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Vogel and McClenahan (1952) tnus s.uggested thðt a prîmary defect of the
cerebral vessels produces local hypoxia and degeneration of the involved
area of the bra i n.
2,4,7 Amn i ot ic- Adhesions
During the nineteenth century fetal constriction by amniotic bands or
adhesîons was held to be responsîble for' many'congenital malformations
(Dareste, 1877). Certainl¡i amnÌotic adhesion to open.brain defects does
occur ín man (Torpin, 1968) as well as in experimental animals. However
this is now usually regarded ês the resul t rãther than the cause of
anencepha I y.
2.4.8 Abnormal Development of the Tai l-Bud
The origîn of the most caudal part of the spinal cord must differ
from that of the rest of the neuraxis, as the posterîor neuropore closes
before the definitive length of the embryonic axis has been achieved. The
terminal section of the cord is apparently developed by growth of the undífferentiated
taíl bud, at least in the chick (Romanoff, 1960; Hami ìton,
1952), the rat (Benrl iff and Gordon, .l965) and perhaps in man (Lemire, 1969).
Crlley (1969) demonstrated an area of overlap and fr,lsìon between these two
sources of neural material in the chick embryo.
tenire (1969) suggests that some neuraì malformations în the lower
lumbar and sacral regíons (especial ly those covered by skin) mig[t arise
by abnormal development of the tail bud material.
2.4.9 Trauma
Reviewing the co¡ lection of embryos studied by Sternberg fi929),
Pol ltzer (1954) note¿ that some narrow mídline braîn or cord defect'showed
a break in continuity between neural tissue and the skìn. He suggested that
these particular lesíons m¡ght be trãumatìc in origin.