Allodynia: Difference between revisions – Physiopedia


 

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== Aetiology/Mechanism ==

== Aetiology/Mechanism ==

Allodynia is considered a sign/symptom, not a disease. It may be a temporary ‘normal’ (adaptive) response to tissue damage for better protection of vulnerable tissues.<ref name=”:3″>Sandkuhler J. [https://journals.physiology.org/doi/epdf/10.1152/physrev.00025.2008 Models and mechanisms of hyperalgesia and allodynia.] Physiological reviews. 2009 Apr;89(2):707-58.</ref> Changes in nervous system processing can result in allodynia persisting long after the original injury has healed, or may occur in the absence of injury. Pain then becomes maladaptive and can have negative effects on quality of life. <ref>Viana F. Nociceptors: thermal allodynia and thermal pain. InHandbook of clinical neurology 2018 Jan 1 (Vol. 156, pp. 103-119). Elsevier.</ref>     

Allodynia is considered a sign/symptom, not a disease. It may be a temporary ‘normal’ (adaptive) response to tissue damage for better protection of vulnerable tissues.<ref name=”:3″>Sandkuhler J. [https://journals.physiology.org/doi/epdf/10.1152/physrev.00025.2008 Models and mechanisms of hyperalgesia and allodynia.] Physiological reviews. 2009 Apr;89(2):707-58.</ref> Changes in nervous system processing can result in allodynia persisting long after the original injury has healed, occur in the absence of injury. then maladaptive and can have negative effects on quality of life. <ref>Viana F. Nociceptors: thermal allodynia and thermal pain. InHandbook of clinical neurology 2018 Jan 1 (Vol. 156, pp. 103-119). Elsevier.</ref>   

A-delta and C-fibres (unmyelinated) are nociceptive (high threshold); A-beta fibres are low threshold and usually not nociceptive<ref name=”:3″ />   

The mechanisms responsible for allodynia include:

 

* ”””

The mechanisms responsible for allodynia include:  

* ”’Activation of silent nociceptors:”’ A-beta fibres communicate with and activate nociceptors (A-delta fibres) through sodium channels<ref name=”:0″ />

 

* ”’Central inhibition errors:”’ Disinhibition of secondary spinal networks <ref>Kuner R. Central mechanisms of pathological pain. Nature medicine. 2010 Nov;16(11):1258-66. </ref>. Mental state can influence the perception of allodynia by altering the inhibition of nociceptive input. ”In other words, a loss of spinal segregation of touch and pain can be a key mechanism of allodynia<ref>Kuner R, Flor H. Structural plasticity and reorganization in chronic pain. Nature Reviews Neuroscience. 2017 Jan;18(1):20-30. </ref>.”

* ”’Long-term potentiation error”’

be by in the :in and (-

* ”’Activation of silent nociceptors:”’ A-beta fibres communicate with and activate nociceptors (A-delta fibres) through sodium channels<ref name=”:0″ />

* ”’Central inhibition errors:”’ Disinhibition of secondary spinal networks<ref>Kuner R. Central mechanisms of pathological pain. Nature medicine. 2010 Nov;16(11):1258-66. </ref>. Mental state can influence the perception of allodynia by altering the inhibition of nociceptive input. ”In other words, a loss of spinal segregation of touch and pain can be a key mechanism of allodynia<ref>Kuner R, Flor H. Structural plasticity and reorganization in chronic pain. Nature Reviews Neuroscience. 2017 Jan;18(1):20-30. </ref>.”

Dynamic/mechanical allodynia is thought to be caused by sensitised low-threshold A-beta fibres that

 

Changes in the dorsal root ganglion cells

 

Central Sensitisation: increase in the excitability of neurons in the CNS – decrease in activation threshold and increase in recruitment of new inputs(can occur with excessive cfibre inputs)

== Conditions ==

== Conditions ==

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Listed below are some conditions that may present with allodynia:

Listed below are some conditions that may present with allodynia:

* [[Neuropathic Pain]]: Allodynia is present in 15-50% of patients with neuropathic pain<ref name=”:0″ />

* [[Neuropathic Pain]]: Allodynia is present in 15-50% of patients with neuropathic pain<ref name=”:0″ />

* [https://www.physio-pedia.com/Diabetic_Neuropathy?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Diabetic Neuropathy]: Often bilateral, distal and symmetrical allodynia

* [https://www.physio-pedia.com/Diabetic_Neuropathy?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Diabetic Neuropathy]: Often bilateral, distal and symmetrical allodynia

* Postherpetic Neuralgia

* Postherpetic Neuralgia

* [https://www.physio-pedia.com/Fibromyalgia?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Fibromyalgia]

* [https://www.physio-pedia.com/Fibromyalgia?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Fibromyalgia]

* [https://www.physio-pedia.com/Trigeminal_Neuralgia?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Trigeminal Neuralgia]

* [https://www.physio-pedia.com/Trigeminal_Neuralgia?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Trigeminal Neuralgia]

* [[Chemotherapy-Induced Peripheral Neuropathy (CIPN)|Chemotherapy induced peripheral neuropathy]]

