Usher syndrome has been historically categorized into one of three classical types based on the patient phenotype. However, the vestibular phenotype does not infallibly predict which Usher genes are mutated. Conversely, the Usher syndrome genotype is not sufficient to reliably predict vestibular function. Here we present a characterization of the vestibular phenotype of 90 patients with clinical presentation of Usher syndrome (59 females), aged 10.9 to 75.5 years, with genetic variants in eight Usher syndromic genes and expand the description of atypical Usher syndrome. We identified unexpected horizontal semicircular canal reactivity in response to caloric and rotational stimuli in 12.5% (3 of 24) and 41.7% (10 of 24), respectively, of our USH1 cohort. These findings are not consistent with the classical phenotypic definition of vestibular areflexia in USH1. Similarly, 17% (6 of 35) of our cohort with USH2A mutations had saccular dysfunction as evidenced by absent cervical vestibular evoked myogenic potentials in contradiction to the classical assumption of normal vestibular function. The surprising lack of consistent genotypic to vestibular phenotypic findings as well as no clear vestibular phenotypic patterns among atypical USH cases, indicate that even rigorous vestibular phenotyping data will not reliably differentiate the three USH types.
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http://dx.doi.org/10.1111/cge.13868 | DOI Listing |
Orphanet J Rare Dis
January 2025
Ophthalmology Department, Centro Hospitalar e Universitário de Coimbra (CHUC), Hospitais da Universidade de Coimbra (HUC), ULS Coimbra, Praceta Prof. Mota Pinto, 3000-075, Coimbra, Portugal.
Background: Syndromic genetic disorders affecting vision can also cause hearing loss, and Usher syndrome is by far the most common etiology. However, many other conditions can present dual sensory impairment. Accurate diagnosis is essential for providing patients with genetic counseling, prognostic information, and appropriate resources.
View Article and Find Full Text PDFJ Sleep Res
December 2024
Department of Otorhinolaryngology, Radboud University Medical Center, Nijmegen, The Netherlands.
This study aimed to improve our understanding of sleep problems as a comorbidity of hereditary deaf-blindness due to Usher syndrome type 2a. Fifteen patients with Usher syndrome type 2a with a conclusive genetic diagnosis and 15 unaffected controls participated in comprehensive sleep and activity assessments for 2 weeks, using the MotionWatch 8 actigraph and consensus sleep diary. Various sleep parameters including sleep opportunity window, sleep latency, sleep efficiency, and self-reported sleep quality were analysed.
View Article and Find Full Text PDFProg Retin Eye Res
December 2024
Department of Ophthalmology, Leiden University Medical Center, Leiden, the Netherlands; Department of Ophthalmology, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Retinitis pigmentosa (RP) is a progressive inherited retinal dystrophy, characterized by the degeneration of photoreceptors, presenting as a rod-cone dystrophy. Approximately 20-30% of patients with RP also exhibit extra-ocular manifestations in the context of a syndrome. This manuscript discusses the broad spectrum of syndromes associated with RP, pathogenic mechanisms, clinical manifestations, differential diagnoses, clinical management approaches, and future perspectives.
View Article and Find Full Text PDFEur J Hum Genet
December 2024
Molecular, Cellular, and Genomic Biomedicine Group, IIS-La Fe, Valencia, Spain.
The AGBL5 gene encodes for the Cytoplasmic Carboxypeptidase 5 (CCP5), an α-tubulin deglutamylase that cleaves the γ-carboxyl-linked branching point of glutamylated tubulin. To date, pathogenic variants in AGBL5 have been associated only with isolated retinitis pigmentosa (RP). Hearing loss has not been reported in AGBL5-caused retinal disease.
View Article and Find Full Text PDFDev Med Child Neurol
December 2024
Edinburgh Clinical Trials Unit, Usher Institute, University of Edinburgh, Edinburgh, UK.
Aim: To extend the findings of a previous clinical trial suggesting combined abacavir (ABC), lamivudine (3TC), and zidovudine (AZT) reduces type I interferon (IFN) signalling in Aicardi-Goutières syndrome (AGS).
Method: This was an open label, non-placebo-controlled phase II clinical trial (NCT04731103) in patients less than 16 years with any of five AGS genotypes. The effect of ABC or 3TC individually, or of combined ABC + 3TC + AZT, on IFN-stimulated gene (ISG) expression (primary outcome) and IFN-alpha protein (secondary outcome) in blood was assessed.
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