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1                                              Subthalamic activity was predominantly led by activity i
2 y ON dopamine, the total duration over which subthalamic and pallidal populations were aligned to pha
3 equency and duration of periods during which subthalamic and pallidal populations were phase-locked t
4 ients with Parkinson's disease to identify a subthalamic area with an analogous electrophysiological
5                                 More ventral subthalamic areas showed predominant connectivity to med
6 icycling and walking led to a suppression of subthalamic beta power (13-35Hz), and this suppression w
7                               The designated subthalamic 'beta' area projected predominantly to motor
8 iological abnormalities, including excessive subthalamic bursts, cortico-subthalamic synchronization,
9 g machine learning techniques we showed that subthalamic connectivity differentiates binge drinkers a
10 se results are the first to demonstrate that subthalamic D5Rs are involved in the pathophysiology of
11 to what has been shown for patients with PD, subthalamic DBS reversibly decreased PAC in a subset of
12 and reduction of cortical synchronization by subthalamic DBS, providing an explanation for their simi
13 atients with Parkinson's disease, on and off subthalamic deep brain stimulation (DBS), focussing on a
14                  We simulated the effects of subthalamic deep brain stimulation both proximally to th
15 haracterize anatomical circuits modulated by subthalamic deep brain stimulation, and infer about the
16  Parkinson's disease with either thalamic or subthalamic electrodes (13 male and two female patients,
17 k performance has its origins in the pallido-subthalamic feedback loop.
18              Gamma oscillations arise in the subthalamic-globus pallidus feedback loop, and occur dur
19  causes reorganization likely takes place at subthalamic levels.
20 t in mid-brain structures, in particular the subthalamic locomotor region (subthalamic nucleus, STN)
21 ponding and emphasized the relevance of this subthalamic network across alcohol misuse.
22 potential therapeutic targets for modulating subthalamic neuron activity in neurological disorders su
23                              The activity of subthalamic neurons is tightly controlled by upstream in
24 idered here (the change in firing pattern of subthalamic neurons through the dopamine-induced change
25 input and downstream structures reveals that subthalamic, not striatal, activity fluctuations correla
26 se patients with electrodes implanted in the subthalamic nuclei for deep brain stimulation.
27 35Hz) beta power changes were analyzed in 22 subthalamic nuclei from 13 Parkinson disease patients (5
28 tion electrodes implanted bilaterally in the subthalamic nuclei of 10 patients with Parkinson's disea
29 ing from dorsal raphe, pedunculopontine, and subthalamic nuclei were tested for synaptic modification
30 lism, and the correlations were strongest in subthalamic nuclei, anterior cingulate, and medial orbit
31 endent upon functioning of the glutamatergic subthalamic nucleus (computing the 'normalization term'
32 ic) profiles in the dorsolateral part of the subthalamic nucleus (i.e. its sensorimotor territory) wa
33                                          The subthalamic nucleus (STh) is a small subcortical structu
34 S) of globus pallidus internus (GPi DBS) and subthalamic nucleus (STN DBS) are effective treatment fo
35                Deep brain stimulation of the subthalamic nucleus (STN DBS) has become an accepted tre
36 tential of high-frequency stimulation of the subthalamic nucleus (STN HFS) for heroin addiction.
37 such speed-accuracy adjustments by recording subthalamic nucleus (STN) activity and electroencephalog
38                 Neural synchrony between the subthalamic nucleus (STN) and cortex is critical for pro
39               Recent evidence implicates the subthalamic nucleus (STN) and globus pallidus internus (
40  but varies as a function of activity in the subthalamic nucleus (STN) and is further modulated by tr
41 le in the genesis of burst discharges in the subthalamic nucleus (STN) and parkinsonian locomotor sym
42    We recorded local field potentials in the subthalamic nucleus (STN) and scalp EEG (modified 10/20
43 ease promotes burst firing of neurons in the subthalamic nucleus (STN) and substantia nigra zona reti
44 connectivity profile of effective DBS to the subthalamic nucleus (STN) and test its ability to predic
45 otor cortex and by a network composed of the subthalamic nucleus (STN) and the external segment of gl
46                                          The subthalamic nucleus (STN) and the zona incerta (ZI) are
47 rnal globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN) are closely related to motor f
48 SMA) and inferior frontal gyrus (IFG) to the subthalamic nucleus (STN) are thought to support this fu
49  chronic deep brain stimulation (DBS) of the subthalamic nucleus (STN) at the commonly used frequency
50                         The striatum and the subthalamic nucleus (STN) constitute the input stage of
51 changes in Parkinson disease (PD) induced by subthalamic nucleus (STN) DBS to determine whether these
52                                              Subthalamic nucleus (STN) deep brain stimulation (DBS) c
53                                              Subthalamic nucleus (STN) deep brain stimulation (DBS) h
54                                              Subthalamic nucleus (STN) deep brain stimulation (DBS) r
55 inson's disease (PD) patients with bilateral subthalamic nucleus (STN) deep brain stimulation underwe
56                            The glutamatergic subthalamic nucleus (STN) exerts control over motor outp
57  local field potential (LFP) activity in the subthalamic nucleus (STN) from electrodes implanted in p
58 ders and deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been reported to improve s
59          Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has no effect on the AER, but
60               The neuronal population of the subthalamic nucleus (STN) has the ability to prolong inc
61          Deep brain stimulation (DBS) of the subthalamic nucleus (STN) improves symptoms of Parkinson
62 cephalography and direct recordings from the subthalamic nucleus (STN) in 17 PD patients.
