| Literature DB >> 31136090 |
Alessandro Ferretti1, Sabina Barresi2, Marina Trivisano1, Andrea Ciolfi2, Maria L Dentici2, Francesca C Radio1, Federico Vigevano1, Marco Tartaglia2, Nicola Specchio1.
Abstract
POGZ (# 614787) encodes a multidomain nuclear protein involved in transcriptional regulation and its defective function has been recently associated with a syndromic neurodevelopmental disorder, known as White-Sutton syndrome (# 616364). While originally epileptic seizures were unreported, it seems that epilepsy represents a recurrent feature in affected subjects. Few data, however, are available on electroclinical features of POGZ-related epilepsy. We report a 5-year-old girl with a de novo inactivating POGZ mutation with a complex neurological phenotype characterized by hypotonia, severe developmental delay, and paroxysmal epileptic and nonepileptic events. Comparing this patient with the previously reported nine cases exhibiting epilepsy as associated feature, we detected that epilepsy onset is mostly during infancy (1-4 years of age), with both focal and generalized seizures. EEGs reveal that epileptic abnormalities mainly are localized in the frontal regions, and seizure control might be reached with one or multiple antiepileptic drugs. Besides dysmorphic features and other comorbidities (microcephaly, intellectual disability, absent speech, sensorineural hearing loss, and autistic spectrum disorder) major brain MR features include cortical and cerebellar atrophy, delayed myelination, and brainstem hypoplasia. Although the small number of patients reported, we were able to delineate primary electroclinical epileptic phenotype related to POGZ mutations. This would be crucial for an early identification and management of the condition.Entities:
Keywords: zzm321990POGZ; White-Sutton syndrome; children; epilepsy
Mesh:
Substances:
Year: 2019 PMID: 31136090 DOI: 10.1002/ajmg.a.61206
Source DB: PubMed Journal: Am J Med Genet A ISSN: 1552-4825 Impact factor: 2.578