Cortical Potentials Evoked by Deep Brain Stimulation in the Subthalamic Area

Abstract

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been used since the mid-1990s as a treatment for patients with Parkinson's disease, and more recently also in other conditions, such as dystonia or obsessive compulsive disorder. Non-invasive studies of cortical evoked potentials (EPs) that follow individual STN–DBS stimuli has provided us with insights about the conduction of the DBS pulses to the cortex. Such EPs have multiple components of different latencies, making it possible to distinguish short-latency and long-latency responses (3–8 ms and 18–25 ms latency, respectively). The available evidence indicates that these short- and long-latency EPs correspond to conduction from the STN stimulation site to the cortical recording location via anti- and orthodromic pathways, respectively. In this review we survey the literature from recording studies in human patients treated with STN–DBS for Parkinson's disease and other conditions, as well as recent animal studies (including our own) that have begun to elucidate details of the pathways, frequency dependencies, and other features of EPs. In addition, we comment on the possible clinical utility of this knowledge.

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

“…Thus, STN DBS, with use of the contacts in the sensorimotor region of the nucleus, may stimulate nearby pallidal-thalamic fibers and cerebellar-thalamic fibers in the zona incerta, and may antidromically activate afferents from GPe, which send (inhibitory) collaterals to GPi. STN DBS may also directly activate the nigrostriatal tract [298], but this is unlikely to be relevant in the treatment of PD because of the degeneration of this pathway in PD.…”

“…STN stimulation has also been found to influence directly cortical neurons via antidromic activation of the corticosubthalamic pathway [298][299][300][301]. In fact, optogenetic studies in rodents have suggested that the antidromic activation of motor cortical input may be responsible for the clinical effects of STN DBS [299,302].…”

“…In fact, optogenetic studies in rodents have suggested that the antidromic activation of motor cortical input may be responsible for the clinical effects of STN DBS [299,302]. While antidromic stimulation of cortex has also been shown in nonhuman primates and in patients, based on short-latency cortical-evoked potentials [298,301,[303][304][305], it is not clear what role they play in the overall behavioral response to STN DBS in patients with movement disorders. Antidromic effects are not likely to play a prominent role in the case of GPi DBS [297,298], which achieves the same motor result as STN DBS.…”

“…While antidromic stimulation of cortex has also been shown in nonhuman primates and in patients, based on short-latency cortical-evoked potentials [298,301,[303][304][305], it is not clear what role they play in the overall behavioral response to STN DBS in patients with movement disorders. Antidromic effects are not likely to play a prominent role in the case of GPi DBS [297,298], which achieves the same motor result as STN DBS. Finally, a recent rodent study of STN DBS showed that STN DBS may also engage cerebellar activity to improve parkinsonian motor symptoms [306].…”

Direct Functional Connectivity between the Thalamus (Vim) and the Contralateral Motor Cortex: Just a Single Case Observation or a Common Pathway in the Human Brain?

“…We use very short latency cortical evoked responses (CER) as evidence of a direct anatomical pathway between the thalamus and the ipsilateral and contralateral cortex. CERs with various latencies have been previously reported from patients undergoing DBS for intractable tremor and from experimental models in primates [1][2][3][4].…”