Evidence map›Paper›PMID 17270046›Full record

ReviewOrphanet journal of rare diseases2007

Cone rod dystrophies.

Christian P Hamel

Open access · goldAbstract readReview
In one paragraph

Review in Orphanet journal of rare diseases, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
227citing papers in PubMed, 1 pooled it
6.0field-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

227 citing papers in PubMed, 1 synthesis or guideline pooled it, 438 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Article
  8. Ciliary Defects in Inherited Retinal Diseases.Advanced genetics (Hoboken, N.J.) · 2026
    Review
  9. Case series: The value of fundus autofluorescence in inherited macular disease.Optometry and vision science : official publication of the American Academy of Optometry · 2026
    Article
  10. Article
  11. Article
  12. American journal of ophthalmology case reports · 2025
    Article
  13. Article
  14. Veterinary sciences · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Novel compound heterozygousExperimental and therapeutic medicine · 2025
    Article
  20. "My child can't see"-workup and management of children with low vision: a joint workshop of the AAPOS Low Vision Rehabilitation and Genetic Eye Diseases Committees.Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus · 2025
    Review

167 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.

Christian P HamelInserm U. 583, Physiopathologie et thérapie des déficits sensoriels et moteurs, Institut des Neurosciences de Montpellier, BP 74103, 80 av, Augustin Fliche, 34091 Montpellier Cedex 05, France. hamel@montp.inserm.fr
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cone rod dystrophies (CRDs) (prevalence 1/40,000) are inherited retinal dystrophies that belong to the group of pigmentary retinopathies. CRDs are characterized by retinal pigment deposits visible on fundus examination, predominantly localized to the macular region. In contrast to typical retinitis pigmentosa (RP), also called the rod cone dystrophies (RCDs) resulting from the primary loss in rod photoreceptors and later followed by the secondary loss in cone photoreceptors, CRDs reflect the opposite sequence of events. CRD is characterized by primary cone involvement, or, sometimes, by concomitant loss of both cones and rods that explains the predominant symptoms of CRDs: decreased visual acuity, color vision defects, photoaversion and decreased sensitivity in the central visual field, later followed by progressive loss in peripheral vision and night blindness. The clinical course of CRDs is generally more severe and rapid than that of RCDs, leading to earlier legal blindness and disability. At end stage, however, CRDs do not differ from RCDs. CRDs are most frequently non syndromic, but they may also be part of several syndromes, such as Bardet Biedl syndrome and Spinocerebellar Ataxia Type 7 (SCA7). Non syndromic CRDs are genetically heterogeneous (ten cloned genes and three loci have been identified so far). The four major causative genes involved in the pathogenesis of CRDs are ABCA4 (which causes Stargardt disease and also 30 to 60% of autosomal recessive CRDs), CRX and GUCY2D (which are responsible for many reported cases of autosomal dominant CRDs), and RPGR (which causes about 2/3 of X-linked RP and also an undetermined percentage of X-linked CRDs). It is likely that highly deleterious mutations in genes that otherwise cause RP or macular dystrophy may also lead to CRDs. The diagnosis of CRDs is based on clinical history, fundus examination and electroretinogram. Molecular diagnosis can be made for some genes, genetic counseling is always advised. Currently, there is no therapy that stops the evolution of the disease or restores the vision, and the visual prognosis is poor. Management aims at slowing down the degenerative process, treating the complications and helping patients to cope with the social and psychological impact of blindness.

Indexed as

ATP-Binding Cassette TransportersCorneal Dystrophies, HereditaryDiagnosis, DifferentialDiagnostic Techniques, OphthalmologicalGenetic TestingHomeodomain ProteinsHumansIntermediate Filament ProteinsMembrane GlycoproteinsMutationNerve Tissue ProteinsPeripherinsRetinitis PigmentosaTrans-ActivatorsTreatment OutcomeABCA4 protein, humanATP-Binding Cassette Transporterscone rod homeobox proteinHomeodomain ProteinsIntermediate Filament ProteinsMembrane GlycoproteinsNerve Tissue ProteinsPeripherinsTrans-Activators

Identifiers

PMID17270046
PMCPMC1808442
OpenAlexW2166621376

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.