Research Review By Dr. Demetry Assimakopoulos&copy


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Date Posted:

March 2017

Study Title:

Recognition and Treatment of Central Sensitization in Chronic Pain Patients: Not Limited to Specialized Care


Nijs J, Goubert D & Ickman K

Author's Affiliations:

Pain in Motion International Research Group, Brussels, Belgium; Department of Physiotherapy, Human Physiology and Anatomy, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel, Brussels, Belgium; Department of Physical Medicine and Physiotherapy, University Hospital Brussels, Brussels, Belgium; Department of Rehabilitation Sciences and Physiotherapy, Universiteit Gent, Ghent, Belgium.

Publication Information:

Journal of Orthopaedics and Sports Physical Therapy 2016; 46(12): 1024-1028.

Background Information:

Simply defined, central sensitization (CS) is the amplification of neural signalling within the CNS, leading to pain hypersensitivity (1, 2). Some clinicians opine that CS is a rare phenomenon in primary care settings, and that treatment of CS is reserved for specialized pain management programs. However, the authors of this article argue that CS is also commonly seen in general practice, and that modern pain neuroscience concepts need to be implemented to provide adequate treatment in this setting. In light of this, the authors discuss the mechanisms underpinning the presentation of CS, define how clinicians can clinically recognize CS, and finally discuss how CS is best clinically treated.


Understanding the Psychophysiology of Central Sensitization (CS):

Many patients suffering from persistent pain lack a clear nociceptive source. In some cases, a source of nociception exists, but is not severe enough to explain the severity (nor anatomical distribution) of pain.

The clinical picture of CS is largely defined by CNS-mediated, heightened responsiveness to sensory stimulation (i.e. mechanical, chemical, light, sound, cold, heat, stress and electricity). These CNS dysfunctions occur because of altered cortical sensory processing, heightened cortical activity, poor functioning of descending anti-nociceptive mechanisms (“the brake” or top-down analgesic pathways), and increased activity of brain-orchestrated nociceptive facilitatory pathways (“the accelerator”). Cognitive-emotional factors, such as fear, catastrophization, stress, hypervigilance, lack of acceptance, depressive thoughts and perceived injustice, will increase facilitatory pathway activity. Put simply, “the brake” isn’t working, and “the accelerator” is much too active in patients with CS. These cortical changes result in exaggerated CNS responses, which present clinically as severe pain to relatively little or even normal somatosensory input, sleep disturbance, and stress intolerance. (WRITER’S NOTE: many of these patients will also disclose light/sound/cold sensitivity, issues with digestion, abdominal pain, or headaches. It is worth noting that many patients will not disclose these other symptoms unless they are directly asked.)

In which patients can we expect to find CS?

While only a minority of patients will develop CS, in the right circumstances, any patient that suffers an injury may develop CNS hypersensitivity. It has been previously shown that individuals with fibromyalgia, whiplash, low back pain, tendinopathy, shoulder pain, osteoarthritis, rheumatoid arthritis, post-cancer treatment pain, lateral epicondylalgia and headache may present with clinical elements of CS. Unfortunately, those with features of CS have poorer prognoses, higher pain severity, and lower quality of life.

Recognition of CS in Clinical Practice:
  1. Rule out Neuropathic Pain: Neuropathic pain arises from a lesion of the central or peripheral nervous system. A clinical suspicion of neuropathic pain is supported by positive clinical examination findings, imaging and/or electrophysiological testing. In some cases, a plausible cause for neuropathic pain may exist (i.e. a spinal cord injury), but cannot fully explain reported symptoms (i.e. widespread pain). In some cases, a patient may have a mixed clinical picture of neuropathic and CS pain.
  2. Pain Experience Disproportionate to the Nature and Extent of Injury or Pathology (5): Clinicians must determine if the extent of a patient’s injury, pathology or dysfunction is capable of creating the patient’s subjective pain experience. For example, a patient may have previously suffered a whiplash injury, and subsequently developed total body pain.
  3. Hypersensitivity of Senses Unrelated to the Musculoskeletal System (5): CS patients may also exhibit altered sensitivity to environmental (light, cold, heat, sound, weather, stress), and chemical (odors, pesticides, medication) sensory inputs. The case for a clinical picture dominated by CS may be strengthened by the results of the Central Sensitization Inventory (6). A score > 40/100 allows correct identification of over 82% of patients with CS pain. However, the chance of a false positive score is also relatively high, which is why the inventory should be used alongside a comprehensive examination. Adaptations of the inventory have been created for post-cancer treatment pain (7) as well as LBP (8). It is also currently being adapted for OA-related pain. However, studies investigating the inventory’s clinical validity are needed.
Treatment Implication of CS in Orthopaedic and Sports Physical Therapy:

It is important to note that treating the site of pain is typically of little value when treating patients with predominant CS-related pain. Bearing this in mind, approaches targeting the brain’s top-down pain inhibitory mechanisms are warranted (9).

Patients with CS-related pain often ruminate about their condition. In such cases, clinicians should begin treatment by teaching the patient about the mechanisms underpinning CS (i.e. pain neuroscience education [PNE]). PNE has been shown to improve patients’ understanding of what is happening in their bodies, and assists in the development of coping strategies (10). Then, active interventions such as stress management, sleep management and graded exercise can be introduced. Manual hands-on therapy often leads to short-term analgesic effects though top-down nociceptive inhibition (11). Finally, the cognitive factors that prolong, and possibly initiate CS in patients with MSK pain (i.e. catastrophizing, anxiety, fear, maladaptive pain beliefs, anger, and perceived injustice) should be identified and targeted. (WRITER’S NOTE: various tools exist to determine the existence and severity of cognitive factors, such as the PHQ-9, Tampa Scale of Kinesiophobia, and Pain Catastrophization Scale. In some cases, using PNE to link these factors to an overall pain experience can validate a patient’s feelings, and re-conceptualize their pain. However, in the case of severe anxiety or depression, referral to other professionals might be required. The take home message here is to understand where your job as a clinician begins and where it ends.)

