Allodynia: Difference between revisions

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<div class="editorbox">'''Original Editors ''' - [[User:Abbi Davis|Abbi Davis]], [[User:Jessica Bradshaw|Jessica Bradshaw]], & [[User:Parker Hall|Parker Hall ]] as part of the [[Arkansas Colleges of Health Education School of Physical Therapy Musculoskeletal 1 Project]]<br>
<div class="editorbox">'''Original Editors ''' - [[User:Abbi Davis|Abbi Davis]], [[User:Jessica Bradshaw|Jessica Bradshaw]], & [[User:Parker Hall|Parker Hall ]] as part of the [[Arkansas Colleges of Health Education School of Physical Therapy Musculoskeletal 1 Project]]<br>
'''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}}</div>
'''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}}</div>


== Overview ==
== Introduction ==
Allodynia is defined as pain resulting from a stimulus, such as a light touch of the skin, that would not normally provoke pain<ref>Definition of ALLODYNIA [Internet]. Merriam-webster.com. 2017 [cited 2022 Apr 9]. Available from: https://www.merriam-webster.com/dictionary/allodynia</ref>. For example, brushing a feather against the arm causes pain where it should only cause a sensation. Allodynia is a type of neuropathic (nerve) pain and is categorized into three types: dynamic (or mechanical) when pain results from an object moving across the skin, thermal which results from mild temperature changes, or tactile (or static) which results from gentle touch or pressure. There is ultimately an error in the nerve communication network.    
Allodynia is defined by the International Association for the Study of Pain (IASP) as      
*
 
<blockquote>''"Pain resulting from a stimulus that does not normally provoke/elicit pain"'' <ref name=":1">IASP. Terminology. Available from: https://www.iasp-pain.org/resources/terminology/ (accessed 12 Dec 2023)</ref> </blockquote>     
 
For example, brushing a feather against the arm causes pain where it should only cause a sensation.<ref name=":0">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/</ref> It is a clinical term to describe this phenomenon of altered '''quality''' of a sensation, and does not imply a mechanism or specific diagnosis.<ref name=":1" />It may however give insight into possible mechanisms at play.    
 
=== Classification ===
Allodynia is categorised into four types<ref name=":2" />:     


== Etiology/Mechanism ==
# '''Dynamic''' '''mechanical''' when pain results from an object moving across the skin (stroking or brushing); mediated by A-beta fibres
Allodynia is considered a symptom, not a disease. It may be a patient's chief complaint. Allodynia is the phenomenon of a non-painful stimulus producing a sharp pain response, which implies an error in neuronal conduction. The mechanism behind this error is unclear. The strongest evidence that exists, thus far, suggests that sensory neuronal fibres may stimulate pain pathways, possibly due to an error in long-term potentiation. However, studies exist that suggest that superficial sensory components may also have involvement. There is also evidence that different mental states can affect the perception of allodynia. There is an analogy of "crisscrossed" fibres, where the actual location of the crisscrossing can vary and may be located almost anywhere along the peripheral to the central nervous system tract. Allodynia can involve both the peripheral nervous system and central nervous system via sensitization, and the mechanism behind the inappropriate pain sensations can evolve. This might partially explain the existing contradictory studies - they may all be measuring allodynia with neuronal confusion at different locations<ref name=":0">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/</ref>.  The expression of allodynia may be as elegantly simple as a consistent increase in sympathetic nervous system activity, which leads to a sensitization of C-fibers. The increase in C-fiber sensitization is also a reflection of disinhibition of secondary spinal networks<ref>Kuner R. Central mechanisms of pathological pain. Nature medicine. 2010 Nov;16(11):1258-66. </ref>. 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>. 
# '''Thermal''' which results from mild temperature changes; mediated by A-delta and C-fibres
# '''Tactile''' (or static) which results from gentle touch or pressure; mediated by A-delta nociceptive fibres


Listed below are some of the most common diseases associated with allodynia:
== 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, and allodynia can also 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|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>Although the exact mechanisms underlying allodynia is the subject of ongoing research, the most accepted hypotheses are presented below.   


