Plasticity is an intrinsic property of the central nervous system, reflecting its capacity to respond in a dynamic manner to the environment and experience via modification of neural circuitry. In the context of healthy development, plasticity is considered beneficial, facilitating adaptive change in response to environmental stimuli and enrichment, with research documenting establishment of new neural connections and modification to the mapping between neural activity and behaviour. Less is known about the impact of this plasticity in the context of the young, injured brain. This review seeks to explore plasticity processes in the context of early brain insult, taking into account historical perspectives and building on recent advances in knowledge regarding ongoing development and recovery following early brain insult, with a major emphasis on neurobehavioural domains. We were particularly interested to explore the way in which plasticity processes respond to early brain insult, the implications for functional recovery and how this literature contributes to the debate between localization of brain function and neural network models. To this end we have provided an overview of normal brain development, followed by a description of the biological mechanisms associated with the most common childhood brain insults, in order to explore an evidence base for considering the competing theoretical perspectives of early plasticity and early vulnerability. We then detail these theories and the way in which they contribute to our understanding of the consequences of early brain insult. Finally, we examine evidence that considers key factors (e.g. insult severity, age at insult, environment) that may act, either independently or synergistically, to influence recovery processes and ultimate outcome. We conclude that neither plasticity nor vulnerability theories are able to explain the range of functional outcomes from early brain insult. Rather, they represent extremes along a 'recovery continuum'. Where a child's outcome falls along this continuum depends on injury factors (severity, nature, age) and environmental influences (family, sociodemographic factors, interventions).

OBJECTIVEType 2 diabetes (T2DM) is associated with brain atrophy and cerebrovascular disease. We aimed to define the regional distribution of brain atrophy in T2DM and to examine whether atrophy or cerebrovascular lesions are feasible links between T2DM and cognitive function.RESEARCH DESIGN AND METHODSThis cross-sectional study used magnetic resonance imaging (MRI) scans and cognitive tests in 350 participants with T2DM and 363 participants without T2DM. With voxel-based morphometry, we studied the regional distribution of atrophy in T2DM. We measured cerebrovascular lesions (infarcts, microbleeds, and white matter hyperintensity [WMH] volume) and atrophy (gray matter, white matter, and hippocampal volumes) while blinded to T2DM status. With use of multivariable regression, we examined for mediation or effect modification of the association between T2DM and cognitive measures by MRI measures.RESULTST2DM was associated with more cerebral infarcts and lower total gray, white, and hippocampal volumes (all P < 0.05) but not with microbleeds or WMH. T2DM-related gray matter loss was distributed mainly in medial temporal, anterior cingulate, and medial frontal lobes, and white matter loss was distributed in frontal and temporal regions. T2DM was associated with poorer visuospatial construction, planning, visual memory, and speed (P ≤ 0.05) independent of age, sex, education, and vascular risk factors. The strength of these associations was attenuated by almost one-half when adjusted for hippocampal and total gray volumes but was unchanged by adjustment for cerebrovascular lesions or white matter volume.CONCLUSIONSCortical atrophy in T2DM resembles patterns seen in preclinical Alzheimer disease. Neurodegeneration rather than cerebrovascular lesions may play a key role in T2DM-related cognitive impairment.