Professor Jo Nijs PhD

Department of Physiotherapy, Human Physiology and Anatomy, Vrije Universiteit Brussel, Belgium

Jo Nijs holds a PhD in rehabilitation science and physiotherapy. He is professor at the Vrije Universiteit Brussel (Brussels, Belgium) and physiotherapist/manual therapist at the University Hospital Brussels. His research and clinical interests are patients with chronic unexplained pain / fatigue and pain-movement interactions. He has (co-)authored 165 peer reviewed publications, obtained €5 million of grant income, supervised 7 PhD projects to completion (excluding 15 ongoing PhD projects) and served more than 170 times as an invited speaker at national and international meetings in 19 different countries (including 20 keynotes). His work has been cited >2000 times (ISI Web of Knowledge). Jo is ranked 1st in the world among chronic fatigue syndrome researchers, 4th in the world among whiplash researchers and 7th in the world among chronic pain researchers (

Website twitter @PaininMotion

The Process of Central Sensitisation

Learning objectives:

At the completion of this lecture, learners will be:

1.      Informed about the mechanisms underlying chronic (central sensitization) pain;

2.      Able to recognize clinical symptom presentations of predominant central sensitization pain;

3.      Understand how the mechanism of central sensitization fits within our understanding of chronic pain in general;

4.      How therapists can influence (i.e. treat) the mechanism of central sensitization in patients with chronic pain.

Some patients with persistent pain have predominant central sensitization pain rather than nociceptive or neuropathic pain. Central sensitization encompasses various related dysfunctions of the central nervous system, all contributing to an increased responsiveness to a variety of stimuli like mechanical pressure, chemical substances, light, sound, cold, heat, stress and electrical stimuli. Such dysfunctions of the central nervous system include altered sensory processing in the brain, malfunctioning of descending anti-nociceptive mechanisms, increased activity of pain facilitatory pathways, and enhanced temporal summation of second pain or wind-up. In addition, the pain (neuro) matrix is overactive in patients with predominant central sensitization pain.

An overview of the evidence regarding central sensitization in patients with persistent pain will be presented, together with guidelines on how to recognize predominant central sensitization pain. Also the implications for clinical reasoning and the treatment of persistent pain will be addressed. 

A variety of treatment strategies specifically target pathophysiological mechanisms known to be involved in central sensitization pain; i.e. they hold – at least theoretically – the capacity to desensitize the central nervous system. Such treatments include pharmacological options, electrotherapy targeting the brain (i.e. transcranial magnetic stimulation), manual therapy,  virtual reality, stress management / neurofeedback training, transcutaneous electrical nerve stimulation, pain neuroscience education, exercise therapy, and cognitive behavioural therapy. Most of these treatment options, when used for treating central sensitization in patients with persistent pain, have their effects through central nervous system modulation, that is, by targeting the brain (top-down approach) rather than peripheral nociceptive input (bottom-up).

Treatment of Pain Sensitisation 

Learning objectives:

At the completion of this lecture, learners will be:

1.      Understand the mechanisms underlying the development of pain memories;

2.      Understand the role of stress and sleep in the etiology and sustainment of central sensitization in people with persistent pain;

3.      Able to integrate modern pain neuroscience into conservative interventions for chronic pain patients;

4.      Hopefully have new ideas on how to approach patients with persistent pain. 


Chronic pain the post prevalent and most costly medical problem in the Western society. It is now well-established that sensitization of the central nervous system is an important feature in many patients with chronic pain, but the etiological mechanisms of this central nervous system dysfunction are poorly understood. This lecture will cover 2 important etiological mechanisms together with their therapeutic implications: aberrant glial activity and development of pain memories.

Recently, an increasing number of animal and human studies suggest that aberrant glial activation takes part in the establishment and/or maintenance of central sensitization. Such glial overactivation results in a low-grade neuroinflammatory state, characterized by high levels of BDNF, IL-1β, TNF-α, which in turn increases the excitability of the central nervous system neurons through mechanisms like long-term potentiation and increased synaptic efficiency. Other mechanisms linking aberrant glial activation to the development of central sensitization include attenuation of the nociceptive inhibitory action of GABA and glycine receptor-mediated inhibition.

Aberrant glial activity in chronic pain might have been triggered by severe stress exposure, and/or sleeping disturbances, each of which are established initiating factors for chronic pain development. Potential treatment avenues include several pharmacological options for diminishing glial activity, as well as conservative interventions like sleep management, stress management and exercise therapy.

The second potential etiological mechanism entails the development of pain memories. Even though nociceptive pathology has often long subsided, the brain of patients with chronic pain has typically acquired a protective (movement-related) pain memory. Exercise therapy for patients with chronic pain is often hampered by such pain memories. Therapists can alter pain memories in patients with chronic pain by integrating pain neuroscience education with exercise interventions. The latter includes applying graded exposure in vivo principles during exercise therapy, for targeting the brain circuitries orchestrated by the amygdala (the memory of fear centre in the brain).

Before initiating exercise therapy, a preparatory phase of intensive pain neuroscience education is required. Next, exercise therapy can address movement-related pain memories by applying the ‘exposure without danger’ principle. By addressing patients’ perceptions about exercises, therapists should try to decrease the anticipated danger (threat level) of the exercises by challenging the nature of, and reasoning behind their fears, assuring the safety of the exercises, and increasing confidence in a successful accomplishment of the exercise. This way, exercise therapy accounts for the current understanding of pain neuroscience, including the mechanisms of central sensitization.