* [[Chemotherapy-Induced Peripheral Neuropathy (CIPN)|Chemotherapy induced peripheral neuropathy]]

* [[Migraine Headache|Migraine]]: Cutaneous allodynia is present in about 60% of people suffering from migraines and indicates central sensitisation.<ref name=”:2″>Mínguez-Olaondo A, Quintas S, Morollón Sánchez-Mateos N, López-Bravo A, Vila-Pueyo M, Grozeva V, Belvís R, Santos-Lasaosa S, Irimia P. [https://www.frontiersin.org/articles/10.3389/fneur.2021.831035/full Cutaneous allodynia in migraine: a narrative review.] Frontiers in neurology. 2022 Jan 21;12:831035.</ref>

* [[Migraine Headache|Migraine]]: Cutaneous allodynia is present in about 60% of people suffering from migraines and indicates central sensitisation.<ref name=”:2″>Mínguez-Olaondo A, Quintas S, Morollón Sánchez-Mateos N, López-Bravo A, Vila-Pueyo M, Grozeva V, Belvís R, Santos-Lasaosa S, Irimia P. [https://www.frontiersin.org/articles/10.3389/fneur.2021.831035/full Cutaneous allodynia in migraine: a narrative review.] Frontiers in neurology. 2022 Jan 21;12:831035.</ref>

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* [[Complex Regional Pain Syndrome (CRPS)]]

* [[Complex Regional Pain Syndrome (CRPS)]]

* [[Chronic Low Back Pain]]

* [[Chronic Low Back Pain]]

* [[Osteoarthritis]]

* [[Osteoarthritis]]

* [[Rheumatoid Arthritis]]

* [[Rheumatoid Arthritis]]

* [[Amputation Pain Rehabilitation|Post-amputation stump pain]]

* [[Amputation Pain Rehabilitation|Post-amputation stump pain]]

* Snake bites

*

== Differential Diagnosis ==

== Differential Diagnosis ==

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Hyperalgesia is the condition of having increased sensitivity to pain or enhanced intensity of pain sensation. There is an exaggerated experience of pain from a stimulus that is normally painful – i.e. an increased response/pain on supra-threshold stimulation (see image)<ref name=”:1″ /> <ref name=”:3″ />.     

Hyperalgesia is the condition of having increased sensitivity to pain or enhanced intensity of pain sensation. There is an exaggerated experience of pain from a stimulus that is normally painful – i.e. an increased response/pain on supra-threshold stimulation (see image)<ref name=”:1″ /> <ref name=”:3″ />.     

Although allodynia and hyperalgesia are distinct clinical terms, they can co-exist.<ref name=”:0″ />     

Although allodynia and hyperalgesia are distinct clinical terms, they can co-exist.<ref name=”:0″ />     

== Assessment ==

== Assessment ==

This article or area is currently under construction and may only be partially complete. Please come back soon to see the finished work! (19/12/2023)

Allodynia is defined by the International Association for the Study of Pain (IASP) as

“Pain resulting from a stimulus that does not normally provoke/elicit pain” [1]

For example, brushing a feather against the arm causes pain where it should only cause a sensation.[2] It is a clinical term to describe this phenomenon of altered quality of a sensation, and does not imply a mechanism or specific diagnosis.[1]It may however give insight into possible mechanisms at play.

Classification[edit | edit source]

Allodynia is categorised into three types[3]:

  1. Dynamic (or mechanical) when pain results from an object moving across the skin (stroking or brushing); mediated by A-beta fibres
  2. Thermal which results from mild temperature changes; mediated by A-delta and C-fibres
  3. Tactile (or static) which results from gentle touch or pressure; mediated by A-delta nociceptive fibres

Allodynia is considered a sign/symptom, not a disease. It may be a temporary ‘normal’ (adaptive) response to tissue damage for better protection of vulnerable tissues.[4] Changes in nervous system processing can result in allodynia persisting long after the original injury has healed, and allodynia can therefore occur in the absence of injury. The pain associated with allodynia is then regarded as maladaptive and can have negative effects on recovery and quality of life. [5]Although the exact mechanisms underlying allodynia is the subject of ongoing research, the most accepted hypotheses are presented below.

The mechanisms responsible for allodynia include:

  • Sensitisation of dorsal horn cells: Increased excitability of wide dynamic range (WDR) neurones
  • Activation of silent nociceptors: Low threshold A-beta fibres are sensitised. These fibres are usually not nociceptive. A-beta fibres communicate with and activate nociceptors (A-delta fibres) through sodium channels, resulting in pain when non-painful mechanical stimuli is applied.[2][4]
  • Central inhibition errors: Disinhibition of secondary spinal networks resulting in central sensitisation[6]. Mental state can influence the perception of allodynia by altering the inhibition of nociceptive input. In other words, a loss of spinal segregation of touch and pain can be a key mechanism of allodynia[7].

