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Multisection Proton MR Spectroscopy for Mesial Temporal Lobe Epilepsy - AJNR News Digest
April 2014
Brain

Multisection Proton MR Spectroscopy for Mesial Temporal Lobe Epilepsy

Aristides Capizzano

Aristides A. Capizzano

Proton MR spectroscopy (MRS) studies of patients with temporal lobe epilepsy (TLE) have consistently shown reduced concentration of the neuronal marker N-acetylaspartate (NAA) in the medial temporal lobe ipsilateral to the seizure focus. These findings not only replicate information available from the presence of hippocampal sclerosis (HS) on conventional MRI, but have also been detected in normal-appearing temporal lobes1–4 and in patients with bilateral HS.5 Furthermore, some of these studies showed that metabolic changes in these difficult clinical cases predict surgical outcome.4,5

Metabolic changes in TLE extend far beyond the areas of neuronal loss on histopathology, as shown by hypometabolism on interictal FDG-PET scans.6 Given the dependence of NAA synthesis on aerobic metabolism, we hypothesized that NAA reductions in TLE could be detected in ipsilateral cerebral cortical areas connected with the hippocampus by using a multisection MRS imaging sequence developed at the San Francisco Veterans Affairs Medical Center MRS laboratory. NAA reductions were consistently detected with high SNR spectra from the temporal operculum, insula, and lateral temporal cortex ipsilateral to the seizure focus. These findings agree with the extensive ipsilateral FDG-PET cerebral hypometabolism seen in TLE.6,7 Follow-up studies replicated the extrahippocampal NAA reduction in TLE,8–10 although the most recent of the latter studies using whole-brain 3D MRS coverage questioned the lateralizing value of these metabolic changes.9 This discrepancy with our study could result from different voxel selection approaches.

MRS can be done in the clinical setting at 1.5 or 3T using commercially available single voxel or multivoxel sequences centered at the hippocampi after manually adjusted local shimming. High-quality spectra can be obtained from the lateral temporal cortex and insula given their improved B0 homogeneity compared with the hippocampal region. However, sampling lateral cortical regions requires multisection or volumetric MRS sequences, whose availability from commercial manufacturers has been limited. Furthermore, multisection, and especially 3D MRS techniques, produce very large datasets that require time-consuming processing for quantitative interpretation, which is a limitation in the clinical arena. These

factors, together with the uncertain reimbursement of clinical MRS studies, have limited the clinical application of MRS in TLE. Notwithstanding these limitations, the authors' conviction is that MRS depicts regions of NAA reduction relevant for TLE lateralization in normal-appearing brain. MRI hardware and postprocessing software improvements, as well as increased availability of broad coverage MRS sequences, will likely result in wider clinical utilization of MRS in TLE.

References

  1. Woermann FG, McLean MA, Bartlett PA, et al. Short echo time single-voxel 1H magnetic resonance spectroscopy in magnetic resonance imaging-negative temporal lobe epilepsy: different biochemical profile compared with hippocampal sclerosis. Ann Neurol 1999;45:369–76
  2. Shih JJ, Weisend MP, Lewine J, et al. Areas of interictal spiking are associated with metabolic dysfunction in MRI-negative temporal lobe epilepsy. Epilepsia 2004;45:223–29
  3. Connelly A, Van Paesschen W, Porter DA, et al. Proton magnetic resonance spectroscopy in MRI-negative temporal lobe epilepsy. Neurology 1998;51:61–66
  4. Suhy J, Laxer KD, Capizzano AA, et al. 1H MRSI predicts surgical outcome in MRI-negative temporal lobe epilepsy. Neurology 2002;58:821–23
  5. Li LM, Cendes F, Antel SB, et al. Prognostic value of proton magnetic resonance spectroscopic imaging for surgical outcome in patients with intractable temporal lobe epilepsy and bilateral hippocampal atrophy. Ann Neurol 2000;47:195–200
  6. Engel J, Jr, Brown WJ, Kuhl DE, et al. Pathological findings underlying focal temporal lobe hypometabolism in partial epilepsy. Ann Neurol 1982;12:518–28
  7. Henry TR, Mazziotta JC, Engel J, Jr. Interictal metabolic anatomy of mesial temporal lobe epilepsy. Arch Neurol 1993;50:582–89
  8. Mueller SG, Suhy J, Laxer KD, et al. Reduced extrahippocampal NAA in mesial temporal lobe epilepsy. Epilepsia 2002;43:1210–16
  9. Mueller SG, Ebel A, Barakos J, et al. Widespread extrahippocampal NAA/(Cr+Cho) abnormalities in TLE with and without mesial temporal sclerosis. J Neurol 2011;258:603–12
  10. Mueller SG, Laxer KD, Cashdollar N, et al. Identification of abnormal neuronal metabolism outside the seizure focus in temporal lobe epilepsy. Epilepsia 2004;45:355–66

 

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