Literature DB >> 25864721

GRIN1 mutations cause encephalopathy with infantile-onset epilepsy, and hyperkinetic and stereotyped movement disorders.

Chihiro Ohba1,2, Masaaki Shiina3, Jun Tohyama4, Kazuhiro Haginoya5, Tally Lerman-Sagie6, Nobuhiko Okamoto7, Lubov Blumkin6, Dorit Lev6, Souichi Mukaida8, Fumihito Nozaki9, Mitsugu Uematsu10, Akira Onuma11, Hirofumi Kodera1, Mitsuko Nakashima1, Yoshinori Tsurusaki1, Noriko Miyake1, Fumiaki Tanaka2, Mitsuhiro Kato12, Kazuhiro Ogata3, Hirotomo Saitsu1, Naomichi Matsumoto1.   

Abstract

OBJECTIVE: Recently, de novo mutations in GRIN1 have been identified in patients with nonsyndromic intellectual disability and epileptic encephalopathy. Whole exome sequencing (WES) analysis of patients with genetically unsolved epileptic encephalopathies identified four patients with GRIN1 mutations, allowing us to investigate the phenotypic spectrum of GRIN1 mutations.
METHODS: Eighty-eight patients with unclassified early onset epileptic encephalopathies (EOEEs) with an age of onset <1 year were analyzed by WES. The effect of mutations on N-methyl-D-aspartate (NMDA) receptors was examined by mapping altered amino acids onto three-dimensional models.
RESULTS: We identified four de novo missense GRIN1 mutations in 4 of 88 patients with unclassified EOEEs. In these four patients, initial symptoms appeared within 3 months of birth, including hyperkinetic movements in two patients (2/4, 50%), and seizures in two patients (2/4, 50%). Involuntary movements, severe developmental delay, and intellectual disability were recognized in all four patients. In addition, abnormal eye movements resembling oculogyric crises and stereotypic hand movements were observed in two and three patients, respectively. All the four patients exhibited only nonspecific focal and diffuse epileptiform abnormality, and never showed suppression-burst or hypsarrhythmia during infancy. A de novo mosaic mutation (c.1923G>A) with a mutant allele frequency of 16% (in DNA of blood leukocytes) was detected in one patient. Three mutations were located in the transmembrane domain (3/4, 75%), and one in the extracellular loop near transmembrane helix 1. All the mutations were predicted to impair the function of the NMDA receptor. SIGNIFICANCE: Clinical features of de novo GRIN1 mutations include infantile involuntary movements, seizures, and hand stereotypies, suggesting that GRIN1 mutations cause encephalopathy resulting in seizures and movement disorders. Wiley Periodicals, Inc.
© 2015 International League Against Epilepsy.

Entities:  

Keywords:  Encephalopathy; GRIN1; Movement disorders; Neurotransmitter disorders; Seizure

Mesh:

Substances:

Year:  2015        PMID: 25864721     DOI: 10.1111/epi.12987

Source DB:  PubMed          Journal:  Epilepsia        ISSN: 0013-9580            Impact factor:   5.864


  35 in total

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