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Kathleen A. Sluka, PT, PhD, FAPTA
3148 Medical LaboratoriesPhone: (319) 384-4442
Dr. Sluka's laboratory studies the peripheral and central mechanisms of chronic musculoskeletal pain, and non-pharmacological treatment for chronic pain. These studies involve the use of animal models of muscle pain developed and characterized in Dr. Sluka's laboratory, as well as projects in human subjects. We use a variety of techniques to address these questions including cell culture, molecular biology, genetic manipulations, behavioral pharmacology, and standard clinical trial methodology. Our overall goals are to improve the management of pain for people with a variety of musculoskeletal pain conditions by discovering the underlying mechanisms that lead to the development of chronic pain, discovering new therapies for pain management, and improving the use of currently available treatment for pain.
Goal: Examine the underlying mechanisms for how exercise can exacerbate
These studies involve examining the mechanisms that contribute to exercise induced pain. In people with chronic pain, acute physical activity and exercise can exacerbate their pain. Our laboratory has developed models of exercise-induced pain that involve applying a fatiguing exercise stimulus in combination with a low-dose muscle insult to produce long-lasting widespread muscle pain. We are currently examining the 1) role of fatigue metabolites - ATP, lactate, and protons - released during the exercise task can sensitize nociceptors to produce pain, 2) the role of the immune system in the development of exercise-induced pain and the differences between sedentary and physically active mice, and 3) sites, neurotransmitters, and receptors in the brainstem that are altered by unaccustomed exercise and can lead to exercise-induced pain - glutamate, serotonin, opioids and their receptors.
Funded by NIH AR061372
Recent Reference: Sluka KA, Danielson J, Rasmussen L, DaSilva LF. Exercise-induced pain requires NMDA receptor activation in the medullary raphe nuclei. Med Sci Sports Exerc. 2012 Mar; 44(3):420-7.
Goal: Examine the underlying mechanisms for how exercise can prevent and reduce pain
Regular physical activity and exercise is an effective treatment for existing chronic pain, and can prevent the development of chronic pain. Our laboratory is examining the underlying mechanisms for how regular physical activity can prevent the development of pain and reduce existing chronic pain using animal models. We exercise animals with running wheels to simulate regular physical activity or on a treadmill to simulate a regular exercise program, and compare these to sedentary animals. We are currently examining 1) the central mechanisms underlying this analgesia: sites, neurotransmitters, and receptors in the brainstem - glutamate, serotonin, opioids and their receptors, and 2) immune mechanisms underlying this analgesia: local and systematic changes in immune cells and cytokines.
Funded by NIH AR 061372
Recent Reference: Vance CG, Rakel BA, Blodgett NP, DeSantana JM, Amendola A, Zimmerman MB, Walsh DM, Sluka KA. Effects of transcutaneous electrical nerve stimulation on pain, pain sensitivity, and function in people with knee osteoarthritis: a randomized controlled trial. Phys Ther. 2012 Jul; 92(7):898-910.
Fibromyalgia activity study with TENS (FAST).
Goal: Test the effectiveness of TENS for pain during activity in people with fibromyalgia
Transcutaneous electrical nerve stimulation (TENS) is a non-pharmacological treatment for chronic pain commonly used by physical therapists. Our laboratory has discovered the underlying mechanisms for how TENS works using animal models and translating these findings into human subjects. We have discovered that TENS reduces central excitability and increases central inhibition in an opioid-dependent manner. We have subsequently shown that TENS is more effective for evoked pain such as hyperalgesia and pain during activity, when compared to resting pain. This two-site clinical trial will test the effects of home usage of TENS during physical activity in people with fibromyalgia on a variety of outcomes measures including pain during movement, fatigue, psychosocial variables, function, and quality of life. We will also test the ability of TENS to restore normal pain physiology including descending inhibition and hyperalgesia measures, and factors that affect response to TENS.
Funded by NIH UM1 AR063381
Sluka KA, O'Donnell JM, Danielson J, Rasmussen LA. Regular physical activity prevents development of chronic pain and activation of central neurons. J Appl Physiol. 2013 Mar 15; 114(6):725-33.
Liebano RE, Rakel B, Vance CG, Walsh DM, Sluka KA. An investigation of the development of analgesic tolerance to TENS in humans. Pain. 2011 Feb; 152(2):335-42.
Electrical stimulation-induced analgesia.
Goal: Understand the underlying mechanisms of different forms of electrical stimulation-induced analgesia including TENS and spinal cord stimulation (SCS).
TENS applies electrical current to the skin for pain control and SCS applies electrical current to the dorsal columns through an implanted lead for pain control. Our laboratory is currently examining the underlying mechanisms and ideal parameters for both TENS and SCS using animal models. These studies include determining the underlying neurotransmitters and receptors involved in the analgesia, the tolerance and underlying mechanisms induced by TENS, and mechanisms to improve efficacy of TENS and SCS by developing both pharmacological and non-pharmacological treatment strategies.
SCS studies funded by Medtronic, Inc.
Sato KL, King EW, Johanek LM, Sluka KA. Spinal cord stimulation reduces hyperssensitivity through activation of opioid receptors in a frequency-dependent manner. Eur J Pain. 2013 Apr; 17(4):551-61.
Sato KL, Sanada LS, Rakel BA, Sluka KA. Increasing intensity of TENS prevents analgesic tolerance in rats. J Pain. 2012 Sep; 13(9):884-90.
Role of ASICs in musculoskeletal pain.
Goal: Understand the role of decreases in pH and activation of acid sensing ion channels (ASICs) in the development of inflammatory and non-inflammatory musculoskeletal pain.
These studies are aimed at understanding factors that initiate and maintain chronic painful conditions. Our prior studies have shown that decreases in pH can induce chronic pain, ASICs are key players in the development of musculoskeletal pain, and that ASICs can modulate synovitis in arthritis. These studies are therefore examining the role of ASICs on the nociceptors that innervate joint and muscle tissue for development in a variety of animal models of pain, as well as the role of ASICs on synoviocytes that line joint tissue for the control of inflammation.
Funded by AR053509
Sluka KA, Rasmussen LA, Edgar MM, O'Donnell JM, Walder RY, Kolker SJ, Boyle DL, Firestein GS. Acid-sensing ion channel 3 deficiency increases inflammation but decreases pain behavior in murine arthritis. Arthritis Rheum. 2013 May;65(5):1194-201. doi: 10.1002/art.37862.
Walder RY, Gautam M, Wilson SP, Benson CJ, Sluka KA. Selective targeting of ASIC3 using artificial miRNAs inhibits primary and secondary hyperalgesia after muscle inflammation. Pain. 2011 Oct;152(10):2348-56.