[Ketogenic diet may control seizures by increasing the binding potential of the benzodiazepine receptor: a speculation from the [11C] flumazenil-PET study].

The ketogenic diet (KD) is a high-fat, low-protein, low-carbohydrate diet which is effective in the treatment of medically refractory epilepsy. Several theories have been proposed to explain the mechanism underlying the anticonvulsant efficacy of the KD, however, the precise anticonvulsant mechanism of the KD is still unknown. We speculated the mechanism underlying the effect of the KD in patients with intractable epilepsy, based on the results of the [11C] flumazenil (FMZ)-positron emission tomography (PET) study. A patient developed frontal lobe epilepsy at the age of 2 years. At the age of 4 years 11 months, she was admitted to our hospital for the initiation of a KD. At the time of admission, she had several epileptic attacks each day: frequent postural tonic seizures, hypermotor seizures, head nodding, and intermittent loss of consciousness (non-convulsive status epilepticus). MR imaging showed no abnormal signal intensity in the brain. With the KD, the seizure frequency reduced dramatically on the fifth day. Interictal [11C] FMZ-PET was performed before and 2 months after the initiation of the KD. Before the KD, the [11C] FMZ-PET images and [11C] FMZ-PET binding potential (BP) images showed extremely low accumulation of FMZ throughout the cerebral cortex. Two months after the initiation of the KD, significantly increased binding potential of [11C] FMZ was observed, implying the increased binding potential of the benzodiazepine receptors, probably due to the anticonvulsant effect of the KD. These PET findings suggested that KD may control seizures by directly or indirectly increasing the binding potential of the benzodiazepine receptors.