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1                                              GPi activity in higher frequency bands ( > 20 Hz) was mo
2                                              GPi DBS also resulted in a significant (P < 0.01) declin
3                                              GPi DBS improved UPDRS motor ratings (36%, P < 0.001) an
4                                              GPi DBS outcomes vary across monogenic dystonias.
5                                              GPi DBS substantially reduced the AER, restoring lost hi
6                                              GPi DBS was associated with lower mean performance on on
7                                              GPi increases and their suppressive effects, perhaps on
8                                              GPi neurons that project to the pre-SMA are located in a
9                                              GPi neurons were slower, bustier, and less regular in dy
10                                              GPi stimulation led to a significant improvement in tic
11                      Forty-five subjects (23 GPi, 22 STN) completed the protocol.
12  a total sample size of 502 PD patients (254 GPi DBS, 248 STN DBS), were included in this meta-analys
13 cts of posterior internal pallidal ablation (GPi pallidotomy) on parkinsonian signs and symptoms were
14 he Short Form Health Survey-36 (SF-36) after GPi DBS in patients with inherited or idiopathic isolate
15 or improvement, measured by UPDRS-III, after GPi DBS, compared to STN DBS (17.5 +/- 13.0 vs 14.6 +/-
16 im was to compare the effects of STN DBS and GPi DBS on the AER.
17 y activates GABA(B) receptors in the GPe and GPi and contributes significantly to the control of the
18  increased the spontaneous firing of GPe and GPi neurons, suggesting that GABA released from the axon
19 types are functionally homologous to GPe and GPi neurons, we recorded from neurons in area X of singi
20 , 4.5-5.5, and 7.0-9.0 msec for both GPe and GPi neurons.
21 emporal firing pattern of neurons in GPe and GPi underlie the beneficial effect of HFS in the STN in
22 d internal segments of the pallidum (GPe and GPi) receive heavy GABAergic innervations from the neost
23 oimmunoradiography) was increased in GPe and GPi, likely reflecting increased striatal input and incr
24 nal segments of the globus pallidus (GPe and GPi, respectively).
25 tagonist)-sensitive responses in the GPe and GPi.
26  GABAergic innervation to the GPe itself and GPi.
27 study revealed no difference between STN and GPi DBS in the change of co-primary mood and cognitive o
28  improvement were observed with both STN and GPi DBS.
29 underlying the therapeutic effect of STN and GPi DBS.
30        We compared beta power in the STN and GPi during rest and movement in 37 people with PD underg
31 ive was to compare beta power in the STN and GPi during rest and movement in people with PD undergoin
32           The findings indicate that STN and GPi evoke a similar motor network pattern, while NAc sho
33             Notably, the role of the STN and GPi extends beyond motor control to emotional regulation
34 ur aim was to assess the role of the STN and GPi in impulsivity using invasive local field potential
35 easures (mood and cognition) between STN and GPi in the optimal DBS state.
36                         In contrast, STN and GPi phase led cortex in the 70-85 Hz band.
37 correlates of impulsivity within the STN and GPi regions.
38 The difference between the effect of STN and GPi stimulation on movement-related activity was mainly
39 P reward processing responses in the STN and GPi uniquely depended on the severity of impulsivity.
40 *, phase, or SW images (P < .05) for STN and GPi visualization.
41 ntrast-to-noise ratios (CNRs) of the STN and GPi were also measured.
42 D diagnosed with ICD, neurons in the STN and GPi would be more responsive to reward-related stimuli a
43  low beta band (8-20 Hz) in both the STN and GPi, but not in M1.
44 s resulted in increased discharge in STN and GPi, comparable with the changes seen after MPTP but did
45 uch as altered discharge patterns in STN and GPi, may play an important role in the generation of par
46 te decreased in GPe but increased in STN and GPi.
47 planted with DBS leads targeting the STN and GPi.
48 er, across all recording sites (M1, STN, and GPi) in PD.
49 tionally defined regions of the striatum and GPi/SNr to determine the relationships between thalamost
50 mmunication can scale with GPi synchrony and GPi-to-VLa convergence, illuminating how synchrony of ba
51 nd significant positive correlations between GPi firing rates and thalamic glucose metabolism in both
52                                    Bilateral GPi Local Field Potentials (LFP) activity was recorded v
53                                         Both GPi and GPe firing frequencies differed significantly wi
54  results suggest that responsiveness to both GPi and STN DBS is similar among different PD motor subt
55 ration and frequency in the GPi and STN, but GPi bursts were stronger and correlated to bradykinesia-
56 njected into localized regions of the caudal GPi in squirrel monkeys.
