We studied 167 patients who had identifiable lesions and temporal or e
xtratemporal partial epilepsy. Pathology included neuronal migration d
isorders (NMIDs) (48), low-grade tumors (52), vascular malformations (
34), porencephalic cysts (16), and gliotic lesions as a result of cere
bral insults early in life (17). MRI volumetric studies using thin (1.
5- or 3-mm) coronal images were performed in all patients and in 44 ag
e-matched normal controls. An atrophic hippocampal formation (HF), ind
icating dual pathology, was present in 25 patients (15%). Abnormal HF
volumes were present in those with lesions involving temporal (17%) bu
t also extratemporal (14%) areas. Age at onset and duration of epileps
y did not influence the presence of HF atrophy. However, febrile seizu
res in early childhood were more frequently, although not exclusively,
found in patients with hippocampal atrophy. The frequency of hippocam
pal atrophy in our patients with low-grade tumors (2%) and vascular le
sions (9%) was low. Dual pathology was far more common in patients wit
h NMDs (25%), porencephalic cysts (31%), and reactive gliosis (23.5%).
Some structural lesions, such as NMDs, are more likely to be associat
ed with hippocampal atrophy, independent of the distance of the lesion
from the HF. In other types of lesions, such as vascular malformation
s, dual pathology was found when the lesion was close to the HF. A com
mon pathogenic mechanism during pre- or perinatal development may expl
ain the occurrence of concomitant mesial temporal sclerosis and other
structural lesions because of either (1) associated developmental abno
rmalities or (2) predisposition to prolonged febrile convulsions. Furt
her clarification of this issue would improve our understanding of the
pathogenesis of mesial temporal sclerosis and lead to more efficient
planning of surgical treatment for lesional epilepsy.