Women with epilepsy have known for some time that female hormones affect seizures. Female sex hormones change the excitability of brain neurons by increasing excitation or inhibition. These hormones act on the cell membrane, changing the threshold for firing, change the rate at which neurons manufacture excitatory and inhibitory brain chemicals, and even change the shape of neurons, altering the way brain cells connect to one another. Steroid molecules: estrogen and progesterone easily pass through the cell membrane and are able to find receptor molecules within the cell. Progesterone can depress brain excitability, and therefore may reduce seizure activity. The other major female sex steroid hormone, estrogen, has an almost opposite effect from progesterone. The most direct, fastest, and obvious effect of estrogen is to increase the excitatory neurotransmitters in brain regions such as the hippocampus which are thought to be responsible for the generation of temporal lobe seizures.

Currently, positron emission tomography (PET) and single photon emission computed tomography (SPECT) are the only noninvasive imaging modalities that can be used to image specific receptor molecules and to quantify their kinetics. By formally comparing the output of the model to the experimentally obtained PET or SPECT data, one can estimate values for the kinetic parameters and thus extract information on binding, or any hypothesized process. The simplest of compartmental models applied to receptor-ligand studies postulates two tissue compartments. These two tissue compartments along with a plasma compartment are arranged in series. The partial volume effect is widely recognized as a limiting factor in the ability to quantify the amount of radioactivity in tissue accurately. The pharmacokinetic approach requires the PET or SPECT data to be analyzed using a mathematical model of radioactivity uptake. PET and SPECT brain imaging studies are divided into two groups: receptor-ligand studies and tracer studies.