betz RR, Mulcahey MJ editors: The Child with a Spinal Cord Injury, American Association of Orthopaedic Surgeons Symposium, Rosemont, IL. pp. 449-458. 1996.
Rudolph, K.S., Fitzgerald, G.K., Snyder-Mackler, L.: Restoration of Dynamic Stability in the ACL deficient Knee. in Lephart, S., Fu, F., editors: Role of Proprioception and Neuromuscular Control in Management in Articular Pathology. Human Kinetics Publisher, Champaign, IL. pp. 393-404, 2000.
Chmielewski, T.L., Rudolph K.S., Axe, M.J., Fitzgerald, G.K., Snyder-Mackler, L. Movement Patterns of individuals with good potential to dynamically stabilize their knees after acute ACL rupture. In: The Many Faces of Osteoarthritis, ed by KE Kuettner and VC Hascall, Raven Press, New York, pp. 461-463. 2002.
Snyder-Mackler L, Schmitt L, Rudolph K, Woodzell W. Electrophysical Agents in Sport and Exercise Injury Management in Physical Therapies in Sport and Exercise. In Kolt and Snyder-Mackler L (eds) Physical Therapies in Sport and Exercise. Churchill Livingstone, pp. 217-232. 2003.
Ling SM, Rudolph KS. Osteoarthritis. In Stephen T. Wegener ST, Basia L, Gall EP (eds) Clinical Care in the Rheumatic Diseases. 3rd Edition. American College of Rheumatology, Atlanta, GA, 2006.

Other scholarly activity

Peer Reviewed Presentations

Funded grants

Active:

Northern New England – Clinical Translational Research Network (PI: Stackhouse) “Influence of Noxious Electrical Stimulation on Chronic Pain-A Pilot Study” 07/01/20 06/30/21; $40,000 direct; 1.2 mos., Role: Co-Investigator

UNE Mini-Grant (PI:Rudolph) “Dual Task Activities and Subjective Cognitive Decline” 01/01/21 - 08/31/23

Completed:

Invited plenary presentation

Research interests

Dr. Rudolph's research interest is neuromuscular control of locomotion and chronic pain. She studies people with joint instability in anterior cruciate ligament deficiency and knee osteoarthritis; people with hemiparesis post-stroke and older adults. She is also interested in developing new technologies for use in rehabilitation including muscle strengthening devices and rehabilitation robots for gait training.

Research topics

Behavioral Neuroscience

Biosignaling

Brain

COM Neuroscience and Pain

Exercise and Resilience

Fear

Learning

Neuroscience

Pain

Sensory Neuron