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Research paper
Surgery for amygdala enlargement with mesial temporal lobe epilepsy: pathological findings and seizure outcome
  1. Noriaki Minami1,2,
  2. Michiharu Morino1,
  3. Takehiro Uda1,
  4. Takashi Komori3,
  5. Yasuhiro Nakata4,
  6. Nobutaka Arai5,
  7. Eiji Kohmura2,
  8. Imaharu Nakano1
  1. 1Department of Neurosurgery, Tokyo Metropolitan Neurological Hospital, Tokyo, Japan
  2. 2Department of Neurosurgery, Kobe University School of Medicine, Kobe, Hyogo, Japan
  3. 3Department of Laboratory Medicine and Pathology (Neuropathology), Tokyo Metropolitan Neurological Hospital, Tokyo, Japan
  4. 4Department of Neuroradiology, Tokyo Metropolitan Neurological Hospital, Tokyo, Japan
  5. 5Brain Pathology Research Center, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
  1. Correspondence to Dr Noriaki Minami, Department of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan; minaminoriaki{at}


Objective Amygdala enlargement (AE) has been suggested to be a subtype of mesial temporal lobe epilepsy (MTLE). However, most reports related to AE have referred to imaging studies, and there have been few reports regarding surgical and pathological findings. The present study was performed to clarify the surgical outcomes and pathology of AE.

Methods Eighty patients with drug-resistant MTLE were treated surgically at the Tokyo Metropolitan Neurological Hospital between April 2010 and July 2013. Of these patients, 11 were diagnosed as AE based on presurgical MRI. Nine patients with AE underwent selective amygdalohippocampectomy, while the remaining two patients underwent selective amygdalotomy with hippocampal transection. Intraoperative EEG was routinely performed. The histopathology of the resected amygdala tissue was evaluated and compared with the amygdala tissue of patients with hippocampal sclerosis.

Results Pathological findings indicated that 10 of 11 specimens had closely clustering hypertrophic neurons with vacuolisation of the background matrix. Slight gliosis was seen in nine specimens, while the remaining two showed no gliotic changes. Intraoperative EEG showed abnormal sharp waves that seemed to originate not from the amygdala but from the hippocampus in all cases. Ten patients became seizure-free during the postoperative follow-up period.

Conclusions 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.


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