Pallidal stimulation suppresses pathological dysrhythmia in the parkinsonian motor cortex
- Authors
- McCairn, Kevin W.; Turner, Robert S.
- Issue Date
- Apr-2015
- Publisher
- AMER PHYSIOLOGICAL SOC
- Keywords
- deep brain stimulation; MPTP; nonhuman primate; Parkinson' s disease; primary motor cortex; globus pallidus
- Citation
- JOURNAL OF NEUROPHYSIOLOGY, v.113, no.7, pp.2537 - 2548
- Journal Title
- JOURNAL OF NEUROPHYSIOLOGY
- Volume
- 113
- Number
- 7
- Start Page
- 2537
- End Page
- 2548
- URI
- http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/956
- DOI
- 10.1152/jn.00701.2014
- ISSN
- 0022-3077
- Abstract
- "Although there is general consensus that deep brain stimulation (DBS) yields substantial clinical benefit in patients with Parkinson's disease (PD), the therapeutic mechanism of DBS remains a matter of debate. Recent studies demonstrate that DBS targeting the globus pallidus internus (GPi-DBS) suppresses pathological oscillations in firing rate and between-cell spike synchrony in the vicinity of the electrode but has negligible effects on population-level firing rate or the prevalence of burst firing. The present investigation examines the downstream consequences of GPi-DBS at the level of the primary motor cortex (M1). Multielectrode, single cell recordings were conducted in the M1 of two parkinsonian nonhuman primates (Macaca fasicularis). GPi-DBS that induced significant reductions in muscular rigidity also reduced the prevalence of both beta (12-30 Hz) oscillations in single unit firing rates and of coherent spiking between pairs of M1 neurons. In individual neurons, GPi-DBS-induced increases in mean firing rate were three times more common than decreases; however, averaged across the population of M1 neurons, GPi-DBS induced no net change in mean firing rate. The population-level prevalence of burst firing was also not affected by GPi-DBS. The results are consistent with the hypothesis that suppression of both pathological, beta oscillations and synchronous activity throughout the cortico-basal ganglia network is a major therapeutic mechanism of GPi-DBS."
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