ライフサイエンスコーパス: STN

1 STN activity was rescued by NMDA receptor antagonism or

2 STN DBS did not protect against alpha-syn-mediated defic

3 STN DBS is neuroprotective against neurotoxicants in ani

4 STN DBS was associated with greater mean reductions on s

5 STN gamma (60-90 Hz) increased most strongly when the ta

6 STN HFS inhibited key brain regions, including the subst

7 STN HFS prevented the re-escalation of heroin intake aft

8 STN neurons containing alpha4beta2 nAChRs (alpha4beta2 n

9 STN neurons exhibited prolonged NMDA receptor-mediated s

10 STN synapses showed a decrease in calcium-permeable AMPA

11 STN-DBS significantly improved the off-medication UPDRS-

12 le size of 502 PD patients (254 GPi DBS, 248 STN DBS), were included in this meta-analysis.

13 The fate mapped E11.5-12.5 STN neuronal population included 20% of neurons with pro

14 Long-term trkB blockade abolished STN DBS-mediated neuroprotection of SN neurons following

15 crease lateral PFC-STN coherence and altered STN neuronal spiking.

16 synchronization in both the motor cortex and STN.

17 to activity at prefrontal electrode Fz, and STN beta activity (13-30 Hz) coupled to electrodes C3/C4

18 suggest that responsiveness to both GPi and STN DBS is similar among different PD motor subtypes, al

19 nals within the striatum, thalamus, GPi, and STN were all associated with increases and decreases in

20 , and between the inferior frontal gyrus and STN, also predicted individual differences in stopping e

21 al ACC, pre-SMA, inferior frontal gyrus, and STN in computing the trade-off between escalating reward

22 the release probability at DR-innervated and STN-innervated synapses, quantified by decreases in pair

23 nge was transiently reduced in both mPFC and STN after dopamine depletion but recovered by day 21.

24 w-frequency oscillatory activity in mPFC and STN before making a response have higher decision thresh

25 However, mPFC and STN both showed peaks in the 45-55 Hz frequency range in

26 ectrophysiology) in healthy participants and STN local field potentials in Parkinson's patients durin

27 er structure in the tract between preSMA and STN correlated with effective connectivity of the same p

28 rength of the interaction between preSMA and STN, and the degree of modulation by the inferior fronta

29 rom thalamus were much stronger to GP-TA and STN neurons than to GP-TI neurons.

30 tched in weight, but those between GP-TA and STN neurons were not; only GP-TI neurons sent substantia

31 Reciprocal connections between GP-TI and STN neurons were matched in weight, but those between GP

32 We applied STN-DBS in an adeno-associated virus (AAV) 1/2-driven hu

33 impedance was lowest in contacts situated at STN border (p=0.03).

34 At <2 and 6 months of age autonomous STN activity was impaired due to activation of KATP chan

35 GT performance in 20 patients with PD before STN surgery with and without dopaminergic treatment and

36 The interstimulus intervals (ISIs) between STN-DBS and TMS that produced cortical facilitation were

37 The relationship between STN activity and decision thresholds critically depends

38 imed to determine if the effect of bilateral STN DBS on dual-task performance in isolated patients wi

39 Previous reports indicate that bilateral STN stimulation in patients with PD amplifies the decrem

40 n stimulation (DBS) surgery of the bilateral STN.

41 atients with dystonia treated with bilateral STN DBS, with average dystonia duration of 10.5 years an

42 l interaction deficits were not corrected by STN-HFS.

43 required to explore the circuitry engaged by STN-HFS, as well as other potential stimulation sites.

44 imb akinesia improvement normally induced by STN DBS.

45 locomotor activity, which was unaffected by STN-HFS.

46 based connectivity between the contralateral STN and motor cortex decreased.

47 In contrast, STN neurons containing alpha7 nAChRs (alpha7 neurons) re

48 N inputs in PD mice, reduced loss of cortico-STN transmission and patterning and improved motor funct

49 ion suggested that downregulation of cortico-STN transmission in PD mice was triggered by increased s

50 , in parkinsonian mice we found that cortico-STN transmission strength had diminished by 50%-75% thro

51 e generally to that of classically described STN neurons.

52 denervation or loss of SNpc neuron, nor did STN DBS elevate p-rpS6 levels further.