63 regulated by the burst-firing pattern of the subthalamic nucleus (STN) in a feed-forward, or efferent
64           Recent studies have implicated the subthalamic nucleus (STN) in decisions that involve inhi
65 ans have demonstrated the involvement of the subthalamic nucleus (STN) in motivational and emotional
66 potential (LFP) activities recorded from the subthalamic nucleus (STN) in patients with deep brain st
67 ingers while recording LFP activity from the subthalamic nucleus (STN) in patients with Parkinson's d
68 ection highlighted the important role of the subthalamic nucleus (STN) in regulating behavior.
69 ng surgery for deep brain stimulation to the subthalamic nucleus (STN) indicate that spectral changes
70                                          The subthalamic nucleus (STN) is a critical excitatory signa
71          Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a highly effective symptoma
72                                          The subthalamic nucleus (STN) is a key area of the basal gan
73                                          The subthalamic nucleus (STN) is a key node in the network t
74   Evidence across species has shown that the subthalamic nucleus (STN) is activated by scenarios invo
75          Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective treatment for
76                                          The subthalamic nucleus (STN) is an element of cortico-basal
77                                          The subthalamic nucleus (STN) is hypothesized to play a cent
78 hown that beta-band desynchronization in the subthalamic nucleus (STN) is reduced just before and dur
79 ated in effortful control over behavior, the subthalamic nucleus (STN) is specifically thought to con
80                                          The subthalamic nucleus (STN) is the main target for neurosu
81          Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is the most common neurosurgic
82                                          The subthalamic nucleus (STN) is thought to play a central r
83                        Gamma activity in the subthalamic nucleus (STN) is widely viewed as a pro-kine
84 nt models of decision making assume that the subthalamic nucleus (STN) mediates this function by elev
85 to different patterns of synaptic input from subthalamic nucleus (STN) neuron.
86                             In Parkinsonism, subthalamic nucleus (STN) neurons and two types of exter
87                     The activity patterns of subthalamic nucleus (STN) neurons are intimately linked
88 ese models suggest that a network of GPe and subthalamic nucleus (STN) neurons computes the normaliza
89                                              Subthalamic nucleus (STN) neurons exhibited low-latency
90  been reported as a pathological activity of subthalamic nucleus (STN) neurons in Parkinson's disease
91 ng methods to predict firing patterns of rat subthalamic nucleus (STN) neurons when their rhythmic fi
92 ypic GABAergic GPe neurons fire antiphase to subthalamic nucleus (STN) neurons, often express parvalb
93 neous rhythmic bursts of spikes generated by subthalamic nucleus (STN) neurons.
94 ior motor thalamus (Vim/Vop) neurons and 123 subthalamic nucleus (STN) neurons.
95 uency (13-30 Hz) oscillatory activity in the subthalamic nucleus (STN) of Parkinson's disease (PD) ha
96 ta and gamma ranges has been recorded in the subthalamic nucleus (STN) of Parkinson's disease (PD) pa
97 e applied glutamate receptor blockers to the subthalamic nucleus (STN) of parkinsonian rats and evalu
98                                          The subthalamic nucleus (STN) of the basal ganglia appears t
99 uppresses motor activity, ostensibly via the subthalamic nucleus (STN) of the basal ganglia.
100  Parkinson's disease (PD) patients to either subthalamic nucleus (STN) or globus pallidus internus (G
101  whereby deep brain stimulation (DBS) of the subthalamic nucleus (STN) or internal globus pallidus (G
102                These models predict that the subthalamic nucleus (STN) provides feedback that normali
103 rget for deep brain stimulation (DBS) of the subthalamic nucleus (STN) remains controversial.
104                     In the BG motor loop the subthalamic nucleus (STN) represents an important struct
105 ion and blockade of neuronal activity in the subthalamic nucleus (STN) results in a hyperkinetic move
106 ral electrocorticography in combination with subthalamic nucleus (STN) single-unit recording to study
107     We studied 14 PD patients with bilateral subthalamic nucleus (STN) stimulation and 16 age-matched
108 medical therapy (BMT); and (2) randomised to subthalamic nucleus (STN) versus globus pallidus interna
109 gyrus, presupplementary motor area (preSMA), subthalamic nucleus (STN), and primary motor cortex duri
110 , globus pallidus interna and externa (GPe), subthalamic nucleus (STN), and substantia nigra pars com
111 tex provides strong excitatory inputs to the subthalamic nucleus (STN), and these cortico-STN inputs
112 d associated brainstem nuclei, including the subthalamic nucleus (STN), globus pallidus, striatum, an
113 projections to ventral tegmental area (VTA), subthalamic nucleus (STN), lateral hypothalamus, among o
114                                          The subthalamic nucleus (STN), which receives excitatory inp
115      We hypothesize that repeated pairing of subthalamic nucleus (STN)-DBS and M1-TMS at specific tim
116 ated and coherent activity in the cortex and subthalamic nucleus (STN).
117 t and indirect pathways, interact within the subthalamic nucleus (STN).
118 were the major GPe cell type innervating the subthalamic nucleus (STN).
119 us (DR), pedunculopontine nucleus (PPN), and subthalamic nucleus (STN).
120 nflict: the medial prefrontal cortex and the subthalamic nucleus (STN).
121 ced by the glutamatergic projection from the subthalamic nucleus (STN).
122 e-supplementary motor area (preSMA), and the subthalamic nucleus (STN).
123 rnal globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN).
124 right inferior frontal cortex (rIFC) and the subthalamic nucleus (STN).
125 e-SMA), inferior frontal gyrus, caudate, and subthalamic nucleus (STN).
126 brain stimulation (DBS, n=164) at either the subthalamic nucleus (STN, n=84) or globus pallidus inter
127          Deep brain stimulation (DBS) of the subthalamic nucleus (STN-DBS) has largely replaced ablat
128  suggests that deep brain stimulation of the subthalamic nucleus (STN-DBS) may have a disease modifyi
129 lation (HFS) via implanted electrodes at the subthalamic nucleus (STN-HFS).
130  average of all the significantly correlated subthalamic nucleus activities accounted for >60% of the
131     The results implicate frequency-specific subthalamic nucleus activities as substantial factors in
132 z) and high-gamma/high-frequency (55-375 Hz) subthalamic nucleus activity and force measures, which e
133                           When recording the subthalamic nucleus activity, we found a clear neural re
134                    The strength of effective subthalamic nucleus afferents and efferents were reduced
135 rom the substantia nigra pars reticulata and subthalamic nucleus along with cortical electroencephalo
136       We show that VP output pathways to the subthalamic nucleus and also to the ventral tegmental ar
137 chronization and oscillatory activity in the subthalamic nucleus and basal ganglia (BG) output nuclei
138 or performing simultaneous recordings of the subthalamic nucleus and cortex using magnetoencephalogra
139 r treated with deep brain stimulation to the subthalamic nucleus and dopaminergic therapy or managed
140 BAergic transmission within the normal human subthalamic nucleus and evidence of GABA innervation thr
141 served that certain phase alignments between subthalamic nucleus and globus pallidus amplified local
142 ronize a network of model neurons comprising subthalamic nucleus and globus pallidus external and sug
143 ed local field potential recordings from the subthalamic nucleus and globus pallidus of five patients
144 connectivity in the orbitofrontal cortex and subthalamic nucleus and greater local connectivity in th
145               Beta band coupling between the subthalamic nucleus and lateral motor areas was not infl
146 ssed synchronization of activity between the subthalamic nucleus and mesial premotor regions, includi
147 ations, and make stronger projections to the subthalamic nucleus and parafascicular nucleus of the th
148  associated with anterior associative-limbic subthalamic nucleus and right dorsolateral prefrontal fu
149  and drug-taking behavior via projections to subthalamic nucleus and substantia nigra pars reticulata
150 tudy, 40 received a bilateral implant in the subthalamic nucleus and their data contributed to the pr
151 fied cell classes projected primarily to the subthalamic nucleus and to the striatum, respectively.
