Hyperalgesia: Difference between revisions

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IASP definition:  
IASP definition:  


<blockquote>"Increased pain from a stimulus that normally provokes pain."<ref name=":0">IASP. Terminology. Available from: https://www.iasp-pain.org/resources/terminology/ (accessed 12 Dec 2023)</ref> </blockquote>Hyperalgesia is a clinical term used to described the phenomenon of an increased pain response to a painful stimuli. It does not imply a single pain mechanism, but is associated with peripheral sensitization and central sensitisation.<ref name=":0" />Hyperalgesia is normal protective response after tissue injury and will usually subside as healing occurs. It may however increase over time in certain conditions, such as neuropathic pain conditions.
<blockquote>"Increased pain from a stimulus that normally provokes pain."<ref name=":0">IASP. Terminology. Available from: https://www.iasp-pain.org/resources/terminology/ (accessed 12 Dec 2023)</ref> </blockquote>Hyperalgesia is a clinical term used to described the phenomenon of an increased pain response to a painful stimuli (such as pin prick, pressure, extreme heat/cold). It does not imply a single pain mechanism, but is associated with peripheral sensitisation and central sensitisation.<ref name=":0" />
 
Hyperalgesia is normal protective response after tissue damage and will usually subside as healing occurs.<ref name=":1">Sandkuhler J. [[Models and mechanisms of hyperalgesia and allodynia]]. Physiological reviews. 2009 Apr;89(2):707-58.</ref> It may however increase over time in certain conditions, such as neuropathic pain conditions.


The interpretation of the phenomenon of hyperalgesia might change with further research.
The interpretation of the phenomenon of hyperalgesia might change with further research.


==Classification==
==Aetiology/Mechanism==
Hyperalgesia may involve a reduction in nociceptive firing threshold, and an increase in the supra-threshold response.<ref name=":1" />The end result is amplified nociception and an increase in pain intensity.
* '''Primary Hyperalgesia:''' Hyperalgesia that occurs at the site of injury and is often a reflection of [[Peripheral Sensitisation|peripheral sensitisation]]. It occurs as a result of reduced activation threshold and increased responsiveness of nociceptors.<ref name=":1" />
* '''Secondary Hyperalgesia:''' Hyperalgesia in an area adjacent to or remote from the site of injury.<ref name=":1" />Maintained by changes in the central processing of sensory information, including sensitisation of the spinal nociceptive neurons and altered descending inhibition.<ref name=":1" />
It is important to remember, that in acute injuries, the finding of hyperalgesia is a normal adaptive response. Since the injured tissue is vulnerable, the nociceptive system adapts by becoming sensitised to ensure tissue protection.<ref name=":1" />In such a case hyperalgesia would be an appropriate shift in pain threshold. It is however possible for this normal response to be exaggerated and does not always reflect the severity of an injury.
 
If hyperalgesia does however occur long after tissue healing has occurred or in the absence of damaged tissue, it is considered maladaptive.
 
=== Risk Factors ===
The following factors may increase the risk of maladaptive hyperalgesia:
 
* '''Diet:''' There is some evidence from animal studies that a diet rich in omega-3 is associated with stronger heat hyperalgesia.<ref name=":1" />
* '''Anxiety and chronic stress:''' A sustained stated of stress may enhance pain sensitivity.<ref name=":1" />
* Chronic Inflammation: Excess fat results in chronic release of inflammatory mediators
 
== Conditions ==
''Skin injury (e.g., a burn) or inflammation causes innocuous heat to become painful. Hypersensitivity to heat is also a prominent sign in systemic inflammatory disorders such as rheumatoid arthritis. In addition, thermal allodynia and hyperalgesia are common symptoms in patients after injury to the somatosensory nervous system, a condition known as neuropathic pain (Colloca et al., 2017). Conditions associated with neuropathic pain include peripheral nerve injuries, chemotherapy, postherpetic''<ref>Viana F. Nociceptors: thermal allodynia and thermal pain. InHandbook of clinical neurology 2018 Jan 1 (Vol. 156, pp. 103-119). Elsevier.</ref>
 
''Cold allodynia and cold hyperalgesia are common signs in various neuropathic conditions, including peripheral neuropathies caused by chemotherapeutic agents (e.g., oxaliplatin and paclitaxel), posttraumatic nerve injury (e.g., complex regional pain syndrome type 2, amputation), and also as a consequence of a stroke (e.g., central poststroke pain) (Jensen and Finnerup, 2014). Cold-evoked pain is also a common occurrence in diabetic neuropathy.''
 
