A subcortical network of dysfunction in TLE measured by magnetic resonance spectroscopy.
OBJECTIVE
The goal of this work was to evaluate the relationship between neuronal injury/loss in the hippocampus, thalamus, and putamen in temporal lobe epilepsy (TLE) patients using (1)H magnetic resonance spectroscopic imaging.


METHODS
(1)H spectroscopic images from the hippocampus and thalamus of controls and patients with TLE were acquired at 4 T. The spectroscopic imaging data were reconstructed using an automated voxel-shifting method based on anatomic landmarks providing four, six, and three loci for the hippocampus, thalamus, and putamen, respectively. For correlation analysis, the hippocampal and striatal loci were averaged to provide single estimates of the entire structure, whereas the thalamus was divided into two regions, an anterior and posterior measure, using the average of three loci each.


RESULTS
The ratio of N-acetyl aspartate to creatine (NAA/Cr), a measure of neuronal injury/loss, was significantly reduced in both the ipsilateral and contralateral hippocampi and thalami. NAA/Cr in the ipsilateral hippocampus was significantly correlated with the ipsilateral and contralateral anterior and posterior thalami, putamen, and contralateral hippocampus. In control subjects, the hippocampi were only correlated with each other.


CONCLUSIONS
The data demonstrate that there is significant neuronal injury/loss in both the ipsilateral and contralateral thalami in temporal lobe epilepsy patients, with greater impairment in the anterior portions of the ipsilateral thalamus. The degree of injury/loss in the ipsilateral and contralateral thalamus and putamen is directly correlated with that of the ipsilateral hippocampus. This is consistent with the hypothesis that the impairment and damage associated with recurrent seizures as measured by N-acetyl aspartate originating in the hippocampus results in injury and impairment in other subcortical structures.
Hetherington
H P
HP
Department of Neurosurgery, Yale University, PO Box 208062, New Haven, CT 06520-8062, USA. hoby.hetherington@yale.edu
Kuzniecky
R I
RI
Vives
K
K
Devinsky
O
O
Pacia
S
S
Luciano
D
D
Vasquez
B
B
Haut
S
S
Spencer
D D
DD
Pan
J W
JW
D000293:Adolescent; D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D003401:Creatine / Q000378:metabolism; D004833:Epilepsy, Temporal Lobe / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009415:Nerve Net / Q000378:metabolism / Q000503:physiopathology*; D011699:Putamen / Q000378:metabolism / Q000503:physiopathology; D013788:Thalamus / Q000378:metabolism / Q000503:physiopathology
D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine