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In order to supplement Dr. Johnson's review we wish to make two
points: I) not all grossly similar lesions should be considered t.
o be due to the same etiology, even if experimentally documented,
and 2) relatively few infections (syphilis, toxoplasmosis,
cytomegalovirus, herpesvirus and rubella) and no immunologic
disorders (except for kernicterus due to hyperbilirubinemia) are
known to affect the developing human nervous system. Admittedly,
since most human malformations are of unproven cause, these two
points are not mutually exclusive. Rather, the challenge remains to
show that any of the experimental models relates to any of the
human diseases. In particular, the porencephaly-hydranencephaly
spectrum could be due to ischemia in the watershed distribution of
one or more branches of the internal carotid ar- teries; and
aqueductal stenosis could be due to secondary blockage by blood
clots or debris related to hemorrhage or necrosis in the germinal
matrix or periventricular white matter, lesions most likely due to
hypoxia-acidosis in premature infant, who die most often of the
concomitant respiratory distress syndrome. REFERENCES Altshuler. G.
: Toxoplasmosis as a cause of hydranencephaly. Am. l. Dis. Child.
125: 251-252 (1973). Beer. A. E. and Billingham. R. E. :
Immunobiology of mammalian reproduction. Adv. Immunol. 14: 1-84
(1971). Berenberg. W. and Nakervis. G. : Long-term follow-up of
cytomegalic inclusion disease of in- fancy. Pediatrics 46: 403-410
(1970). Boniuk. M. and Zimmerman. L. E. : Ocular pathology in the
rubella syndrome. Arch. Ophthalmo!. 77: 455-473 (1967).
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