53 na incerta (quantified bradykinesia), dorsal STN (mood, anxiety), and inferior STN/substantia nigra (

54 BS throughout, and mood improved with dorsal STN DBS.

55 INTERPRETATION: Effective STN DBS for PD is associated with a specific connectivit

56 We evaluated STN DBS in a parkinsonian model that displays alpha-synu

57 und to be narrow (E10.5-E14.5) with very few STN neurons born at E10.5 or E14.5.

58 Patients who were eligible for STN-DBS were given the choice of undergoing surgery or c

59 additionally assumes that the feedback from STN-GPe circuit to cortex is important for maintaining t

60 hanges in oscillatory activity recorded from STN between ultradian sleep states to determine whether

61 surprise signals occur, and that the fronto-STN circuits for doing this, at least for stopping and c

62 Furthermore, STN burst-firing and beta oscillations are two independe

63 Glutamatergic STN neurons provide the major excitatory drive to the ou

64 er of functional GABAA receptor-mediated GPe-STN inputs.

65 ctivation of STN NMDA receptors triggers GPe-STN inputs to strengthen abnormally, contributing to the

66 ne the causal roles of VP --> VTA and VP --> STN pathways in context-induced reinstatement and reacqu

67 at silencing either the VP --> VTA or VP --> STN pathways is sufficient to reduce both reinstatement

68 work suggests that LFP recordings from human STN differentiate between sleep cycle states, and sleep-

69 2) receptor subunits within the normal human STN.

70 isual and emotional information in the human STN, and provide evidence of separate processing of the

71 opulations of principal neurons in the human STN.

72 es more readily than neuronal cell bodies in STN, which may help explain anatomic variation in stimul

73 nce was significantly higher for contacts in STN, at baseline (111 Omega vs STN border, p=0.03; 169 O

74 y of DBS electrodes chronically implanted in STN, impedance is lower at the rostral STN border and in

75 able to identify an independent increase in STN theta-delta activity triggered by conflict.

76 Data show increases in STN and MCx 29-36 Hz LFP spectral power and coherence af

77 ne selectively affects alpha4beta2 nAChRs in STN: this treatment increased the number of alpha4beta2

78 are regulated by different NMDA receptors in STN.

79 tral STN border and in white matter, than in STN.

80 , suggesting a noncanonical role for trkB in STN DBS-mediated behavioral effects.

81 e, we show that trial-by-trial variations in STN low-frequency oscillatory activity predict adjustmen

82 a), dorsal STN (mood, anxiety), and inferior STN/substantia nigra (UPDRS tremor, working memory).

83 ng that NMDA receptor activity can influence STN output.

84 This could result from intra-STN feedback excitation.

85 Intracranially, STN activity is also increased post surprise, especially

86 decision making by recording intraoperative STN and prefrontal cortex (PFC) electrophysiology as par

87 found increased beta activity in both local STN LFP and sensorimotor cortical EEG and in the couplin

88 In preclinical models, STN DBS provides neuroprotection for substantia nigra (S

89 ic acetylcholine receptors (nAChRs) in mouse STN.

90 ed optogenetics to activate or inhibit mouse STN to test its putative causal role.

91 uence of the medial prefrontal cortex (mPFC)-STN pathway on decision thresholds during high cautiousn

92 oscillatory activity and corresponding mPFC-STN coupling are involved in determining how much eviden

93 In the Spare-the-Nephron (STN) Study, kidney transplant recipients randomized abou

94 neurons, and innervated the striatum but not STN.

95 ency stimulation of the subthalamic nucleus (STN HFS) for heroin addiction.

96 djustments by recording subthalamic nucleus (STN) activity and electroencephalography in 11 Parkinson

97 l synchrony between the subthalamic nucleus (STN) and cortex is critical for proper information proce

98 evidence implicates the subthalamic nucleus (STN) and globus pallidus internus (GPi) in reward and pu

99 tion of activity in the subthalamic nucleus (STN) and is further modulated by trial-by-trial measures

100 field potentials in the subthalamic nucleus (STN) and scalp EEG (modified 10/20 montage) during sleep

101 of effective DBS to the subthalamic nucleus (STN) and test its ability to predict outcome in an indep

102 network composed of the subthalamic nucleus (STN) and the external segment of globus pallidus (GPe).

