Abstract

BackgroundAlthough neuroanatomical and cognitive sequelae of low birthweight and preterm birth have been investigated, little is understood as to the likely prevalence of a history of low birthweight or preterm birth, or neuroanatomical correlates of such a history, within the special educational needs population. Our aim was to address these issues in a sample of young people receiving additional learning support.MethodsOne hundred and thirty-seven participants aged 13–22 years, receiving additional learning support, were recruited via their schools or colleges and underwent structural magnetic resonance imaging (MRI). Obstetric records, available in 98 cases, included birthweight and gestational data in 90 and 95 cases, respectively. Both qualitative and quantitative voxel-based analyses of MRI data were conducted.ResultsA history of low birthweight and preterm birth was present in 13.3% and 13.7% of cases, respectively. Low birthweight and preterm birth were associated with specific qualitative anomalies, including enlargement of subarachnoid cisterns and thinning of the corpus callosum. Low birthweight was associated with reduced grey matter density (GMD) in the superior temporal gyrus (STG) bilaterally, left inferior temporal gyrus and left insula. Prematurity of birth was associated with reduced GMD in the STG bilaterally, right inferior frontal gyrus and left cerebellar hemisphere. Comparison of subjects with no history of low birthweight or preterm birth with a previously defined control sample of cognitively unimpaired adolescents (n = 72) demonstrated significantly greater scores for several anomalies, including thinning of the corpus callosum, loss of white matter and abnormalities of shape of the lateral ventricles.ConclusionAlthough a two-fold increased prevalence of a history of low birthweight and preterm birth exists within the special educational needs population, other aetiological factors must be considered for the overwhelming majority of cases. Neuroanatomical findings within this sample include qualitative anomalies of brain structure and grey matter deficits within temporal lobe structures and the cerebellum that persist into adolescence. These findings suggest a neurodevelopmental mechanism for the cognitive difficulties associated with these obstetric risk factors.

Highlights

  • Neuroanatomical and cognitive sequelae of low birthweight and preterm birth have been investigated, little is understood as to the likely prevalence of a history of low birthweight or preterm birth, or neuroanatomical correlates of such a history, within the special educational needs population

  • Obstetric data was available for 98 participants: these participants did not differ from those in whom obstetric data was unavailable in term of gender (χ2 = 0.006, df = 1, p = 0.939), age (F = 0.059, p = 0.809) or intelligence quotient (IQ) (F = 1.193, p = 0.277)

  • A recent US Institute of Medicine report estimated that preterm birth in the US cost society US$26.6 billion in 2005, with US$1.1 billion representing the cost of provision of special educational services, and stated the need for outcome studies extending into adolescence [45]

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Summary

Introduction

Neuroanatomical and cognitive sequelae of low birthweight and preterm birth have been investigated, little is understood as to the likely prevalence of a history of low birthweight or preterm birth, or neuroanatomical correlates of such a history, within the special educational needs population. Preterm birth is associated with similar qualitative anomalies, including ventricular dilatation, white matter loss and corpus callosal thinning [13], as well as periventricular leukomalacia and basal ganglia haemorrhage [14], and quantitative abnormalities in terms of reduced hippocampal and caudate volumes [15,16,17], reduced cerebellar volumes [18,19], reduced cortical grey matter volumes in parieto-occipital regions [20], thinning of the corpus callosum [21], increased temporal lobe gyrification [22] and enlargement of the occipital and temporal horns and body of the lateral ventricles [20,23]

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