Types of Pain

Before writing about my framework for my subjective I think it is important to summarise pain. Recent reflection on my clinical knowledge of pain made me realise how poor my knowledge was. I have since realised the importance, from a diagnosis, management and prognosis aspect, of being able to identify what pain(s) are contributing to the patients presentation. In addition to this we need to also look for mechanisms contributing to, or amplifying, the patients pain.  I will include some references at the end of this post.

So what are the types of pain?

Woolf (2004 and 2010) and Costigan et al (2009) divide pain into the following types:

  • Nociceptive
  • Inflammatory
  • Pathological – subdivided into Neuropathic and Dysfunctional/Functional

Nociceptive Pain is defined as:

  • Physiological pain produced by noxious stimuli that activate high-threshold nociceptor neurons.(Costigan et al 2009).
  • Sensation associated with the detection of potentially tissue-damaging noxious stimuli and is protective (Woolf 2010).

Inflammatory Pain is defined as:

  • Pain hypersensitivity due to peripheral tissue inflammation involving the detection of active inflammation by nociceptors and a sensitization of the nociceptive system (Costigan et al 2009).
  • Inflammatory pain is associated with tissue damage and the infiltration of immune cells and can promote repair by causing pain hypersensitivity until healing occurs (Woolf 2010).
Pathological Pain is defined as:
  • Pathological pain is a disease state caused by damage to the nervous system (neuropathic) or by its abnormal function (dysfunctional) (Woolf 2010).
Neuropathic Pain is defined as:
  • Spontaneous pain and hypersensitivity to pain in association with damage to or a lesion of the nervous system (Woolf 2004).
  • Maladaptive plasticity caused by a lesion or disease affecting the somatosensory system alters nociceptive signal processing so that pain is felt in the absence of a stimulus, and responses to innocuous and noxious stimuli are enhanced (Costigan et al 2009).

Dysfunctional/Functional Pain is defined as:

  • Hypersensitivity to pain resulting from abnormal central processing of normal input (Woolf 2004).
  • Amplification of nociceptive signaling in the absence of either inflammation or neural lesions (Costigan et al 2009).
  • Conditions that evoke dysfunctional pain include fibromyalgia, irritable bowel syndrome, tension type headache, temporomandibular joint disease, interstitial cystitis, and other syndromes in which there exists substantial pain but no noxious stimulus and no, or minimal, peripheral inflammatory pathology (Woolf, 2010).

In addition to the pain types mentioned above, it is also important to be aware of additional pain mechanisms. These being Peripheral Sensitisation and Central Sensitisation. Based on my readings these are mechanisms, not types of pain. I, incorrectly, used to think of central sensitisation as a type of pain.

Peripheral Sensitisation:

  • Inflammatory mediators reduce threshold for activation of nociceptors (sensitised terminal).
  • Can result in allodynia and hyperalgesia (primary).
    • (Costigan et al 2009)
Central Sensitisation:
  • Pathophysiological mechanism that is common in inflammatory, neuropathic and dysfunctional/functional pain.
  • Can result in allodynia and hyperalgesia (primary and secondary).
    • (Costigan et al 2009)

I like the following analogy by Woolf (2010) to sum up:

“if pain were a fire alarm, the nociceptive type would be activated appropriately only by the presence of intense heat, inflammatory pain would be activated by warm temperatures, and pathological pain would be a false alarm caused by malfunction of the system itself.”

 The purpose of this post was to cover the basic definitions of pain, the types of pain and mechanisms of pain states. What I haven’t covered yet is how as clinicians we can identify types of pain via the subjective and objective examinations.

Subsequent posts will cover this.


  • Costigan M, Scholz J, Woolf CJ (2009). Neuropathic pain: a maladaptive response of the nervous system to damage. Annu. Rev. Neurosci. 32 (1-32).
  • Woolf CJ (2004) Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med.140 (441-451).
  • Woolf CJ (2010) What is this thing called pain?. The Journal of Clinical Investigation. 120:11 (3742-3744)
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 Sessional Academic at Curtin University. The views expressed on this blog are his own.

Post a Comment

%d bloggers like this: