Evidence map›Paper›PMID 19655104›Full record

ReviewHandbook of experimental pharmacology2009

Visceral pain: the neurophysiological mechanism.

Jyoti N Sengupta

Abstract readReview
In one paragraph

Review in Handbook of experimental pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
31.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

90 citing papers in PubMed, 190 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Opioid analgesics for sedation-based gastrointestinal endoscopy.World journal of gastrointestinal pharmacology and therapeutics · 2025
    Review
  12. Article
  13. Article
  14. The Acute Abdomen: Structured Diagnosis and Treatment.Deutsches Arzteblatt international · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Jyoti N SenguptaDivision of Gastroenterology and Hepatology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53051, USA. sengupta@mcw.edu
Medical College of Wisconsin · US

Funding

Mechanisms of Esophageal PainR01DK062312 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI SENGUPTA, JYOTI N · 2004 to 2008
$1.2M
Neural Plasticity and the Development of Overlapping Pelvic PainR56DK089493 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI BANERJEE, BANANI B, SENGUPTA, JYOTI N · 2010 to 2010
$543k
NIDDK NIH HHS R01 DK062312NIDDK NIH HHS R01 DK062312-A2NIDDK NIH HHS R56 DK089493
6 · The paper itself

Abstract

The mechanism of visceral pain is still less understood compared with that of somatic pain. This is primarily due to the diverse nature of visceral pain compounded by multiple factors such as sexual dimorphism, psychological stress, genetic trait, and the nature of predisposed disease. Due to multiple contributing factors there is an enormous challenge to develop animal models that ideally mimic the exact disease condition. In spite of that, it is well recognized that visceral hypersensitivity can occur due to (1) sensitization of primary sensory afferents innervating the viscera, (2) hyperexcitability of spinal ascending neurons (central sensitization) receiving synaptic input from the viscera, and (3) dysregulation of descending pathways that modulate spinal nociceptive transmission. Depending on the type of stimulus condition, different neural pathways are involved in chronic pain. In early-life psychological stress such as maternal separation, chronic pain occurs later in life due to dysregulation of the hypothalamic-pituitary-adrenal axis and significant increase in corticotrophin releasing factor (CRF) secretion. In contrast, in early-life inflammatory conditions such as colitis and cystitis, there is dysregulation of the descending opioidergic system that results excessive pain perception (i.e., visceral hyperalgesia). Functional bowel disorders and chronic pelvic pain represent unexplained pain that is not associated with identifiable organic diseases. Often pain overlaps between two organs and approximately 35% of patients with chronic pelvic pain showed significant improvement when treated for functional bowel disorders. Animal studies have documented that two main components such as (1) dichotomy of primary afferent fibers innervating two pelvic organs and (2) common convergence of two afferent fibers onto a spinal dorsal horn are contributing factors for organ-to-organ pain overlap. With reports emerging about the varieties of peptide molecules involved in the pathological conditions of visceral pain, it is expected that better therapy will be achieved relatively soon to manage chronic visceral pain.

Indexed as

Action PotentialsAfferent PathwaysAnalgesicsAnimalsBehavior, AnimalDisease Models, AnimalHumansHyperalgesiaMechanotransduction, CellularPainPain MeasurementPain ThresholdReceptors, NeurotransmitterSensory Receptor CellsVisceraAnalgesicsReceptors, Neurotransmitter

Identifiers

PMID19655104
PMCPMC3156094
OpenAlexW1548699817

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.