Central sensitization is defined as ‘an augmentation of responsiveness of central pain-signalling neurons to input from low-threshold mechanoreceptors’ (Nijs 2009)
The evolution of chronic pain has been shown to have strong association with the process of central sensitization, in which there is enhanced sensitivity to various modes of painful and non-painful stimuli (Buchgreitz et al 2006).
Staud (2006) has described the ways in which peripheral pain impulses can lead to central sensitization. In many chronic pain states, including chronic migraine, irritable bowel syndrome,fibromyalgia syndrome, repetitive, persistent or recurrent peripheral nociceptive features can lead to neuroplastic changes in the spinal cord and brain, that results in central sensitization and consequent pain.
Yi-Meng Xu et al (2010) have explained that even the nociceptive input from latent trigger points can contribute to central sensitization, and that only minimal nociceptive input (resulting from touch, pressure or heat) may be required to maintain the chronic pain state, once central sensitization has evolved.
A generalized central sensitization is identified as operating in fibromyalgia syndrome which is also common accompanying diagnosis in patients with chronic headache. Yunus (2007) has described the overlap of a number of chronic pain as Central Sensitivity Syndromes – asserting that in such conditions hyperexitability exists of central neurons resulting from the influence of various neurotransmitter and neurochemical activities, with this (central sensitization) itself being contingent – for both development and maintenance – on abnormal or continued peripheral inputs.
Background to sensitization
Selye (1984) defined both the general adaptation syndrome (GAS) affecting the individual as a whole, and the local adaptation syndrome (LAS), affecting a local area of the body that is subjected to stressors demanding adaptation. The GAS and LAS models explain how adaptation progresses, over time, with modifications to function occurring, leading eventually to adaptive capacity becoming exhausted, and symptoms emerging.
Neuromusculoskeletal adaptive changes involved in such processes can be seen to represent a record of the body’s attempts to adapt and adjust to the multiple and varied stresses which have been imposed upon it, over time. The results of repeated postural and traumatic insults over a lifetime, combined with the somatic effects of emotional and psychological origin, will often present a confusing pattern of tense, shortened, bunched, fatigued and, ultimately, fibrous soft-tissues.
Some of the many forms of biomechanical stressors that affect the body include the following (Lewit 2009).
- Congenital and inborn factors, such as short or long leg, small hemi-pelvis, fascial influences
- Overuse, misuse and abuse factors, such as injury, or inappropriate or repetitive patterns of use involved in work, sport or activities of daily life (Schamberger 2002)
- Immobilization, disuse (irreversible changes can occur after just 8 weeks) (Cramer et al 2010)
- Postural stress patterns
- Inappropriate breathing patterns (O’Sullivan & Beales 2007)
- Chronic negative emotional states such as depression, anxiety, etc.
- Reflexive influences (trigger points, facilitated spinal regions) (Giamberardino et al 2007)
Widespread functional changes develop – for example, affecting respiratory function and posture – with implications for the total economy of the body. (Timmons & Ley 1994)
In the presence of a constant neurological feedback of impulses to the CNS/brain, from neural reporting stations, there will be increased levels of psychological arousal and a reduction in the ability of the individual, or local hypertonic tissues, to relax effectively, with consequent reinforcement of hypertonicity, and inevitably relative ischemia – an environment ideal for myofascial trigger point evolution (Shah 2005).
Functional patterns of use, of a biologically unsustainable nature, are likely to evolve, leading to chronic musculoskeletal problems and pain. (Crockett et al 2002) At this stage, restoration of normal function would require therapeutic input to address both the multiple changes that have occurred, as well as there being a need for re-education of the individual as to how to use the body, to breathe, and to display posture in more sustainable ways.
For more on the topic of adaptation the following two links will take you to some of my blog postings on this subject:
Additional and associated articles on the subject can be found on my website www.leonchaitow.com
Soft tissue changes
Soft-tissue changes involving pain, hyper- or hypotonicity, joint dysfunction, antagonist muscle imbalances, overactive synergist muscles, lead to localized areas of hyper-reactivity, in the form of myofascial trigger points, and/or neural entrapment. (Lewit 2009) Additionally, pain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread pain. Another example of a local musculoskeletal disorder associated with chronic pain, frequently seen in manual therapy practice, is arthritis, possibly causing continuous activation of local nociceptors that initiate or sustain, central sensitization
Reducing the nociceptive barrage
Yunus (2007) has suggested that effective manual therapy in sub-acute cases of musculoskeletal dysfunction should be capable of limiting the afferent barrage of noxious input to the central nervous system, so preventing chronicity. Nijs et al (2009) goes further and affirms the importance of decreasing the afferent nociceptive barrage of trigger points, by means of soft-tissue mobilization, in comprehensive care of cases of chronic pain.