152 iven by a neural network, which includes the subthalamic nucleus and ventrolateral thalamus and has b
153                         The striatum and the subthalamic nucleus are the main entry points for cortic
154 ived bilateral deep brain stimulation of the subthalamic nucleus at the National Institutes of Health
155 a-amplitude are coupled to, and precede, the subthalamic nucleus beta-trough.
156                             Accordingly, the subthalamic nucleus can be considered a key component of
157 ect of bilateral delivery of AAV2-GAD in the subthalamic nucleus compared with sham surgery in patien
158  The identification of a hyperdirect cortico-subthalamic nucleus connection highlighted the important
159 tral striatum to right anterior ventromedial subthalamic nucleus consistent with previous observation
160  internal segment of the globus pallidus and subthalamic nucleus correlated strongly with the number
161 oup scanned on and off treatment with either subthalamic nucleus deep brain stimulation (n = 14) or i
162 c efficacy of STN DBS.SIGNIFICANCE STATEMENT Subthalamic nucleus deep brain stimulation (STN DBS) is
163                                              Subthalamic nucleus deep brain stimulation (STN DBS) pro
164                                    Bilateral subthalamic nucleus deep brain stimulation (STN-DBS) has
165 Parkinson's Disease patients both on and off subthalamic nucleus deep brain stimulation (STN-DBS), wh
166 onism with severe dyskinesias, and underwent subthalamic nucleus deep brain stimulation 8 years after
167                   Specifically, we show that subthalamic nucleus deep brain stimulation modulates all
168  subthalamic nucleus, respectively, and that subthalamic nucleus deep brain stimulation predominantly
169  results highlight that clinically effective subthalamic nucleus deep brain stimulation suppresses sy
170 ng magnetoencephalography (during concurrent subthalamic nucleus deep brain stimulation).
171 y described clinically in some patients with subthalamic nucleus deep brain stimulation.
172 paradigm to test the hypothesis that pairing subthalamic nucleus deep-brain stimulation (STN-DBS) wit
173  deep brain stimulation to the region of the subthalamic nucleus disrupts decision making when multip
174 oxygen-level-dependent response in the right subthalamic nucleus during an impulsiveness task.
175 eoperatively, (2) the day after insertion of subthalamic nucleus electrodes, (3) three weeks later, p
176 hat coordinated reset neuromodulation of the subthalamic nucleus has both acute and sustained long-la
177 levations in beta activity (13-35 Hz) in the subthalamic nucleus have been demonstrated to correlate
178  white matter structures in proximity to the subthalamic nucleus have been implicated in the clinical
179 hods that modulate production of GABA in the subthalamic nucleus improve basal ganglia function in pa
180 ed BCI-controlled adaptive DBS (aDBS) of the subthalamic nucleus in 8 PD patients.
181     In conclusion, our results implicate the subthalamic nucleus in a modulation of outcome value in
182 ecificity of the anterior associative-limbic subthalamic nucleus in decisional impulsivity.
183 ouis Benabid for elucidating the role of the subthalamic nucleus in mediating the motor dysfunction o
184 riatal, and hyperdirect connections with the subthalamic nucleus in modulating waiting and stopping a
185 a better understanding about the role of the subthalamic nucleus in non-motor functions is needed.
186        Recent work has shown that DBS of the subthalamic nucleus in Parkinson's disease greatly reduc
187          Deep brain stimulation (DBS) of the subthalamic nucleus in Parkinson's disease is known to c
188 , and second, the critical importance of the subthalamic nucleus in successful decision making when m
189 ase, suggesting a more pervasive role of the subthalamic nucleus in the control of human decision-mak
190 sibility that cortical connectivity with the subthalamic nucleus in the high and low beta bands may r
191 or regions were predominantly coupled to the subthalamic nucleus in the high beta frequency range, bu
192 tion suppresses synchrony locally within the subthalamic nucleus in the low beta oscillatory range an
193 e that the amplitude of beta activity in the subthalamic nucleus increases in proportion to burst dur
194 imulation of estimated predominant non-motor subthalamic nucleus induced hypomanic behaviour.
