Effect of fetal hydrocephalus on the distribution patterns of calcium-binding proteins in the human occipital cortex.

Neuronal pathology in the cerebral cortex (CC) of fetal hydrocephalus brains is quite subtle when applying routine Nissl staining. This study is aimed at investigating alterations of interneurons which can be immunolabelled by antibodies against the calcium-binding proteins calretinin (CR), calbindin (CB) and parvalbumin (PV). The subplate (SP) subjacent to the cortex anlage is included as this transient zone plays a pivotal role in the establishment of cortical connections. Nine occipital lobes from cases of fetal hydrocephalus and 9 controls were categorized according to age: 21-25 weeks of gestation (group 1) and 32-36 weeks (group 2). No differences in the distribution, number and morphology of CR-immunoreactive (ir) neurons are seen when comparing hydrocephalic with control brains of group 1. In severely altered hydrocephalic brains of group 2, the distribution and number of CR-, PV- and CB-ir nerve cells are not altered; however, they appear shrunken and processes are less immunolabelled. In extremely altered tissue PV-, CB-ir neurons cannot be detected, whereas the number of CR-ir somata is not reduced. The data indicate that subpopulations of interneurons of the CC may be differentially damaged. The alterations observed in the SP may implicate a possible impairment of transient neuronal circuitries that are essential for the development of cortical connections. On the whole, these neuronal alterations may account for residual deficits observed after shunting.