Referred pain from somatic and visceral structures

Procacci, Paolo; Maresca, Marco

doi:10.1007/s11916-999-0032-y

Cited by 27 publications

(19 citation statements)

References 17 publications

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“…This is supported by recent evidence that sympathetic blockade at the ganglion impar dramatically improves daily, unprovoked pain, but not provoked pain, among women with generalized vulvodynia (Abstract, District VII Annual clinical meeting ACOG 2005, in submission). In addition, coexistence of vaginismus supports greater CNS involvement among treatment failures, as the pelvic floor hypertonicity occurs via central neurogenic inflammation (27,31,32). It has been reported that vestibulectomy specimens have neural hyperplasia as compared with controls (86,87).…”

Section: Mechanistic Approachmentioning

confidence: 99%

“…For example, experimentally induced inflammation of the colon or uterus produces inflammation not only in the intentionally targeted organ but also in the bladder and the skin and animals with endometriosis have reduced bladder capacity, vaginal hyperalgesia, and increased visceral pain (28)(29)(30)(31)(32). This process requires intact CNS connections and is mediated by neurogenic inflammation; visceral and somatic pathology can be induced by inflammatory CNS lesions alone, and both referred pain and pathology can be prevented by surgically interrupting the neural connections (26,29,(30)(31)(32)(33).…”

Section: Coexistence Of Other Pain Syndromementioning

confidence: 99%

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Vulvodynia: New Thoughts on a Devastating Condition

Gunter

2007

Obstetrical &Amp; Gynecological Survey

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Section: Mechanistic Approachmentioning

confidence: 99%

Section: Coexistence Of Other Pain Syndromementioning

confidence: 99%

Vulvodynia: New Thoughts on a Devastating Condition

Gunter

2007

Obstetrical &Amp; Gynecological Survey

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“…In visceral pain conditions, neurogenic infl ammation seems to be a factor in the mechanism of referred pain [120] . For example, pain from myocardial infarction may sometimes induce a left seapulohumoral periarthritis, an infl ammatory condition in the referred zone [121] .…”

Section: Neurogenic Infl Ammation In Pancreatitis and Its Relationshimentioning

confidence: 99%

Role of Neurogenic Inflammation in Pancreatitis and Pancreatic Pain

Vera–Portocarrero¹,

Westlund²

2005

Neurosignals

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Pain arising from pancreatic diseases can become chronic and difficult to treat. There is a paucity of knowledge regarding the mechanisms that sensitize neural pathways that transmit noxious information from visceral organs. In this review, neurogenic inflammation is presented as a possible amplifier of the noxious signal from peripheral organs including the pancreas. The nerve pathways that transmit pancreatic pain are also reviewed as a conduit of the amplified signals. It is likely that components of these visceral pain pathways can also be sensitized after neurogenic inflammation.

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“…The afferent barrage from the internal organ is likely to activate a number of viscerosomatic reflexes toward the periphery, responsible for both the increased sensitivity and the modification of thickness and consistency of deep body wall tissues [2,17,34]. Further experimental studies on other animal models of the condition (such as the rat model of referred muscle hyperalgesia from uterine inflammation) [49,50] will hopefully help to clarify this issue.…”

Section: Pathophysiologic Aspectsmentioning

confidence: 99%

“…However, several forms of referred pain from somatic structures are also very commonly detected in the clinical setting, such as referred pain from other muscles and referred pain from joints [2]. Whatever the origin of the symptom, in the referred zones physical and instrumental procedures often reveal a condition of secondary hyperalgesia (increased sensitivity to pain) in skeletal muscles, which arises in relation to the algogenic pathology.…”

mentioning

confidence: 99%

Referred muscle pain: Clinical and pathophysiologic aspects

Vecchiet

Giamberardino

1999

Current Review of Pain

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Referred pain, that is, pain perceived in an area other than that in which the noxious stimulation takes place, is very frequent in the clinical setting. There are various forms of referred muscle pain from viscera and from somatic structures. Examples of the latter are referred pain from one muscle to another muscle (as in myofascial pain syndromes) and referred pain from joints (as in osteoarthritis of the knee). Whatever the origin of the symptom, a condition of secondary hyperalgesia very often takes place in the referred zones, together with trophic tissue changes. Referred muscle pain from viscera without hyperalgesia is explained on the basis of the convergence of visceral and somatic afferent fibers on the same central neurons. Referred muscle pain from viscera with hyperalgesia is not completely understood; it is hypothesized that it is due to both central (sensitization process) and peripheral (intervention of reflex arcs) mechanisms. Referred muscle pain from other muscles or from joints is not easily explained by the mechanism of "central convergence" in its original form, because in dorsal horn neurons there is little convergence from deep tissues. It has been proposed that convergent connections from deep tissues to dorsal horn neurons are not present from the beginning but are opened by nociceptive input from skeletal muscle, and referral to myotomes outside the lesion is due to a spread of central sensitization to adjacent spinal segments.

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Referred pain from somatic and visceral structures

Cited by 27 publications

References 17 publications

Vulvodynia: New Thoughts on a Devastating Condition

Vulvodynia: New Thoughts on a Devastating Condition

Role of Neurogenic Inflammation in Pancreatitis and Pancreatic Pain

Referred muscle pain: Clinical and pathophysiologic aspects

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