57 hemes to target fibers ventral to the caudal GPi or at the rostral pole of GPi appear to be misguided
58       The fiber bundle ventral to the caudal GPi was mainly devoid of labeling.
59 en, and the ventrolateral part of the caudal GPi; 2) a "limbic" circuit involves the rostral one-thir
60                         We sought to compare GPi DBS outcomes among the most common monogenic dystoni
61                      In contrast, decreasing GPi volumes were associated with decreasing levels of ir
62  In this study, we investigate how different GPi-DBS frequencies modulate evoked potential (EP) chara
63 ge was observed in any of these areas during GPi stimulation.
64 th antidromic activation not observed during GPi DBS, raise questions about its role as the primary m
65                                     Finally, GPi theta effects were uniform across conditions, with i
66 owed a higher proportion of regularly firing GPi cells compared with the other groups (p<0.001).
67  these findings suggest a potential role for GPi's synchronized activity in shaping feedback processi
68       Enrolled patients received surgery for GPi DBS and then were randomly assigned in a 1:1 ratio (
69 ric synapses (type S2), which originate from GPi.
70 strate that, perhaps unexpectedly, GABAergic GPi and SNr inputs converge with those from the Cb.
71 t inhibition in the GPe, whereas the STN-GPe-GPi inhibitory response dominates over the STN-GPi excit
72 ysiological situations: simulations show how GPi-VLa communication can scale with GPi synchrony and G
73 rt of antiphase homotopic synchrony in human GPi, potentially related to incorporating and processing
74 iated claims of hyper- versus hypofunctional GPi output in PD versus dystonia, and provided cellular-
75 on and Wisconsin Card Sorting (STN improved, GPi worse with stimulation).
76             We found a significant change in GPi activity between daytime and nighttime in most subje
77                            The difference in GPi activity between "on" and "on with dyskinesias" sugg
78 xcitation followed by a strong inhibition in GPi neurons.
79 d frequency-dependent modulation observed in GPi suggests that optimal stimulation parameters should
80 cy-dependent effects were most pronounced in GPi recordings, followed by STN and VO, suggesting that
81 n most subjects (82.4%), with a reduction in GPi activity at nighttime in 56.2% of recordings and an
82 voked a predominantly inhibitory response in GPi neurons.
83 t to identify the optimal targeting sites in GPi and STN for reversal of parkinsonian signs through a
84 tion to motor and associative territories in GPi was confirmed by examining the corresponding regions
85 dial extent of the sensorimotor territory in GPi and the lateral portion of the sensorimotor territor
86 anges generally began earlier in VLa than in GPi.
87 profitable response is identified, increased GPi activity suppresses alternative responses, sharpenin
88 trode data from the globus pallidus interna (GPi) and globus pallidus externa (GPe) in children under
89 ease (PD), with the globus pallidus interna (GPi) commonly targeted.
90 ucleus (STN) versus globus pallidus interna (GPi) DBS surgery.
91 c nucleus (STN) vs. globus pallidus interna (GPi) deep brain stimulation (DBS) in Parkinson disease.
92 als from MEs in the globus pallidus interna (GPi) in two of the cases.
93 ted that DBS of the globus pallidus interna (GPi) might.
94  and/or ipsilateral globus pallidus interna (GPi) or scalp EEG during voluntary movements of a hand-h
95 c nucleus (STN) and globus pallidus interna (GPi), high beta MRD and gamma (40-80 Hz) movement-relate
96 leus (STN, n=84) or globus pallidus interna (GPi, n=80), using standardised neuropsychological tests.
97 ulation of the globus pallidus pars interna (GPi DBS).
98 or part of the globus pallidus pars interna (GPi) contralateral to the moving hand, which was paralle
99 review was the globus pallidus pars interna (GPi).
100  to the primate external (GPe) and internal (GPi) pallidal segments.
101 imulation (DBS) of globus pallidus internus (GPi DBS) and subthalamic nucleus (STN DBS) are effective
102 ) thalamus (n=51), globus pallidus internus (GPi) (n=47), nucleus accumbens/anterior limb of the inte
103 c nucleus (STN) or globus pallidus internus (GPi) affects levels of impulsivity.
104 icacy of bilateral globus pallidus internus (GPi) DBS in patient's with severe Tourette's syndrome.
105 leus (STN) DBS and globus pallidus internus (GPi) DBS.