* [https://www.physio-pedia.com/Fibromyalgia?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Fibromyalgia]
The mechanisms responsible for allodynia include:
* [https://www.physio-pedia.com/Trigeminal_Neuralgia?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Trigeminal Neuralgia]
* '''Sensitisation of dorsal horn cells:''' Increased excitability of  second order neurons in the spinal cord<ref name=":4" />
* [https://www.physio-pedia.com/Diabetic_Neuropathy?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Diabetic Neuropathic Pain]
* '''Sensitisation of mechanoreceptors:''' Low threshold A-beta fibres become sensitised. These fibres are usually not [[Nociception|nociceptive]] (rather mechanoreceptors). A-beta fibres communicate with and activate nociceptors (A-delta fibres) through various mechanisms (phenotypic switching, sprouting and opening of postsynaptic excitatory pathways), resulting in pain when non-painful mechanical stimuli is applied. As a result there is a loss of segregation of touch and pain. <ref name=":0" /><ref name=":3" /><ref>Kuner R, Flor H. Structural plasticity and reorganization in chronic pain. Nature Reviews Neuroscience. 2017 Jan;18(1):20-30. </ref>
* Migraine Associated Allodynia
* '''[[Pain Descending Pathways|Central inhibition]] errors:''' A change in the balance of [[Descending Inhibition|descending inhibitory]] and facilitating pathways from the brain to the spinal cord can result in [[Central Sensitisation|central sensitisation]]<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.  
These mechanisms can be facilitated by persistent peripheral nociceptive input, resulting in sensitisation, or can be as a direct result of damage/disease of the peripheral or central nervous system.<ref name=":4">Jensen TS, Finnerup NB. A[https://www.sciencedirect.com/science/article/pii/S1474442214701024 llodynia and hyperalgesia in neuropathic pain: clinical manifestations and mechanisms.] The Lancet Neurology. 2014 Sep 1;13(9):924-35.</ref>


*  
== Conditions ==
Allodynia is often associated with conditions that involve sensitisation of the skin. Common examples include sunburn, [[Inflammation Acute and Chronic|inflammation]] or trauma.<ref name=":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|neuropathic pain]] conditions.<ref name=":1" />Certain types of allodynia (eg. thermal allodynia) are more often associated with specific conditions - for example, cold allodynia is very common in post-stroke pain and chemotherapy neuropathy, whereas mechanical allodynia is more common in neuralgias and other neuropathies .<ref name=":4" />
 
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" />
* [[Neuropathies|Neuropathies:]] Eg. [[Carpal Tunnel Syndrome]]
* Polyneuropathy such as [[HIV-related Neuropathy]] and [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
* [[Brachial Plexus Injury]]
* Postherpetic Neuralgia
* [https://www.physio-pedia.com/Fibromyalgia?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Fibromyalgia]<ref name=":4" />
* [https://www.physio-pedia.com/Trigeminal_Neuralgia?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Trigeminal Neuralgia] and postherpetic neuralgia<ref name=":4" />
* [[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>
* [[Central Sensitisation]]
* [[Peripheral Sensitisation]]
* [[Complex Regional Pain Syndrome (CRPS)]]
* [[Chronic Low Back Pain]]
* [[Osteoarthritis]]<ref name=":4" />
* [[Rheumatoid Arthritis]]
* [[Amputation Pain Rehabilitation|Post-amputation stump pain]]<ref name=":4" />
* Central nervous system disorders: [[Post-Stroke Pain|Post-stroke pain]], [[Multiple Sclerosis (MS)|Multiple Sclerosis]], [[Spinal Cord Injury]]<ref name=":4" />


== Differential Diagnosis ==
== Differential Diagnosis ==
[[File:Allodynia.gif|thumb|Allodynia vs. Hyperalgesia<ref>Garvey J, Abolade A, Etherton J, Jackson K, Hampton L, Thomas E, et al. Allodynia.gif [Internet]. Physiopedia. 2016 [cited 2022 Apr 8]. Available from: [[:File:Allodynia.gif|https://www.physio-pedia.com/File:Allodynia.gif]] </ref> ]]Another sensory condition that is often a differential diagnosis to allodynia is [[Pain Behaviours#sts=Hyperalgesia?utm source=physiopedia&utm medium=search&utm campaign=ongoing internal|hyperalgesia]]. Hyperalgesia is the condition of having increased sensitivity to pain or enhanced intensity of pain sensation<ref>Medical Definition of HYPERALGESIA [Internet]. www.merriam-webster.com. [cited 2022 Apr 9]. Available from: https://www.merriam-webster.com/medical/hyperalgesia</ref>. Patients do not necessarily perceive high pressure as pain, but the stimulus that would normally be perceived as low pain is sensed at a higher pain level. Patients respond to pain stimulus in the same way that they would if they did not have the condition, but it is an exaggerated response<ref name=":0" />. The cause of both allodynia and hyperalgesia is unknown. 
[[File: Allodynia.gif|thumb|Allodynia vs. Hyperalgesia ]]Another clinical term that needs to be differentiated from allodynia, is [[Pain Behaviours#sts=Hyperalgesia?utm source=physiopedia&utm medium=search&utm campaign=ongoing internal|hyperalgesia]]. Where allodynia refers to changes in the '''quality''' of sensation, hyperalgesia refers to changes in the '''intensity''' of the sensation of pain.<ref name=":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)<ref name=":1" /> <ref name=":3" />.  
 
