2014
DOI: 10.1111/jon.12106
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Temporal Lobe Epilepsy with Unilateral Amygdala Enlargement: Morphometric MR Analysis with Clinical and Pathological Study

Abstract: Cortical dysplasia may be one of the pathological diagnoses in AE, and in some patients it may extend to the temporal pole.

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Cited by 25 publications
(51 citation statements)
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“…Some reports discussed amygdala volumetry, confirming the existence of AE 7–11 25. To the best of our knowledge, there have been few reports regarding surgical and pathological findings in MTLE with AE, probably because patients with MTLE with AE tend to be less symptomatic and surgery is less likely to be indicated 12 25. Hence, the present study was performed to clarify the intraoperative EEG findings of the amygdala, the pathological findings and the surgical outcome of MTLE with AE.…”
Section: Discussionmentioning
confidence: 87%
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“…Some reports discussed amygdala volumetry, confirming the existence of AE 7–11 25. To the best of our knowledge, there have been few reports regarding surgical and pathological findings in MTLE with AE, probably because patients with MTLE with AE tend to be less symptomatic and surgery is less likely to be indicated 12 25. Hence, the present study was performed to clarify the intraoperative EEG findings of the amygdala, the pathological findings and the surgical outcome of MTLE with AE.…”
Section: Discussionmentioning
confidence: 87%
“…In a previous report, 8 of 12 surgical cases of AE were pathologically diagnosed as focal cortical dysplasia (FCD) 12. Two pathological cases of AE were also reported previously; the temporal cortex was examined in these cases and disorganisation of the cortical layer and dysmorphic neurons was observed, suggesting the existence of FCD 25. Cytoskeletal impairments, such as hypertrophic neurons, are sometimes observed in cortical dysplasia 29.…”
Section: Discussionmentioning
confidence: 89%
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“…However, AE is observed at high rates in the amygdala contralateral to seizure onset (Coan et al, 2013) and epileptogenic activity appears to arise from the hippocampus, not the enlarged amygdala (Minami et al, 2015). Prior AE studies included only TLE patients that had concordant EEG findings (Kim et al, 2012; Kimura et al, 2015; Sone et al, 2015; Takaya et al, 2014) or did not specify whether they applied this selection criterion (Coan et al, 2013; Lv et al, 2014; Mitsueda-Ono et al, 2011). To address this unresolved issue, we compare rates of AE, defined quantitatively, across a large sample of individuals with normal MRI and either localization related epilepsy (LRE), IGE, or no epilepsy [i.e., healthy controls (HC)].…”
Section: 1 Introductionmentioning
confidence: 99%
“…Indeed, the stimulation of the left hippocampus, amygdala, and insula induce asystole in humans (7). Recently, unilateral amygdala enlargements have been found in patients with temporal lobe epilepsy (8), and its pathophysiological roles are currently being investigated.…”
Section: Discussionmentioning
confidence: 99%