Musculoskeletal Pain and Motor Control Laboratory

Musculoskeletal Pain and Motor Control Laboratory

Head of Laboratory: Thomas Graven-Nielsen, Professor (TGN)


The main objective is translational research on musculoskeletal pain focusing on the sensory manifestations and perturbed motor function involved in deep tissue pain. Mechanisms of muscle pain transduction, transmission, processing, perception and motor control interactions are studied in healthy subjects and pain patients.
The approach is to induce experimental deep-tissue pain and assess quantitatively the responses by psychophysical, biomechanical, physiological, and electrophysiological methods. This approach translates known mechanisms from basic animal studies to pain patients via human pain models in healthy subjects.
An improved understanding of musculoskeletal pain mechanisms under normal and pathological conditions is essential for developing more rational diagnostic and treatment strategies. Furthermore, the experimental techniques are important in screening new drugs and predict analgesic efficacy.


                               Induction and assessment of deep tissue hyperalgesia and referred pain

Main Research Areas

  1. Models of deep-tissue pain
    The peripheral apparatus of musculoskeletal pain consists of nociceptors that can be excited by algesic substances (e.g., hypertonic saline, capsaicin, glutamate), ischaemic exercise, eccentric exercise and external stimuli (e.g. mechanical, thermal and electrical). Stimulus intensity (i.e. strength, volume, concentration), temporal and spatial summation, and nociceptor density are the main determinants of the muscle pain sensation. Mechanisms involved in experimental muscle pain have been explored and confirmed the mechanical, chemical and thermal modalities known from animal studies. The aim is to develop novel and realistic human models of musculoskeletal pain.
  2. Deep-tissue hyperalgesia
    In clinical muscle pain deep-tissue hyperalgesia and soreness are frequent. Experimental muscle pain leads to a variety of changes in deep and superficial tissue sensitivity in the local and referred muscle pain area. Neurophysiological models based on sensitisation and/or desensitisation of receptors or central neural structures are proposed to be involved in the somatosensory sensitivity changes after muscle pain. The aim is to develop robust experimental models of deep-tissue hyperalgesia and by that clarify mechanisms involved in deep tissue hyperalgesia, such as trigger points in myofascial pain patients.
  3. Referred pain
    Referred pain is perceived at a site adjacent to or at a distance from the nociceptive origin. A typical example is referred pain evoked by activation of trigger points in musculoskeletal pain patients. Muscle pain evokes referred pain that typically is felt as a deep sensation, delayed compared to the muscle pain, inhibited over time with constant muscle pain and is correlated to the local muscle pain intensity. Somatosensory afferent activity from the referred pain area is not a necessary condition for referred pain. Referred deep-tissue hyperalgesia has previously been reported especially in soft-tissue referred pain areas. This laboratory has proposed a neurophysiological model of referred pain by providing new knowledge on involvement of peripheral afferent input from the referred pain area, temporal aspects of local and referred pain and referred sensitivity changes. The aim is to explore further aspects of referred pain and by that refine the model for referred pain.
  4. Quantitative sensory assessment
    Quantitative sensory assessment of deep structures involves two separate topics: (1) Standardized activation of the muscle nociceptive system and (2) quantitative assessment of the evoked sensory and motor responses. The aim is to develop robust techniques to assess fundamental parameters related to deep tissue pain such as referred pain and temporal summation in clinical and pharmaceutical translational studies.
  5. Effect of deep-tissue pain on motor control
    The interactions between muscle pain and motor control depend on the specific motor task. In general, muscle pain causes no increase in muscle activity at rest and reduces maximal voluntary contraction and endurance time during submaximal contractions. Moreover, muscle pain causes a change in co-ordination during dynamic exercises and new motor control strategies are used. On the motor unit level decreased firing is observed during muscle pain. The aim is to develop models of the motor control changes caused by muscle pain by advanced electrophysiological techniques, such as matrix EMG and intramuscular recordings of motor units or reflex studies to assess the central motor control components.

Key Collaborators

  • School of Physiotherapy, Curtin University of Technology, Perth, Australia
  • Division of Physiotherapy, The University of Queensland, Brisbane, Australia
  • Inst. f. Anatomie und Zellbiologie III, Universität Heidelberg, Heidelberg, Germany
  • Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada
  • Department of Oral Physiology, Faculty of Dentistry, University of Toronto, Toronto, Canada
  • Physical Therapy and Rehabilitation Science, The University of Iowa, Iowa City, IA, USA
  • Department of Neuroscience II, Division of Stress Recognition and Response, Research Institute of Environmental Medicine, Nagoya University, Japan
  • Department of Physical Therapy, University of Missouri-Columbia, Columbia, USA
  • The Parker Institute, Dept. of Rheumatology, Frederiksberg Hospital, Copenhagen, Denmark
  • Department of Rehabilitation Medicine, Faculty of Health Sciences, Linköping University Hospital, Sweden


Fredrik Bajers Vej 7D, 3-113