Evidence map›Paper›PMID 29649050›Full record

ArticleOtology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology2018

Temporal Bone Histopathology in Cockayne Syndrome.

Ophir Handzel, Joseph B Nadol

Abstract readCase Reports
In one paragraph

Article in Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 53% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
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

2 authors at 2 institutions in 2 countries.

Ophir HandzelCochlear Implant Center, Department of Otolaryngology/Head, Neck & Maxillofacial Surgery, Tel-Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel-Aviv, Israel.
Joseph B NadolOtopathology Laboratory, Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts.
Massachusetts Eye and Ear Infirmary · USTel Aviv Sourasky Medical Center · IL

Funding

NIDCD National Temporal Bone, Hearing and Balance Pathology Resource RegistryU24DC013983 · NIDCD · MASSACHUSETTS EYE AND EAR INFIRMARY · PI LIBERMAN, M. CHARLES, QUESNEL, ALICIA M · 2014 to 2025
$6.5M
NIDCD NIH HHS U24 DC013983
6 · The paper itself

Abstract

: Cockayne syndrome (CS) is a rare autosomal recessive syndrome resulting in defective DNA repair. Its features include cachectic dwarfism, hearing loss, skin hypersensitivity to sunlight, premature aging, and dementia. Presented is a right temporal bone of a patient who died at the age of 29 years. The clinical course was compatible with type 1 CS, the classical form. Homozygous missense variant in the ERCC6 gene (Excision Repair Cross-Complementation group 6) was found, compatible with CS complementation group B. Five years before his death he complained of tinnitus. An audiogram 3 and a 1/2 years before his death demonstrated a moderate symmetrical sensorineural hearing loss at 2 to 8 kHz. The speech reception threshold was 20 dB, and the word recognition score was 100% on the right.Histopathology revealed a near normal population of inner hair cells except in the basal 5 mm of the cochlea, and mild loss of outer hair cells particularly at the base of the cochlea. Severe atrophy of the spiral ligament and atrophy of stria vascularis and spiral prominence was present. There was loss of Claudius cells, outer sulcus cells, and mesenchymal cells on the scala tympani side of the basilar membrane and loss of cellularity of the limbus. There was a moderate loss of Scarpa's and spiral ganglion neurons, with the most severe loss in the basal segment. The vestibular neuro-epithelium was nearly intact, with the exception of mild loss in the saccule. The vestibular perilymphatic, and to a lesser extent endolymphatic spaces, were filled with filamentous material and osteoid. The patient had better hearing and a larger complement of neurons compared with the few published case reports.Neurodegenerative symptoms are likely attributed to the effect of intramitochondrial reactive oxygen species. The pathogenesis of hearing loss in CS may shed light on other causes of hearing loss, such as that induced by noise.

Indexed as

AdultAutopsyCochleaCockayne SyndromeHearing Loss, SensorineuralHumansMaleTemporal Bone

Identifiers

PMID29649050
PMCPMC5940547
OpenAlexW2797067548

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.