Surgery for amygdala enlargement with mesial temporal lobe epilepsy: pathological findings and seizure outcome

Minami, Noriaki; Morino, Michiharu; Uda, Takehiro; Komori, Takashi; Nakata, Yasuhiro; Arai, Nobutaka; Kohmura, Eiji; Nakano, Imaharu

doi:10.1136/jnnp-2014-308383

Cited by 44 publications

(79 citation statements)

References 35 publications

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“…An enlarged amygdala has been found to contain focal cortical dysplasia (Kimura et al, 2015; Mitsueda-Ono et al, 2011; Takaya et al, 2014), long-term epilepsy associated tumors (Kim et al, 2012), or the results of neuroinflammatory processes (Minami et al, 2015). Most studies report a higher age of seizure onset for patients with AE than patients with hippocampal sclerosis or TLE without AE; however, this is highly variable, which may be due to small sample sizes and inconsistent ascertainment methods (Beh et al, 2016).…”

Section: 5 Discussionmentioning

confidence: 99%

“…Amygdala enlargement (AE) is reported on MRI in patients with nonlesional temporal lobe epilepsy (TLE) at rates that range from 12% to 63% (Bower et al, 2003; Coan et al, 2013; Minami et al, 2015). This has led to the hypothesis that AE represents a distinct subtype of TLE (Lv et al, 2014).…”

Section: 1 Introductionmentioning

confidence: 99%

“…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).…”

Section: 1 Introductionmentioning

confidence: 99%

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Amygdala enlargement: Temporal lobe epilepsy subtype or nonspecific finding?

et al. 2017

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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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Section: 5 Discussionmentioning

confidence: 99%

Section: 1 Introductionmentioning

confidence: 99%

Section: 1 Introductionmentioning

confidence: 99%

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Amygdala enlargement: Temporal lobe epilepsy subtype or nonspecific finding?

et al. 2017

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“…In such patients with refractory epileptic symptoms, a surgical approach could be an option in the future (10).…”

Section: Discussionmentioning

confidence: 99%

Cardiac Asystole Triggered by Temporal Lobe Epilepsy with Amygdala Enlargement

et al. 2016

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A 25-year-old previously healthy man was hospitalized for syncope. While standing, he suddenly lost consciousness, followed by a generalized tonic clonic seizure. An electrocardiogram demonstrated asystole. No cardiac abnormalities were detected on the echocardiogram, cardiac magnetic resonance imaging (MRI), positron emission tomography, or a coronary angiogram. An electrophysiological study showed normal sinus node and atrioventricular node function. An electroencephalogram revealed small spike waves in the frontotemporal region. Brain MRI demonstrated a left-sided amygdala enlargement. To the best of our knowledge, this is the first case of temporal lobe epilepsy with an amygdala enlargement that induced cardiac asystole. Case ReportA 25-year-old previously healthy man was hospitalized due to a recent history of syncope with a generalized tonic clonic seizure (GTC). He had experienced prodromes consisting of chest discomfort and flashbacks of visual memory. He was currently receiving carbamazepine (CBZ, 400 mg/ day), as prescribed by another medical facility. No abnormal physical findings were noted except for skin rashes on his trunk. His initial electrocardiogram (ECG) and electroencephalogram (EEG) were normal; magnetic resonance imaging (MRI) of the brain also showed no abnormalities. A laboratory examination revealed moderate liver injury along with mild eosinophilia. At this time, CBZ was discontinued due to potential allergic reactions. After 21 days of admission, while standing beside his bed and talking to his physician, he felt prodromes and suddenly lost consciousness, followed by a GTC that lasted for approximately 30 s. He recovered spontaneously without resuscitation. ECG monitoring at this time demonstrated asystole (5 s and 9 s, respectively, Fig. 1A). On the next day, asystole occurred twice along with prodromes (Fig. 1B). However, he did not lose consciousness and no GTC was observed. He was then transferred to the cardiology department for an evaluation of bradyarrhythmia. Results from Holter ECG monitoring, a signal-averaged ECG, and the head-up tilting test were normal. No cardiac abnormalities were detected on the echocardiogram, cardiac MRI with gadolinium contrast agent, fluorodeoxyglucose positron emission tomography/computed tomography, or coronary angiogram. An electrophysiological study showed normal sinus node function and atrial ventricular node function. A repeat EEG showed small spike waves in the fronto-temporal region (Fig. 2). Antiepileptic medication with zonisamide (ZNS, 400 mg/day) was initiated, and the symptoms disappeared. A permanent cardiac pacemaker was not implanted due to the patient's refusal. Subsequently, he was transferred to the neurosurgery department at the Juntendo University Hospital. Repeat MRI of the brain demonstrated a left-sided amygdala enlargement

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“…Furthermore, both atrophy and hypertrophy of the amygdalae have been reported in adults with epilepsy (Cendes et al, 1994, Minami et al, 2015) and linked to interictal psychopathology (Tebartz van Elst et al, 1999). Increased amygdala volume has also been reported in children with chronic focal (Daley et al, 2008) and generalized epilepsy (Schreibman Cohen et al, 2009) and associated with anxiety disorders and depression.…”

Section: Introductionmentioning

confidence: 99%

Disruptions in cortico-subcortical covariance networks associated with anxiety in new-onset childhood epilepsy

Garcia‐Ramos

Lin

Bonilha

et al. 2016

NeuroImage: Clinical

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Anxiety disorders represent a prevalent psychiatric comorbidity in both adults and children with epilepsy for which the etiology remains controversial. Neurobiological contributions have been suggested, but only limited evidence suggests abnormal brain volumes particularly in children with epilepsy and anxiety. Since the brain develops in an organized fashion, covariance analyses between different brain regions can be investigated as a network and analyzed using graph theory methods. We examined 46 healthy children (HC) and youth with recent onset idiopathic epilepsies with (n = 24) and without (n = 62) anxiety disorders. Graph theory (GT) analyses based on the covariance between the volumes of 85 cortical/subcortical regions were investigated. Both groups with epilepsy demonstrated less inter-modular relationships in the synchronization of cortical/subcortical volumes compared to controls, with the epilepsy and anxiety group presenting the strongest modular organization. Frontal and occipital regions in non-anxious epilepsy, and areas throughout the brain in children with epilepsy and anxiety, showed the highest centrality compared to controls. Furthermore, most of the nodes correlating to amygdala volumes were subcortical structures, with the exception of the left insula and the right frontal pole, which presented high betweenness centrality (BC); therefore, their influence in the network is not necessarily local but potentially influencing other more distant regions. In conclusion, children with recent onset epilepsy and anxiety demonstrate large scale disruptions in cortical and subcortical brain regions. Network science may not only provide insight into the possible neurobiological correlates of important comorbidities of epilepsy, but also the ways that cortical and subcortical disruption occurs.

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Surgery for amygdala enlargement with mesial temporal lobe epilepsy: pathological findings and seizure outcome

Abstract: Histopathologically, clustering hypertrophic neurons and vacuolation with slight gliosis or without gliosis were considered to be pathological characteristics of AE. Amygdalohippocampectomy or hippocampal transection with amygdalotomy is effective for seizure control in patients with AE.

Cited by 44 publications

References 35 publications

Amygdala enlargement: Temporal lobe epilepsy subtype or nonspecific finding?

Amygdala enlargement: Temporal lobe epilepsy subtype or nonspecific finding?

Cardiac Asystole Triggered by Temporal Lobe Epilepsy with Amygdala Enlargement

Disruptions in cortico-subcortical covariance networks associated with anxiety in new-onset childhood epilepsy

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