106 c nucleus (STN) or globus pallidus internus (GPi) deep brain stimulation (DBS), found that stimulatio
107 osimulation of the globus pallidus internus (GPi) in individuals with Parkinson's disease induces lon
108  nucleus (STN) and globus pallidus internus (GPi) in reward and punishment processing, and deep brain
109  nucleus (STN) and globus pallidus internus (GPi) is an effective treatment for parkinsonian motor si
110 ation (DBS) of the globus pallidus internus (GPi) is an established treatment for dystonia, yet the n
111 ted differences in globus pallidus internus (GPi) neuronal activity, and short- and long-term plastic
112 ures targeting the globus pallidus internus (GPi) to treat medically intractable hypokinetic and hype
113  beta power in the globus pallidus internus (GPi), an equally effective DBS target.
114 mic nucleus (STN), globus pallidus internus (GPi), and globus pallidus externus (GPe) during their pe
115 ta activity in the globus pallidus internus (GPi), another effective target for deep brain stimulatio
116 gle neurons in the globus pallidus internus (GPi), the primary BG output nucleus, in nonhuman primate
117 ion of the BG, the globus pallidus internus (GPi).
118 ave focused on the globus pallidus internus (GPi).
119  explored in human Globus Pallidus internus (GPi).
120 d thalamic nuclei (globus pallidus-internus [GPi] and ventrolateral anterior nucleus [VLa]) in monkey
121        This retrospective study investigates GPi circadian rhythms in a large cohort of subjects with
122  best stimulation target for a PD patient is GPi or STN.
123 lated interaction between DA release in left GPi and pre-SMA, a mechanism that may also apply to othe
124              In contrast, HF-2 neurons, like GPi neurons, discharged continuously without bursts or l
125    Dyskinesias result from an imbalanced low GPi discharge, a circumstance that may be susceptible to
126                                   The median GPi firing frequency was higher in the primary group tha
127 three DBS targets (STN, subthalamic nucleus; GPi, globus pallidus internus; NAc, nucleus accumbens) e
128 30% of the volume of the dentate and <15% of GPi.
129                            A subset (29%) of GPi neurons showed learning-related effects, decreasing
130 thophysiology and the mechanism of action of GPi DBS.
131 led along the medial and inferior borders of GPi at centrorostral levels were traceable to the medial
132 ed to compare oscillatory characteristics of GPi between dystonia and Parkinson's Disease (PD).
133 es than on T2w images for differentiation of GPi from the internal capsule and external globus pallid
134                        The overall effect of GPi DBS on UPDRS III was not significantly different fro
135                                The effect of GPi DBS was similar to STN DBS except for depression, ho
136 opeduncular nucleus (EP), the rat homolog of GPi, in a unilateral 6-hydroxydopamine lesioned female S
137 ationship between the depth of modulation of GPi neurons and forearm rotation amplitude, direction, o
138 ted no differences in the firing patterns of GPi neurons from DYT1 and DYT6 patients.
139  to the caudal GPi or at the rostral pole of GPi appear to be misguided.
140 ntral striatum, and the rostromedial pole of GPi; and 3) an "associative"circuit exists between the c
141 terior ventrolateral sensorimotor portion of GPi and to less selectively target STN, centrally, the i
142 bers originating from the caudal portions of GPi, including the motor territory, do not course ventro
143 ating from motor and associative portions of GPi, small quantities of the anterograde/ retrograde tra
144 ignificant in comparison with stimulation of GPi.
145  involves the caudate-receiving territory of GPi (dorsal one-third), the dorsolateral Pf (Pfdl), and
146 discrete regions in the central territory of GPi and the lateral portion of STN are sufficient to ame
147 , in particular, from the motor territory of GPi has important clinical relevancy.
148 onal cerebral glucose utilization on and off GPi stimulation.
149 e effect of age, sex and disease duration on GPi DBS outcomes.
150 9 patients were randomised to STN (n=147) or GPi (n=152) DBS surgery.
151 stimulation of either the STN (18 nuclei) or GPi (28 nuclei).
152 ubjects were randomized to unilateral STN or GPi DBS.
153 facilitatory decreases in internal pallidal (GPi) activity are primarily greater under sensory-trigge
154  procedures targeting the internal pallidum (GPi) and the subthalamic nucleus (STN) have led to major
155 trical stimulation of the internal pallidum (GPi) or the subthalamic nucleus (STN) improves clinical
156 and external segment of the globus pallidus (GPi and GPe, respectively) in two rhesus monkeys rendere
157  nucleus (STN) and internal globus pallidus (GPi) (P < 0.001), as well as in the dorsal pons and prim
158 ojections from the internal globus pallidus (GPi) and glutamatergic inputs from motor cortices.
