Nociplastic pain

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Nociplastic pain
Other namesCentral sensitisation
Widespread Pain Index Areas.svg
Fibromyalgia is the classic example of nociplastic pain, [1] being diagnosed when pain is felt in four different quadrants of the body using measures such as the Widespread Pain Index shown
Specialty Neurology
DurationShort to long-term [2]
Diagnostic method Clinical history, description of pain [3]
Treatment Exercise, medication, psychological therapies, pain neuroscience education [4]


Nociplastic painakacentral sensitisation is the consensus semantic term used by medical researchers to describe a third category of pain that is mechanistically distinct from nociceptive pain, due to inflammation and tissue damage, and neuropathic pain, due to nerve damage. [5] It may occur in combination with the other types of pain or in isolation. Its location may be generalised or multifocal and it can be more intense than would be expected from any associated physical cause. [3]

Contents

Its causes are not fully understood but it is thought to be a dysfunction of the central nervous system whose processing of pain signals may have become distorted or sensitised. [3] [6]

The concept and term was formally added to the taxonomy of the International Association for the Study of Pain following the recommendation of a task force in 2017. [7] The root terms are Latin nocēre, meaning to hurt, and Greek πλαστός, meaning development or formation in a medical context.

This type of pain typically arises in some chronic pain conditions, with the archetypal condition being fibromyalgia. It may be a factor in long COVID. [8] [9] Exercise is commonly prescribed for such conditions. [10] Nociplastic pain has also been hypothesized to play a role in the persistence of medically unexplained symptoms. [6]

Definition

Nociplastic pain is a longterm complex pain, one of three mechanisms of pain, defined by the International Association for the Study of Pain as "pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain". [2] The other two mechanisms are nociceptive pain and neuropathic pain. [2] Widespread pain and increased pain have been suggested as important clinical features. [2]

Central sensitization is a broader term referring to a hyperexcitability of the nervous system, usually including hyperalgesia (increased sensitivity to pain), and allodynia (painful perception of non-painful stimuli). [6]

An even broader term is that of central sensitivity syndromes, referring to syndromes characterized by the hyperexcitement of central neurons. These include fibromyalgia, irritable bowel syndrome, headaches, chronic fatigue syndrome [11] and temporomandibular disorder. [12]

Mechanism

Its causes are not fully understood but it is thought to be a dysfunction of the central nervous system whose processing of pain signals may have become distorted or sensitised. [3] Specific central nervous system locations that have been suggested are nociceptive neurons, spinal and supraspinal structures, the dorsal horn and others. [6]

Diagnosis

It is diagnosed by its clinical features and lack of response to regular painkillers. [3] Pain is experienced in several body parts, and is often widespread and intense. [3] There may be associated tiredness, and difficulties with memory, mood and sleep. [3] It can occur on its own in conditions such as tension headache or fibromyalgia, or combined with other pain categories such as in chronic back pain. [3]

Tools to measure central sensitization include sensory tests to painful stimuli, magnetic resonance imaging and measures of cytokines and neurotrophines in the blood and urine. [6] Self-report questionnaires such as the Central Sensitization Inventory [13] and the Sensory Hypersensitivity Scale [14] are also used. [6]

Treatment

Treatment generally requires both physical and psychological therapies, along with pain neuroscience education. [4]

Related Research Articles

<span class="mw-page-title-main">Pain</span> Type of distressing feeling

Pain is a distressing feeling often caused by intense or damaging stimuli. The International Association for the Study of Pain defines pain as "an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage."

<span class="mw-page-title-main">Fibromyalgia</span> Chronic pain of unknown cause

Fibromyalgia is a medical syndrome which commonly presents as chronic widespread pain, accompanied by fatigue, waking unrefreshed, and cognitive symptoms. Other symptoms include headaches, lower abdominal pain or cramps, and depression. People with fibromyalgia can also experience insomnia and a general hypersensitivity. The cause of fibromyalgia is unknown, but is believed to involve a combination of genetic and environmental factors. Environmental factors may include psychological stress, trauma, and certain infections. Since the pain appears to result from processes in the central nervous system, the condition is referred to as a "central sensitization syndrome".

