The phenotype of bilateral hippocampal sclerosis and its management in “real life” clinical settings

Sen, Arjune; Dugan, Patricia; Perucca, Piero; Costello, Daniel J.; Choi, Hyunmi; Bazil, Carl W.; Radtke, Rod; Andrade, Danielle M.; Depondt, Chantal; Heavin, Sinéad B.; Adcock, Jane; Pickrell, William Owen; McGinty, Ronan N.; Nascimento, Fábio A.; Smith, Philip E. M.; Rees, Mark I.; Kwan, Patrick; O’Brien, Terence J.; Goldstein, David B.; Delanty, Norman

doi:10.1111/epi.14436

Cited by 7 publications

(5 citation statements)

References 34 publications

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“…There is, however, significant topographic and phenotypic heterogeneity in hippocampal degeneration, creating difficulties in establishing strict criteria for widespread use. Moreover, hippocampal sclerosis is a pathological endpoint associated with various underlying disease processes, including epilepsy, hypoxia, hypoglycaemia, certain infections, and numerous neurodegenerative conditions (Josephs et al , 2007; Thom et al , 2009; Yokota et al , 2010; Malek-Ahmadi et al , 2013; Murray et al , 2013; Ling et al , 2017; Popkirov et al , 2017; Sen et al , 2018). Having originated in a 19th century study of epilepsy by Wilhelm Sommer (Sommer, 1880; Thom, 2009), the term hippocampal sclerosis is still used widely by radiologists and pathologists in the context of seizure disorders (Isnard and Bourdillon, 2015; Thom and Sisodiya, 2015).…”

Section: Introductionmentioning

confidence: 99%

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Nelson

Dickson

Trojanowski

et al. 2019

Brain

1,040

1,035

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Nelson et al. describe a recently recognized brain disorder that mimics the clinical features of Alzheimer’s disease: L imbic-predominant A ge-related T DP-43 E ncephalopathy (LATE). They review the literature and present consensus-based recommendations of an international, multidisciplinary working group, providing guidelines for diagnosis and staging of LATE neuropathological changes.

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Section: Introductionmentioning

confidence: 99%

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Nelson

Dickson

Trojanowski

et al. 2019

Brain

1,040

1,035

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“…Another nonspecific histopathologic hallmark that has been associated with dementia, and that is directly related to TDP-43 proteinopathy, is HS pathology. This ill-defined pathologic endpoint has been associated with various underlying disease categories including epilepsy, hypoxia/ anoxia, infectious diseases, and various neurodegenerative conditions [52,[126][127][128]. The term HS is applied in clinical radiology, usually in relation to seizure disorders, and ~90% of PubMed hits for the search term "hippocampal sclerosis" are papers related to seizure disorders.…”

Section: Downstream Effects: Insights and Controversies In An Evolvinmentioning

confidence: 99%

Tau and TDP-43 proteinopathies: kindred pathologic cascades and genetic pleiotropy

Chornenkyy

Fardo

Nelson

2019

Laboratory Investigation

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We review the literature on Tau and TDP-43 proteinopathies in aged human brains and the relevant underlying pathogenetic cascades. Complex interacting pathways are implicated in Alzheimer's disease and related dementias (ADRD), wherein multiple proteins tend to misfold in a manner that is "reactive," but, subsequently, each proteinopathy may contribute strongly to the clinical symptoms. Tau proteinopathy exists in brains of individuals across a broad spectrum of primary underlying conditions-e.g., developmental, traumatic, and inflammatory/infectious diseases. TDP-43 proteinopathy is also expressed in a wide range of clinical disorders. Although TDP-43 proteinopathy was first described in the central nervous system of patients with amyotrophic lateral sclerosis (ALS) and in subtypes of frontotemporal dementia (FTD/FTLD), TDP-43 proteinopathy is also present in chronic traumatic encephalopathy, cognitively impaired persons in advanced age with hippocampal sclerosis, Huntington's disease, and other diseases. There is also evidence of cellular co-localization between Tau and TDP-43, suggesting common pathways or protein interactions facilitating misfolding in one protein by the other. Multiple pleiotropic gene variants can alter risk for Tau or TDP-43 pathologies, and certain gene variants (e.g., APOE ε4, Huntingtin triplet repeats) are associated with increases of both Tau and TDP-43 proteinopathies.

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“…In these instances, other regions of archicortex, such as paralimbic cortex or insula, should serve as internal reference. Identification of bilateral pathology will have important treatment consequences, for example, bilateral MTS may preclude surgical resection in many cases 38,39 …”

Section: Hippocampal Digitationsmentioning

confidence: 99%

Anatomical Variations, Mimics, and Pitfalls in Imaging of Patients with Epilepsy

Hassankhani

Stein

Haboosheh³

et al. 2020

Journal of Neuroimaging

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Epilepsy is among one of the most common neurologic disorders. The role of magnetic resonance imaging (MRI) in the diagnosis and management of patients with epilepsy is well established, and most patients with epilepsy are likely to undergo at least one or more MRI examinations in the course of their disease. Recent advances in high‐field MRI have enabled high resolution in vivo visualization of small and intricate anatomic structures that are of great importance in the assessment of seizure disorders. Familiarity with normal anatomic variations is essential in the accurate diagnosis and image interpretation, as these variations may be mistaken for epileptogenic foci, leading to unnecessary follow‐up imaging, or worse, unnecessary treatment. After a brief overview of normal imaging anatomy of the mesial temporal lobe, this article will review a few important common and uncommon anatomic variations, mimics, and pitfalls that may be encountered in the imaging evaluation of patients with epilepsy.

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The phenotype of bilateral hippocampal sclerosis and its management in “real life” clinical settings

Cited by 7 publications

References 34 publications

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Tau and TDP-43 proteinopathies: kindred pathologic cascades and genetic pleiotropy

Anatomical Variations, Mimics, and Pitfalls in Imaging of Patients with Epilepsy

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