Cited by 94Pain Mechanisms and TreatmentsPain Management and TreatmentIon Channels and Receptors

The DOI matches its Crossref record.

Mechanisms of sympathetic pain

McMahon, S B·1991·British Medical Bulletin

Abstract

In some chronic pain states, notably causalgia and reflex sympathetic dystrophy, activity in sympathetic efferent neurones can exacerbate the pain and sympathectomies relieve it. These patients are said to have sympathetically maintained pain (SMP). In normal tissue, activity in postganglionic sympathetic efferents does not produce pain, nor is it capable of activating nociceptive sensory neurones. It can, however, induce modest firing in some mechanoreceptors. SMP is often held to result from a vicious circle of events which include changes in peripheral and central somatosensory processes, and most importantly a positive feedback element in the form of sympathetic efferent neurones which, by activating sensory neurones in the periphery, completes the vicious circle. Several specific hypotheses have been advanced as to the primary pathophysiological cause of pain in these patients. Suggestions, largely deriving from observations on animal models, include: ephaptic transmission, adrenergic receptors on sensory neurones, indirect coupling of sympathetic and sensory neurones, sensitization of nociceptive afferents, and, in the central nervous system, sensitization of dorsal horn neurones. All these suggestions have some supporting evidence, but none are able to adequately explain all the disturbances seen in patients with SMP.

Overview

Integrity signals

Registry

Crossref · 10.1093/oxfordjournals.bmb.a072494

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Findings from the rat model suggest that central sensitization, a process thought to underlie pain hypersensitivity, is an important mechanism that contributes with peripheral sensitization to the association between endometriosis and pain.

    “These rat model findings suggest that central sensitization, a process thought to underlie pain hypersensitivity, is an important mechanism”
  • Physical proximity between sensory and sympathetic fibers within the cysts suggests a functional coupling between them.

    “Furthermore, the physical proximity between sensory and sympathetic fibers within the cysts suggests a functional coupling between them [28,36].”

    From Endocannabinoid involvement in endometriosis. (2010) · cites this paper as [36]

Citations

Cited by

Sorted by citations

Metadata

Authors
McMahon, S. B.
Affiliations
St Thomas' Hospital (GB)
Corresponding author
McMahon, S B
Venue
British Medical Bulletin
Published
1991-07
Volume
47
Issue
3
Pages
584-600
ISSN
  • 0007-1420 (ISSN-L)
  • 1471-8391
OpenAlex
W1906123128
Cited by
93
References
0
Citations by year
2026: 1 · 2024: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2017: 3 · 2016: 1 · 2015: 2 · 2014: 3 · 2013: 3 · 2012: 3
FWCI
1.69
Type
journal article
Language
en
Open access
closed
Locations
  • British Medical Bulletin (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords
sympathetically maintained pain, complex regional pain syndrome, causalgia, nociceptors, ephaptic transmission, pain pathophysiology
MeSH terms
Chronic Disease, Humans, Models, Neurological, Pain, Sympathetic Nervous System

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review