Multimodality imaging in partial epilepsies

Current Opinion in Neurology

Volumn 17, Issue 2, 2004, Pages 165-172

  Knowlton, Robert C ^a  

^a UNIVERSITY OF ALABAMA AT BIRMINGHAM   (United States)

Author keywords

Epilepsy; Imaging; MRI; MRS; PET; SPM

Indexed keywords

CARBON 11; FLUMAZENIL; FLUORODEOXYGLUCOSE F 18; N METHYLTRYPTOPHAN;

BRAIN BLOOD FLOW; BRAIN METABOLISM; DIFFUSION WEIGHTED IMAGING; ELECTROENCEPHALOGRAPHY; EPILEPSY; EPILEPTOGENESIS; FOCAL EPILEPSY; HUMAN; MAGNETOENCEPHALOGRAPHY; NEUROIMAGING; NEURORADIOLOGY; NUCLEAR MAGNETIC RESONANCE IMAGING; NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY; PATHOPHYSIOLOGY; POSITRON EMISSION TOMOGRAPHY; REVIEW; SINGLE PHOTON EMISSION COMPUTER TOMOGRAPHY;

BRAIN DAMAGE, CHRONIC; BRAIN MAPPING; CEREBRAL CORTEX; CHILD; DISEASE PROGRESSION; ELECTROENCEPHALOGRAPHY; EPILEPSIES, PARTIAL; HIPPOCAMPUS; HUMANS; IMAGE PROCESSING, COMPUTER-ASSISTED; MAGNETIC RESONANCE IMAGING; MAGNETIC RESONANCE SPECTROSCOPY; MAGNETOENCEPHALOGRAPHY; SCLEROSIS; SENSITIVITY AND SPECIFICITY; TEMPORAL LOBE; TOMOGRAPHY, EMISSION-COMPUTED;

EID: 1842557960     PISSN: 13507540     EISSN: None     Source Type: Journal    
DOI: 10.1097/00019052-200404000-00014     Document Type: Review

References (54)