Although allodynia and hyperalgesia are distinct clinical terms, they can and often do co-exist.<ref name=":0" />  
 
== Assessment ==
 
=== '''Subjective Assessment''' ===
* Obtain a history of [[diabetes]], herpes, chemotherapy, [[Human Immunodeficiency Virus (HIV)|HIV,]] surgical procedures - any of these could contribute to neuropathic pain
* Take note of current medications as some medications can cause neuropathic pain (eg. [[Antiretrovirals and HIV|antiretroviral]] treatment and [[Chemotherapy-Induced Peripheral Neuropathy (CIPN)|chemotherapy]])
* Is the pain associated with touch or stroking or temperature changes?<ref name=":0" />
* Mental health screening to determine stress levels and detect [[depression]] and/or [[Generalised Anxiety Disorder|anxiety]] - this could affect [[Pain Descending Pathways|central inhibition pathways]]
 
=== '''Objective Assessment''' ===
* Always compare to 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 [[Dermatomes|dermatomal]] or peripheral nerve pattern, and whether it is bilateral
* Testing for allodynia forms part of '''[[Quantitative Sensory Testing (QST)|Quantitative Sensory Testing]]''' - see the page for a more detailed description of assessment and interpretation
* If allodynia is present, a [[Neurological Assessment|neurological examination]] (reflexes, muscle strength etc.) is indicated to determine whether nerve damage could be the underlying cause


==Treatment==
==Treatment==
There are multiple ways that healthcare providers can help treat allodynia. Providers can either treat the condition that is causing allodynia or try to reduce the pain. The treatment options for allodynia can be categorized as medications including topic creams, mental health counselling, physical therapy, and medical procedures. Some oral medications that can help manage allodynia include anticonvulsants (used to treat seizures), triptans (used to treat migraines), and some antidepressants. Topical creams that can help manage allodynia will typically have lidocaine or capsaicin as the active ingredient. Counselling may be recommended if signs of depression are detected. [[Biofeedback]], mindfulness training, and [[Cognitive Behavioural Therapy|cognitive behavioural therapy]] can change the way a person responds to pain. The psychologically informed physical therapist can include pain neuroscience education (PNE) and cognitive functional therapy. Physical therapists can help manage allodynia with [[desensitization]] and/or mirror therapy. A nerve block injection may be recommended to reduce pain in a specific nerve or nerve group. Surgery may be needed if these treatments are unsuccessful in managing allodynia. The surgeon implants a device that will deliver electricity directly to the spinal cord to stimulate it. These low levels of electricity help reduce pain<ref>Cleveland Clinic. Allodynia. [cited 2022 Apr 8]. Available from: https://my.clevelandclinic.org/health/symptoms/21570-allodynia </ref>.
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]]). It is important  to remember that various mechanisms can be involved in the [[Central Sensitisation|central sensitisation]] that allodynia is a sign of. The presence of allodynia should alert the clinician to investigate nerve pathology and central mechanisms, and treatment should target the mechanisms involved.  
 
