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AJNR Awards, New Junior Editors, and more. Read the latest AJNR updates

Research ArticleBRAIN

MR Imaging in the Presurgical Workup of Patients with Drug-Resistant Epilepsy

Horst Urbach, Jörg Hattingen, Joachim von Oertzen, Cordelia Luyken, Hans Clusmann, Thomas Kral, Martin Kurthen, Johannes Schramm, Ingmar Blümcke and Hans H. Schild
American Journal of Neuroradiology June 2004, 25 (6) 919-926;
Horst Urbach
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Jörg Hattingen
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Joachim von Oertzen
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Cordelia Luyken
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Hans Clusmann
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Thomas Kral
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Martin Kurthen
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Johannes Schramm
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Ingmar Blümcke
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Hans H. Schild
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  • Fig 1.
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    Fig 1.

    Scarring of the left superior frontal gyrus. Axial 5-mm-thick (a–c) and coronal 3-mm-thick (d) FLAIR fast spin-echo images show an atrophic and hyperintense lesion in the right superior frontal gyrus (solid-head arrows in a–d). Note also a tiny increase in signal intensity and the atrophy in the depth of the right frontal superior sulcus (open-head arrows in a, c, and d)

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    Fig 2.

    Schematic depiction of method used in MR imaging lesion detection.

  • Fig 3.
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    Fig 3.

    Focal cortical dysplasia of the Taylor balloon cell type (FCDBC). Images in a and b show a small lesion in the depth of the left frontal superior sulcus (arrow). Image in c shows a huge lesion and a small lesion (arrow) in the right parietal and occipital lobe. Image in d shows a lesion under an atrophic left superior frontal gyrus. The MR imaging hallmark of FCDBC is a subcortical hyperintensity tapering toward the lateral ventricle. It is clearly visible (arrow), but because of atrophy of the superior frontal gyrus, the lesion was mistaken for gyral scarring.

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    Fig 4.

    Focal polymicrogyria in the left frontal lobe. Contiguous, 3-mm-thick, coronal FLAIR fast spin-echo sections (a–c) show a deep superior frontal sulcus with a slightly irregular contour and a normal signal intensity of the cortex (arrow). Planar surface-reconstructed view (d) generated from a 1.1-mm-thick, 3D, T1-weighted gradient-echo sequence confirms the distorted anatomy (arrow). Histopathologic sections show loss of neocortical architecture (MAP2 [e]) compared with that of adjacent six–layered cortex (nematoxylin–eosin straining [f]).

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    Fig 5.

    PXA of the right temporal lobe. The lesion shows typical meningeocerebral contrast enhancement (arrows), cystic parts, and surrounding edema.

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    Fig 6.

    Anaplastic (limbic) astrocytoma of WHO grade III. Coronal 3-mm-thick FLAIR fast spin-echo sections show increased volume and signal intensity of both temporopolar cortices, the amygdala, hippocampi, thalami, and left parietal cortex. Because repeated CSF investigation showed a slightly increased protein content (54–95 mg/dL) and 6–8 cells per microliter, limbic encephalitis was suspected.

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    Fig 7.

    Schematic diagram depicting reasons not to operate on patients with MR imaging lesions.

Tables

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    TABLE 1:

    MR lesion type and seizure outcome

    Outcome/Engel IA Class
    MR with lesion
     Hippocampal sclerosis104 (50%)65/93 (70%)
     Ectopic white matter neurons3 (1%)2/3 (66%)
     FCD with balloon cells17 (8%)13/16 (81%)
     FCD without balloon cells5 (2%)2/4 (50%)
     Polymicrogyria1 (0.5%)0/1 (0%)
     Ganglioglioma21 (10%)15/21 (71%)
     DNT10 (5%)7/9 (78%)
     PXA4 (2%)3/3 (100%)
     Glioma II, III8 (6%)6/7 (86%)
     Cavernoma15 (7%)11/15 (73%)
     Hemimegalencephaly2 (1%)1/2 (50%)
     Meningeoangiomatosis1 (0.5%)1/1 (100%)
     Ulegyria, cortical, or glial scar9 (4%)3/9 (33%)
     Tuber cinereum hamartoma2 (1%)1/2 (50%)
    MR without lesion
     NAD10/1
     Reactive gliosis63/6
     Ectopic white matter neurons22/2
    • Note.—NAD indicates nothing abnormal detected.

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    TABLE 2:

    Lesion type and MR diagnosis

    Histopathologic FindingsMR Findings
    Hippocampal sclerosis101 hippocampal sclerosis, 3 atrophy, no sclerosis
    Ectopic white matter neurons2 poor gray-white matter demarcation, 1 FCD without BC, 2 NAD
    FCD with balloon cells (FCDBC)14 FCDBC, 2 cortical/glial scar, 1 equivocal findings
    FCD without balloon cells3 FCD without BC, 2 ganglioglioma
    Polymicrogyria1 Polymicrogyria
    Ganglioglioma16 ganglioglioma, 4 FCD without BC, 1 DNT
    DNT8 DNT, 1 ganglioglioma, 1 FCD without BC
    PXA1 PXA, 3 ganglioglioma
    Glioma II, III5 glioma, 2 ganglioglioma, 1 limbic encephalitis
    Cavernoma15 cavernoma
    Enzephalitis (Rasmussen, limbic)5 encephalitis, 1 NAD
    Hemimegalencephaly2 hemimegalencephaly
    Meningeoangiomatosis1 ganglioglioma
    Ulegyria, cortical, or glial scar7 cortical/glial scar, 1 ganglioglioma, 1 DNT
    Tuber cinereum hamartoma2 tuber cinereum hamartoma
    Reactive gliosis6 NAD
    Normal1 NAD
    • Note.—NAD indicates nothing abnormal detected.

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American Journal of Neuroradiology: 25 (6)
American Journal of Neuroradiology
Vol. 25, Issue 6
1 Jun 2004
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Cite this article
Horst Urbach, Jörg Hattingen, Joachim von Oertzen, Cordelia Luyken, Hans Clusmann, Thomas Kral, Martin Kurthen, Johannes Schramm, Ingmar Blümcke, Hans H. Schild
MR Imaging in the Presurgical Workup of Patients with Drug-Resistant Epilepsy
American Journal of Neuroradiology Jun 2004, 25 (6) 919-926;

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MR Imaging in the Presurgical Workup of Patients with Drug-Resistant Epilepsy
Horst Urbach, Jörg Hattingen, Joachim von Oertzen, Cordelia Luyken, Hans Clusmann, Thomas Kral, Martin Kurthen, Johannes Schramm, Ingmar Blümcke, Hans H. Schild
American Journal of Neuroradiology Jun 2004, 25 (6) 919-926;
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