We tested the hypothesis that very-low-birth-weight (<1.5 kg) infants with perinatal growth failure whose head size is not normal by eight months of age (corrected for prematurity) have significantly poorer growth and neurocognitive abilities at school age than very-low-birth-weight children with a normal head size at eight months. We also hypothesized that these differences would persist even after control for major neurologic impairment and perinatal and sociodemographic risk factors.

We tested the hypothesis that very low birth weight (VLBW > 1.5 kg) children would have significantly poorer neurocognitive abilities at school age than would normal birth weight full-term age mates, that differences would persist after control for neurologic impairment and social risk, and that VLBW would interact with social risk. Two hundred forty-nine VLBW children and a randomly selected sample of 363 normal birth weight age mates born 1977 through 1979 were tested at 8 years. A neurologic examination and tests of intelligence, language, speech, reading, mathematics, spelling, visual and fine motor abilities, and behavior were performed. Twenty-four (10%) VLBW had a major neurologic abnormality compared with none of the controls. VLBW had significantly poorer scores on all tests, with the exception of speech and the total behavior score. These differences persisted among VLBW children without major neurologic abnormality, with the exception of social competence, reading, and spelling. Even normal IQ, neurologically normal VLBW had significantly poorer scores than did controls in expressive language, memory, visuomotor, and fine motor function, and measures of hyperactivity. When social risk was controlled in multiple regression analyses, VLBW still had an adverse effect on all outcome measures with the exception of speech. Social risk was, however, the major determinant of outcome. We found an interaction between VLBW and social risk only in verbal IQ and in the opposite direction than hypothesized.

Developmental apraxia of speech (DAS)is a putative diagnostic category for children whose speech errors presumedly (a) differ from the errors of children with developmentalspeech delay (SD)and (b) resemble the errors of adults with acquired apraxia of speech. The studies reported in this series (Shriberg, Aram, & Kwiatkowski, 1997a, 1997b) concern both premises, with primary focus on the first—that children with DAS can be differentiated from children with SD on the basis of one or more reliable differences in their speech error profiles. Immediate goals are to identify a diagnostic marker for DAS and to consider implications for research and clinical practice. A long-term goal is to identify the phenotype marker for DAS, on the assumption that it may be a genetically transmitted disorder. This first paper reviews relevant descriptive and theoretical perspectives. Findings from a local ascertainment study support the clinical functionality of the termsuspectedDAS.

The present study examined invented spelling of pinyin (a phonological coding system for teaching and learning Chinese words) in relation to subsequent Chinese reading development. Among 296 Chinese kindergartners in Beijing, independent invented pinyin spelling was found to be uniquely predictive of Chinese word reading 12 months later, even with Time 1 syllable deletion, phoneme deletion, and letter knowledge, in addition to the autoregressive effects of Time 1 Chinese word reading, statistically controlled. These results underscore the importance of children’s early pinyin representations for Chinese reading acquisition, both theoretically and practically. The findings further support the idea of a universal phonological principle and indicate that pinyin is potentially an ideal measure of phonological awareness in Chinese.