Universlty of Manitoba, ln Partîal Fulfiìlment - MSpace at the ...

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and Lassman, 1972). ln the sirnple form there is a local ized absence of
spinous processes for a few ségments, usually without neurological ínvolvenìent.
The spina blfida occuìta syndrome consists of neural arch defects
overlylng an abnormal (dysplastic) cord or nerve roots.
The relåtion of occult to cystic forms of spÌna bifida is not clear.
Lorber anc Levtck (r967) found that parents oi chirdren with myelomeningocele
showed an lncreased frequency of spina bifida occulta, suggest¡ng
some etlologlcal connection. several mutant mice wîth open neural defects
may also show spina bifida occulta (Gruneberg, I963).
ln the present chick embryos mesodermal defects, which m¡ght later
result ln spina bifida occul ta,. were seen in experimental embryos with
rryeloschlsis or closed cords. Many 12 day chick embryos exhibited spina
blfida occulta but the pôthogenesis of the lesion was not investigated.
Trypan blue-induced dysraphism of rats can result in exencephaly,
spina bifida manifesta and spina bifida occulta in older embryos. The
early development of the defects is associated with extensive blebformatlon
and hematomas which later disappear, so that small open defects
mîght possibly close ât .later stêges. (Rokos et al., .|970; 1975; Lendon,
1968; 1976).
Rokos ani Knowles (1976) demonstrated a high regulative abílîty in
chlck embryos after opening the roof plate of the neural tube on the third
day. Smal I incísions showed rapid closure and reconstitution. Larger
înclslons produced an everted neural lesîon, at which the cut edges of neural
tube and ectoderm often fused together in 2-4 hours. Thus spìna bífida
occulta could originate e¡ ther as a primary mesodermal defect, or by closure
of a smâl I neural defect. lnvestigation of windowed chick embryos after 72