Visceral Pain: Difference between revisions

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Visceral pain is initially described as vague, central sensation felt anterior or posterior, accompanied by various neurovegetative symptoms such as malaise, nausea, sweating, palour , anxiety, and sense of impending doom (โ€˜true visceral painโ€™). Eventually this subsides, and is followed by a variety of symptoms and signs perceived in somatic areas receiving the same innervation. Skin, subcutis and muscle are all involved. Initially, the ''symptoms'' of pain rather than pain itself is felt. As time progresses, signs start to develop. The muscle layer is earliest and most commonly involved layer. However, the skin and subcutaneous layers are also commonly involved with hyperalgesia, and sudomotor signs. These symptoms and signs can persist even when the visceral insult has resolved. These symptoms and signs may also, in turn, influence visceral symptoms.
Visceral pain is initially described as vague, central sensation felt anterior or posterior, accompanied by various neurovegetative symptoms such as malaise, nausea, sweating, palour , anxiety, and sense of impending doom (โ€˜true visceral painโ€™). Eventually this subsides, and is followed by a variety of symptoms and signs perceived in somatic areas receiving the same innervation. Skin, subcutis and muscle are all involved. Initially, the ''symptoms'' of pain rather than pain itself is felt. As time progresses, signs start to develop. The muscle layer is earliest and most commonly involved layer. However, the skin and subcutaneous layers are also commonly involved with hyperalgesia, and sudomotor signs. These symptoms and signs can persist even when the visceral insult has resolved. These symptoms and signs may also, in turn, influence visceral symptoms.


{| class="wikitable"
|+From Cervero et al 1999<ref>{{#pmid:10382712}}</ref>
|-
! Symptoms & Signs!! Neurobiology
|-
| Not evoked from all viscera || Not all viscera are innervated by sensory receptors.
|-
| Not linked to injury|| Functional properties of visceral sensory afferents
|-
| Referred to body wall|| Viscerosomatic convergence in central pain pathways
|-
| Diffuse and poorly localised|| Few sensory visceral afferents. Extensive divergence in central nervous system
|-
| Intense motor and autonomic reactions|| Mainly a warning system, with substantial capacity for amplification
|}
==References==
[[Category:Pain Physiology]]
[[Category:Pain Physiology]]
[[Category:Abdominal Wall]]
[[Category:Abdominal Wall]]

Revision as of 19:18, 13 July 2020

Vagal afferents convey predominantly physiological information, while spinal afferents convey noxious stimuli.

There are likely to be three types of nociceptive sensory receptors: High threshold noxious, Low threshold innocuous to noxious, while some are silent and recruited by tissue injury and inflammation.

All can be sensitized, and drive central sensitisation that can persist even after the initial insult has resolved. Damage and inflammation also affects normal motility and secretion, producing changes to the nociceptor environment. While ascending pathways include the spinothalamic tract, the dorsal column is more important in nociceptive transmission. Ascending tracts synapse at the thalamus, limbic centres, and the somatosensory cortex. There is no somatotropic representation in the cortex. Pain is represented in the secondary somatosensory cortex. Visceral pain elicits nausea and hypotension, the opposite to somatic pain.

Peripheral sensitisation can occur, but the mechanisms differ from cutaneous sensitisation. Functional visceral disturbance can persist even after the initial insult has resolved. While with central sensitisation, NMDA receptors are likely to play significant role.

Visceral pain is initially described as vague, central sensation felt anterior or posterior, accompanied by various neurovegetative symptoms such as malaise, nausea, sweating, palour , anxiety, and sense of impending doom (โ€˜true visceral painโ€™). Eventually this subsides, and is followed by a variety of symptoms and signs perceived in somatic areas receiving the same innervation. Skin, subcutis and muscle are all involved. Initially, the symptoms of pain rather than pain itself is felt. As time progresses, signs start to develop. The muscle layer is earliest and most commonly involved layer. However, the skin and subcutaneous layers are also commonly involved with hyperalgesia, and sudomotor signs. These symptoms and signs can persist even when the visceral insult has resolved. These symptoms and signs may also, in turn, influence visceral symptoms.

From Cervero et al 1999[1]
Symptoms & Signs Neurobiology
Not evoked from all viscera Not all viscera are innervated by sensory receptors.
Not linked to injury Functional properties of visceral sensory afferents
Referred to body wall Viscerosomatic convergence in central pain pathways
Diffuse and poorly localised Few sensory visceral afferents. Extensive divergence in central nervous system
Intense motor and autonomic reactions Mainly a warning system, with substantial capacity for amplification

References

  1. โ†‘ Cervero & Laird. Visceral pain. Lancet (London, England) 1999. 353:2145-8. PMID: 10382712. DOI.