Exencephaly is said to precede anencephaly resulting from failure of the rostral neuropore closure. In order to verify if the exencephaly induced after neural tube closure would also lead to anencephaly, exencephaly was induced in rat fetuses by maternal administration of a single dose (15 mg/kg) of cyclophosphamide on day 12 of gestation and pregnancy was prolonged by uterine ligation until postconception (PC) day 24. Fetal death was found to increase with prolongation of gestation and no sign of recovery from growth retardation was observed. Alizarin red-S-stained skeletal preparations substantiated the persistence of skull malformations in the exencephalic fetuses. Histological observations of the mesenchyme and the brain indicated degenerative changes that were intensifying with time. The ventricular system expanded progressively; the ependyma was denuded and neural mass lay free in the ventricle. The choroid plexus appeared to be elaborate and extensive. The haemorrhagic capillary network around the brain tissue was highly proliferative and appeared to penetrate the former from the exterior. Tissue necrosis seemed to progress unabated. Cystic spaces appeared beneath the base of the brain and became progressively large and it appeared as if the brain was being pushed out of the shallow cranial fossae. By PC day 24, most of the brain tissue had degenerated, thus giving clearly the appearance of the anencephalic condition.