**Abstract**

This chapter will cover the neuroimaging techniques and their application to the diagnostic work up and management of adults and children with new onset or chronic epilepsy. We will focus on the specific indications and requirements of different imaging techniques for the diagnosis and pre-surgical work up of pharmacoresistant focal epilepsies. We will discuss the sensitivity, specificity and prognostic value of imaging features, benign variants and artefacts, and the possible diagnostic significance of non-epileptogenic lesions. This chapter is intended to be relevant for day-to-day practice in average clinical circumstances, with emphasis on MRI and most commonly used functional neuroimaging techniques.

**Keywords:** MRI, epilepsy, temporal, extratemporal, SPECT, PET

## **1. Introduction**

The advent of neuroimaging has provided powerful tools for the identification of epileptogenic lesions preoperatively. This has increased the number of surgical candidates and improved postsurgical outcomes [1–3]. The approach of presurgical evaluation in patients with potential epileptogenic lesions has also radically changed, absolving the need for invasive neurophysiologic techniques.

Magnetic resonance imaging is currently the best available tool for identification of epileptogenic lesions, newer scanning techniques such as 3T magnets, functional MRI (fMRI), and diffusion tensor imaging (DTI) are giving clinicians more insight into the presumptive pathology. More importantly these techniques allow precise 3D anatomic localization of the lesion and its relationship to adjacent structures and network connectivity (brain connectome). Novel imaging results are giving us more information about cortical function and/or dysfunction in patients with epilepsy in order to predict postoperative deficits and odds of seizure freedom. This has given a lot of hope to patients previously diagnosed with refractory epilepsy with no identifiable culprit.

## **2. MRI**

3T MRI scanners are now widely available and replacing 1.5T scanners for epilepsy protocol imaging. Increase in the magnetic field strength in 3T MRI improves the signal-to-noise ratio and contrast-to-noise ratio, thereby improving the detection

of elusive lesions such as malformations of cortical development (MCD) [4–7]. Challenges of ultra-high-field imaging include far greater radiofrequency signal inhomogeneities, higher energy deposition in tissue, and more pronounced imaging artifacts at soft tissue–air and soft tissue–bone interfaces. 3T MRI also has increased device incompatibility [4, 8, 9] compared to older machines.

Most MRI studies for evaluation of epilepsy would first include a sagittal T1-weighted spin-echo acquisition in order to position the slices of the subsequent pulse sequences. Two kinds of protocols were commonly used in epilepsy imaging in the past, the temporal lobe protocol and extratemporal protocol. However, these protocols would often neglect substantial parts of the non-targeted area of the brain. Some centres now advocate a more comprehensive protocol [10, 11]. Supplementary imaging sequences include T2\* gradient echo, DWI, sagittal 3D TSE T2/FLAIR, contrast imaging and post-processing techniques such as voxel based morphometry. FLAIR has a specific advantage over T2 for lesions in periventricular, hippocampal and subpial cortex locations due to proximity to the brain-CSF interface. Other lesions readily identified by FLAIR include subtle hyperintensities blurring the gray-white junction of MCD, subcortical foci of gliotic hyperintensity in areas of encephalomalacia, and the extent of infiltration of low-grade neoplasms. Limitations of FLAIR include CSF pulsation induced motion artifacts causing blurring of the medial temporal regions and contrast suppression obscuring visualization of small foci of heterotopic gray matter. Also of note is that contrast on fast FLAIR seems to be most limiting in patients with immature white matter i.e. young children (<2 years). Conventional spin density images tend to be more helpful in this age group.

Signal characteristics of immature myelin in infants and young children can pose significant challenges in interpretation of studies obtained in infancy. Lesions such as MCDs and cortical tubers have varying signal characteristics depending on the developmental stage of the myelin of the lesions and the surrounding brain. In infants, the dysplastic cortex and adjacent subcortical regions may appear hypointense on T2-weighted images and hyperintense on T1 sequences, contrary to the reverse pattern seen in older children and adults [12–14]. In some patients these lesions tend to become less obvious or rarely "vanish" on follow-up imaging [15] thus reviewing only the most recent images may fail to detect the lesions. Conversely, a "new lesion" of MCD may be detected on follow-up imaging due to the poor background contrast of the bright immature myelin on the T2 images [16]. Follow-up MRI during 2nd year of life or later may unmask areas of MCD with decreased or absent subcortical myelin. Cortical tubers of tuberous sclerosis may be more evident on follow-up imaging. Apart from changes in myelination, increased growth of tubers and dystrophic calcification may contribute to their better visibility on followup imaging. Serial MRIs are helpful in other epileptic disorders such as Rasmussen encephalitis and Sturge-Weber syndrome to demonstrate progressive regional or hemispheric cortical atrophy.

#### **2.1 Susceptibility weight imaging (SWI)**

SWI techniques exploit differences in magnetic susceptibility of tissue components such as deoxygenated blood, iron, and calcium to provide additional information in epileptogenic lesions containing blood products. This can be useful for cavernomas, certain posttraumatic epilepsies, and Sturge-Weber syndrome. SWI is superior to T2\* Gradient Echo (GRE) in detection of remote hemorrhages. Cortical gyral abnormalities in Sturge-Weber syndrome can represent venous stasis-related

hypoxia, and their SWI findings seem to correspond to the hypometabolic areas detected on FDG-PET. Thus, SWI has the potential to show functional information in addition to anatomical details in Sturge-Weber syndrome [17, 18].