<span class="mw-page-title-main">Itch</span> Sensation that causes desire or reflex to scratch

Itch is a sensation that causes a strong desire or reflex to scratch. Itches have resisted many attempts to be classified as any one type of sensory experience. Itches have many similarities to pain, and while both are unpleasant sensory experiences, their behavioral response patterns are different. Pain creates a withdrawal reflex, whereas itches leads to a scratch reflex.

<span class="mw-page-title-main">Peripheral neuropathy</span> Nervous system disease affecting nerves beyond the brain and spinal cord

Peripheral neuropathy, often shortened to neuropathy, refers to damage or disease affecting the nerves. Damage to nerves may impair sensation, movement, gland function, and/or organ function depending on which nerve fibers are affected. Neuropathies affecting motor, sensory, or autonomic nerve fibers result in different symptoms. More than one type of fiber may be affected simultaneously. Peripheral neuropathy may be acute or chronic, and may be reversible or permanent.

<span class="mw-page-title-main">Hyperalgesia</span> Abnormally increased sensitivity to pain

Hyperalgesia is an abnormally increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves and can cause hypersensitivity to stimulus. Prostaglandins E and F are largely responsible for sensitizing the nociceptors. Temporary increased sensitivity to pain also occurs as part of sickness behavior, the evolved response to infection.

Neuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system. Neuropathic pain may be associated with abnormal sensations called dysesthesia or pain from normally non-painful stimuli (allodynia). It may have continuous and/or episodic (paroxysmal) components. The latter resemble stabbings or electric shocks. Common qualities include burning or coldness, "pins and needles" sensations, numbness and itching.

<span class="mw-page-title-main">Referred pain</span> Pain perceived at a location other than the site of the painful stimulus

Referred pain, also called reflective pain, is pain perceived at a location other than the site of the painful stimulus. An example is the case of angina pectoris brought on by a myocardial infarction, where pain is often felt in the left side of neck, left shoulder, and back rather than in the thorax (chest), the site of the injury. The International Association for the Study of Pain has not officially defined the term; hence, several authors have defined it differently. Referred pain has been described since the late 1880s. Despite an increasing amount of literature on the subject, the biological mechanism of referred pain is unknown, although there are several hypotheses.

Sensitization is a non-associative learning process in which repeated administration of a stimulus results in the progressive amplification of a response. Sensitization often is characterized by an enhancement of response to a whole class of stimuli in addition to the one that is repeated. For example, repetition of a painful stimulus may make one more responsive to a loud noise.

<span class="mw-page-title-main">Allodynia</span> Feeling of pain from stimuli which do not normally elicit pain

Allodynia is a condition in which pain is caused by a stimulus that does not normally elicit pain. For example, sunburn can cause temporary allodynia, so that usually painless stimuli, such as wearing clothing or running cold or warm water over it, can be very painful. It is different from hyperalgesia, an exaggerated response from a normally painful stimulus. The term comes from Ancient Greek άλλος (állos) 'other', and οδύνη (odúnē) 'pain'.

<span class="mw-page-title-main">Group C nerve fiber</span> One of three classes of nerve fiber in the central nervous system and peripheral nervous system

Group C nerve fibers are one of three classes of nerve fiber in the central nervous system (CNS) and peripheral nervous system (PNS). The C group fibers are unmyelinated and have a small diameter and low conduction velocity, whereas Groups A and B are myelinated. Group C fibers include postganglionic fibers in the autonomic nervous system (ANS), and nerve fibers at the dorsal roots. These fibers carry sensory information.

Pain tolerance is the maximum level of pain that a person is able to tolerate. Pain tolerance is distinct from pain threshold. The perception of pain that goes in to pain tolerance has two major components. First is the biological component—the headache or skin prickling that activates pain receptors. Second is the brain’s perception of pain—how much focus is spent paying attention to or ignoring the pain. The brain’s perception of pain is a response to signals from pain receptors that sensed the pain in the first place.