195                Deep brain stimulation of the subthalamic nucleus is an effective treatment for Parkin
196                Deep brain stimulation of the subthalamic nucleus is an established treatment for the
197              We show that stimulation of the subthalamic nucleus is causally implicated in increasing
198                                Moreover, the subthalamic nucleus is critical to balance inhibitory an
199  variability, functional organization of the subthalamic nucleus is difficult to investigate in vivo
200                                          The subthalamic nucleus is implicated in inhibitory function
201 pears at odds with the current view that the subthalamic nucleus is important for adjusting behaviour
202 ese results provide strong evidence that the subthalamic nucleus is involved in response inhibition,
203 t spread of current to nonmotor areas of the subthalamic nucleus may be responsible for declines in c
204  that low-frequency neuronal activity in the subthalamic nucleus may encode the information required
205 ms tested, including cortical astrocytes and subthalamic nucleus neurons and in measures of long-term
206 lationship using extracellular recordings of subthalamic nucleus neurons from 19 PD patients undergoi
207 ocal field potentials were recorded from the subthalamic nucleus of 12 patients with advanced Parkins
208 ients received bilateral implantation in the subthalamic nucleus of a constant-current DBS device.
209 ants underwent bilateral implantation in the subthalamic nucleus of a multiple-source, constant-curre
210 ocal field potentials were recorded from the subthalamic nucleus of eight Parkinson's disease patient
211 rded local field potential activity from the subthalamic nucleus of humans undergoing functional neur
212 es by recording the neuronal activity of the subthalamic nucleus of patients with Parkinson's disease
213                            We found that the subthalamic nucleus of the basal ganglia has a substanti
214 ests that the modulatory relationship of the subthalamic nucleus on intracerebellar connectivity is l
215     Yet only the change in strength of local subthalamic nucleus oscillations correlates with the deg
216                               First that the subthalamic nucleus plays a role in adjusting response t
217 -DOPA, and were associated with increases in subthalamic nucleus power over a broad gamma range.
218 , direct, and basal ganglia afferents to the subthalamic nucleus predicted clinical status and therap
219                 Motor cortical coupling with subthalamic nucleus predominantly involved driving of th
220                  Constant-current DBS of the subthalamic nucleus produced significant improvements in
221  basal ganglia pathways, and the hyperdirect subthalamic nucleus projections.
222  patients with deep brain stimulation of the subthalamic nucleus region did not slow down appropriate
223 tterns in the striatum, globus pallidus, and subthalamic nucleus related to sensory and motor events
224 ectivity with the ventrolateral thalamus and subthalamic nucleus showed inverse correlation with keta
225            These abnormalities improved with subthalamic nucleus stimulation (p < 0.005) but not levo
226 nts with idiopathic Parkinson's disease with subthalamic nucleus stimulation were analysed on externa
227 ssive coupling may be reduced by therapeutic subthalamic nucleus stimulation.
228 in the anterior frontal cortex, striatum and subthalamic nucleus suggests the striatal afferent conne
229 ety of bilateral infusion of AAV2-GAD in the subthalamic nucleus supports its further development for
230 uency band having much shorter net delays to subthalamic nucleus than those in the lower beta band.
231 wever, suppression of the sensitivity of the subthalamic nucleus to its hyperdirect afferents by deep
232                           Stimulation of the subthalamic nucleus was associated with dysarthria, fati
233 ociated suppression in their coupling to the subthalamic nucleus was not found to correlate with moto
234 ming asymmetric synapses in the dorsolateral subthalamic nucleus was reduced by 55.1% and 27.9%, resp
235 ral cortices, striatum, substantia nigra and subthalamic nucleus were assessed.
236 as associated with lower connectivity of the subthalamic nucleus with ventral striatum and subgenual
237 ence of different functional circuits within subthalamic nucleus' portions deemed to be appropriate a
238 lysis exploring the effect of atrophy in the subthalamic nucleus, a cerebellar input source, confirme
239 r in all regions except the dentate nucleus, subthalamic nucleus, and corpus callosum of multiple sys
240 ementary motor area, inferior frontal gyrus, subthalamic nucleus, and inferior parietal cortex.
241 subthalamic nucleus, ramping activity of the subthalamic nucleus, and movement-related activity of th
242 Hz, a similar, though weaker, oscillation in subthalamic nucleus, and strong phase coherence between
243 n the external and internal globus pallidus, subthalamic nucleus, and ventral motor thalamic nuclei.
244 eiving more inputs from the globus pallidus, subthalamic nucleus, and zona incerta.
