LAUSR

with slight hyperintensity on FLAIR (Fig. 1c), but not on diffusion-weighted images. Laboratory tests were negative for anti-glutamic acid decarboxylase (GAD) antibodies and anti-voltage-gated potassium channel (VGKC) complexes. Routine CSF analysis was normal. Positron emission tomography with [11C]-Pittsburgh compound B suggested MCI was due to Alzheimer’s disease (AD) (Fig. 2a). He was administered levetiracetam 1500 mg/day and carbamazepine 300 mg/day, resulting in seizure cessation. After 10 months of seizure freedom, an MRI showed decreased left amygdala volume (Fig. 1d); however, cognitive function continued to decline and he was diagnosed with AD. SPECT performed around the peri-ictal condition (numerous fits/ day) showed decreased rCBF in the left medial temporal region but not in the amygdala (Fig. 2b). SISCOM analysis showed restricted hyperperfusion in the left amygdala and right thalamus (Fig. 2c). We demonstrated changes in amygdala volume and rCBF in a patient with elderly onset TLE. AE appeared gradually, peaking at seizure onset and declining after treatment (Fig. 1e). Previous studies indicate that AE is pathologically heterogeneous [1–3]. Because AE abated after anti-epileptic treatment, AE in our patient reflected a seizure-related physiological response rather than the presence of a neoplasm. Although autoimmune pathology could have been a possible etiology [3, 6], GAD antibodies or anti-VGKC complexes were not detected, and AE remitted without immunosuppressive therapy. As epileptogenicity has been shown to induce volumetric changes on MRI [7], we hypothesized the change in amygdala volume was likely seizure-related. Using SISCOM analysis, we found peri-ictal focal hyperperfusion in the left amygdala, suggesting epileptogenesis. The spread of Dear Sirs,