NORMALIZATION OF NEURONAL METABOLIC DYSFUNCTION AFTER SURGERY FOR TEMPORAL-LOBE EPILEPSY - EVIDENCE FROM PROTON MR SPECTROSCOPIC IMAGING

Citation
F. Cendes et al., NORMALIZATION OF NEURONAL METABOLIC DYSFUNCTION AFTER SURGERY FOR TEMPORAL-LOBE EPILEPSY - EVIDENCE FROM PROTON MR SPECTROSCOPIC IMAGING, Neurology, 49(6), 1997, pp. 1525-1533
Citations number
36
Journal title
ISSN journal
00283878
Volume
49
Issue
6
Year of publication
1997
Pages
1525 - 1533
Database
ISI
SICI code
0028-3878(1997)49:6<1525:NONMDA>2.0.ZU;2-K
Abstract
Surgery is a safe and effective treatment for patients with temporal l obe epilepsy (TLE) who do not respond adequately to anticonvulsant med ication and in whom the seizure generator can be identified and safely removed. Proton MR spectroscopic imaging (MRSI) can image and quantif y neuronal damage in patients with TLE based on reduced signals from N -acetylaspartate (NAA), a compound localized exclusively in neurons. W e performed proton MRSI in patients with TLE before and after surgical treatment to determine whether NAA or other resonance intensities cha nged in the temporal lobes of patients with TLE after surgery, and whe ther these changes correlated with surgical outcome. N-acetylaspartate resonance intensity relative to creatine (NAA/Cr) was abnormally low preoperatively in at least one temporal lobe in all 14 patients examin ed. It was low ipsilaterally in the patients who became seizure free a nd bilaterally in those who did not. Postoperatively, it increased to the normal range on the side of surgery in all patients who became sei zure free. In the one patient who became seizure free and who had low NAA/Cr in both temporal lobes before surgery, NAA/Cr values in the con tralateral, unoperated temporal lobe also increased to the normal rang e. Ln contrast, NAA relative intensity ratios did not change in those patients who continued to have seizures after surgery. The creatine re sonance intensity (Cr) in the temporal lobes was high, relative to the brainstem, in seven patients preoperatively. After surgery, the Cr re mained high in two patients, both of whom continued to have seizures. We conclude that NAA (and Cr) abnormalities in TLE do not result solel y from neuronal loss and gliosis but can be reversible after postsurgi cal control of seizures. This implies that the NAA and Cr abnormalitie s in patients with TLE, at least in part, are dynamic markers of both local and remote physiologic dysfunction associated with ongoing seizu res.