Brain‐responsive neurostimulation treatment in patients with GAD65 antibody–associated autoimmune mesial temporal lobe epilepsy

Abstract Glutamic acid decarboxylase 65‐kilodalton isoform (GAD65) antibodies have been associated with multiple nonneurological and neurological syndromes including autoimmune epilepsy (AE). Although immunotherapy remains the cornerstone for the treatment of AE, those with GAD65 Ab‐associated AE (G...

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Main Authors: Anteneh M Feyissa, Emily A. Mirro, Angela Wabulya, William O. Tatum, Kaitlyn E. Wilmer‐Fierro, Hae Won Shin
Format: Article
Language:English
Published: Wiley 2020-06-01
Series:Epilepsia Open
Subjects:
Online Access:https://doi.org/10.1002/epi4.12395
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spelling doaj-d46873d38f97467b8f610e65a63ae68e2020-11-25T03:53:59ZengWileyEpilepsia Open2470-92392020-06-015230731310.1002/epi4.12395Brain‐responsive neurostimulation treatment in patients with GAD65 antibody–associated autoimmune mesial temporal lobe epilepsyAnteneh M Feyissa0Emily A. Mirro1Angela Wabulya2William O. Tatum3Kaitlyn E. Wilmer‐Fierro4Hae Won Shin5Department of Neurology Mayo Clinic Florida Jacksonville FloridaNeuroPace, Inc. Mountain View CaliforniaDepartment of Neurology University of North Carolina at Chapel Hill Chapel Hill North CarolinaDepartment of Neurology Mayo Clinic Florida Jacksonville FloridaNeuroPace, Inc. Mountain View CaliforniaDepartment of Neurology University of North Carolina at Chapel Hill Chapel Hill North CarolinaAbstract Glutamic acid decarboxylase 65‐kilodalton isoform (GAD65) antibodies have been associated with multiple nonneurological and neurological syndromes including autoimmune epilepsy (AE). Although immunotherapy remains the cornerstone for the treatment of AE, those with GAD65 Ab‐associated AE (GAD65‐AE) remain refractory to immunotherapy and antiseizure medication (ASM). Outcomes of epilepsy surgery in this patient population have also been unsatisfactory. The role of neuromodulation therapy, particularly direct brain‐responsive neurostimulation therapy, has not been previously examined in GAD65‐AE. Here, we describe four consecutive patients with refractory GAD‐65‐associated temporal lobe epilepsy (GAD65‐TLE) receiving bilateral hippocampal RNS System treatment. The RNS System treatment was well tolerated and effective in this study cohort. Three patients had a >50% clinical seizure reduction, and one patient became clinically seizure‐free following resective surgery informed by the RNS System data with continued RNS System treatment. In all four of our patients, the long‐term ambulatory data provided by the RNS System allowed us to gain objective insights on electrographic seizure lateralization, patterns, and burden as well as guided immunotherapy and ASM optimization. Our results suggest the potential utility of the RNS System in the management of ASM intractable GAD65‐AE.https://doi.org/10.1002/epi4.12395autoimmune epilepsybrain‐responsive neurostimulationdrug‐resistant epilepsyGAD65 antibodytemporal lobe epilepsy
collection DOAJ
language English
format Article
sources DOAJ
author Anteneh M Feyissa
Emily A. Mirro
Angela Wabulya
William O. Tatum
Kaitlyn E. Wilmer‐Fierro
Hae Won Shin
spellingShingle Anteneh M Feyissa
Emily A. Mirro
Angela Wabulya
William O. Tatum
Kaitlyn E. Wilmer‐Fierro
Hae Won Shin
Brain‐responsive neurostimulation treatment in patients with GAD65 antibody–associated autoimmune mesial temporal lobe epilepsy
Epilepsia Open
autoimmune epilepsy
brain‐responsive neurostimulation
drug‐resistant epilepsy
GAD65 antibody
temporal lobe epilepsy
author_facet Anteneh M Feyissa
Emily A. Mirro
Angela Wabulya
William O. Tatum
Kaitlyn E. Wilmer‐Fierro
Hae Won Shin
author_sort Anteneh M Feyissa
title Brain‐responsive neurostimulation treatment in patients with GAD65 antibody–associated autoimmune mesial temporal lobe epilepsy
title_short Brain‐responsive neurostimulation treatment in patients with GAD65 antibody–associated autoimmune mesial temporal lobe epilepsy
title_full Brain‐responsive neurostimulation treatment in patients with GAD65 antibody–associated autoimmune mesial temporal lobe epilepsy
title_fullStr Brain‐responsive neurostimulation treatment in patients with GAD65 antibody–associated autoimmune mesial temporal lobe epilepsy
title_full_unstemmed Brain‐responsive neurostimulation treatment in patients with GAD65 antibody–associated autoimmune mesial temporal lobe epilepsy
title_sort brain‐responsive neurostimulation treatment in patients with gad65 antibody–associated autoimmune mesial temporal lobe epilepsy
publisher Wiley
series Epilepsia Open
issn 2470-9239
publishDate 2020-06-01
description Abstract Glutamic acid decarboxylase 65‐kilodalton isoform (GAD65) antibodies have been associated with multiple nonneurological and neurological syndromes including autoimmune epilepsy (AE). Although immunotherapy remains the cornerstone for the treatment of AE, those with GAD65 Ab‐associated AE (GAD65‐AE) remain refractory to immunotherapy and antiseizure medication (ASM). Outcomes of epilepsy surgery in this patient population have also been unsatisfactory. The role of neuromodulation therapy, particularly direct brain‐responsive neurostimulation therapy, has not been previously examined in GAD65‐AE. Here, we describe four consecutive patients with refractory GAD‐65‐associated temporal lobe epilepsy (GAD65‐TLE) receiving bilateral hippocampal RNS System treatment. The RNS System treatment was well tolerated and effective in this study cohort. Three patients had a >50% clinical seizure reduction, and one patient became clinically seizure‐free following resective surgery informed by the RNS System data with continued RNS System treatment. In all four of our patients, the long‐term ambulatory data provided by the RNS System allowed us to gain objective insights on electrographic seizure lateralization, patterns, and burden as well as guided immunotherapy and ASM optimization. Our results suggest the potential utility of the RNS System in the management of ASM intractable GAD65‐AE.
topic autoimmune epilepsy
brain‐responsive neurostimulation
drug‐resistant epilepsy
GAD65 antibody
temporal lobe epilepsy
url https://doi.org/10.1002/epi4.12395
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