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Jo Hajnal

Publications and source records attributed to Jo Hajnal.

3 recordsLinked to original sources

Abnormal deep grey matter development following preterm birth detected using deformation-based morphometry.

Preterm birth is a leading risk factor for neurodevelopmental and cognitive impairment in childhood and adolescence. The most common known cerebral abnormality among preterm infants at term equivalent age is a diffuse white matter abnormality seen on magnetic resonance (MR) images. It occurs with a similar prevalence to subsequent impairment, but its effect on developing neural systems is unknown. MR images were obtained at term equivalent age from 62 infants born at 24-33 completed weeks gestation and 12 term born controls. Tissue damage was quantified using diffusion-weighted imaging, and deformation-based morphometry was used to make a non-subjective survey of the whole brain to identify significant cerebral morphological alterations associated with preterm birth and with diffuse white matter injury. Preterm infants at term equivalent age had reduced thalamic and lentiform volumes without evidence of acute injury in these regions (t = 5.81, P < 0.05), and these alterations were more marked with increasing prematurity (t = 7.13, P < 0.05 for infants born at less than 28 weeks) and in infants with diffuse white matter injury (t = 6.43, P < 0.05). The identification of deep grey matter growth failure in association with diffuse white matter injury suggests that white matter injury is not an isolated phenomenon, but rather, it is associated with the maldevelopment of remote structures. This could be mediated by a disturbance to corticothalamic connectivity during a critical period in cerebral development. Deformation-based morphometry is a powerful tool for modelling the developing brain in health and disease, and can be used to test putative aetiological factors for injury.

Adolescent↗

Abnormal cortical development after premature birth shown by altered allometric scaling of brain growth.

BACKGROUND: We postulated that during ontogenesis cortical surface area and cerebral volume are related by a scaling law whose exponent gives a quantitative measure of cortical development. We used this approach to investigate the hypothesis that premature termination of the intrauterine environment by preterm birth reduces cortical development in a dose-dependent manner, providing a neural substrate for functional impairment. METHODS AND FINDINGS: We analyzed 274 magnetic resonance images that recorded brain growth from 23 to 48 wk of gestation in 113 extremely preterm infants born at 22 to 29 wk of gestation, 63 of whom underwent neurodevelopmental assessment at a median age of 2 y. Cortical surface area was related to cerebral volume by a scaling law with an exponent of 1.29 (95% confidence interval, 1.25-1.33), which was proportional to later neurodevelopmental impairment. Increasing prematurity and male gender were associated with a lower scaling exponent (p < 0.0001) independent of intrauterine or postnatal somatic growth. CONCLUSIONS: Human brain growth obeys an allometric scaling relation that is disrupted by preterm birth in a dose-dependent, sexually dimorphic fashion that directly parallels the incidence of neurodevelopmental impairments in preterm infants. This result focuses attention on brain growth and cortical development during the weeks following preterm delivery as a neural substrate for neurodevelopmental impairment after premature delivery.

Biometry↗

Diffusion-weighted magnetic resonance imaging in term perinatal brain injury: a comparison with site of lesion and time from birth.

OBJECTIVE: The aim of this study was to establish a more objective method for confirming tissue injury in term neonates who present with early seizures that are believed to be hypoxic-ischemic in origin. METHODS: We studied the relationship between contemporaneous diffusion-weighted magnetic resonance imaging and conventional magnetic resonance imaging in 63 symptomatic term-born neonates and 15 control term infants performed in the neonatal period. Apparent diffusion coefficients (ADC) were obtained for multiple regions of the brain. RESULTS: ADC values in the 15 control infants were 1 (1-1.15) (median [range]) x 10(-3)/mm2/second in the thalami and 1.1 (1-1.3) x 10(-3)/mm2/second in the lentiform nuclei, 1.5 (1.3-1.7) x 10(-3)/mm2/second in the centrum semiovale, 1.6 (1.46-1.7) x 10(-3)/mm2/second in the anterior white matter (WM), and 1.55 (1.35-1.85) x 10(-3)/mm2/second in the posterior WM with little variation over time. ADC values were significantly reduced in the first week after severe injury to either WM or basal ganglia and thalami (BGT), but values normalized at the end of the first week and then increased during week 2. ADC values were either normal or increased in moderate BGT and WM lesions when compared with controls. ADC values < 1.1 x 10(-3)/mm2/second were always associated with WM infarction and values <0.8 x 10(-3)/mm2/second with thalamic infarction. CONCLUSION: A reduced ADC soon after delivery allows the presence of tissue infarction to be confirmed at a time when conventional imaging changes may be subtle. However, as both moderate WM and BGT lesions may have normal or increased ADC values, a normal ADC value during the first week does not signify normal tissue. ADC values should always be measured in combination with visual analysis of both conventional and diffusion-weighed images for maximum detection of pathologic tissue, and the timing of the scan needs to be taken into account when interpreting the results.

Brain↗