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Alcoholic Fetopathy and Embryopathy

Alcohol can also be especially cytotoxic and neu-rotoxic to embryos and fetuses, since alcohol penetrates the blood-placental barrier and because the enzyme system of the fetus or embryo is still undeveloped (West et al. 1990). The impact is multifarious. Moreover, physical dependence begins from the time of intrauterine intoxication.

Among the reported sequelae are intrauterine hypotrophy, craniofacial dysmorphy, and extracranial skeletal malformation (Clarren and Smith 1978; Majewski 1979; Streissguth et al. 1980; Rosett and Weiner 1984). The brain is subject to neuronal migration inhibition with neuroglial heterotopia and internal hydrocephalus. Extensive experimental studies describe, above all, migration inhibition in the cerebellum (Volk 1980).

Wisniewski et al. (1983) (see also Archibald et al. 2001) list the following neuropathological changes caused by alcoholic fetopathy and embryopathy (Fig. 18.8):

— Microcephaly

— Hydrocephalus

— Cerebellar malformations, especially of the cer-ebellar vermis

— Abnormalities (agenesis) of the corpus callosum and the anterior commissure

— Disproportionality and reduced basal ganglia volume

— Hypoplasia of the optic nerve and globe of the eye (microphthalmia)

— Loss or deficiency of retinal ganglion cells

— Meningeal glioneuronal heterotopia

— Neuronal microdysplasia

It is now known that alcohol - at least in animals -can cause massive intrauterine cell death; this nerve cell death is apparently caused by the blockade of the NMDA receptors on the one hand and activation of the GABA receptor on the other (Ikonomidou et al. 2000).

Fig. 18.8a-c. Fetal alcohol syndrome, which is characterized cortex = heterotopia (b) and microdysgenesis of the pallidum by craniofacial dysmorphy (a), microcephaly and hydrocephalus (b, c Nissl stain; magnification b Xl,000; c X300) as well as retarded migration of Purkinje cells in the cerebellar

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