<span class="mw-page-title-main">TRPM8</span> Protein-coding gene in the species Homo sapiens

Transient receptor potential cation channel subfamily M (melastatin) member 8 (TRPM8), also known as the cold and menthol receptor 1 (CMR1), is a protein that in humans is encoded by the TRPM8 gene. The TRPM8 channel is the primary molecular transducer of cold somatosensation in humans. In addition, mints can desensitize a region through the activation of TRPM8 receptors.

Na<sub>v</sub>1.8 Protein-coding gene in the species Homo sapiens

Nav1.8 is a sodium ion channel subtype that in humans is encoded by the SCN10A gene.

Psychogenic pain is physical pain that is caused, increased, or prolonged by mental, emotional, or behavioral factors, without evidence of physical injury or illness.

<span class="mw-page-title-main">Wide dynamic range neuron</span>

The wide dynamic range (WDR) neuron was first discovered by Mendell in 1966. Early studies of this neuron established what is known as the gate control theory of pain. The basic concept is that non-painful stimuli block the pathways for painful stimuli, inhibiting possible painful responses. This theory was supported by the fact that WDR neurons are responsible for responses to both painful and non-painful stimuli, and the idea that these neurons could not produce more than one of these responses simultaneously. WDR neurons respond to all types of somatosensory stimuli, make up the majority of the neurons found in the posterior grey column, and have the ability to produce long range responses including those responsible for pain and itch.

<span class="mw-page-title-main">Pain in crustaceans</span> Ethical debate

There is a scientific debate which questions whether crustaceans experience pain. It is a complex mental state, with a distinct perceptual quality but also associated with suffering, which is an emotional state. Because of this complexity, the presence of pain in an animal, or another human for that matter, cannot be determined unambiguously using observational methods, but the conclusion that animals experience pain is often inferred on the basis of likely presence of phenomenal consciousness which is deduced from comparative brain physiology as well as physical and behavioural reactions.

Diffuse noxious inhibitory controls (DNIC) or conditioned pain modulation (CPM) refers to an endogenous pain modulatory pathway which has often been described as "pain inhibits pain". It occurs when response from a painful stimulus is inhibited by another, often spatially distant, noxious stimulus.

<span class="mw-page-title-main">Pain in cephalopods</span> Contentious issue

Pain in cephalopods is a contentious issue. Pain is a complex mental state, with a distinct perceptual quality but also associated with suffering, which is an emotional state. Because of this complexity, the presence of pain in non-human animals, or another human for that matter, cannot be determined unambiguously using observational methods, but the conclusion that animals experience pain is often inferred on the basis of likely presence of phenomenal consciousness which is deduced from comparative brain physiology as well as physical and behavioural reactions.

Ocular neuropathic pain is a spectrum of disorders of ocular pain which are caused by damage or disease affecting the nerves. Ocular neuropathic pain is frequently associated with damaged or dysfunctional corneal nerves, but the condition can also be caused by peripheral or centralized sensitization. The condition shares some characteristics with somatic neuropathic pain in that it is similarly associated with abnormal sensations (dysesthesia) or pain from normally non-painful stimuli (allodynia), but until recent years has been poorly understood by the medical community, and frequently dismissed by ophthalmologists who were not trained to identify neuropathic pain as a source of unexplained eye pain beyond objective findings noted on slit-lamp examination.

Epigenetics of chronic pain is the study of how epigenetic modifications of genes affect the development and maintenance of chronic pain. Chromatin modifications have been found to affect neural function, such as synaptic plasticity and memory formation, which are important mechanisms of chronic pain. In 2019, 20% of adults dealt with chronic pain. Epigenetics can provide a new perspective on the biological mechanisms and potential treatments of chronic pain.

