Vulnerability of the hippocampus to traumatic brain injury (TBI) in adults is related to severity of injury and white matter atrophy. The objectives of this study were to determine features of anthropometry and cerebral morphometry late after TBI in childhood and to assess whether hippocampal volume is related to severity of initial ictus and changes in white matter at follow-up. Thirty-three patients underwent magnetic resonance imaging 4.9 y after severe TBI that necessitated intensive care; 23 had mechanical ventilation and intracranial pressure monitoring longer than 3 d. Magnetic resonance imaging analyses included volume of brain, hemisphere, ventricles, and hippocampal and perihippocampal regions; spatial distribution of voxel-based morphometry differences in white matter; and eigenvalues of diffusion tensor imaging diffusivity. Patients with longer intensive care ictus had smaller-than-expected occipitofrontal head circumference. Eight of these, identified by voxelbased morphometry, had periventricular white matter loss and smaller-than-expected brain volume for OFC, suggesting "atrophy"; the remainder had expected volume for a smaller OFC, suggesting "growth disturbance." Ninety-three percent of the variation in right hippocampal volume was accounted for by factors related to severity of injury and white matter atrophy. It is concluded that anthropometry and cerebral morphometric measurements late after severe A key factor in preserving cognitive abilities during aging is brain growth during childhood (1,2). Larger head size is associated with better performance, and, in adults, a difference as small as 1.3 SD (~2 cm) is of major significance. It is also suggested that factors that promote brain growth may protect against cognitive decline (2). However, a corollary to this idea must also be the potential effect of impaired growth in childhood and risk for lesser cognitive function throughout adulthood, with detrimental implications in old age. Traumatic brain injury (TBI) is relatively common in children and adolescents (3), and in recent years, there has been much work on the close relationship between findings on magnetic resonance imaging (MRI) and functional and behavioral outcomes. The hippocampus and white matter have been a particular focus. For example, in adults who survive TBI, MRI findings show that the degree of hippocampal atrophy is related to severity of initial injury (4) and subsequent white matter atrophy (5). In children, however, only a trend (p ϭ 0.09) toward smaller right hippocampal volume has been found in more severe cases (6).Hippocampal volume and its relations can serve as a "bioassay" of previous or ongoing pathology and development. For

In severe paediatric traumatic brain injury (TBI), a common focus of treatment is raised intracranial pressure (ICP). We have previously reported frontal cerebral vulnerability with executive deficits from raised ICP in paediatric TBI. Now, using diffusion tensor imaging (DTI) in a different population, we have examined fractional anisotropy (FA), and mean, axial and radial diffusivity (MD, AD, RD) in 4 regions of the corpus callosum (CC) and in both inferior frontal regions. Our aim was to examine during the chronic phase of TBI whether the CC cross-sectional area correlated with regional DTI metrics of white matter microstructure, with global outcome ratings of function (Functional Independence Measure and Multiattribute Health Status Classification) and with performance in the Rey-Osterrieth Complex Figure (ROCF) test. We examined 33 paediatric TBI cases who were followed, on average, 4.9 years after severe injury. All cases had received mechanical ventilation during their acute treatment and, a priori, they were assigned to a non-ICP or a raised ICP group. Twenty-two participants had mainly right-sided injury at the time of acute ictus. The findings confirm that severe TBI in childhood, complicated by intracranial hypertension, results in CC vulnerability. In the chronic phase of recovery, it is reduced in the cross-sectional area, it is more compact and thinned, and the anterior region is disproportionately small. Late after raised ICP, we have also found that individuals exhibit regional microstructural abnormality with combined reduced FA and increased MD, AD and RD. Smaller size and such microstructural changes in the anterior CC were associated with similar right-sided (rather than left-sided) frontal microstructural changes in the ICP group. Taken together, this evidence points to an interaction between raised ICP-related brain tissue perturbation and focal frontal extracallosal injury, leading to anterior CC regional vulnerability, most likely wallerian degeneration. At long-term follow-up, this lack of white matter integrity in the anterior CC is correlated with functional outcome, particularly in aspects of social interaction and the copy component of the ROCF test, which suggests that the CC-to-forebrain function warrants further study in chronic TBI.