Partial epilepsy: A pictorial review of 3 TESLA magnetic resonance imaging features

Abstract

Epilepsy is a disease with serious consequences for patients and society. In many cases seizures are sufficiently disabling to justify surgical evaluation. In this context, Magnetic Resonance Imaging (MRI) is one of the most valuable tools for the preoperative localization of epileptogenic foci. Because these lesions show a large variety of presentations (including subtle imaging characteristics), their analysis requires careful and systematic interpretation of MRI data. Several studies have shown that 3 Tesla (T) MRI provides a better image quality than 1.5 T MRI regarding the detection and characterization of structural lesions, indicating that high-field-strength imaging should be considered for patients with intractable epilepsy who might benefit from surgery. Likewise, advanced MRI postprocessing and quantitative analysis techniques such as thickness and volume measurements of cortical gray matter have emerged and in the near future, these techniques will routinely enable more precise evaluations of such patients. Finally, the familiarity with radiologic findings of the potential epileptogenic substrates in association with combined use of higher field strengths (3 T, 7 T, and greater) and new quantitative analytical post-processing techniques will lead to improvements regarding the clinical imaging of these patients. We present a pictorial review of the major pathologies related to partial epilepsy, highlighting the key findings of 3 T MRI.

Figure 1

Hippocampal sclerosis in a 31-year-old man with refractory right mesial temporal sclerosis. A) coronal T2-weighted image and B) coronal FLAIR images, both perpendicular to the long axis of the hippocampus. These images show a hyperintense signal, the loss of digitations and atrophy in the right hippocampal head (white arrow).

Figure 2

Bilateral hippocampal sclerosis and “dual pathology” in a 34-year-old woman. A) Coronal FLAIR image showing bilateral hippocampal atrophy and hyperintensity as well as a hyperintense lesion in the right superior temporal gyrus. B) Coronal T1-weighted image after a contrast administration revealed a nodular mass enhancement situated at the gray-matter-white-matter junction (white arrows); this mass might correspond to a developmental neoplasm. This lesion appeared stable on consecutive MRI scans.

Figure 3

A typical MRI of focal transmantle cortical dysplasia in a 34-year-old woman. A) A coronal T2-weighted image demonstrating focal hyperintensity and the thickening of the right frontal cortex with a loss of demarcation between the gray and white matter (white arrow). B) A coronal T2 FLAIR showing a band of abnormal signal intensity extending from the cortex to the lateral ventricle (white arrows).

Figure 4

Focal cortical dysplasia type IIB of Palmini in a 10-year-old girl. A) An axial T2-weighted image demonstrating a focal thickening of the right parietal cortex (white arrows). B) An automated analysis of cortical thickness generated by Freesurfer using a volumetric T1-weighted image. These measurements clearly show a significant focal area of cortical thickening in the right superior parietal region that corresponds to the lesion observed in the T2-weighted sequence.

Figure 5

Tuberous sclerosis in a 21-year-old female with drug-resistant partial epilepsy. A) Axial FLAIR images show hyperintense cortical tubers with a band of abnormal signal intensity from the cortex to the lateral ventricle (white arrows) and B) multiple subependymal hamartome (green arrows) with a hyperintense signal.

Figure 6

A MRI of a ganglioglioma in a 45-year-old man with refractory left partial mesial temporal lobe epilepsy. A) A coronal T2-weighted image and B) a contrast-enhanced coronal T1-weighted image showing a solid-cystic lesion in the mesial left temporal lobe with intense enhancement of the soft tissue component (white arrows).

Figure 7

Familial cerebral cavernous malformations caused by a KRIT1 gene mutation in a 36-year-old woman with multiple epileptic foci (video-EEG) and chronic partial epilepsy. A) Coronal T2-weighted images show the typical appearance of a type 2 cavernoma (white arrows) characterized by mixed signal intensity with a hemosiderin ring. B) An axial T2*-weighted gradient-echo sequence revealing two type 4 cavernomas (black arrows) in the right temporal lobe, only observed using this sequence.

Figure 8

Rasmussen encephalitis confirmed via biopsy in a 37-year-old woman with refractory partial motor epilepsy. A) An axial T2-weighted image and B) a coronal T2-weighted image showing atrophy and gliosis of the right frontal lobe.

Figure 9

Sturge-Weber syndrome in a 14-year-old boy with multiple epileptic foci in the right cerebral hemisphere (video-EEG) and chronic partial epilepsy. A) An axial T2-weighted image showing right cerebral hemiatrophy (white arrows). B) An axial T1-weighted sequence after gadolinium injection, demonstrating leptomeningeal enhancement of the fronto-parietal region (white arrows). C) Axial SWI revealing cortical calcification in the frontal lobe, appearing as signal voids (white arrows).

Figure 10

Disseminated parenchymal neurocysticercosis in a 23-year-old man with intractable epilepsy and multiple epileptic foci (video-EEG). A) An axial T2 FLAIR sequence showing multiple vesicular cysts, some with scolex inside (white arrows). B) An axial T2 FLAIR image revealing perilesional edema in the right frontal lobe (white arrow). C) An axial TC shows multiple calcified lesions. These findings characterize the different phases of neurocysticercosis, which are pathognomonic of this disease.