References

  1. Chimenti RL, Frey-Law LA, Sluka KA (May 2018). "A Mechanism-Based Approach to Physical Therapist Management of Pain". Physical Therapy. 98 (5): 302–314. doi:10.1093/ptj/pzy030. PMC   6256939 . PMID   29669091.
  2. 1 2 3 4 Wåhlén K (2020). "Introduction: chronic pain". The pain profile in fibromyalgia: Painomic studies of pain characteristics and proteins in blood. Sweden: Linköping University. p. 9. ISBN   978-91-7929-783-1.
  3. 1 2 3 4 5 6 7 8 Fitzcharles MA, Cohen SP, Clauw DJ, Littlejohn G, Usui C, Häuser W (May 2021). "Nociplastic pain: towards an understanding of prevalent pain conditions". Lancet. 397 (10289): 2098–2110. doi:10.1016/S0140-6736(21)00392-5. PMID   34062144. S2CID   235245552.
  4. 1 2 Zafereo J (2020). "17. Physical therapy for pain management". In Noe CE (ed.). Pain Management for Clinicians: A Guide to Assessment and Treatment. Switzerland: Springer. pp. 445–448. ISBN   978-3-030-39982-5.
  5. Fitzcharles MA, Cohen SP, Clauw DJ, Littlejohn G, Usui C, Häuser W (May 2021). "Nociplastic pain: towards an understanding of prevalent pain conditions". Lancet. 397 (10289): 2098–2110. doi:10.1016/s0140-6736(21)00392-5. PMID   34062144. S2CID   235245552.
  6. 1 2 3 4 5 6 den Boer, Carine; Dries, Linne; Terluin, Berend; van der Wouden, Johannes C.; Blankenstein, Annette H.; van Wilgen, C. Paul; Lucassen, Peter; van der Horst, Henriëtte E. (February 2019). "Central sensitization in chronic pain and medically unexplained symptom research: A systematic review of definitions, operationalizations and measurement instruments". Journal of Psychosomatic Research. 117: 32–40. doi:10.1016/j.jpsychores.2018.12.010. PMID   30665594. S2CID   58565532.
  7. IASP Council Adopts Task Force Recommendation for Third Mechanistic Descriptor of Pain, International Association for the Study of Pain, 14 November 2017
  8. Clauw DJ, Häuser W, Cohen SP, Fitzcharles MA (August 2020). "Considering the potential for an increase in chronic pain after the COVID-19 pandemic". Pain. 161 (8): 1694–1697. doi:10.1097/j.pain.0000000000001950. PMC   7302093 . PMID   32701829.
  9. Linda Geddes (28 June 2021), "The pain that can't be seen – Sufferers of chronic pain have long been told it's all in their head. We now know that's wrong", The Guardian
  10. Ferro Moura Franco K, Lenoir D, Dos Santos Franco YR, Jandre Reis FJ, Nunes Cabral CM, Meeus M (January 2021). "Prescription of exercises for the treatment of chronic pain along the continuum of nociplastic pain: A systematic review with meta-analysis" (PDF). European Journal of Pain. 25 (1): 51–70. doi:10.1002/ejp.1666. hdl: 10067/1726510151162165141 . PMID   32976664. S2CID   221937920.
  11. Yunus, Muhammad B. (June 2007). "Fibromyalgia and Overlapping Disorders: The Unifying Concept of Central Sensitivity Syndromes". Seminars in Arthritis and Rheumatism. 36 (6): 339–356. doi:10.1016/j.semarthrit.2006.12.009. PMID   17350675.
  12. Mezhov, Veronica; Guymer, Emma; Littlejohn, Geoffrey (December 2021). "Central sensitivity and fibromyalgia". Internal Medicine Journal. 51 (12): 1990–1998. doi: 10.1111/imj.15430 . ISSN   1444-0903. PMID   34139045. S2CID   235471910.
  13. Scerbo, Thomas; Colasurdo, Joseph; Dunn, Sally; Unger, Jacob; Nijs, Jo; Cook, Chad (April 2018). "Measurement Properties of the Central Sensitization Inventory: A Systematic Review". Pain Practice. 18 (4): 544–554. doi: 10.1111/papr.12636 . PMID   28851012. S2CID   206247498.
  14. Dixon, Eric A.; Benham, Grant; Sturgeon, John A.; Mackey, Sean; Johnson, Kevin A.; Younger, Jarred (June 2016). "Development of the Sensory Hypersensitivity Scale (SHS): a self-report tool for assessing sensitivity to sensory stimuli". Journal of Behavioral Medicine. 39 (3): 537–550. doi:10.1007/s10865-016-9720-3. ISSN   0160-7715. PMC   4854764 . PMID   26873609.