Purpose: Increased availability of surgically resected epileptogenic tissue
s reveals often unsuspected cortical dysplasia (CD). There is some controve
rsy about the ontogenic stages in which these occur. Although most take pla
ce during neuroblast proliferation and migration, there is some evidence fo
r some CD occurring during postmigrational intrinsic cortical organization.
It has been shown that various kinds of focal cortical manipulations in ra
ts, if performed within 3-4 postnatal days, lead to the genesis of various
cortical malformations including a four-layered microgyrus or an unlayered
CD. It is not known whether such events also might occur in the human brain
.
Methods: Two children sustained minor head trauma within 3-4 postnatal days
and later developed intractable epilepsy, which was relieved by surgery. N
europathologic analysis of the resected tissues revealed an unsuspected mic
rodysplastic cortex immediately adjacent to a focal, modest meningeal fibro
sis, presumably secondary to the old closed head trauma.
Results: The main histologic features were a disorganized, unlayered cortex
; abnormal clusters of neurons, often with complex, randomly oriented proxi
mal dendritic patterns with absent apical orientation; the presence of a nu
mber of heterotopic small and large neurons in the white matter; absence of
inflammatory infiltrates, of hemosiderine, of reactive gliosis, or of an e
xcessive number of blood vessels. The morphologic features in these surgica
l specimens suggest that these focal malformations occur because of a regio
nal disorder of postmigrational intrinsic cortical remodeling.
Conclusions: The clinical histories and the pathologic findings lend some s
upport to the hypothesis that minor morbid events occuring in the immediate
postnatal period may lead to microdysplasia in the human similar to those
induced in rat pups. The animal model could be helpful to clarify the genes
is of some cases of CD and of the epileptogenicity often manifesting later
in life.