1. Duncan JS. Neuroimaging in epilepsy: quality and not just quantity is important: current resources for neuroimaging could be used more efficiently. J Neurol Neurosurg Psychiatry 2003; 73:612-613.
2. Von Oertzen J, Urbach H, Jungbluth S, et al. Standard magnetic resonance imaging is inadequate for patients with refractory focal epilepsy [Comment]. J Neurol, Neurosurg Psychiatry 2002; 73:643-647.
3. Tassi L, Colombo N, Garbelli R, et al. Focal cortical dysplasia: neuropathological subtypes, EEG, neuroimaging and surgical outcome. Brain 2002; 125:1719-1732.
4. Yang KH, Kim DS, Choi JU. The reversible focal MRI abnormalities in complex partial seizure: technical instruction. Childs Nerv Syst 2002; 18:722-724.
5. 11C]-flumazenil PET in mesial temporal lobe epilepsy. Neurology 2001; 56:897-906.
6. 11C]flumazenil binding in temporal lobe epilepsy with normal MRI. Brain 2002; 125:2257-2271.
7. Hammers A, Koepp MJ, Richardson MP, et al. Grey and white matter flumazenil binding in neocortical epilepsy with normal MRI: a PET study of 44 patients. Brain 2003; 126:1300-1318. PET flumazenil binding was measured in 44 patients with neocortical partial epilepsy and normal MRI. The work presents major clinical implications for the possible detection of cryptic microdysgenesis and migrational abnormalities that may have prognostic significance for surgical treatment.
8. 11C]methyl-L- tryptophan positron emission tomography. Ann Neurol 1998; 44:858-866.
9. 11C]-methyl-L- tryptophan PET identifies the epileptogenic tuber and correlates with interictal spike frequency. Epilepsy Res 2003; 52:203-213.
10. Zubal IG, Spencer SS, Imam K, et al. Difference images calculated from ictal and interictal technetium-99m-HMPAO SPECT scans of epilepsy. J Nucl Med 1995; 36:684-689.
11. O'Brien TJ, So EL, Mullan BP, et al. Subtraction SPECT co-registered to MRI improves postictal SPECT localization of seizure foci. Neurology 1999; 52:137-146.
12. Valenti MP, Froelich S, Armspach JP, et al. Contribution of SISCOM imaging in the presurgical evaluation of temporal lobe epilepsy related to dysembryoplastic neuroepithelial tumors. Epilepsia 2002; 43:270-276.
13. Lee D, Kim H-J, Lee B, et al. Evaluation of ictal brain SPECT using statistical parametric mapping in temporal lobe epilepsy. Eur J Nucl Med 2000; 27:1658-1665.
14. Chang DJ, Zubal IG, Gottschalk C, et al. Comparison of statistical parametric mapping and SPECT difference imaging in patients with temporal lobe epilepsy. Epilepsia 2002; 43:68-74.
15. Wieshmann UC, Symms MR, Shorvon SD. Diffusion changes in status epilepticus. Lancet 1997; 350:493-494.
16. Wieshmann UC, Clark CA, Symms MR, et al. Water diffusion in the human hippocampus in epilepsy. Magn Reson Imag 1999; 17:29-36.
17. Hugg J, Butterworth E, Kuzniecky R. Diffusion mapping applied to mesial temporal lobe epilepsy: preliminary observations. Neurology 1999; 53:173-176.
18. Eriksson SH, Rugg-Gunn FJ, Symms MR, et al. Diffusion tensor imaging in patients with epilepsy and malformations of cortical development. Brain 2001; 124:617-626.
19. Rugg-Gunn FJ, Eriksson SH, Symms MR, et al. Diffusion tensor imaging of cryptogenic and acquired partial epilepsies. Brain 2001; 124:627-636.
20. Konstantinos A, Hermann BP, Rogers BP, et al. Diffusion tensor MRI in temporal lobe epilepsy. Magn Reson Imag 2002; 20:511-519.
21. Rugg-Gunn FJ, Eriksson SH, Symms MR, et al. Diffusion tensor imaging in refractory epilepsy. Lancet 2002; 359:1748-1751.
22. Ebersole JS. Magnetoencephalography/magnetic source imaging in the assessment of patients with epilepsy. Epilepsia 1997; 38 (Suppl 4):S1-S5.
23. Moore KR, Funke ME, Constantino T, et al. Magnetoencephalographically directed review of high-spatial-resolution surface-coil MR images improves lesion detection in patients with extratemporal epilepsy. Radiology 2002; 225:880-887.
24. Zhang W, Simos PG, Ishibashi H, et al. Multimodality neuroimaging evaluation improves the detection of subtle cortical dysplasia in seizure patients. Neurol Res 2003; 25:53-57.
25. Eliashiv DS, Elsas SM, Squires K, et al. Ictal magnetic source imaging as a localizing tool in partial epilepsy. Neurology 2002; 59:1600-1610.