* '''Pharmacologic:''' Anticonvulsants (such as gabapentin), triptans (used to treat migraines), and some antidepressants are most effective for [[Neuropathic Pain Medication|neuropathic]] conditions. [[NSAIDs]] may also be effective where persistent inflammation is present.<ref name=":4" /> Topical creams that can help manage allodynia will typically contain lidocaine or capsaicin as the active ingredient, but there is limited evidence of its effectiveness.<ref name=":0" /> [[Opioids]] should be avoided.
* '''Psychosocial interventions:''' Counselling may be recommended if signs of depression are detected. [[Biofeedback]], [[mindfulness]] training, and [[Cognitive Behavioural Therapy|cognitive behavioural therapy]] can influence descending inhibition and therefore alter pain perception.
* '''Physiotherapy''': The psychologically informed physiotherapist can include [[Pain Neuroscience Education (PNE)|pain neuroscience education]] (PNE) and cognitive functional therapy. Physiotherapist can help manage allodynia with [[desensitization|desensitisation]] and/or [[Graded Motor Imagery|graded motor imagery]].  
* '''Other procedures:''' A nerve block injection may be recommended to reduce pain in a specific nerve or nerve group.<ref name=":0" />
 
== Conclusion ==
Allodynia is a clinical sign that indicates sensitisation of the nervous system. It is common in neuropathic and [[Chronic Pain|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.


== Prevention ==
== Resources ==
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 via checkups, maintaining a healthy weight, having a balanced diet, and having good sleep hygiene.
'''[http://www.headache.mobi/uploads/1/1/7/5/11757140/asc-12.pdf 12 Item Allodynia Symptom checklist]''' (for Migraine)


== References  ==
== References  ==
<references />
<references />
[[Category:Pain]]
[[Category:Pain]]
[[Category:Arkansas Colleges of Health Education School of Physical Therapy Musculoskeletal 1 Project]]
[[Category: Arkansas Colleges of Health Education School of Physical Therapy Musculoskeletal 1 Project]]
[[Category:Conditions]]
[[Category:Neuropathy]]

Latest revision as of 13:23, 20 December 2023

Introduction[edit | edit source]

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 four types[3]:

  1. Dynamic 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

Aetiology/Mechanism[edit | edit source]

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 also 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 second order neurons in the spinal cord[6]
  • Sensitisation of mechanoreceptors: Low threshold A-beta fibres become sensitised. These fibres are usually not nociceptive (rather mechanoreceptors). A-beta fibres communicate with and activate nociceptors (A-delta fibres) through various mechanisms (phenotypic switching, sprouting and opening of postsynaptic excitatory pathways), resulting in pain when non-painful mechanical stimuli is applied. As a result there is a loss of segregation of touch and pain. [2][4][7]
  • Central inhibition errors: A change in the balance of descending inhibitory and facilitating pathways from the brain to the spinal cord can result in central sensitisation[8]. Mental state can influence the perception of allodynia by altering the inhibition of nociceptive input.

These mechanisms can be facilitated by persistent peripheral nociceptive input, resulting in sensitisation, or can be as a direct result of damage/disease of the peripheral or central nervous system.[6]

Conditions[edit | edit source]

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]Certain types of allodynia (eg. thermal allodynia) are more often associated with specific conditions - for example, cold allodynia is very common in post-stroke pain and chemotherapy neuropathy, whereas mechanical allodynia is more common in neuralgias and other neuropathies .[6]

Listed below are some conditions that may present with allodynia:

Differential Diagnosis[edit | edit source]

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]

Assessment[edit | edit source]

Subjective Assessment[edit | edit source]

  • 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 - this could affect central inhibition pathways

Objective Assessment[edit | edit source]

  • Always compare to 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

Treatment[edit | edit source]

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). It is important to remember that various mechanisms can be involved in the central sensitisation that allodynia is a sign of. The presence of allodynia should alert the clinician to investigate nerve pathology and central mechanisms, and treatment should target the mechanisms involved.

  • Pharmacologic: 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.[6] Topical creams that can help manage allodynia will typically contain 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 influence descending inhibition and therefore alter pain perception.
  • Physiotherapy: The psychologically informed physiotherapist can include pain neuroscience education (PNE) and cognitive functional therapy. Physiotherapist can help manage allodynia with desensitisation 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]

Conclusion[edit | edit source]

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.

Resources[edit | edit source]

12 Item Allodynia Symptom checklist (for Migraine)

References[edit | edit source]

  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. 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 6.8 Jensen TS, Finnerup NB. Allodynia and hyperalgesia in neuropathic pain: clinical manifestations and mechanisms. The Lancet Neurology. 2014 Sep 1;13(9):924-35.
  7. Kuner R, Flor H. Structural plasticity and reorganization in chronic pain. Nature Reviews Neuroscience. 2017 Jan;18(1):20-30.
  8. Kuner R. Central mechanisms of pathological pain. Nature medicine. 2010 Nov;16(11):1258-66.