O-2-23 - Expression of vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) in meningiomas and associated peritumoral edema

Abstract

Deep brain stimulation (DBS) was first used to treat essential tremor and the movement disorders associated with Parkinson disease. Its success led to its consideration as treatment for a wide variety of applications, including other neurologic as well as psychiatric and cognitive impairments. Extensive research conducted over the past 20 years has attempted to explain the as-yet uncertain mechanisms of DBS, with a focus on its effects on neuronal and astrocytic activity at the cellular, regional, and network level within the basal ganglia thalamocortical circuitry. Based on experimental evidence and theoretical considerations, five potentially co-occurring mechanisms have been proposed. DBS may produce local changes in the stimulated brain nuclei, as well as distal changes in efferent outputs and target nuclei.These theories of mechanism may not be exclusionary. Determining the degree to which some or all of these cellular and circuitry mechanisms account for the therapeutic efficacy as well as the potential adverse effects of DBS has been an important matter of debate. A review of the literature suggests that DBS mechanisms of action may be too complex to be supported by a single hypothesis, and they cannot be reduced to a simple question of inactivation or inhibition of neuronal activity and neurotransmission. This review summarizes each of these theories and advances in the understanding of the action of DBS, particularly as they relate to the modulation of neuronal spike generation, oscillatory network activity, and enhanced neurotransmission in the basal ganglia–thalamocortical circuit.