26. Jager L, Werhahn KJ, Hoffmann A, et al. Focal epileptiform activity in the brain: detection with spike-related functional MR imaging - preliminary results. Radiology 2002; 223:860-869.
27. Deblaere K, Backes WH, Hofman P, et al. Developing a comprehensive presurgical functional MRI protocol for patients with intractable temporal lobe epilepsy: a pilot study. Neuroradiology 2002; 44:667-673.
28. Binder JR, Swanson SJ, Hammeke TA, et al. Determination of language dominance using functional MRI: a comparison with the Wada test. Neurology 1996; 46:978-984.
29. Detre J, Maccotta L, King D, et al. Functional MRI lateralization of memory in temporal lobe epilepsy. Neurology 1998; 50:926-932.
30. Binder JR, Swanson SJ, Hammeke TA, et al. Determination of language dominance using functional MRI: a comparison with the Wada test. Neurology 1996; 46:978-984.
31. Benson R, FitzGerald D, LeSueur L, et al. Language dominance determined by whole brain functional MRI in patients with brain lesions. Neurology 1999; 52:798-809.
32. Wellmer J, von Oertzen J, Schaller C, et al. Digital photography and 3D MRI-based multimodal imaging for individualized planning of resective neocortical epilepsy surgery. Epilepsia 2002; 43:1543-1550.
33. Mathern GW, Babb TL, Vickrey BG, et al. The clinical-pathogenic mechanisms of hippocampal neuron loss and surgical outcomes in temporal lobe epilepsy. Brain 1995; 118:105-118.
34. Kobayashi E, Sousa SC, Lopes-Cendes I, et al. Seizure outcome and hippocampal atrophy in familial mesial temporal lobe epilepsy. Neurology 2001; 56:166-172.
35. Kobayashi E, D'Agostino D, Lopes-Cendes I, et al. Hippocampal atrophy and T2-weighted signal changes in familial mesial temporal lobe epilepsy. Neurology 2003; 60:405-409. This remarkable work reveals a high frequency of hippocampal atrophy/ hippocampal sclerosis (even bilateral) in 99 out of 142 patients with familial MTLE - present in all groups, including those with well-controlled seizures. A major conclusion to be considered is that hippocampal abnormality may be genetically determined and is not necessarily associated with poor seizure control.
36. Kobayashi E, Li LM, Lopes-Cendes I, et al. Magnetic resonance imaging evidence of hippocampal sclerosis in asymptomatic, first-degree relatives of patients with familial mesial temporal lobe epilepsy. Arch Neurol 2002; 59:1891-1894.
37. Keller SS, Wieshmann UC, Mackay CE, et al. Voxel based morphometry of grey matter abnormalities in patients with medically intractable temporal lobe epilepsy: effects of side of seizure onset and epilepsy duration. J Neurol, Neurosurg Psychiatry 2002; 73:648-655. This remarkable study using voxel-based morphometry further supports two proposed concepts or hypotheses: that an initial early insult (e.g. PFC) is predominantly responsible for the development of hippocampal sclerosis, and recurrent seizures over time are responsible for secondary injury.
38. Theodore WH, DeCarli C, Gaillard WD. Total cerebral volume is reduced in patients with localization-related epilepsy and a history of complex febrile seizures. Arch Neurol 2003; 60:250-252. MRI-based volumetry was performed in 40 patients with intractable TLE. This study indicates that even secondary brain effects may be more related to an early insult/injury rather than recurrent seizures.
39. Briellmann RS, Berkovic SF, Syngeniotis A, et al. Seizure-associated hippocampal volume loss: a longitudinal magnetic resonance study of temporal lobe epilepsy. Ann Neurol 2002; 51:641-644. Serial MRI hippocampal volumetry was performed prospectively in 24 patients with newly diagnosed TLE shortly after onset and 3.5 years later. This work should be interpreted in the context of other work documenting the evolution of hippocampal sclerosis shortly after an early insult, such as PFC.
40. Fuerst D, Shah J, Shah A, et al. Hippocampal sclerosis is a progressive disorder: a longitudinal volumetric MRI study. Ann Neurol 2003; 53:413-416. Serial MRI hippocampal volumetry was performed in 12 patients with chronic TLE with hippocampal sclerosis. This work is important in demonstrating the progression of hippocampal atrophy in chronic TLE, but it should not be interpreted to account for the cause of hippocampus sclerosis.
