Mitochondria morphopathological changes in human congenital hydrocephalus, Arnold-Chiari malformation and postmeningitis hydrocephalus. An electron microscopic study

Vuia1 reported two twin brothers diagnosed with congenital spongy degeneration of the brain featured by accumulation of lamellar bodies within the mitochondria, and free in the cellular cytoplasm with tendency to form inclusions of the multilamellar or finger-print type. Watanabe2 described in a 51/2-year-old boy with congenital myopathy associated with communicating hydrocephalus myofibrillar disorganization and Z-band streaming with decrease or absence of mitochondria. These Authors considered that common pathogenetic mechanism may have been involved in the development of both the myopathy and the hydrocephalus. Kaur and Ling3 found swelling and disintegration of mitochondria in ricin-induced hydrocephalus in postnatal rats. Madhavi and Jacob4 carried out a morphometry study of mitochondria in the choroidal ependyma of hydrocephalic guinea pigs, and observed that the inner membrane of the mitochondria including cristae exhibited a significant decrease in the hydrocephalic animals. According to these Authors, this reduction in the surface area could probably be attributed to the reduced activity of choroid ependymal cells in obstructive hydrocephalus. Castejón5 distinguished variable degrees of mitochondrial swelling in human hydrocephalic cerebral cortex. Boillat et al.6 described distorted mitocondria in the deep cortical pyramidal cells of infant rats with inherited hydrocephalus. Castejón et al.7 examined in details the pathological changes of mitochondria in the edematous human cerebral cortex associated to severe and complicated brain trauma, tumors, and in a preliminary way the human hydrocephalus.