103 ntal gyrus (IFG) to the subthalamic nucleus (STN) are thought to support this function, but the conne

104 The striatum and the subthalamic nucleus (STN) constitute the input stage of the basal ganglia (BG

105 Subthalamic nucleus (STN) deep brain stimulation (DBS) can improve motor comp

106 Subthalamic nucleus (STN) deep brain stimulation (DBS) represents a well-esta

107 The glutamatergic subthalamic nucleus (STN) exerts control over motor output through nuclei of

108 l (LFP) activity in the subthalamic nucleus (STN) from electrodes implanted in patients with Parkinso

109 timulation (DBS) of the subthalamic nucleus (STN) has been reported to improve sleep architecture in

110 timulation (DBS) of the subthalamic nucleus (STN) has no effect on the AER, but a previous case sugge

111 ronal population of the subthalamic nucleus (STN) has the ability to prolong incoming cortical excita

112 t-firing pattern of the subthalamic nucleus (STN) in a feed-forward, or efferent-only, mechanism.

113 ies have implicated the subthalamic nucleus (STN) in decisions that involve inhibiting movements.

114 the involvement of the subthalamic nucleus (STN) in motivational and emotional processes; however, p

115 ities recorded from the subthalamic nucleus (STN) in patients with deep brain stimulation (DBS) elect

116 g LFP activity from the subthalamic nucleus (STN) in patients with Parkinson's disease who had underg

117 The subthalamic nucleus (STN) is a critical excitatory signaling center within th

118 timulation (DBS) of the subthalamic nucleus (STN) is a highly effective symptomatic therapy for motor

119 The subthalamic nucleus (STN) is a key area of the basal ganglia circuitry regula

120 cies has shown that the subthalamic nucleus (STN) is activated by scenarios involving stopping or pau

121 The subthalamic nucleus (STN) is an element of cortico-basal ganglia-thalamo-cort

122 The subthalamic nucleus (STN) is hypothesized to play a central role in the rapid

123 The subthalamic nucleus (STN) is the main target for neurosurgical treatment of m

124 timulation (DBS) of the subthalamic nucleus (STN) is the most common neurosurgical treatment for Park

125 Gamma activity in the subthalamic nucleus (STN) is widely viewed as a pro-kinetic rhythm.

126 making assume that the subthalamic nucleus (STN) mediates this function by elevating decision thresh

127 at a network of GPe and subthalamic nucleus (STN) neurons computes the normalization term in Bayes' e

128 firing patterns of rat subthalamic nucleus (STN) neurons when their rhythmic firing was densely pert

129 as been recorded in the subthalamic nucleus (STN) of Parkinson's disease (PD) patients and linked to

130 eceptor blockers to the subthalamic nucleus (STN) of parkinsonian rats and evaluated locomotor behavi

131 The subthalamic nucleus (STN) of the basal ganglia appears to have a potent role

132 ity, ostensibly via the subthalamic nucleus (STN) of the basal ganglia.

133 (PD) patients to either subthalamic nucleus (STN) or globus pallidus internus (GPi) deep brain stimul

134 timulation (DBS) of the subthalamic nucleus (STN) remains controversial.

135 euronal activity in the subthalamic nucleus (STN) results in a hyperkinetic movement syndrome, simila

136 ry motor area (preSMA), subthalamic nucleus (STN), and primary motor cortex during response inhibitio

137 m nuclei, including the subthalamic nucleus (STN), globus pallidus, striatum, and substantia nigra.

138 l tegmental area (VTA), subthalamic nucleus (STN), lateral hypothalamus, among others, and the roles

139 hat repeated pairing of subthalamic nucleus (STN)-DBS and M1-TMS at specific time intervals will lead

140 ivity in the cortex and subthalamic nucleus (STN).

141 tal gyrus, caudate, and subthalamic nucleus (STN).

142 ys, interact within the subthalamic nucleus (STN).

143 ll type innervating the subthalamic nucleus (STN).

144 tine nucleus (PPN), and subthalamic nucleus (STN).

145 S, n=164) at either the subthalamic nucleus (STN, n=84) or globus pallidus interna (GPi, n=80), using

146 timulation (DBS) of the subthalamic nucleus (STN-DBS) has largely replaced ablative therapies for Par

147 anted electrodes at the subthalamic nucleus (STN-HFS).

148 At 12 months of age approximately 30% of STN neurons had been lost, as in HD.

149 f dopamine, excessive cortical activation of STN NMDA receptors triggers GPe-STN inputs to strengthen

150 ition of the STN and increased activation of STN NMDA receptors.

151 Next we showed that brief activation of STN projection neurons was sufficient to interrupt or pa

152 We recorded the activities of STN, Type-I GP (GP-TI) and Type-A GP (GP-TA) neurons in

153 In addition, the spontaneous activity of STN neurons in R6/2 mice was reduced and neurons exhibit

154 to a particular function of the activity of STN neurons.

155 eta oscillations entrain spiking activity of STN, striatal cholinergic interneurons and BG downstream

156 Spectral analysis of STN local field potentials revealed elevated beta power

157 expectedly reduced the functional benefit of STN DBS on a short timescale that is inconsistent with c

158 Using Western blotting of STN tissue punches, we demonstrated that GluN2D is expre

159 urons, indicating an additional diversity of STN neurons: responses to electrical stimulation.

160 The effect of STN DBS on cognitive function in dystonia patients is le

161 This study suggests the effect of STN DBS on working memory and attention may be much less

162 In order to investigate the effect of STN stimulation on impulsive decision making, we used th

163 roprotective and disease-modifying effect of STN-DBS in a mechanistically relevant model of PD.

164 Our aim was to compare the effects of STN DBS and GPi DBS on the AER.

165 ssion is impaired, resembling the effects of STN lesioning or inactivation.

166 neuroprotective and symptomatic efficacy of STN DBS.SIGNIFICANCE STATEMENT Subthalamic nucleus deep

167 data establish that cortical entrainment of STN neural activity is disrupted in R6/2 mice and may be

168 These findings provide further evidence of STN involvement in impulsive behaviour in the PD populat

169 from the Dbx1 microdomain, at the expense of STN and PM populations.

170 e aim in this study to examine the impact of STN-DBS on the survival of patients with severe PD.

171 Increases of STN LFO power preceding the response predicted increased

172 We propose that the involvement of STN in reactive control is restricted to its ventromedia

173 Knockdown of STN NMDA receptors, which also suppresses proliferation

174 Repeated pairing of STN-DBS and M1-TMS at short ( approximately 3 ms) and me

175 We found that repeated pairing of STN-DBS with TMS at short ( approximately 3 ms) and medi

176 efficacy and disease-modifying potential of STN DBS.

177 nstructions, while cue-induced reductions of STN beta power decreased thresholds irrespective of inst

178 ictly segregated to a ventromedial region of STN.

179 Our results highlight the pivotal role of STN divergent projections in BG physiology and pathophys

180 physiological evidence for the exact role of STN during adjustment of decision thresholds is lacking.

181 xpression and produced a robust silencing of STN neurons as measured using whole-cell recording ex vi

182 This suggests that a subpopulation of STN neurons forms a local glutamatergic network, which t

183 We found that specific subsets of STN neurons have activity consistent with causal roles i

184 erate plateau potentials, similar to that of STN neurons without local axon collaterals and more gene

185 a dendritic arbor that differed from that of STN neurons without local axon collaterals.

186 ecordings, allowed identifying a new type of STN neurons that possess a highly collateralized intrins

187 and three weeks later received four weeks of STN DBS or electrode implantation that remained inactive

188 that VP neurons projecting to either VTA or STN are recruited during context-induced reinstatement o

189 uppresses proliferation of GABAergic pallido-STN inputs in PD mice, reduced loss of cortico-STN trans

190 val since baseline (completion of the parent STN study at 24 months posttransplant).

191 Cortically patterned STN neuronal activity was less phase-locked in R6/2 mice

192 potentiation, and less effectively patterned STN activity.

193 es were associated with increase lateral PFC-STN coherence and altered STN neuronal spiking.

194 nstrated that GluN2D is expressed in the rat STN throughout development [age postnatal day 7 (P7)-P60

195 rtical plasticity can be induced by repeated STN and M1 stimulation at specific intervals.

196 ed in STN, impedance is lower at the rostral STN border and in white matter, than in STN.