41. Salmenpera T, Kalviainen R, Partanen K, et al. Hippocampal and amygdaloid damage in partial epilepsy: a cross-sectional MRI study of 241 patients. Epilepsy Res 2001; 46:69-82.
42. Scott RC, King MD, Gadian DG, et al. Hippocampal abnormalities after prolonged febrile convulsion: a longitudinal MRI study. Brain 2003; 126:2551-2557. MRI was performed in 14 children between 4 and 8 months of age of a PFC who had previously been studied within 5 days of the event. These are the best data available on evolving hippocampal sclerosis in patients with PFC. Future MRI studies on this cohort should be very revealing on the important issue of hippocampal injury and the evolution of hippocampal sclerosis.
43. Gaillard WD, Kopylev L, Weinstein S, et al. Low incidence of abnormal (18)FDG-PET in children with new-onset partial epilepsy: a prospective study. Neurology 2002; 58:717-722.
44. Knowlton RC, Laxer KD, Klein G, et al. In vivo hippocampal glucose metabolism in mesial temporal lobe epilepsy. Neurology 2001; 57:1184-1190.
45. Vielhaber S, Von Oertzen JH, Kudin AF, et al. Correlation of hippocampal glucose oxidation capacity and interictal FDG-PET in temporal lobe epilepsy. Epilepsia 2003; 44:193-199. This work represents a substantial attempt to understand the metabolic disturbances in MTLE, with findings supporting the hypothesis that impaired mitochondrial metabolism is the primary cause of the relative hypometabolism detected with FDG-PET.
46. Kunz W, Kudin A, Vielhaber S, et al. Mitochondrial complex I deficiency in the epileptogenic focus of patients with temporal lobe epilepsy. Neurology 2000; 48:766-773.
47. Kuzniecky R, Palmer C, Hugg J, et al. Magnetic resonance spectroscopic imaging in temporal lobe epilepsy: neuronal dysfunction or cell loss? Arch Neurol 2001; 58:2048-2053.
48. Knowlton RC, Abou-Khalil B, Sawrie SM, et al. In vivo hippocampal metabolic dysfunction in human temporal lobe epilepsy. Arch Neurol 2002; 59:1882-1886. Hippocampal FDG uptake and NAA were measured in vivo with PET and MRS in 29 patients with MTLE. Neither the normalized hippocampal FDG metabolic index nor hippocampal FDG asymmetry correlated with NAA measures. The absence of correlation was interpreted to reflect a hypothesized differential effect of varying degrees of disturbed cellular energy metabolism on the mechanisms of glucose use and the biosynthesis of NAA.
49. Petroff OAC, Errante LD, Jung KH, et al. N-acetyl-aspartate, total creatine, and myo-inositol in the epileptogenic human hippocampus. Neurology 2003; 60:1646-1651. This work strongly supports the conclusion that decreased NAA in MTLE reflects altered metabolism - not merely neuronal loss or gliosis. The numerous possible mechanisms for mitochondrial disturbances that could be responsible for decreased NAA in epileptogenic tissue are appropriately discussed, and include not just abnormalities in NAA synthesis, but also transporters between neural and glial cells required in NAA catabolism.
50. Hugg JW, Kuzniecky RI, Gilliam FG, et al. Normalization of contralateral metabolic function following temporal lobectomy demonstrated by 1H magnetic resonance spectroscope imaging. Ann Neurol 1996; 40:236-239.
51. Cendes F, Andermann F, Dubeau F, et al. Normalization of neuronal metabolic dysfunction after surgery for temporal lobe epilepsy: evidence from proton MR spectroscopic imaging. Neurology 1997; 49:1525-1533.
52. Capizzano AA, Vermathen P, Laxer KD, et al. Multisection proton MR spectroscopy for mesial temporal lobe epilepsy. Am J Neuroradiol 2002; 23:1359-1368.
53. Guye M, Le Fur Y, Confort-Gouny S, et al. Metabolic and electrophysiological alterations in subtypes of temporal lobe epilepsy: a combined proton magnetic resonance spectroscopic imaging and depth electrodes study. Epilepsia 2002; 43:1197-1209.
54. Archer JS, Briellman RS, Syngeniotis A, et al. Spike-triggered fMRI in reading epilepsy: involvement of left frontal cortex working memory area. Neurology 2003; 60:415-421.