We studied glucose metabolism in brain tissue surrounding cavernous an
gioma in 22 patients, using PET, and evaluated its relation to the siz
e, sire and epileptogenic nature of the vascular malformation, as well
as to the post-surgical seizure outcome. Preoperatively, 18 patients
suffered recurrent seizures, the origin of which could be clearly rela
ted to the vascular malformation in 14. Brain metabolism surrounding c
avernous angiomas was normal in 18 patients (82%), and significantly d
ecreased in four (18%). In these four patients, but in none of the 18
other cases, the vascular malformation disrupted connections between p
aralimbic areas and the adjacent temporal neocortex where hypometaboli
sm was most pronounced. The latter did not correlate with the size nor
with the epileptogenic nature of the cavernomas. Sixteen epileptic pa
tients underwent surgical removal of their cavernoma, without resectio
n of the surrounding cortex. Ar 1-year postoperatively, seizures have
relapsed in seven patients (44%), including those four whose epilepsy
could not be clearly related to the vascular malformation. Conversely,
the four patients with perilesional hypometabolism on preoperative PE
T were seizure free postoperatively. Hypometabolism in brain tissue su
rrounding cavernomas is a rare finding which seems more likely to refl
ect deafferentation than the epileptogenic process itself.