These mechanisms can be facilitated by persistent peripheral nociceptive input, resulting in sensitisation, or be as a direct result of damage/disease of the peripheral or central nervous system.[8]

Allodynia is often associated with conditions that involve sensitisation of the skin. Common examples include sunburn, inflammation or trauma.[1]Allodynia is a normal protective response after tissue injury has occurred and will usually subside as healing progresses. It may however increase over time in certain conditions, such as neuropathic pain conditions.[1]

Listed below are some conditions that may present with allodynia:

Allodynia vs. Hyperalgesia

Another clinical term that needs to be differentiated from allodynia, is hyperalgesia. Where allodynia refers to changes in the quality of sensation, hyperalgesia refers to changes in the intensity of the sensation of pain.[1]

Hyperalgesia is the condition of having increased sensitivity to pain or enhanced intensity of pain sensation. There is an exaggerated experience of pain from a stimulus that is normally painful – i.e. an increased response/pain on supra-threshold stimulation (see image)[1] [4].

Although allodynia and hyperalgesia are distinct clinical terms, they can and often do co-exist.[2]

Subjective Assessment:

  • Obtain a history of diabetes, herpes, chemotherapy, HIV, surgical procedures – any of these could contribute to neuropathic pain
  • Take note of current medications as some medications can cause neuropathic pain (eg. antiretroviral treatment and chemotherapy)
  • Is the pain associated with touch or stroking or temperature changes[2]
  • Mental health screening to determine stress levels and detect depression and/or anxiety

Objective Assessment:

  • Always compare the the unaffected side or a body site distant from the affected area (especially if there is bilateral involvement)
  • Light touch: With the patient’s eyes closed, use a cotton swab/Q-tip to gently stroke the affected area and then the opposite side/unaffected and note whether the patient feels pain
  • Temperature: Use a cold metal coin for cold, and then heat it in your pocket for heat – determine whether the patient feels pain with cold/hot touch
  • If allodynia is present, determine whether it follows a dermatomal or peripheral nerve pattern, and whether it is bilateral
  • Testing for allodynia forms part of Quantitative Sensory Testing – see the page for a more detailed description of assessment and interpretation
  • If allodynia is present, a neurological examination (reflexes, muscle strength etc.) is indicated to determine whether nerve damage could be the underlying cause

Providers shoulder treat/manage the underlying condition that is causing the allodynia, as well as manage the pain associated with it. Also see Neuropathic Pain

  • Medication: Anticonvulsants (such as gabapentin), triptans (used to treat migraines), and some antidepressants are most effective for neuropathic conditions. NSAIDs may also be effective where persistent inflammation is present. Topical creams that can help manage allodynia will typically have lidocaine or capsaicin as the active ingredient, but there is limited evidence of its effectiveness.[2] Opioids should be avoided.
  • Psychosocial interventions: Counselling may be recommended if signs of depression are detected. Biofeedback, mindfulness training, and cognitive behavioural therapy can change the way a person responds to pain.
  • Physiotherapy: The psychologically informed physiotherapist can include pain neuroscience education (PNE) and cognitive functional therapy. Physiotherapist can help manage allodynia with desensitization and/or graded motor imagery.
  • Other procedures: A nerve block injection may be recommended to reduce pain in a specific nerve or nerve group.[2]

Allodynia can not be directly prevented, however, one can lower the risk of acquiring a condition that causes allodynia. Risk management includes exercising regularly, monitoring health, managing mental health , maintaining a healthy weight, having a balanced diet, and having good sleep hygiene.

Allodynia is a clinical sign that indicates sensitisation of the nervous system. It is common in neuropathic and chronic pain conditions, and may be influenced by emotional state. It can also have a significant negative impact on quality of life and requires early detection and multidisciplinary management.

12 Item Allodynia Symptom checklist (for Migraine)

  1. 1.0 1.1 1.2 1.3 1.4 1.5 IASP. Terminology. Available from: https://www.iasp-pain.org/resources/terminology/ (accessed 12 Dec 2023)
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 He Y, Kim PY. Allodynia [Internet]. PubMed. Treasure Island (FL): StatPearls Publishing; 2016 [cited 2022 Apr 9]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537129/
  3. 3.0 3.1 Mínguez-Olaondo A, Quintas S, Morollón Sánchez-Mateos N, López-Bravo A, Vila-Pueyo M, Grozeva V, Belvís R, Santos-Lasaosa S, Irimia P. Cutaneous allodynia in migraine: a narrative review. Frontiers in neurology. 2022 Jan 21;12:831035.
  4. 4.0 4.1 4.2 Sandkuhler J. Models and mechanisms of hyperalgesia and allodynia. Physiological reviews. 2009 Apr;89(2):707-58.
  5. Viana F. Nociceptors: thermal allodynia and thermal pain. InHandbook of clinical neurology 2018 Jan 1 (Vol. 156, pp. 103-119). Elsevier.
  6. Kuner R. Central mechanisms of pathological pain. Nature medicine. 2010 Nov;16(11):1258-66.
  7. Kuner R, Flor H. Structural plasticity and reorganization in chronic pain. Nature Reviews Neuroscience. 2017 Jan;18(1):20-30.
  8. 8.0 8.1 8.2 8.3 8.4 8.5 Jensen TS, Finnerup NB. Allodynia and hyperalgesia in neuropathic pain: clinical manifestations and mechanisms. The Lancet Neurology. 2014 Sep 1;13(9):924-35.

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