Evidence map›Paper›PMID 32219415›Full record

ReviewBritish medical bulletin2020

Understanding the genetic basis of congenital insensitivity to pain.

Ichrak Drissi, William Aidan Woods, Christopher Geoffrey Woods

Open access · hybridAbstract readReview
In one paragraph

Review in British medical bulletin, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Thalamic CGRP neurons define a spinothalamic pathway for affective pain.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Pain Management with Natural Products: Neurophysiological Insights.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Review
  12. Homozygosity for a RareInternational journal of molecular sciences · 2024
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  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

3 authors at 2 institutions in 1 country.

Ichrak DrissiCambridge Institute for Medical Research, University of Cambridge, Cambridge Biomedical Campus, The Keith Peters Building, Hills Road, Cambridge CB2 0XY, UK.
William Aidan WoodsSchool of Medicine, David Weatherall building, University Road, Keele University, Staffordshire ST5 5BG, UK.
Christopher Geoffrey WoodsCambridge Institute for Medical Research, University of Cambridge, Cambridge Biomedical Campus, The Keith Peters Building, Hills Road, Cambridge CB2 0XY, UK.
University of Cambridge · GBKeele University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

INTRODUCTION OR

backgroundCongenital insensitivity to pain (CIP) is caused by extremely rare Mendelian genetic disorders. CIP individuals demonstrate the unexpectedly severe consequences of painlessness. Although only a small number of causative conditions and genes are known, most have led to profound insights into human nociception. CIP gene discovery is catalyzing the manufacture of completely new classes of analgesics, and these are needed as alternatives to synthetic highly potent opioids. SOURCES OF DATA: Pubmed.gov peer-reviewed journal articles and reviews. AREAS OF AGREEMENT: The importance of nerve growth factor-tropomyosin receptor kinase A (NGF-TRKA) signalling for nociceptor genesis and subsequent pain sensing.New analgesics can be generated from knowledge of the NGF-TRKA nociceptor pathway.Increased susceptibility to Staphylococcus aureus infection is a consequence of deficient NGF-TRKA signalling.Mutations in the voltage-gated sodium channels SCN9A and SCN11A can cause congenital painlessness, and in contradistinction, other mutations can cause episodic neuropathic pain. SCN9A/Nav1.7 is an analgesic target. SCN11A/Nav1.9 is unlikely to be an analgesic target.There are further Mendelian causes of painlessness to be discovered. AREAS OF CONTROVERSY: Which NGF-TRKA intracellular signalling pathways operate in nociceptor development and which in post-natal pain sensing?Why have no clinically effective Nav1.7 antagonist been generated? SCN9A-CIP causes analgesia, at least in part, through endogenous opioids.Why do all CIP phenotypes involve a complete loss of all types of nociception? AREAS TIMELY FOR DEVELOPING RESEARCH: PRDM12 as an analgesic target.Discovery of the function and analgesic potential of new CIP genes.Can NGF-TRKA be used in the treatment of S. aureus?

Indexed as

Drug DiscoveryNociceptionHumansNerve Tissue ProteinsPain Insensitivity, CongenitalPharmacogenomic TestingSignal TransductionNerve Tissue Proteinscongenital painlessnessnociceptor developmentnociceptor functionpain genes

Identifiers

PMID32219415
PMCPMC7227775
OpenAlexW3013271261

What OpenQuestion holds

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LicenceCC BY-NC
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.