Morphological and Advanced Imaging of Epilepsy: Beyond the Basics

Abstract

The etiology of epilepsy is variable and sometimes multifactorial. Clinical course and response to treatment largely depend on the precise etiology of the seizures. Along with the electroencephalogram (EEG), neuroimaging techniques, in particular, magnetic resonance imaging (MRI), are the most important tools for determining the possible etiology of epilepsy. Over the last few years, there have been many developments in data acquisition and analysis for both morphological and functional neuroimaging of people suffering from this condition. These innovations have increased the detection of underlying structural pathologies, which have till recently been classified as "cryptogenic" epilepsy. Cryptogenic epilepsy is often refractory to anti-epileptic drug treatment. In drug-resistant patients with structural or consistent functional lesions related to the epilepsy syndrome, surgery is the only treatment that can offer a seizure-free outcome. The pre-operative detection of the underlying structural condition increases the odds of successful surgical treatment of pharmacoresistant epilepsy. This article provides a comprehensive overview of neuroimaging techniques in epilepsy, highlighting recent advances and innovations and summarizes frequent etiologies of epilepsy in order to improve the diagnosis and management of patients suffering from seizures, especially young patients and children.

Keywords: cortical malformations; diffusion tensor imaging; epilepsy; hippocampal sclerosis; magnetic resonance imaging (MRI); positron emission topography-computed tomography (PET-CT); single positron emission computed tomography (SPECT); spectroscopy.

Figure 1

33-year-old female with MERRF (myoclonic epilepsy with ragged red fibers) and myoclonic epilepsy. Axial T2 (a), Fluid-attenuated inversion recovery (FLAIR) (b) and Diffusion weighted imaging (DWI) (c) trace images (b = 1000) show cortical thickening in the right frontal (arrow) and bilateral pericingulate region (arrowhead) with subcortical white matter hyperintensity and restricted diffusion (ADC images not shown). Magnetic Resonance (MR) spectrum (d) at short TE (35 ms) at the level of right pericingulate lesion (region of interest of 1 cm diameter) shows lactate peak at 1.33 ppm (curved arrow) consistent with mitochondrial encephalopathy.

Figure 2

14-year-old female with parieto-occipital polymicrogyria. Sagittal T1 magnetization/prepared-2-rapid-acquisition-gradient-echo (MP2RAGE) (a) image showing numerous small gyri involving the parasagittal parieto-occipital region (arrow) and calcarine sulcus (black arrow) with mild cortical hyperintensity (arrowheads) on axial FLAIR (b) images suggestive of polymicrogyria.

Figure 3

Patient with tuberosis sclerosis complex: the interictal Single-photon emission computed tomography (SPECT) and fluorodeoxyglucose-positron emission tomography (FDG-PET) (fused with MRI FLAIR images) show multiple hypometabolic foci, corresponding to the multiple tubers. Ictal SPECT shows ictal hyperperfusion of the superior right frontal tuber.

Figure 4

36-year-old woman. The right hippocampus is smaller than the left (arrows) as seen on coronal T2WI (a), FLAIR (b) and MP2RAGE (c) and shows hyperintensity on T2WI and FLAIR. There is also flattening and loss of the normal undulations of the right hippocampus, suggestive of hippocampal sclerosis.

Figure 5

10-year-old girl with cortical dysplasia. There is thickening of the cortex on the left mesial fronto-parietal region (arrows in (a) to (f)) associated to funnel-shaped hyperintensity of the surrounding white matter (arrows in (b,e)). Note blurring between the white and gray matter interface (f).

Figure 6

6-month-old baby. Axial T2WI slices through the lateral ventricles (a) and occipital lobes (b) demonstrate a distinct lack of normal brain gyration with a smooth and thickened appearance of the cortex and unfolded gyri, most pronounced in both parietal, temporal and occipital lobes (arrows) consistent with lissencephaly. Note the posterior-anterior gradient with some rudimental sulcation seen in the frontal lobes. Band heterotopia can be clearly seen in the parietal regions on sagittal T1 IR (c) with cobblestone appearance (arrow).