Clinical Application & Conclusions:

CS is an incredibly difficult issue to manage in clinical practice. It can be present in numerous MSK conditions, and is generally associated with poor clinical outcomes. The authors of this paper argue that clinicians providing manual and rehabilitative management in community settings are capable of treating CS, and provide an algorithm for recognizing this clinical phenomenon. First, clinicians should determine if neuropathic pain is present and able to explain the clinical picture. If not, clinicians must then determine if the patient’s pain experience is disproportionate to the tissue injury. If pain is diffuse, the patient’s pain is likely explained by CS. If pain is not diffuse, the Central Sensitization Inventory Score can be used – a score of > 40/100 points to a clinical picture dominated by central sensitization.

Clinical Commentary on CS Treatment from Dr. Assimakopoulos:

Even the best clinicians can be stumped by CS. The key is to not be married to one approach with these patients. If CS truly is a complex, multifactorial neurophysiological phenomenon, it is likely that no one treatment is best. Having more tools in the tool box means you might eventually find one that a patient will accept. The important thing is to treat the whole person. This includes creating a positive, non-judgemental and inviting environment for the patient.

PNE is frequently used as the starting point for CS patients. However, it is important to note that some patients are not ready to hear that they are centrally sensitized, and are committed to the discovery of a nociceptive source to explain their pain. PNE is a good way of laying the foundation for treatment. Just be careful; sometimes patients are just not ready to hear that their nervous system has become hypersensitive. Tread carefully and figure out why before you proceed.

Another tip for treatment might be to assist the patient in creating functional goals. I used the term ”assist” the patient on purpose – patients become attached to goals when they conceive of them. Simply guide them down the path to attaining them. For instance, if one of their goals is to be able to snowshoe with their family, the clinician’s job is to help the patient appropriately scale down the goal into realistic and achievable chunks. Once they begin to attain these goals, their fear and perception of fragility decrease. Focus the patient on achieving their goals and improving function –this has to be their barometer for improvement (albeit, easier said than done).

Lastly, clinicians MUST adjust their expectations for treatment. Changes in function and CS-related pain do not occur over night. Change may take months or years. It is expected that the patient will have good and bad days, or even weeks. In these cases, it is important to use a wide lens – after months of treatment, are they functioning better than they were when they initiated treatment? If the answer to that question is “yes”, then you’re on the right track.

Study Methods:

This was a clinical commentary. Therefore, no study methods were discussed, nor statistical analysis performed.

Study Strengths / Weaknesses:

The authors provide readers with an easy-to-use algorithm that can be used in any clinic tomorrow.

The authors failed to describe any of the possible physical examination, imaging or electrophysiological findings indicative of neuropathic pain. Additionally, they did not describe the possible physical examination findings clinically seen in centrally sensitized patients. Additionally, it is uncertain whether their criteria for determining the presence of CS have been tested for different types of validity, sensitivity or specificity. This is perhaps because of a lack of a gold standard for clinically identifying CS.

Additional References:

  1. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011; 152: S2-S15.
  2. IASP Task Force on Taxonomy. Part III: pain terms, a current list with definitions and notes on usage. In: Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd ed. Seattle, WA: IASP Press; 1994: 209-214.
  3. Van Oosterwijck J, Nijs J, Meeus M, et al. Evidence for central sensitization in chronic whiplash: a systematic literature review. Eur J Pain 2013; 17: 299-312.
  4. Clauw DJ, Arnold LM, McCarberg BH. The science of fibromyalgia. Mayo Clin Proc 2011; 86: 907-911.
  5. Nijs J, Torres-Cueco R, van Wilgen CP, et al. Applying modern pain neuroscience in clinical practice: criteria for the classification of central sensitization pain. Pain Phys 2014; 17: 447-457.
  6. Mayer TG, Neblett R, Cohen H, et al. The development and psychometric validation of the Central Sensitization Inventory. Pain Pract 2012; 12: 276-285.
  7. Nijs J, Apeldoorn A, Hallegraeff H, et al. Low back pain: guidelines for the clinical classification of predominant neuropathic, nociceptive, or central sensitization pain. Pain Phys 2015; 18: E333-E346.
  8. Nijs J, Leysen L, Adriaenssens N, et al. Pain following cancer treatment: guidelines for the clinical classification of predominant neuropathic, nociceptive and central sensitization pain. Acta Oncol 2016; 55: 659-663.
  9. Nijs J, Malfliet A, Ickmans K, Baert I, Meeus M. Treatment of central sensitization in patients with ‘unexplained’ chronic pain: an update. Expert Opin Pharmacother 2014; 15: 1671-1683.
  10. Louw A, Zimney K, Puentedura EJ, Diener I. The efficacy of pain neuroscience education on musculoskeletal pain: a systematic review of the literature. Physiother Theory Pract 2016; 32: 332- 355.
  11. Courtney CA, Steffen AD, Fernández-de-las- Peñas C, et al. Joint mobilization enhances mechanisms of conditioned pain modulation in individuals with osteoarthritis of the knee. J Orthop Sports Phys Ther 2016; 46: 168-176.