Blümcke I, Coras R (2015)
Publication Type: Authored book
Publication year: 2015
Publisher: Cambridge University Press
ISBN: 9781139525312
DOI: 10.1017/CBO9781139525312.020
Most surgically resected epileptogenic brain lesions are detectable by high-resolution MRI at 1.5 or 3 T, such as long-term epilepsy-associated tumors and hippocampal sclerosis of malformations of cortical development (MCD), and MRI visibility is a favorable predictor of postsurgical seizure control. However, recent studies suggest that comparable seizure control can be achieved after epilepsy surgery in patients with MRI-negative TLE, with 55% of patients remaining free of disabling seizures after a mean follow-up of 2 years [1] to 5.8 years [2]. In this chapter, we will discuss the spectrum of histopathological changes that can be observed in tissue specimens obtained from patients with MRI-negative focal epilepsy, with particular emphasis on the cellular architecture that hides such lesions from detection with currently available MRI protocols. However, neither the European Epilepsy Brain Bank nor the German Neuropathology Reference Center for Epilepsy Surgery allow us yet to reliably retrieve clinical information of how many operated patients were reported MRI negative. The increasing interest in this matter will help us to close this knowledge gap in the near future. MRI-negative FCDs The most prominent example for a structural brain abnormality identifiable in MRI-negative focal epilepsies may be focal cortical dysplasia (FCD) type IIa (Figure 19.1); FCDs represent a composite group of cortical malformations [3], which are increasingly recognized as a frequent morphological substrate for severe therapy-refractory epilepsy in children and young adults. However, not all FCD variants can be reliably detected by high-resolution MRI [4; 5]. The term FCD was originally coined by Taylor and colleagues in 1971 describing ten patients with microscopic evidence for dysmorphic neurons [6]. In half of these patients, the authors also described balloon cells. The current ILAE classification separate both variants into FCD type IIa (dysmorphic neurons, no balloon cells) and IIb (dysmorphic neurons and balloon cells) [3]. Yet, there is no distinguishing evidence for the clinical course, etiology and molecular-genetic or biological pathomechanisms of type IIa and IIb FCDs [5]. Furthermore, dysmorphic neurons are very similar between both variants and cannot be distinguished by morphometric analysis [7]. It is solely the presence of balloon cells, accompanied by lack of myelin and oligodendrocytes that makes the difference between the two subtypes of type II FCDs.
APA:
Blümcke, I., & Coras, R. (2015). Histopathology findings in MRI-negative focal epilepsy. Cambridge University Press.
MLA:
Blümcke, Ingmar, and Roland Coras. Histopathology findings in MRI-negative focal epilepsy. Cambridge University Press, 2015.
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