Recognizing and Treating Central Sensitization: Part 1

As a physical therapist, one of the most complicated and frustrating disorders for me to treat was chronic pain. This was until I began to study the neural mechanisms behind pain and begin to understand the much more complex system at play in many of my patient’s conditions. A recent classification system has been developed to help other medical professionals determine what neural mechanisms are contributory to a patient’s pain. The old model of defining pain is time based and describes pain as either acute (<3 months) or chronic (>3 months). This system is obviously easily adminisered and labeled but due to the relatively unpredictable nature of pain, this classification has little validity in its actual relationship to a condition’s triggering of a pain output. The newly proposed alternative pain classification system has been validated and appears to be a better option when applying a label. The system has shown that clinicians are able to discriminate pain as either nociceptive, peripheral neuropathic or central sensitization. As physical therapists, we often do a rather good job at recognizing, understanding and treating conditions which are nociceptive or peripheral neuropathic but often label individuals in central sensitization as difficult, noncompliant, etc. This is likely because the pain is difficult to isolate, doesn’t make sense anatomically and is often associated with psychological variables. In this series of articles, I want to describe how central sensitization occurs, how we can recognize and more importantly, how we can intervene to treatment.

Central sensitization is an augmentation of responsiveness of central neurons to input from nociceptors. In simpler terms, it is a hypersensitivity of the central nervous system to stimuli. It is believed that this process occurs over time because of changes which take place in the nervous system, making it more reactive to stimuli to prevent further damage to injured tissues. There are several diagnoses which have shown to be related to this including: chronic low back and whiplash associated disorders, temporomandibular disorders, myofascial pain syndromes, osteoarthritis, rheumatoid arthritis, chronic fatigue syndrome, fibromyalgia and irritable bowel syndrome.

A recent study has classified disorders involving central sensitization as having consistent signs and symptoms including:

  • Pain that is disproportionate to the nature or extent of injury/pathology
  • Disproportionate, non-mechanical, unpredictable pattern of pain provocation in response to aggravating/easing factors
  • Strong association with maladaptive psychological factors
  • Diffuse/non-anatomic areas of pain/tenderness to palpation

Other characteristics often related to central sensitization include hypersensitivity to: bright light, touch, noise, pesticides, mechanical pressure, medication and temperature.

In our clinical examination of patients with expected central sensitization, there are several recommendations to assist in the confirmation of a diagnosis. Due to hypersensitivity to stimuli, it is recommended that we assess pain pressure thresholds at sites remote from the symptomatic site. As one of the characteristics being non-anatomic areas of pain, pain or sensitivity is often elicited by tissues which are segmentally unrelated to the injured tissue. This spreading of sensitivity is known as widespread (or secondary) hyperalgesia and is indicative of hyper excitability of central nociceptive pathways. A tool called an algometer is rather inexpensive and can measure the amount of force necessary to elicit an output of pain. You simply place it on the skin, push and it will give you a reading of when the patient begins to subjectively tell you they feel pain. Assessment of a thermal stimuli such as hot or cold often elicits a similar response.

Another way we can assess for central sensitization is to assess an individual’s response to exercise. Typically, when we exercise there is an endogenous opiod release and activation of supraspinal anti-nociceptive pathway mechanisms which can stay augmented up to 30 minutes post exercise. In individuals with central sensitization, this process does not work correctly and there is an increased pain perception in response to exercise which lowers ones pain pressure threshold. Due to this response, one should be cautious when having their patients perform strenuous activities.

Next month, I will present how to take this information and develop treatment interventions for individuals who are experiencing pain in a state of central sensitization.

Smart KM, Blake C, Staines A, et al. Self-reported pain severity, quality of life, disability, anxiety and depression in patients classified with nociceptive, peripheral neuropathic and central sensitisation pain. The discriminant validity of mechanism-based classification of low back (+-leg) pain. Manual Therapy 2012: 17; 119-125.

Nijs J, Van Boudewijn H, Oostendrop RAB. Recognition of central sensitization in patients with musculoskeeltal pain: application of pain neurophysiology in manual therapy practice. Manual Therapy 2010: 15; 135-141.

Nijs J, Van Houdenhove B. From acute musculoskeletal pain to chronic widespread pain and fibromyalgia: application of pain neurophysiology in manual therapy practice. Manual Therapy 2009:14; 3-12.

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