BRAIN CME Beyond Mesial Temporal Sclerosis: Optimizing MRI Evaluation in Focal Epilepsy Elliott R. Friedman, MD, and Nitin Tandon, MD CME Credit The American Society of Neuroradiology (ASNR) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The ASNR designates this enduring material for a maximum of 1 AMA PRA Category 1 Credit TM . Physicians should claim only the credit commensurate with the extent of their participation in the activity. To obtain credit for this activity, an online quiz must be successfully completed and submitted. ASNR members may access this quiz at no charge by logging into eCME at http://members.asnr.org. Nonmembers may pay a small fee to access the quiz and obtain credit via http://members.asnr.org/ecme. ABSTRACT Epilepsy is one of the most common neurologic disorders in the United States. The impor- tance of accurately detecting structural causes of epilepsy cannot be overstated. MRI findings initially misdiagnosed as “lesion negative” may result in delayed definitive surgical treatment and increased morbidity because patients with underlying structural lesions are more likely to be refractory to medical therapy. Under-reporting of pertinent MR imaging findings in epilepsy is due to either a failure of imaging to adequately depict the abnormality or an inability to recognize the abnormality when present. The purpose of this article is to describe optimal epilepsy MR imaging and to review common focal epileptogenic lesions, with an emphasis on subtle abnormalities. Learning Objective: Describe the sequences necessary to optimize detection of epilepto- genic lesions on MRI and identify common focal epileptogenic lesions. INTRODUCTION Epilepsy is one of the most common neu- rologic conditions in the world, with an estimated worldwide prevalence of 50 mil- lion people. 1 Epilepsy affects more than 2 million Americans. 2 Sixty to seventy per- cent of patients with newly diagnosed epi- lepsy will enter long-term remission with AEDs and, in most, on a single medication. In fact, response to the first AED has been shown to be the most useful predictor of prognosis with pharmacologic treatment. The 30%– 40% of patients with difficult- to-control epilepsy are more likely to have an underlying structural lesion. 3 Many medically refractory patients can be effectively treated with surgical resec- tions. The success of epilepsy surgery is di- rectly correlated with the ability to define and subsequently resect the epileptogenic zone. The epileptogenic zone is defined as the minimum amount of brain parenchyma that must be resected or completely discon- nected to entirely alleviate seizures. Theo- retically, the epileptogenic zone includes the seizure-onset zone and a potential seizure-onset zone, which includes the cor- tex involved in early seizure spread. 4 Epilepsy surgery is more effective when a structural lesion causally related to the epilepsy is identified. Depending on the se- ries, 20%–30% of patients with temporal lobe epilepsy and 20%– 40% of patients with extratemporal epilepsy have no clear ABBREVIATIONS KEY AED = antiepileptic drug AVM = arteriovenous malformation DNET = dysembryoplastic neuroepithelial tumor FCD = focal cortical dysplasia FOV = field of view HS = hippocampal sclerosis IHI= ipsilateral hippocampal inversion MCF = middle cranial fossa SPECT = single-photon emission tomography Received May 27, 2012; accepted after revision December 5. From the Departments of Diagnostic and Interventional Imaging (E.R.F.) and Neurosurgery (N.T.), The University of Texas Health Science Center at Houston, Houston, Texas. Paper previously presented as an Educational Exhibit at: 49th Annual Meeting of the American Society of Neuroradiology, June 4 –9, 2011; Seattle, Washington. Please address correspondence to Elliott Friedman, MD, Department of Diagnostic and Interventional Imaging, University of Texas HSC Houston, 6431 Fannin St, Suite MSB 2.130B, Houston, TX 77030; e-mail: Elliott.Friedman@uth.tmc.edu http://dx.doi.org/10.3174/ng.2130053 60 | Neurographics 3:60 – 69 Jun 2012 www.neurographics.com