Central Sensitisation

I briefly discussed Central Sensitisation (CS) in a previous post on pain. CS has, at times, been a confusing topic.

As mentioned in my last post on pain, based on my readings, CS is not a type of pain, it is a mechanism relating to pain.

Understanding the mechanism is helpful in understanding the symptoms.

So what are the mechanisms of CS?

Nijs and Van Houdenhove (2009) summarise the mechanism involved in CS:

  • Sustained stimulation of unmyelinated C fibres and thinly myelinated A delta fibre primary afferents increases the responsiveness of neurons in spinal cord pain pathways.
  • This leads to sensitisation and eventual disinhibition of WDR neurons.A beta and C fibres converge at the WDR therefore sensitization of the WDR leads to enhanced synaptic efficacy of A beta fibres.
  • The result being that innocuous tactile sensations are coded as pain (allodynia).

Woolf (2011) describes the mechanisms as:

  • Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitisation.
  • Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation.

These mechanisms can then paint a picture of what the signs and symptoms of CS might be. We can, via the subjective and objective examinations, determine if our patients may have a CS component to their presentation.

Woolf (2011) suggests the presence of:

  • Allodynia – pain mediated by Aβ fibres & represents increased responsiveness of spinothalamic tract to innocuous stimuli.
  • Primary hyperalgesia – increased response & prolonged after effect to a local noxious stimulus.
  • Secondary hyperalgesia – spread of pain sensitivity to areas with no demonstrable pathology ie receptive field expansion which enables input from non-injured tissue to produce pain.
  • Temporal summation/wind up –  progressively increasing pain to a repeated stimulus.

Smart et al (2011) concluded from their study that:

  • Patients with “disproportionate, nonmechanical, unpredictable pattern of pain provocation in response to multiple/nonspecific aggravating/easing factors,” were over 30 times more likely to be classified with a dominance of CS than non-CS.

Curatolo (2011) sums up CS:

  • There is clear evidence that groups of patients with different chronic pain conditions display on average altered central pain processing. The main manifestations of this phenomenon are an exaggerated pain perception after low-input stimulation and an enlargement of the pain areas.
  • Curatolo also concludes that:  “Quantification of the role of disturbances in central pain processing for the determination of symptoms in individual patients, as well as the development of targeted treatment modalities, are challenges of future translational research”.

So we don’t have any “gold standard” procedures/protocols yet to diagnose Central Sensitisation.

There is some suggestion that we can use Neuropathic Pain Questonairres. Woolf (2011) summarises recent research linking a central pain mechanism component (i.e. CS) to Neuropathic pain. The key information Woolf (2011) summarises being:
  • Conditions like carpal tunnel syndrome have revealed enhanced bilateral sensitivity and an extraterritorial spread of symptoms in patients with unilateral or single nerve entrapment, supporting a contribution of central sensitisation.
  • (Given that) centrally acting drugs that normalize enhanced neural activity, are the current first line treatments for neuropathic pain, reinforces the importance of the central component of the pain.
Thanks for reading.

References:

  • Curatolo M (2011) Diagnosis of altered central pain processing. Spine 36:25S   (S200–S204).
  • Nijs J, Van Houdenhove B (2009) From acute musculoskeletal pain to chronic widespread pain and fibromyalgia: application of pain neurophysiology in manual therapy practice. Manual Therapy 14 (3-12).
  • Smart KM, Blake C, Staines A,  Doody C 2011, The discriminative validity of “nociceptive,” “peripheral neuropathic,” and “central sensitisation” as mechanisms- based classifications of musculoskeletal pain. Clin J Pain 2011;00:000–000.
  • Woolf  CJ 2011 Central sensitization: Implications for the diagnosis and treatment of pain. Pain 152 S2–S15
Posted in: Clinical Reasoning, Pain

About the Author:

Mark is a Specialist Musculoskeletal Physiotherapist who consults at both Insight Physiotherapy and Pain Options, in Perth, Western Australia. He specialises in the assessment and management of persistent/chronic musculoskeletal pain. In addition to his clinical role he maintains regular involvement in education of the profession having held a Teaching Fellow position at the University of Western Australia for 10 years and regularly presenting at courses and seminars through the Australian Physiotherapy Association and private education sector. Mark is also a Facilitator for the Australian College of Physiotherapists Specialisation Training Program and a Branch Councillor on the Western Australian Branch of the Australian Physiotherapy Association.

Post a Comment

%d bloggers like this: