| Literature DB >> 25895915 |
Gali Heimer1, Yair Sadaka2, Lori Israelian3, Ariel Feiglin4, Alessandra Ruggieri2, Christian R Marshall2, Stephen W Scherer2, Esther Ganelin-Cohen5, Dina Marek-Yagel6, Michal Tzadok5, Andreea Nissenkorn5, Yair Anikster7, Berge A Minassian8, Bruria Ben Zeev9.
Abstract
We describe the molecular basis of a distinctive syndrome characterized by infantile stress-induced episodic weakness, ataxia, and sensorineural hearing loss, with permanent areflexia and optic nerve pallor. Whole exome sequencing identified a deleterious heterozygous c.2452 G>A, p.(E818K) variant in the ATP1A3 gene and structural analysis predicted its protein-destabilizing effect. This variant has not been reported in context with rapid-onset dystonia parkinsonism and alternating hemiplegia of childhood, the 2 main diseases associated with ATP1A3. The clinical presentation in the family described here differs categorically from these diseases in age of onset, clinical course, cerebellar over extrapyramidal movement disorder predominance, and peripheral nervous system involvement. While this paper was in review, a highly resembling phenotype was reported in additional patients carrying the same c.2452 G>A variant. Our findings substantiate this variant as the cause of a unique inherited autosomal dominant neurologic syndrome that constitutes a third allelic disease of the ATP1A3 gene.Entities:
Keywords: CAPOS; alternating hemiplegia of childhood; deafness; intermittent weakness; rapid-onset dystonia parkinsonism
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Year: 2015 PMID: 25895915 DOI: 10.1177/0883073815579708
Source DB: PubMed Journal: J Child Neurol ISSN: 0883-0738 Impact factor: 1.987