197 Our data show STN-HFS suppresses excessive self-grooming in two autism

198 Subthalamic nucleus deep brain stimulation (STN DBS) is increasingly used in mid- to late-stage Park

199 Subthalamic nucleus deep brain stimulation (STN DBS) protects dopaminergic neurons of the substantia

200 subthalamic nucleus deep brain stimulation (STN-DBS) has been shown to improve motor function, motor

201 subthalamic nucleus deep-brain stimulation (STN-DBS) with motor cortical transcranial magnetic stimu

202 subthalamic nucleus deep brain stimulation (STN-DBS), while they performed an instrumental learning

203 (PD) and tend to improve after subthalamic (STN) stimulation after a marked reduction of dopaminergi

204 Dbx1 microdomain gives rise to subthalamic (STN), premammillary (PM) and posterior hypothalamic (PH)

205 In summary, STN gamma activity may support flexible motor control as

206 n stimulated, with peak p values in superior STN/zona incerta (quantified bradykinesia), dorsal STN (

207 eadmill walking task to compare synchronized STN local field potential (LFP) activity with activity i

208 ticular PD motor subtypes and by DBS target (STN vs GPi).

209 ts during a perceptual decision-making task; STN low-frequency oscillatory (LFO) activity (2-8 Hz), c

210 Our data confirm that STN-DBS, using an MRI-guided/MRI-verified technique, rem

211 These results demonstrate that STN DBS does not protect the nigrostriatal system agains

212 We demonstrate that STN DBS in male rats activates signaling downstream of t

213 Together, our results demonstrate that STN low-frequency oscillatory activity and corresponding

214 tington's disease (HD) by demonstrating that STN activity is reduced and less phase-locked to cortica

215 tion to examine the therapeutic effects that STN HFS may have on relapse in humans with heroin addict

216 We found that STN LFP activities in the gamma (55-90 Hz) and beta (13-

217 We found that STN-HFS significantly suppressed excessive self-grooming

218 These results show that STN-DBS can modulate cortical plasticity.

219 s used to interrupt licking, and showed that STN inhibition reduced the disruptive effect of surprise

220 These results suggest that STN DBS increases BDNF-trkB signaling to contribute to t

221 The results suggest that STN integrates activity from both motor and cognitive ne

222 These findings suggest that STN-DBS does not act as an indiscriminate informational

223 The STN has strong connections between the basal ganglia and

224 simultaneous recordings from cortex and the STN in humans, single-unit recordings in humans, high-re

225 diffusivity in tracts between preSMA and the STN, and between the inferior frontal gyrus and STN, als

226 cillations between prefrontal cortex and the STN, which may provide a preferential "window in time" f

227 illation are generated in the cortex and the STN-GPe circuits resonates at this frequency.

228 vation interrupts behavior, and blocking the STN blunts the interruptive effect of surprise.

229 Crucially, the STN and lateral PFC beta decrease was significantly atte

230 ndividual neurons was recorded in either the STN (n=100) or the GPi (n=100).

231 from intraoperative microrecordings from the STN during affective picture presentation in patients wi

232 le units and local field potentials from the STN exhibit oscillatory entrainment to low-frequency (0.

233 In vivo recordings from the STN of anesthetized adult rats demonstrated that the spi

234 downstream polysynaptic inhibition from the STN to the motor cortex.

235 elationship between neuronal activity in the STN and cortex in an animal model of HD.

236 s with PD diagnosed with ICD, neurons in the STN and GPi would be more responsive to reward-related s

237 units contribute to synaptic activity in the STN and may represent potential therapeutic targets for

238 ta band (15-30 Hz) activity decreased in the STN and PFC, and this decrease was progressively enhance

239 equency-specific oscillatory activity in the STN and voluntary flexion of either the index or little

240 n we reduced Vglut2 expression levels in the STN by 40%, leaving Pitx2 expression intact.

241 High-frequency electrical stimuli in the STN effectively alleviate motor symptoms in movement dis

242 suggesting that the beta suppression in the STN LFP during sustained contraction serves as a proxy f

243 elated suppression of beta-band power in the STN LFP was significantly modulated by effort, but not b

244 as synaptic NMDA receptor activation in the STN of rat brain slices.

245 variables improved with DBS anywhere in the STN region, but several motor, cognitive, and affective

246 ggesting that Vglut2-expressing cells in the STN regulate dopaminergic transmission.

247 rmed in vivo extracellular recordings in the STN to measure single-unit activity and local field pote

248 de of the exaggerated 29-36 Hz rhythm in the STN was modulated by paw movement.

