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Magnetic Resonance Spectroscopic Imaging in Temporal Lobe Epilepsy
Neuronal Dysfunction or Cell Loss?
Ruben Kuzniecky, MD;
Cheryl Palmer, MD;
James Hugg, PhD;
Roy Martin, PhD;
Steve Sawrie, PhD;
Richard Morawetz, MD;
Edward Faught, MD;
Robert Knowlton, MD
Arch Neurol. 2001;58:2048-2053.
Background Magnetic resonance spectroscopy (MRS) has demonstrated consistent metabolic abnormalities in temporal lobe epilepsy. The reason for decreases in N-acetylated compounds are thought to be related to neuronal hippocampal cell loss as observed in hippocampal sclerosis. However, mounting evidence suggest that the N-acetylated compound decreases may be functional and reversible.
Objective To establish whether the metabolic changes measured by MRS correlate to hippocampal cell loss in temporal lobe epilepsy.
Subjects and Methods We prospectively performed quantitative hippocampal MR imaging volumetry and MRS imaging in 33 patients with intractable mesial temporal lobe epilepsy who were undergoing surgery. A neuronal-glial ratio of cornu ammonis and fascia dentata was obtained and correlated while validating the pathologic analysis by comparisons with specimens of age-matched autopsy control-case hippocampus (n = 14).
Results The neuronal-glial ratio of the patient group was statistically significantly lower than in the control group for the cornu ammonis region (P<.001). Correlations of hippocampal volumes with cornu ammonis and neuronal-glial ratios revealed a significant interdependence (P<.01). However, correlations of the resected hippocampal creatine–N-acetylated compound ratio with the cornu ammonis or fascia dentata neuronal-glial ratios showed no significant interdependence (P>.8).
Conclusions Our findings support the concept that the metabolic dysfunction measured by MRS imaging and the hippocampal volume loss detected by MR imaging volumetry do not have the same neuropathologic basis. These findings suggest that the MRS imaging metabolic measures reflect neuronal and glial dysfunction rather than neuronal cell loss as previously assumed.
From the Departments of Neurology (Drs Kuzniecky, Hugg, Martin, Sawrie, Faught, and Knowlton), Pathology (Dr Palmer), and Neurosurgery (Dr Morawetz), University of Alabama at Birmingham Epilepsy Center.
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