Neuromuscular therapies (NMT) aim to reduce the effects of adaptation/compensation as described above, by enhancing musculoskeletal function – including improved posture, respiratory function, and general mobility and stability, and by reducing noxious inputs resulting from the active presence of, for example, myofascial trigger points.
Recognizing Central Sensitization in patients
Nijls et al (2010) have summarized the many associated features of central sensitization;
- Hypersensitivity to bright light
- Hypersensitivity to touch
- Hypersensitivity to noise
- Hypersensitivity to pesticides
- Hypersensitivity to mechanical pressure
- Hypersensitivity to medication
- Hypersensitivity to temperature (high and low)
The presence of some or all of these symptom, together with information gathered during the history taking and the medical diagnosis, and confirmatory results from assessments listed below, can all help in recognition of the existence, in a given patient, of central sensitization. In this assessment the following tests have been suggested (Yunus 2007):
- Assessment of pressure pain thresholds at sites remote from the symptomatic site
- Assessment of sensitivity to touch during manual palpation at sites remote from the symptomatic site
- Assessment of sensitivity to vibration at sites remote from the symptomatic site
- Assessment of sensitivity to heat at sites remote from the symptomatic site
- Assessment of sensitivity to cold at sites remote from the symptomatic site
- Assessment of pressure pain thresholds during and following exercise
- Assessment of joint end feel
- Brachial plexus provocation test
Symptom exacerbation, at both symptomatic and distant sites, indicates central sensitization. It is important to note that a variety of other indications may also suggest this, including increased pain during, or following, exercise
A fundamental principle emerges from current understanding of the sensitization process – sensitization can be reversed.
Affaitati et al (2011) have clearly demonstrated – in fibromyalgia – that therapeutic strategies that reduce the overall stress burden, whether these relate to biomechanics, biochemistry or psychosocial features, will reduce central sensitization.
Affaitati G Costantini R Fabrizio A et al 2011 Effects of treatment of peripheral pain generators in fibromyalgia patients Original Research Article European Journal of Pain 15(1):61-69
Buchgreitz L Lyngberg L Bendtsen A et al 2006 Frequency of headache is related to sensitization: A population study, Pain 123:1–2 19-27
Cramer G et al 2010 Zygapophyseal joint adhesions after induced hypomobility. Journal of Manipulative and Physiological Therapeutics 33:508-518
Crockett HC, Gross LB, Wilk KE et al 2002 Osseous adaptation and range of motion at the gleno-humeral joint in professional baseball pitchers. American Journal of Sports Medicine 30(1):20–26
Giamberardino M A Tafuri E Savini A et al 2007 Contribution of Myofascial Trigger Points to Migraine Symptoms The Journal of Pain 8(11):869-878
Lewit K 2009 Manipulative Therapy: Musculoskeletal Medicine Churchill Livingstone, Edinburgh
Nijs, J Van Houdenhove B 2009 From acute musculoskeletal pain to chronic widespread pain andfibromyalgia: Application of pain neurophysiology in manual therapy practiceManual Therapy 14:3-12
Nijls J, Van Houdenhove B, Oostendorp R. 2010 Recognition of central sensitization in patients with musculoskeletal pain: Application of pain neurophysiology in manual therapy practice. Man Ther 15: 135-141
O’Sullivan P Beales D 2007 Changes in pelvic floor and diaphragm kinematics and respiratory patterns in subjects with sacroiliac joint pain following a motor learning intervention: A case series Manual Therapy 12:209–218
Selye H: The stress of life, New York, 1984, McGraw-Hill
Staud R 2006 Biology and therapy of fibromyalgia: pain in fibromyalgia syndrome. Arthritis Research and Therapy 8: 208
Schamberger W 2002 The malalignment syndrome, Edinburgh, Churchill Livingstone.
Shah JP, Phillips TM, Danoff JV, Gerber LH 2005 An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. J Appl Physiol
Yi-Meng Xu, Hong-You Ge, Lars Arendt-Nielsen et al 2010 Sustained Nociceptive Mechanical Stimulation of Latent Myofascial Trigger Point Induces Central Sensitization in Healthy Subjects The Journal of Pain, 11(12):1348-1355
Yunus M 2007 Fibromyalgia and overlapping disorders: the unifying concept
of central sensitivity syndromes. Seminars in Arthritis and Rheumatology 36:330-356