Genotypic and phenotypic characteristics of juvenile/adult onset vanishing white matter: a series of 14 Chinese patients.


Journal

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
ISSN: 1590-3478
Titre abrégé: Neurol Sci
Pays: Italy
ID NLM: 100959175

Informations de publication

Date de publication:
Aug 2022
Historique:
received: 13 01 2022
accepted: 14 03 2022
pubmed: 8 4 2022
medline: 6 8 2022
entrez: 7 4 2022
Statut: ppublish

Résumé

Vanishing white matter (VWM) is one of the most prevalent leukoencephalopathies and is caused by recessive mutations in gene eIF2B1-5. The onset may vary from an antenatal disorder that is rapidly fatal to an adult-onset disorder with chronic progressive deterioration. Based on a comprehensive study of 14 juvenile/adult patients diagnosed in our department as well as a review of 71 previously reported cases of genetically confirmed juvenile/adult-onset VWM since 2001, we attempted to delineate the clinical symptoms, disease evolution, episodic aggravation, associated symptoms, MRI findings and genotypic characteristics of adult VWM. The onset age of neuropsychiatric symptoms was 23.4 ± 10.6 years, and the mean follow-up time was 8.1 ± 4.8 years. Major clinical symptoms included headache, epilepsy, cognitive decline, cerebellar ataxia, and urinary disturbances. Episodic aggravation was found in 42.9% of the patients in our series. Molecular studies revealed fourteen novel missense mutations. Diffuse abnormal signals characterized by T1-weighted hypointensity and T2-weighted hyperintensity were observed in the supratentorial white matter. The symmetrical leukoencephalopathy must be considered in patients of any age with premature ovarian failure or optic neuropathy. The VWM disease spectrum consists of characteristic imaging findings in combination with extremely wide variability in VWM patients.

Sections du résumé

BACKGROUND BACKGROUND
Vanishing white matter (VWM) is one of the most prevalent leukoencephalopathies and is caused by recessive mutations in gene eIF2B1-5. The onset may vary from an antenatal disorder that is rapidly fatal to an adult-onset disorder with chronic progressive deterioration.
METHODS METHODS
Based on a comprehensive study of 14 juvenile/adult patients diagnosed in our department as well as a review of 71 previously reported cases of genetically confirmed juvenile/adult-onset VWM since 2001, we attempted to delineate the clinical symptoms, disease evolution, episodic aggravation, associated symptoms, MRI findings and genotypic characteristics of adult VWM.
RESULTS RESULTS
The onset age of neuropsychiatric symptoms was 23.4 ± 10.6 years, and the mean follow-up time was 8.1 ± 4.8 years. Major clinical symptoms included headache, epilepsy, cognitive decline, cerebellar ataxia, and urinary disturbances. Episodic aggravation was found in 42.9% of the patients in our series. Molecular studies revealed fourteen novel missense mutations. Diffuse abnormal signals characterized by T1-weighted hypointensity and T2-weighted hyperintensity were observed in the supratentorial white matter.
CONCLUSIONS CONCLUSIONS
The symmetrical leukoencephalopathy must be considered in patients of any age with premature ovarian failure or optic neuropathy. The VWM disease spectrum consists of characteristic imaging findings in combination with extremely wide variability in VWM patients.

Identifiants

pubmed: 35389136
doi: 10.1007/s10072-022-06011-0
pii: 10.1007/s10072-022-06011-0
doi:

Substances chimiques

Eukaryotic Initiation Factor-2B 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

4961-4977

Informations de copyright

© 2022. Fondazione Società Italiana di Neurologia.

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Auteurs

Yuting Ren (Y)

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.

Xueying Yu (X)

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.

Bin Chen (B)

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.

Hefei Tang (H)

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.

Songtao Niu (S)

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.

Xingao Wang (X)

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.

Hua Pan (H)

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.

Zaiqiang Zhang (Z)

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China. ttyy0142011@126.com.

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