Magnetic resonance imaging – MRI

Neuroimaging is crucial in evaluating patients with focal epilepsy, to identify the structural basis of the seizures. MRI is generally the method of choice. In the last decade, expertise and technical improvements have yielded increased sensitivity in detecting epileptogenic lesions, but even high‐resolution qualitative MRI does not reveal significant pathology in 20–30% of patients with chronic focal epilepsy.

The clinical value of MRI depends strongly on the expertise of those obtaining and interpreting the images. Standard MRI based on axial images and read by radiologists unfamiliar with epilepsy investigations fail to detect up to 50% of focal epileptogenic lesions (Von Oertzen et al., 2002). Therefore, a report of “MRI negativity” may mislead, and good candidates for epilepsy surgery may not be referred appropriately (Fig. 2).

Figure 2 Open in figure viewer PowerPoint MR images of left‐sided hippocampal sclerosis. (A) Sagittal T 1 with a line demonstrating the orientation of the coronal images perpendicular to the long axis of the hippocampus, corresponding to the level of the coronal T 1 in D. (B) Coronal FLAIR image illustrating the atrophy and T 2 hyperintensity. (C) Coronal T 2 confirming the FLAIR images. (D) T 1 ‐weighted image.

Most patients referred for epilepsy surgery have MTLE, and HS is the most common histopathologic finding in the resected tissue. In the early 1990s, it was recognized that MRI could detect HS (Jackson et al., 1990; Berkovic et al., 1991). The standard MRI protocol for temporal lobe abnormalities uses coronal slices perpendicular to the long axis of the hippocampus. The MRI features of HS include reduced hippocampal volume, increased signal intensity on T 2 ‐weighted imaging, and disturbed internal architecture (Jackson et al., 1990, 1993; Woermann et al., 1998). Furthermore, temporal lobe atrophy, dilatation of the temporal horn, and blurring of the gray–white matter interface may accompany HS (Meiners et al., 1994; Moran et al., 2001). The hyperintense signal change on T 2 ‐weighted images can be enhanced by using FLAIR (a fluid‐attenuated inversion recovery pulse sequence), but since this can give false‐positive results, FLAIR findings must be confirmed with T 2 ‐weighted images. T 1 ‐weighted images provide detailed information on hippocampal anatomy and gyral patterns and a clear contrast between gray and white matter.

Reduced hippocampal volumes on MRI correlate with lower neuron cell counts in the hippocampus (Bronen et al., 1991; Lencz et al., 1992; Van Paesschen et al., 1997). The increased T 2 signal in HS probably reflects gliosis; one study showed this was influenced mainly by gliosis in the dentate gyrus (Briellmann et al., 2002).

HS may accompany lesions located outside the hippocampus and even outside the temporal lobe—so called “dual pathology.” Early ischemic lesions, hemiatrophy, low‐grade tumors, vascular malformations, and malformations of cortical development can be associated with HS and are mostly ipsilateral (Hofman et al., 2011). Neocortical thinning may also accompany HS (Bonilha et al., 2010; Labate et al., 2011a) (Fig. 3).

Figure 3 Open in figure viewer PowerPoint Dual pathology. (A) Coronal FLAIR image demonstrating right‐sided hippocampal sclerosis and hemiatrophy in a 7‐year old girl. (B) Coronal T 1 images illustrating loss of internal structure in the right temporal pole. After right‐sided TLR, histopathology showed hippocampal sclerosis and heterotopic neurons in the white matter. The patient is seizure‐free since surgery, now for 9 months.

It is important not to miss bilateral HS: when symmetric, it can be difficult to detect on MR. When suspected, volumetric quantification can help. Hippocampal volumes are measured manually or using automated methods. Manual measurement of hippocampal volume involves segmenting the hippocampus on serial sections of a T 1 ‐weighted MR scan acquired perpendicular to the long axis of the hippocampus (Jack et al., 1990; Cook et al., 1992; Watson et al., 1992). Expert manual volumetry is more sensitive than automated methods but requires a trained operator. If not available, automated methods can also be valuable (Pardoe et al., 2009).

MRI features of HS must be carefully assessed and interpreted in their clinical context. Despite the strong relationship between HS and the severity of the epilepsy in MTLE, some patients with well‐controlled MTLE have MRI signs of HS (Labate et al., 2011b). Hippocampal hyperintense FLAIR signal occurs in about one third of normal controls (Labate et al., 2010) but is never associated with hippocampal atrophy. A unilateral enlarged temporal horn, common in HS, also occurs frequently in controls and should not be considered pathologic in isolation (Menzler et al., 2010).

Tertiary epilepsy centers are starting to use new MR methods with increased sensitivity. The so‐called PROPELLER sequence (Periodically Rotated Overlapping Parallel Lines with Enhanced Reconstruction) has excellent contrast between gray and white matter and compensates for subjects moving during the scan (Eriksson et al., 2008). Higher field‐strength MRI scanners (commonly 3T and, for research purposes, 7T) have a higher yield, especially when evaluating malformations of cortical development, but also produce more pronounced artifacts due to greater field inhomogeneity. The added value for diagnosing HS could be through its improved detection of even very small intrahippocampal structural changes and through demonstrating regional differences in hippocampal atrophy (Breyer et al., 2010). However, when MTLE is the likely cause of chronic drug‐resistant epilepsy, a standard MRI protocol for temporal lobe abnormalities on a 1.5‐T scanner is adequate (Symms et al., 2004; Jeukens et al., 2009; Woermann & Vollmar, 2009; Hashiguchi et al., 2010). Sending MR images to epilepsy centers for second opinion is an underutilized resource, both for checking protocol adequacy and for image interpretation.