Synaptogenesis in the Fetal Corpus Striatum, Globus Pallidus, and Substantia Nigra: Correlations With Striosomes of Graybiel and Dyskinesias in Premature Infants

Abstract Synaptogenesis can be detected in tissue sections by immunoreactivity for synaptophysin, a synaptic vesicle glycoprotein that serves as a marker of synaptic maturation. Reactivity was prospectively studied postmortem in sections of the striatum, globus pallidus, and substantia nigra in 172 normal human fetuses and neonates of 6 to 41 weeks' gestation. Caudate nucleus and putamen show patchy reactivity beginning at 13 weeks' gestation around some intracapsular neurons; the pattern is well developed in all regions before midgestation. Near-uniform reactivity throughout the striatum is achieved by 34 weeks, but subtle patchiness is still perceived at term. The globus pallidus shows uniform reactivity without stria from 13 weeks and the substantia nigra from 9 weeks. Synaptic patchiness in the fetal corpus striatum appears to correspond to the ''striosomes of Graybiel'' that define adjacent neurotransmitter-rich and neurotransmitter-poor zones. Clinical correlation is proposed with dystonic postures and athetoid movements observed in normal preterm neonates of 26 to 32 weeks. Keywords corpus striatum, dyskinesias, globus pallidus, striosomes of Graybiel, substantia nigra, synaptogenesis, synaptophysin, caudate, putamen Received October 25, 2011. Accepted for publication January 31, 2012. The temporal and spatial sequence of synaptogenesis can be demonstrated reliably in formalin-fixed, paraffin-embedded sections of human fetal brain using synaptophysin immunocytochemistry

Fetal opercular cavernous angioma causing cerebral cleft: contralateral primitive vascular anomaly and subicular dysgenesis

We describe a 22-week female fetus after pregnancy was terminated because of fetal magnetic resonance imaging showing a large left cerebral hemispheric cleft suggestive of porencephaly or schizencephaly. Postmortem examination revealed a large cavernous angioma of the left opercular region with evidence of previous hemorrhage and extensive cerebral infarction. In the right hemisphere, another vascular malformation within the frontal germinal matrix consisted of an aggregate of primitive vessels not yet canalized. Selective dysgenesis of the right subiculum also was demonstrated. This case illustrates not only a severe encephaloclastic effect of cavernous angioma in fetal brain but also the importance of fetal autopsy to help correlate and explain fetal neuroimaging. Potential future prenatal treatment of fetal angiomata requires precise in utero diagnosis