Childhood-onset progressive dystonia associated with pathogenic truncating variants in CHD8.
Diane DoummarMarco TrevenLeila QebiboDavid DevosJamal GhoumidClaudia RavelliGottfried KranzMartin KrennDiane DemaillyLaura CifJean-Baptiste DavionFritz ZimprichLydie BurglenMichael ZechPublished in: Annals of clinical and translational neurology (2021)
Originally described as a risk factor for autism, CHD8 loss-of-function variants have recently been associated with a wider spectrum of neurodevelopmental abnormalities. We further expand the CHD8-related phenotype with the description of two unrelated patients who presented with childhood-onset progressive dystonia. Whole-exome sequencing conducted in two independent laboratories revealed a CHD8 nonsense variant in one patient and a frameshift variant in the second. The patients had strongly overlapping phenotypes characterized by generalized dystonia with mild-to-moderate neurodevelopmental comorbidity. Deep brain stimulation led to clinical improvement in both cases. We suggest that CHD8 should be added to the growing list of neurodevelopmental disorder-associated genes whose mutations can also result in dystonia-dominant phenotypes.
Keyphrases
- deep brain stimulation
- parkinson disease
- obsessive compulsive disorder
- multiple sclerosis
- end stage renal disease
- early onset
- copy number
- ejection fraction
- newly diagnosed
- chronic kidney disease
- autism spectrum disorder
- early life
- prognostic factors
- peritoneal dialysis
- genome wide
- intellectual disability
- congenital heart disease
- dna methylation
- single cell
- gene expression
- young adults
- childhood cancer