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AJNR - American Journal of Neuroradiology

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

Horst Urbach^a, Jörg Hattingen^a, Joachim von Oertzen^b, Cordelia Luyken^c, Hans Clusmann^c, Thomas Kral^c, Martin Kurthen^b, Johannes Schramm^c, Ingmar Blümcke^d and Hans H. Schild^a

^a Department of Radiology, University of Bonn Medical Center, Germany
^b Department of Epileptology, University of Bonn Medical Center, Germany
^c Department of Neurosurgery, University of Bonn Medical Center, Germany
^d Department of Neuropathology, University of Bonn Medical Center, Germany

View larger version (137K): [in a new window]   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)

View larger version (28K): [in a new window]   FIG 2. Schematic depiction of method used in MR imaging lesion detection.

View larger version (176K): [in a new window]   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.

View larger version (108K): [in a new window]   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]).

View larger version (122K): [in a new window]   FIG 5. PXA of the right temporal lobe. The lesion shows typical meningeocerebral contrast enhancement (arrows), cystic parts, and surrounding edema.

View larger version (154K): [in a new window]   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.

View larger version (28K): [in a new window]   FIG 7. Schematic diagram depicting reasons not to operate on patients with MR imaging lesions.