245 rdson syndrome had less neuronal loss in the subthalamic nucleus, but more severe neuronal loss in th
246 taucipir uptake in globus pallidus, putamen, subthalamic nucleus, midbrain, and dentate nucleus relat
247 emporally regulated sensory responses of the subthalamic nucleus, ramping activity of the subthalamic
248  by the hyperdirect and indirect pathways to subthalamic nucleus, respectively, and that subthalamic
249 particular the subthalamic locomotor region (subthalamic nucleus, STN) and the periaqueductal grey (P
250 rmer from the somatosensory/motor cortex and subthalamic nucleus, which may explain their short-laten
251 tical nodes and is posited to project to the subthalamic nucleus, with a putative global suppressive
252 ucleus predominantly involved driving of the subthalamic nucleus, with those drives in the higher bet
253 ally and spectrally segregated resting state subthalamic nucleus-cortical networks.
254                                          The subthalamic nucleus-globus pallidus network is a potenti
255 ct evidence points to the involvement of the subthalamic nucleus-the most common target for deep brai
256 ts localized within the anterior and ventral subthalamic nucleus.
257 atients, after deep brain stimulation of the subthalamic nucleus.
258  in 4 patients with PD undergoing DBS of the subthalamic nucleus.
259 tual conditions in the cerebellum, pons, and subthalamic nucleus.
260  overlap the labeled neurons observed in the subthalamic nucleus.
261 emotionally evoked activity to right ventral subthalamic nucleus.
262 ter-related hypotheses about the role of the subthalamic nucleus.
263 acy of bilateral constant-current DBS of the subthalamic nucleus.
264 in stimulation of the limbic and associative subthalamic nucleus.
265 caudate and left putamen/globus pallidus and subthalamic nucleus.
266 onnections of the pre-supplementary area and subthalamic nucleus.
267 atory input from the 'limbic' regions of the subthalamic nucleus.
268 ith anterior and posterior subregions of the subthalamic nucleus.
269 des mapped onto a mesial-lateral axis of the subthalamic nucleus.
270 l circuits accompanied by hyperactivation of subthalamic nucleus/putaminal regions.
271                                              Subthalamic principal neurons were found to express GABA
272 on through both GABAA and GABAB receptors on subthalamic principal neurons.
273 utamate transporter 1-positive (i.e. cortico-subthalamic) profiles in the dorsolateral part of the su
274 or a partial loss of the hyperdirect cortico-subthalamic projection in MPTP-treated parkinsonian monk
275 motor and sensory cortices, that the cortico-subthalamic projections have a large-scale functional or
276 he following two questions about the cortico-subthalamic projections using the lentivirus anterograde
277 n, at the single neuron level, the important subthalamic role in motor control and coordination and i
278                               The well-known subthalamic somatotopy showed a large overlap of feet an
279 f the cortical motor network, and highlights subthalamic stimulation as a network-modulating therapy.
280 timulation in Parkinson's disease, P=0.0078, subthalamic stimulation in Parkinson's disease, P=0.0312
281 ven increasing interest in the potential for subthalamic stimulation in psychiatric disorders and the
282 bjects with obsessive compulsive disorder on subthalamic stimulation may be less likely to check for
283                                 Accordingly, subthalamic stimulation may release bilateral cortical c
284                                              Subthalamic stimulation reduces motor disability and imp
285                                              Subthalamic stimulation shifts evidence accumulation in
286                                              Subthalamic stimulation was superior to medical therapy
287 l stimulation and in 56% of those undergoing subthalamic stimulation, with no significant between-gro
288  Parkinson's disease and its modulation with subthalamic stimulation.
289  clinical and reaction time improvement from subthalamic stimulation.
290 ive effects as a function of localization of subthalamic stimulation.
291 son's disease (PD) and tend to improve after subthalamic (STN) stimulation after a marked reduction o
292 , whereas the Dbx1 microdomain gives rise to subthalamic (STN), premammillary (PM) and posterior hypo
293 luding excessive subthalamic bursts, cortico-subthalamic synchronization, and in situ beta synchroniz
294 ded to electrical stimulation of the cortico-subthalamic system in parkinsonian monkeys.
295      To find out whether the primate cortico-subthalamic system is also subject to functionally relev
296 veractivation and synchronization of cortico-subthalamic transmission alone sufficiently and instanta
297 e found that inhibition of NMDAergic cortico-subthalamic transmission ameliorates parkinsonian motor
298 tor cortex stimulation revealed that cortico-subthalamic transmission is deranged in PD and directly
299 ways, our data suggest that deranged cortico-subthalamic transmission via the NMDA receptor also play
300 r and lower extremity movement kinematics in subthalamic units and observed evidence for re-routing t

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