Figure 7

(a) 25-year-old female with Tuberosis Sclerosis Complex (TSC). Axial CT image (a) shows multiple calcified subependymal nodules (arrows). (b–e) Another 23-year-old female with TSC. Axial T1 weighted image (b) showing multiple subependymal hyperintense nodules (arrows). Coronal FLAIR (c) with curvilinear multiplanar reformat (d) shows multiple cortical tubers with radiating subcortical white matter hyperintensity (arrowheads). PET CT (e) shows hypometabolic areas corresponding to cortical tubers in bilateral occipito-temporal and left temporal region (arrows). (f) 14-year-old male with TSC. Coronal reformat of 3D T1 post contrast image (black arrowhead) shows enhancing subependymal giant cell astrocytoma abutting the floor of frontal horn of left lateral ventricle.

Figure 8

31-year-old woman. Axial T1 Gd (a) and T2WI (b) demonstrate a large meningioma arising from the left tentorium cerebelli (arrows). The mass exerts significant mass effect on the adjacent brain parenchyma with vasogenic edema (arrowhead) of the left temporal and occipital white matter.

Figure 9

Right frontal cavernoma. Axial CT image (a) shows right frontal periventricular hyperdensity (arrow) abutting the frontal horn of the lateral ventricle. Axial T2 (b), FLAIR (c), GRE (d) and DWI (e) trace images (b = 1000) show peripheral hypointense rim with central hyperintensity (arrow). Axial T1 VIBE post-contrast image (f) shows mild enhancement (arrow) consistent with cavernoma.

Figure 10

20-year-old female with epilepsy. Axial T2 weighted (a) and coronal FLAIR (b) images show irregularity of the contour of the left lateral ventricle with ex vacuo dilatation, hyperintensity and paucity of periventricular white matter (arrowhead) in the frontal region suggestive of sequalae of perinatal insult i.e., periventricular leukomalacia.

Figure 11

35-year-old woman with herpes encephalitis. Non-contrast CT (a) shows low attenuation in the right mesial temporal region (white arrows). DWI b1000 (b) and ADC map (c) confirm bilateral but asymmetrical restricted diffusion in the mesial temporal areas (white arrows and arrowhead). No haemorrhage is identified on T2* (d). There are signal abnormalities on FLAIR (e,f), most pronounced in the right mesial temporal lobe (white arrow), right insula (black arrowhead) and right frontal lobe (black arrow). MRI performed 2 months later (g,h) shows bilateral areas of encephalomalacia (white arrows and arrowhead), more pronounced on the right, despite treatment.

Figure 12

18-year-old female with medically refractory epilepsy. Coronal T2 (a) and FLAIR (b) images show hemispherical parenchymal volume loss and cortical thinning (asterisk) on the left side with resultant ex vacuo dilatation of the frontal (arrow) and temporal horns (arrowhead) of the left lateral ventricle, consistent with Rasmussen’s encephalitis.

Figure 13

50-year-old woman. Symmetrical hyperintensity is identified on coronal T2WI (a) and FLAIR (b) in both hippocampi (arrows). No abnormal enhancement is seen on 3D T1 Gd (c). This is a case of autoimmune limbic encephalitis.

Figure 14

68-year-old woman with left temporal meningoencephalocele. Axial 3D high-ponderated T2 sequence (a) shows herniation of abnormal brain parenchyma, meninges and cerebrospinal fluid (arrow) into a defect of the greater wing of the sphenoid bone, best seen on CT in the bone window (arrowhead in (b)). This is further illustrated by a 3D cinematic rendering of the 3D T2 acquisition with a left posterior-anterior oblique vantage point (c), which demonstrates the full caudal extent of the meningoencephalocele within the sphenoid bone (arrow).