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.
Content:
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.
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