Amyloid deposition in adults with drug‐resistant temporal lobe epilepsy

Objective Pathological amyloid‐β (Aβ) accumulation and hyperphosphorylated tau proteins have been described in resected temporal lobe specimens of epilepsy patients. We aimed to determine cerebrospinal fluid (CSF) Aβ1‐42 and p181‐tau levels and cerebral Aβ deposits on positron emission tomography (Aβ PET) and correlate these findings with cognitive performance in adults with drug‐resistant temporal lobe epilepsy (TLE). Methods In this cross‐sectional study, we enrolled individuals with drug‐resistant TLE who were 25–55 years old. Each participant underwent 18F‐flutemetamol PET, determination of CSF Aβ1‐42, p181‐tau, and total tau, and a comprehensive neuropsychological assessment. We evaluated normalized standard uptake value ratios (SUVRs) for different brain regions on Aβ PET. Results Thirty patients (mean age = 41.9 ± SD 8.1 years, 57% men) were included. The median disease duration was 9.5 (interquartile range = 4–24) years. Twenty‐six patients (87%) had a clinically significant cognitive impairment on neuropsychological evaluation, 18 (69%) of the amnesic type. On Aβ PET, high uptake was observed in both mesial temporal regions (ipsilateral: SUVR z‐score = .90, 95% confidence interval [CI] = .60–1.20; contralateral: SUVR z‐score = .92, 95% CI = .57–1.27; p