Recording Motor Defects of Children with Cerebral Palsy
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dilatation of the cerebral ventricles and widening of cortical sulci. These features were visible as early as five days after onset of neurological symptoms (patient 2), became marked over the next few months and then remained stationary. In two cases areas of white-matter hypodensity were present around the frontal and occipital horns from onset, and persisted. although less marked, to the last examinations. The initial CT scans for patients 2 and 3 showed mild hypodensity in both lenticular nuclei, which was not visible on later examinations (Fig. I). On all scans, except the initial one for patient 2, a small rounded area of increased density was visible, a fer enhancement, in the posterior half of the left thalamus. CT scan images in glutaric aciduria are drferent from the punched-out areas of hypodensity seen in acute bilateral striatal necrosis. This is in agreement with pathological reports which indicate neuronal loss and gliosis, without cavitation2.
[1] M. Norenberg,et al. Glutaric acidemia as a cause of striatal necrosis in childhood , 1983, Annals of neurology.
[2] J. Aicardi,et al. Acute neurological dysfunction associated with destructive lesions of the basal ganglia in children , 1982, Annals of neurology.
[3] M. Norenberg,et al. Glutaric aciduria: biochemical and morphologic considerations. , 1977, The Journal of pediatrics.