Need for systematic synthetic phonics teaching within the early reading curriculum

Both the New Zealand Ministry of Education's Literacy Experts Group and the Australian National Inquiry into the Teaching of Literacy have recently acknowledged the centrality of systematic instruction in synthetic phonics to early reading instruction, but this conclusion remains contentious in some circles. This paper briefly summarises empirical research in basic psychology and evidence-based evaluation studies supporting the inclusion of systematic synthetic phonics instruction within the early reading curriculum, allowing practising psychologists to develop an informed opinion on this issue.

I-Spi: innovative shared practical ideas: a support guide for literacy and numeracy in the early years of schooling, for home tutor/supervisors in distance education

Innovative Shared Practical Ideas (I-Spi) is a guide to help you and your children learn together. It is designed to affirm, support and strengthen your role as home tutor/supervisors in your daily learning sessions with your children. In this guide particular emphasis is given to the value of talk, formal and informal early literacy and numeracy practices (including ideas from distance school lessons, from home tutor/supervisors, research, and beyond), assessment of these practices together with informal assessment ideas for gauging your children’s literacy and numeracy progress, and stepping in and building on strategies

Clinical and molecular genetics of myoclonic-astatic epilepsy and severe myoclonic epilepsy in infancy (Dravet syndrome)

The majority of severe epileptic encephalopathies of early childhood are symptomatic where a clear etiology is apparent. There is a small subgroup, however, where no etiology is found on imaging and metabolic studies, and genetic factors are important. Myoclonic-astatic epilepsy (MAE) and severe myoclonic epilepsy in infancy (SMEI), also known as Dravet syndrome, are epileptic encephalopathies where multiple seizure types begin in the first few years of life associated with developmental slowing. Clinical and molecular genetic studies of the families of probands with MAE and SMEI suggest a genetic basis. MAE was originally identified as part of the genetic epilepsy syndrome generalized epilepsy with febrile seizures plus (GEFS(+)). Recent clinical genetic studies suggest that SMEI forms the most severe end of the spectrum of the GEFS(+). GEF(+) has now been associated with molecular defects in three sodium channel subunit genes and a GABA subunit gene. Molecular defects of these genes have been identified in patients with MAE and SMEI. Interestingly, the molecular defects in MAE have been found in the setting of large GEFS(+) pedigrees, whereas, more severe truncation mutations arising de novo have been identified in patients with SMEI. It is likely that future molecular studies will shed light on the interaction of a number of genes, possibly related to the same or different ion channels, which result in a severe phenotype such as MAE and SMEI. (C) 2001 Elsevier Science B.V. All rights reserved.