159 the internal segment of the globus pallidus (GPi) and in the substantia nigra (SN) of cynomolgus monk
160 the internal segment of the globus pallidus (GPi) and the cerebellar nuclei (Cb) to the thalamus in t
161 ic ablation of the internal globus pallidus (GPi) for Parkinson's disease causes resting metabolic ch
162 the internal segment of the globus pallidus (GPi) from an awake Parkinson's disease patient undergoin
163 the internal segment of the globus pallidus (GPi) improves Parkinson's disease and increases frontal
164 cal (PM) areas and internal globus pallidus (GPi) in 26 patients with Parkinson's disease undergoing
165 the internal segment of the globus pallidus (GPi) recorded during this procedure were significantly l
166 c nucleus (STN) or internal globus pallidus (GPi) reduces dyskinesias remain largely unknown.
167 the internal segment of the globus pallidus (GPi) was recorded intraoperatively in the same patients
168  scores of STN and internal globus pallidus (GPi) were recorded by two neuroradiologists on all image
169  nucleus (STN) and internal globus pallidus (GPi) with magnetoencephalography, tractography and compu
170 TN, internal segment of the globus pallidus (GPi), and primary motor cortex (M1) in three female rhes
171 the internal segment of the globus pallidus (GPi), and substantia nigra pars reticulata (SNr).
172 tivity through the internal globus pallidus (GPi), external globus pallidus, motor cortex, thalamus,
173 the internal segment of the globus pallidus (GPi).
174 the internal segment of the globus pallidus (GPi).
175 the internal segment of the globus pallidus (GPi).
176 nervation from the internal globus pallidus (GPi).
177 the internal segment of the globus pallidus (GPi).
178  nucleus (STN) and internal globus pallidus (GPi).
179 ation (DBS) at the internal globus pallidus (GPi).
180 5 participants) STN and 26 (22 participants) GPi nuclei.
181 that exhibit activity similar to the primate GPi, and non-thalamus-projecting neurons that exhibit ac
182                      Simultaneously recorded GPi-VLa pairs rarely showed short-time-scale spike-to-sp
183               A higher proportion of regular GPi cells was also seen in patients with fixed/tonic dys
184 not the proposed GABA/glutamate co-releasing GPi neurons, are responsible for encoding negative value
185 e prominent onto GABA/glutamate co-releasing GPi neurons.
186 ere phase synchronous between left and right GPi with an antiphase clustering of phase differences.
187 charges of globus pallidus internal segment (GPi) neurons in monkeys performing a visually driven for
188 tus of the globus pallidus internal segment (GPi) plays a key role in mediating the effects of antipa
189 nglia, the globus pallidus internal segment (GPi) projects to the thalamus and brainstem nuclei there
190 ing in the globus pallidus internal segment (GPi), and lateral hypothalamic area (LHA), respectively.
191 he external segment (GPe), internal segment (GPi), and ventral pallidum (VP)-in 8 HD cases compared w
192 eus (STN) and the internal pallidal segment (GPi) and in the development of parkinsonian motor signs.
193 culata (SNpr) and internal pallidal segment (GPi).
194                   The inhibition of the SNpr/GPi should, in turn, disinhibit the thalamus to facilita
195                        We observed that some GPi neural pairs oscillated synchronously at the tremor
196                         Finally, spontaneous GPi bursts and pauses were both followed by small, slow
197 us pallidus internus deep brain stimulation (GPi DBS) on health-related quality of life (HRQoL) in pa
198 i inhibitory response dominates over the STN-GPi excitatory response in the GPi.
199 al activity led or lagged behind that in STN/GPi were similar, around 20 ms, regardless of the overal
200  MRD and low gamma (40-60 Hz) MRS in the STN/GPi.
201    There were regions within and surrounding GPi and CM thalamus that improved tics for some patients
202 ative signals within the striatum, thalamus, GPi, and STN were all associated with increases and decr
203                  Additionally, we found that GPi tremor-related activity at a given site could fluctu
204                   These results suggest that GPi may initiate reward-related signals through its effe
205                        Our data suggest that GPi/ACC ULF-STDP selectively decreases DMS D1-MSN hypera
206                                          The GPi firing frequency showed a positive correlation with
207 ation involving the ventral thalamus and the GPi (statistical parametric map: P < 0.05, corrected).
208 he STN and coherence between the STN and the GPi was dominated by activity at 70-85 Hz, which increas
209 TN and the coherence between the STN and the GPi were dominated by activity with a frequency of <30 H
210 allidal relay nucleus of the thalamus by the GPi.
211                             In contrast, the GPi was less affected, with a 38% reduction in overall v
212 eral nucleus pars oralis (VLo) following the GPi injections or in the central portion of the ventral
213 reotactic MRI determined coordinates for the GPi target.
