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Magnetic resonance imaging (MRI) has proved to be a valuable tool for monitoring development and pathology in the preterm brain. This imaging modality is useful for assessing numerous pathologies including periventricular leukomalacia, intraventricular haemorrhage/germinal layer haemorrhage, and periventricular haemorrhagic infarction, and can help to predict outcome in these infants. MRI has also allowed the detection of posterior fossa lesions, which are not easily seen with ultrasound. Additionally, and perhaps most relevant, quantitative MR studies have shown differences between the normal appearing preterm brain cit term equivalent age and term born infants, confirming that the brain develops differently in the ex utero environment. Further studies using quantifiable MR techniques will improve our understanding of the effects of the ex utero environment, including aspects of neonatal intensive care on the developing brain.
The developing brain is vulnerable to injury from many causes, resulting in significant mortality and morbidity despite recent improvements in neonatal intensive care, and at 30 months corrected age impairment can be identified in one half of all infants born at 25 weeks gestational age (GA) or less. (1) However, even those with no identifiable disability at this age may experience learning difficulties when they enter mainstream school or have behavioural problems in adolescence. (2-5)
The neuropathological correlates for neurodevelopmental impairments are incompletely defined. Most of our knowledge comes from ultrasound, which shows a relation between periventricular haemorrhagic infarction (PHI) and periventricular leucomalacia (PVL) and the development of cerebral palsy. There are, however, no pathological or imaging correlates for the spectrum of neurocognitive impairments seen in the child who was born preterm.
Magnetic resonance imaging (MRI) provides an ideal and safe technique for imaging the developing brain. It is non-invasive and non-ionising and allows considerable differentiation of structures within the immature brain, showing the extensive maturation that occurs from 23 to 40 weeks gestation while these vulnerable infants are receiving intensive care. MRI shows the well recognised pathologies seen on ultrasound and in addition allows the detection of more subtle abnormalities.
MRI OF THE NORMAL PRETERM BRAIN
MRI provides excellent detail of the immature brain with good delineation of the cortex, white matter, and central grey matter structures. (6,7) In the immature brain we have found that a T2 weighted fast spin echo (FSE) sequence gives the best contrast between different structures. The cortex is seen as high signal intensity on T1 weighted imaging and low signal on T2 weighted imaging, reflecting its high cellular density. Serial imaging allows the maturation of cortical folding to be assessed and scored. (6,7) At 24 weeks GA the surface of the brain appears smooth apart from the parieto-occipital fissure, central sulci, cingulate sulci, calcarine sulci, and very wide Sylvian fissures (fig 1). Sulcation and gyration develop at different rates in different regions of the brain. At any given age prior to term, the folding of the central sulcus is the most advanced, followed by the medial occipital lobe, The parietal lobe is the next most advanced, followed by the frontal and posterior temporal lobes. The anter ior temporal region is the least well developed. By term the cortex has extensive folding with the formation of tertiary sulci.
Unmyelinated cerebral white matter is shown as high signal intensity on T2 weighted imaging and low signal on T1 weighted imaging. On T2 weighted Mm, bands of low signal intensity are visible within the white matter, situated anterior, posterior, and lateral to the lateral ventricles. (6) These represent relatively dense regions of glial cells migrating from the germinal matrix to the cerebral cortex (8) (fig 2). At around 30 weeks GA, while the periventricular white matter remains high signal intensity, the low signal bands become difficult to visualise, presumably because the majority of the migrating cells have reached the cortex at this age. (9) In addition to these areas of low signal intensity, areas of extremely high signal intensity on T2 weighted FSE images are visualised around the anterior horns of the lateral ventricles between 24 and 36 weeks GA. Similar high signal intensity areas in the shape of arrowheads are visualised in the posterior periventricular white matter at this GA. (6) Histological ly, these extremely high signal intensity areas are comprised of dense fibre bundles, which have a relatively low cellular density. (8)
The germinal matrix is visible up to around 32 weeks GA as a prominent structure along the margins of the lateral ventricles (fig 2). After this age, small residual areas of germinal matrix are visualised at the anterolateral angles of the lateral ventricles and adjacent to the head of the caudate nucleus and in the roof of the temporal horn, a site not readily visualised with ultrasound. The germinal matrix is shown as high signal intensity on T1 weighted imaging …