Chapter 78 How does DBS work

Publisher Summary This chapter discusses the mechanisms of the action of deep brain stimulation (DBS) and provides some arguments for and against the stimulation or inhibition of target neural structures. The case for DBS inhibiting or blocking target neurons and their axons is supported by several observations. First, the clinical effects of DBS mimic those of lesions in the same target. Second, the positron emission tomography (PET) studies of pallidotomy and GPi DBS suggest that both activate motor areas consistent with the notion that both remove the excessive inhibitory outflow from the globus pallidus to thalamus and to cortex. To study the issue of subthalamic nucleus (STN) DBS releasing glutamate, the investigators inserted electrodes and applied stimulation in the STN and collected rnicrodialysate in the external segment of the globus pallidus in these animals. They have shown that with the application of chronic STN stimulation at frequencies of 130 Hz, there is a rise in the levels of glutamate in the ipsilateral globus pallidus reaching 3–4 folds higher than resting levels. This data is consistent with the notion that the stimulation of the STN in this circumstance drives STN neurons and causes them to release glutamate at their axon terminals.