214 we discovered that GABAergic inputs from the GPi and SNr converge onto single motor thalamic cells wi
215                   EPs were recorded from the GPi and subthalamic nucleus (STN) of basal ganglia, and
216 oelectrode recording data collected from the GPi during deep brain stimulation surgery, we compared n
217  GPe ( approximately 400 ms long) and in the GPi (60 ms long).
218 ed to Parkinson's tremor first arises in the GPi and is then propagated to the cerebello-thalamo-cort
219 ere similar in duration and frequency in the GPi and STN, but GPi bursts were stronger and correlated
220 functions were anatomically separable in the GPi but not in the STN.
221 inical associations were present only in the GPi cohort.
222 ests that patterned neuronal activity in the GPi is important in the mechanism of hyperkinetic disord
223           Increased (18)F-dopa uptake in the GPi is seen in early PD which then is lost in advanced P
224 that, relative to the STN, beta power in the GPi may be readily detected, modulates more with movemen
225       Relative to the STN, beta power in the GPi may be readily detected, modulates more with movemen
226              We recorded single cells in the GPi of parkinsonian monkeys continuously through the "of
227 s suggest that circadian fluctuations in the GPi vary across individuals and that increased power at
228                                       In the GPi, labeling was most pronounced along the ventral, lat
229 r beta power during rest and movement in the GPi, which also had more beta desynchronization during m
230  over the STN-GPi excitatory response in the GPi.
231 ectrodes implanted in the STN and six in the GPi.
232  neurons (p<0.05) in the STN, but not in the GPi.
233 ces by stimulating D1-MSN afferents into the GPi and ACC glutamatergic projections to the DMS in a ti
234 tion was significant for the STN but not the GPi group.
235 nly in the dorsal and ventral borders of the GPi and that their activity was strongly modulated by ex
236 sing that includes the bottom-up role of the GPi in reward salience and the top-down role of the STN
237 ular nucleus (EPN, the rodent homolog of the GPi).
238 ted with deep brain stimulation (DBS) of the GPi.
239 as recorded in either the STN (n=100) or the GPi (n=100).
240           A less well known fact is that the GPi also projects to the lateral habenula (LHb) which is
241 ollectively, these findings suggest that the GPi neurons that we studied were not significantly invol
242 activity) drove network activity through the GPi, which effectively influenced the cerebello-thalamo-
243            Together, this could point to the GPi as a potentially effective target for beta-based ada
244            Together, this could point to the GPi as a potentially effective target for beta-based ada
245 ve the nigropallidal dopamine pathway to the GPi but not to the external segment of the globus pallid
246 d function of the dopamine projection to the GPi serves, we propose, to maintain a more normal patter
247  improvement in OCB than regions inferior to GPi.
248        Regions within, superior or medial to GPi were associated with a greater improvement in OCB th
249 motor subtype may have a greater response to GPi DBS with respect to gait.
250  patients appear to respond less robustly to GPi-DBS than their DYT1 counterparts, most likely reflec
251 O) nucleus of the thalamus during unilateral GPi stimulation at 55, 85, 185, and 250 Hz.
252 ither medical therapy (N = 18) or unilateral GPi pallidotomy (N = 18).
253 , stimulation of the posterior-ventrolateral GPi was associated with improved dystonia.
254 imilar for patients randomised to STN versus GPi DBS (1.5% vs 0.7%; Fisher's exact p=0.61), but sever
255  PD motor subtypes and by DBS target (STN vs GPi).
256 sociative" territory of the nucleus, whereas GPi neurons that project to the SMA are located in a mor
257 n (DBS) for dystonia and investigate whether GPi and GPe firing rates differ between dystonia types.
258 parkinsonian patients, 6 with STN and 6 with GPi stimulators, we used H2(15)O positron emission tomog
259                         The reduced AER with GPi DBS could be explained by retrograde stimulation of
260                    Clinical improvement with GPi DBS is associated with reduced expression of an abno
261 significantly less frequent in patients with GPi DBS than STN DBS with homogeneous studies (pooled RR
262 how how GPi-VLa communication can scale with GPi synchrony and GPi-to-VLa convergence, illuminating h
263 th PD (130 recordings from 93 subjects) with GPi activity chronically recorded in their home environm
264 ly confirmed monogenic dystonia treated with GPi DBS documenting pre-surgical and post-surgical asses
265 atients with DYT1 dystonia also treated with GPi-DBS by the same team.
266                                       Within GPi, neurons labeled from leg M1 were located in dorsal
267  finding, some paired recording sites within GPi showed periods of transient synchronization.

 
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