249 EPSCs in the STN were mediated primarily by AMPA and NMDA receptors a

250 s of loss responsive neurons (p<0.05) in the STN, but not in the GPi.

251 mechanisms of cholinergic modulation in the STN, we studied cellular and circuit aspects of nicotini

252 of synaptic excitation and inhibition in the STN, which contributes to parkinsonian activity and moto

253 monstration of associative plasticity in the STN-M1 circuits in PD patients using this novel techniqu

254 low deactivation time course of EPSCs in the STN.

255 d two largely divergent microcircuits in the STN; these are regulated in part by either alpha4beta2 o

256 To explore this potential linkage, the STN was studied in BAC transgenic and Q175 knock-in mous

257 ransmission, leading to disinhibition of the STN and increased activation of STN NMDA receptors.

258 rnal globus pallidus (GPe) inhibition of the STN are critical for normal movement and are greatly per

259 ht explain why deep-brain stimulation of the STN can impair subjects' ability to slow down responses

260 nstrated that optogenetic stimulation of the STN excited its major projection targets.

261 ce during movement and support a role of the STN in the control of motor effort to be attributed to a

262 We argue that a major function of the STN is to broadly pause behavior and cognition when stop

263 t cortical inputs and synchronization of the STN neuronal population.

264 The influence of the STN on continue-evoked activity in the pre-SMA was predi

265 While increased oscillatory activity of the STN predicts elevated decision thresholds during high le

266 ted by blocking different connections of the STN-GPe circuit.

267 s described for anatomic subdivisions of the STN.

268 an excitatory influence of the preSMA on the STN, thereby amplifying the downstream polysynaptic inhi

269 iques to firstly, visualize and quantify the STN neurochemical organization based on neuronal markers

270 g stopping or pausing, yet evidence that the STN causally implements stops or pauses is lacking.

271 ese results provide strong evidence that the STN is both necessary and sufficient for such forms of b

272 inputs from the motor cortex directly to the STN and that rescuing this loss alleviates Parkinsonian

273 rat: 1) whether cortical projections to the STN and ZI have independent functional organizations or

274 ation, the GPe needs to send feedback to the STN equal to a particular function of the activity of ST

275 emonstrate that motor cortical inputs to the STN heterosynaptically regulate, through activation of p

276 ontal cortical areas directly project to the STN via so-called hyperdirect pathways.

277 e, a homeostatic mechanism, intrinsic to the STN, balances cortical excitation by adjusting the stren

278 these data argue that dysfunction within the STN is an early feature of HD that may contribute to its

279 tribution of a limited population within the STN is sufficient to achieve results similar to STN lesi

280 linated axons, and axon terminals within the STN.

281 first order dynamic linear model with these STN LFP features as inputs can be used to decode the tem

282 ntromedial portion, further implicating this STN subdivision in impulse control disorders.

283 Thus STN activation interrupts behavior, and blocking the STN

284 neurons sent substantial connections back to STN.

285 red by UPDRS-III, after GPi DBS, compared to STN DBS (17.5 +/- 13.0 vs 14.6 +/- 14.9, p = 0.02), with

286 ng that PAC may be predictive of response to STN DBS.

287 is sufficient to achieve results similar to STN lesions and high-frequency stimulation, but with few

288 a function of communication from pre-SMA to STN when choices differ subtly in reward values, allowin

289 Patients undergoing STN-DBS had significantly longer survival and were signi

290 l (LFP) recordings in PD subjects undergoing STN-DBS over the course of a full-night's sleep.

291 ergic deficits had developed, rats underwent STN-DBS electrode implantation ipsilateral to the vector

292 A cohort of 41 patients who underwent STN-DBS were followed for a minimum period of 5 years, w

293 matter, p<0.001) and over time (90 Omega vs STN border, p<0.001; 54 Omega vs white matter, p<0.001).

294 r contacts in STN, at baseline (111 Omega vs STN border, p=0.03; 169 Omega vs white matter, p<0.001)

295 Whether STN DBS can be protective in other models of synucleinop

296 logy and pathophysiology and may explain why STN is such an effective site for invasive treatment of

297 A training dataset of 51 PD patients with STN DBS was combined with publicly available human conne

298 Ten PD human patients with STN-DBS were studied in the on-medication state with DBS

299 pport complete functional segregation within STN, because movement improved with DBS throughout, and

300 ion time reaching movements with and without STN-DBS.