The changing landscape in epilepsy imaging: Unmasking subtle and unique entities
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Neuroradiology - Review
P: 503-515
September 2022

The changing landscape in epilepsy imaging: Unmasking subtle and unique entities

Diagn Interv Radiol 2022;28(5):503-515
1. Department of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, Connecticut, USA
2. Department of Radiology Abbott Northwestern Hospital, Minneapolis, Mminnesota, USA
3. Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
4. Department of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut, USA
No information available.
No information available
Received Date: 23.03.2021
Accepted Date: 09.07.2021
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ABSTRACT

Dramatic changes have occurred recently in the field of epilepsy, including a fundamental shift in the etiology of epileptogenic substrates found at surgery. Hippocampal sclerosis is no longer the most common etiology found at epilepsy surgery and this decrease has been associated with an increase in the incidence of focal cortical dysplasia and encephaloceles. Significant advances have been made in molecular biology and genetics underlying the basis of malformations of cortical development, and our ability to detect epileptogenic abnormalities with MR imaging has markedly improved. This article begins with a discussion of these trends and reviews imaging techniques essential for detecting of subtle epilepsy findings. Representative examples of subtle imaging findings are presented, which are often overlooked but should not be missed. These include temporal lobe encephaloceles, malformations of cortical development (and especially focal cortical dysplasia), hippocampal sclerosis, hippocampal malformation (also known as HIMAL), ulegyria, autoimmune encephalitis, and Rasmussen’s encephalitis. Recent findings on the pathophysiology and genetic underpinnings of several causes of localization-related epilepsy are incorporated. For instance, it has been recently found that focal cortical dysplasia IIb, tuberous sclerosis, hemimegalencephaly, and gangliogliomas are all the result of mutations of the mTOR pathway for cell growth.