Immunohistochemical evaluation of neuronal maturation in untreated fetal hydrocephalus

The prognosis of fetal hydrocephalus is poor and the results of intrauterine decompression have so far been unsatisfactory. Although several factors have been known to affect the prognosis of intrauterine hydrocephalus, few histological studies of preterm hydrocephalus and no immunohistochemical analyses have been reported to date. In eight fetal cases of untreated preterm hydrocephalus, the authors morphologically studied neuronal maturation by means of immunohistochemical and specific myelin staining techniques. The patients' gestational ages at death ranged from 20 to 40 weeks (mean, 30 weeks). There were two cases of simple form of hydrocephalus, two of cerebral dysgenesis (hydranencephaly and holoprosencephaly), and four of hydrocephalus secondary to intraventricular hemorrhage. Relatively primitive neuronal developmental processes, such as neuronal cell proliferation and migration, were found to be altered by rapidly progressive simple form of intrauterine hydrocephalus, whereas the neuronal maturation disorder was obviously the primary condition in dysgenetic hydrocephalus. Hydrocephalus itself, however, caused additional damage in the presence of delayed but slowly progressing neuronal development. Secondary hydrocephalus initially reflects impairment of previously normal neuronal maturation. In this situation, too, hydrocephalus per se further compromised the potential for continued neuronal development. The results of this study imply that the pathoembryological concepts of fetal hydrocephalus are not so simple. Early decompression may preserve the potential for further neuronal maturation in fetal hydrocephalus.