Anny Reyes1, Thomas Thesen2, Ruben Kuzniecky3, Orrin Devinsky3, Carrie R McDonald4, Graeme D Jackson5, David N Vaughan6, Karen Blackmon7. 1. New York University School of Medicine, Department of Neurology, Epilepsy Division, New York, NY, 10016, United States. Electronic address: anr086@ucsd.edu. 2. New York University School of Medicine, Department of Neurology, Epilepsy Division, New York, NY, 10016, United States; New York University School of Medicine, Department of Radiology, New York, NY,10016, United States. 3. New York University School of Medicine, Department of Neurology, Epilepsy Division, New York, NY, 10016, United States. 4. University of California San Diego, Center for Multimodal Imaging and Genetics (CMIG), San Diego, CA 92093, United States. 5. The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Victoria, 3084, Australia. 6. The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Victoria, 3084, Australia; Austin Health, Department of Neurology, Melbourne, Victoria, Australia. 7. New York University School of Medicine, Department of Neurology, Epilepsy Division, New York, NY, 10016, United States; St. Georges University School of Medicine, Department of Behavioral Sciences, St. Georges, Grenada.
Abstract
OBJECTIVE: Amygdala enlargement (AE) is observed in patients with temporal lobe epilepsy (TLE), which has led to the suggestion that it represents a distinct TLE subtype; however, it is unclear whether AE is found at similar rates in other epilepsy syndromes or in healthy controls, which would limit its value as a marker for focal epileptogenicity. METHODS: We compared rates of AE, defined quantitatively from high-resolution T1-weighted MRI, in a large multi-site sample of 136 patients with nonlesional localization related epilepsy (LRE), including TLE and extratemporal (exTLE) focal epilepsy, 34 patients with idiopathic generalized epilepsy (IGE), and 233 healthy controls (HCs). RESULTS: AE was found in all groups including HCs; however, the rate of AE was higher in LRE (18.4%) than in IGE (5.9%) and HCs (6.4%). Patients with unilateral LRE were further evaluated to compare rates of concordant ipsilateral AE in TLE and exTLE, with the hypothesis that rates of ipsilateral AE would be higher in TLE. Although ipsilateral AE was higher in TLE (19.4%) than exTLE (10.5%), this difference was not significant. Furthermore, among the 25 patients with unilateral LRE and AE, 13 (52%) had either bilateral AE or AE contralateral to seizure onset. CONCLUSION: Results suggest that AE, as defined with MRI volumetry, may represent an associated feature of nonlesional localization related epilepsy with limited seizure onset localization value.
OBJECTIVE:Amygdala enlargement (AE) is observed in patients with temporal lobe epilepsy (TLE), which has led to the suggestion that it represents a distinct TLE subtype; however, it is unclear whether AE is found at similar rates in other epilepsy syndromes or in healthy controls, which would limit its value as a marker for focal epileptogenicity. METHODS: We compared rates of AE, defined quantitatively from high-resolution T1-weighted MRI, in a large multi-site sample of 136 patients with nonlesional localization related epilepsy (LRE), including TLE and extratemporal (exTLE) focal epilepsy, 34 patients with idiopathic generalized epilepsy (IGE), and 233 healthy controls (HCs). RESULTS:AE was found in all groups including HCs; however, the rate of AE was higher in LRE (18.4%) than in IGE (5.9%) and HCs (6.4%). Patients with unilateral LRE were further evaluated to compare rates of concordant ipsilateral AE in TLE and exTLE, with the hypothesis that rates of ipsilateral AE would be higher in TLE. Although ipsilateral AE was higher in TLE (19.4%) than exTLE (10.5%), this difference was not significant. Furthermore, among the 25 patients with unilateral LRE and AE, 13 (52%) had either bilateral AE or AE contralateral to seizure onset. CONCLUSION: Results suggest that AE, as defined with MRI volumetry, may represent an associated feature of nonlesional localization related epilepsy with limited seizure onset localization value.
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