== Differential Diagnosis ==
 
==Assessment==
Hyperalgesia to various painful stimuli can be assessed, and forms part of [[Quantitative Sensory Testing (QST)|Quantitative Sensory Testing]] (QST).
 
== Treatment ==
'''Acute injuries'''


* '''Primary Hyperalgesia:''' hyperalgesia that occurs at the site of injury and is often a reflection of peripheral sanitations. It occurs as a result of reduced activation threshold and increased responsiveness of silent nociceptors
* The focus is to minimise the development of sustained hyperalgesia
* '''Secondary Hyperalgesia:''' Sensitisation of the spinal nociceptive neurons


==Sub Heading 3==
'''Chronic pain'''


==Resources==
==Resources==

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Introduction[edit | edit source]

IASP definition:

"Increased pain from a stimulus that normally provokes pain."[1]

Hyperalgesia is a clinical term used to described the phenomenon of an increased pain response to a painful stimuli (such as pin prick, pressure, extreme heat/cold). It does not imply a single pain mechanism, but is associated with peripheral sensitisation and central sensitisation.[1]

Hyperalgesia is normal protective response after tissue damage and will usually subside as healing occurs.[2] It may however increase over time in certain conditions, such as neuropathic pain conditions.

The interpretation of the phenomenon of hyperalgesia might change with further research.

Aetiology/Mechanism[edit | edit source]

Hyperalgesia may involve a reduction in nociceptive firing threshold, and an increase in the supra-threshold response.[2]The end result is amplified nociception and an increase in pain intensity.

  • Primary Hyperalgesia: Hyperalgesia that occurs at the site of injury and is often a reflection of peripheral sensitisation. It occurs as a result of reduced activation threshold and increased responsiveness of nociceptors.[2]
  • Secondary Hyperalgesia: Hyperalgesia in an area adjacent to or remote from the site of injury.[2]Maintained by changes in the central processing of sensory information, including sensitisation of the spinal nociceptive neurons and altered descending inhibition.[2]

It is important to remember, that in acute injuries, the finding of hyperalgesia is a normal adaptive response. Since the injured tissue is vulnerable, the nociceptive system adapts by becoming sensitised to ensure tissue protection.[2]In such a case hyperalgesia would be an appropriate shift in pain threshold. It is however possible for this normal response to be exaggerated and does not always reflect the severity of an injury.

If hyperalgesia does however occur long after tissue healing has occurred or in the absence of damaged tissue, it is considered maladaptive.

Risk Factors[edit | edit source]

The following factors may increase the risk of maladaptive hyperalgesia:

  • Diet: There is some evidence from animal studies that a diet rich in omega-3 is associated with stronger heat hyperalgesia.[2]
  • Anxiety and chronic stress: A sustained stated of stress may enhance pain sensitivity.[2]
  • Chronic Inflammation: Excess fat results in chronic release of inflammatory mediators

Conditions[edit | edit source]

Skin injury (e.g., a burn) or inflammation causes innocuous heat to become painful. Hypersensitivity to heat is also a prominent sign in systemic inflammatory disorders such as rheumatoid arthritis. In addition, thermal allodynia and hyperalgesia are common symptoms in patients after injury to the somatosensory nervous system, a condition known as neuropathic pain (Colloca et al., 2017). Conditions associated with neuropathic pain include peripheral nerve injuries, chemotherapy, postherpetic[3]

Cold allodynia and cold hyperalgesia are common signs in various neuropathic conditions, including peripheral neuropathies caused by chemotherapeutic agents (e.g., oxaliplatin and paclitaxel), posttraumatic nerve injury (e.g., complex regional pain syndrome type 2, amputation), and also as a consequence of a stroke (e.g., central poststroke pain) (Jensen and Finnerup, 2014). Cold-evoked pain is also a common occurrence in diabetic neuropathy.

Differential Diagnosis[edit | edit source]

Assessment[edit | edit source]

Hyperalgesia to various painful stimuli can be assessed, and forms part of Quantitative Sensory Testing (QST).

Treatment[edit | edit source]

Acute injuries

  • The focus is to minimise the development of sustained hyperalgesia

Chronic pain

Resources[edit | edit source]

  • bulleted list
  • x

or

  1. numbered list
  2. x

References[edit | edit source]

  1. 1.0 1.1 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 2.7 Sandkuhler J. Models and mechanisms of hyperalgesia and allodynia. Physiological reviews. 2009 Apr;89(2):707-58.
  3. Viana F. Nociceptors: thermal allodynia and thermal pain. InHandbook of clinical neurology 2018 Jan 1 (Vol. 156, pp. 103-119). Elsevier.