Evidence map›Paper›PMID 22356223›Full record

ReviewClinical drug investigation2012

Pain mechanisms in patients with chronic pain.

Diego Fornasari

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical drug investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Development, refinement, and validation of an equine musculoskeletal pain scale.Frontiers in pain research (Lausanne, Switzerland) · 2023
    Article
  11. Article
  12. Article
  13. Application of Bioinformatics Methods to Identify Key Genes and Functions in Chronic Pelvic Pain.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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.

Diego FornasariDepartment of Pharmacology, School of Medicine, Università degli Studi di Milano and CNR-Institute of Neuroscience, Milan, Italy. diego.fornasari@unimi.it
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms involved in the development of chronic pain are varied and complex. Pain processes are plastic and unrelieved pain may lead to changes in the neural structure involved in pain generation. Nociceptive pain announces the presence of a potentially damaging stimulus that occurs when noxious stimuli activate primary afferent neurons. Neuropathic pain is initiated or caused by a primary lesion or dysfunction in the nervous system resulting from trauma, infection, ischaemia, cancer or other causes such as chemotherapy. The exact mechanisms involved in the pathophysiology of chronic pain are not well understood, but rapid and long-term changes are thought to occur in parts of the central nervous system that are involved in the transmission and modulation of pain following injury. Peripheral and central sensitization of sensory nerve fibres are the primary reasons for hypersensitivity to pain after injury, and mainly occur in inflammatory and neuropathic pain. During these processes the sensation of pain is enhanced as a result of changes in the environment, the nerve fibres and modifications of the functional properties and the genetic programme of primary and secondary afferent neurons. Non-steroidal anti-inflammatory drugs and opioid analgesics are two of the most common classes of drugs used for the treatment of pain. Response to drug treatment shows significant interindividual variability and can lead to side effects. The neurobiological mechanisms that cause pain may account for the different types of pain observed. Identification of these mechanisms may allow us to move from an empirical therapeutic approach to one that it is specifically targeted at the particular mechanisms of the type of pain experienced by an individual patient.

Indexed as

Analgesics, OpioidAnimalsAnti-Inflammatory Agents, Non-SteroidalChronic PainHumansNeoplasmsNervous System DiseasesNeuralgiaPain ManagementPain MeasurementAnalgesics, OpioidAnti-Inflammatory Agents, Non-Steroidal

Identifiers

PMID22356223
OpenAlexW1979126890

What OpenQuestion holds

Textmetadata
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.