The theoretical basis for DBS of the GPi or STN in Parkinson’s disease was developed in the late 1980's and early 1990's. In Parkinson's disease, loss of dopamine-producing cells leads to excessive and abnormally patterned activity in both the GPi and the STN. "Pacing" of these nuclei with a constant, steady-frequency electrical pulse is thought to correct this excessive and abnormal activity. DBS does not act directly on dopamine producing cells and does not affect brain dopamine levels. Instead, it compensates for one of the major secondary effects of dopamine loss, the excessive and abnormally patterned electrical discharge in the GPi or the STN. The exact mechanism by which the constant frequency stimulation pulse affects nearby brain cells has not however yet been determined.