Temporal lobe epilepsy with amygdala enlargement: a subtype of temporal lobe epilepsy

Abstract

BackgroundSome recent studies suggest that some imaging-negative temporal lobe epilepsy (TLE) had significant amygdala enlargement (AE). Contradictory data were also reported in previous studies regarding the association between AE and TLE. The present study was to investigate the clinical characters of a group of TLE with AE and compare the amygdala volume of the same patient before and after antiepileptic drugs treatment by a larger sample size.MethodsThis study recruited 33 mesial TLE patients with AE and 35 healthy volunteers. The clinical history, seizure semiology, electroencephalogram (EEG), fluorodeoxyglucose-positron emission tomography (FDG-PET) and amygdala volume were investigated. The amygdala volume were compared between ipsilateral and contralateral sides, TLE patients and 35 healthy controls, and patients at first and follow-up visit by 3.0 T MRI.ResultsAverage seizure onset age was 42.0 years (SD 14.3). All patients had complex partial seizures, fourteen had occasional generalized tonic-clonic seizures which often happened during sleep. Ninety percent patients suffered from anxiety or depression. Thirty percent patients had memory decline. Interictal epileptiform discharges appeared predominantly in the anterior or inferior temporal area ipsilateral to AE. Interictal FDG-PET showed regional glucose hypometabolism in the ipsilateral temporal lobe. No hippocampal sclerosis (HS) was suspected in all patients. 22 patients demonstrated good seizure control and significantly reduced volume of the enlarged amygdala after treatment (P < 0.01). The other 11 patients showed initial response to treatment, followed by a gradual increase in seizure frequency over time, and no volume change of the enlarged amygdala after treatment.ConclusionsTLE with AE probably represents a distinct nosological and probably less homogeneous syndrome which is most likely a subtype of TLE without ipsilateral HS. The chronic and long lasting inflammatory processes or focal cortical dysplasia could lead to amygdala enlargement possibly.

Statistical shape analysis of temporal lobe in mesial temporal sclerosis patients

“…Temporal neocortex atrophy in patients with temporal lobe epilepsy was first recognized in the 1950s [11]. This 'sclerosis' was identified in approximately 11 % of surgically treated patients [18].…”

“…Many different applications based on volume, area and shape measurements have been used on anatomical brain structures to measure changes caused by neurovascular diseases [11,12,17]. Recently, statistical shape analysis has become more important in the medical and biological sciences [7].…”

Neuroimaging of epilepsy

“…Bitemporal hypometabolism is associated with less-well-localized ictal epileptiform onset and may be a negative surgical prognostic indicator (Koutroumanidis et al, 2000; Joo et al, 2004; Kim et al, 2006). Patients with TLE and enlarged amygdala, but not MTS, have been reported to have ipsilateral hypometabolism (Lv et al, 2014). …”

Contribution of amygdala pathology to comorbid emotional disturbances in temporal lobe epilepsy

“…In contrast, increased dysthymia, depression, and psychosis of epilepsy seem to correlate with amygdala enlargement in patients with TLE (Tebartz van Elst et al, ; Richardson et al, ). Recent studies further indicate that TLE with amygdala enlargement may be a subtype of TLE without ipsilateral HS (Mitsueda‐Ono et al, ; Lv et al, ). In some mesial TLE patients with an increased amygdala volume and enhanced T2/FLAIR signal on the MRI, limbic autoimmune encephalitis was the underlying cause; these patients also showed affective symptoms and disturbances in recent memory (Soeder et al, ; Lv et al, ).…”

“…Recent studies further indicate that TLE with amygdala enlargement may be a subtype of TLE without ipsilateral HS (Mitsueda-Ono et al, 2011;Lv et al, 2014). In some mesial TLE patients with an increased amygdala volume and enhanced T2/FLAIR signal on the MRI, limbic autoimmune encephalitis was the underlying cause; these patients also showed affective symptoms and disturbances in recent memory (Soeder et al, 2009;Lv et al, 2014). Autoimmune encephalitis, including limbic forms, is often associated with antibodies against intracellular or membranous molecules (e.g., onconeuronal, voltage-gated potassium channel complexes, GM1 gangliosides, glutamic acid decarboxylase [GAD], and transmitter receptors) or defects in cellular immunity (Liimatainen et al, 2013;Ehling et al, 2015;Melzer et al, 2015).…”