To this end, we employed drug-resistant temporal lobe epilepsy (TLE) as a model disease with a well-characterised, regional P-gp up-regulation in the temporal lobe (TL) [12–14] and compared the brain kinetics of [11C]metoclopramide between drug-resistant TLE patients (n = 8), drug-sensitive focal epilepsy patients (n = 5), and healthy subjects (n = 15). Here, PGP is linked to temporal lobe epilepsy.