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1 ever, a lack of in vivo evidence of GABA/Glu thalamic abnormalities in the CHR state.
2   Simultaneous recordings revealed that both thalamic activity and the current state of cortex predic
3 nous ictal firing characterizes cortical and thalamic activity at the population level, individual co
4 r demonstrate that individual differences in thalamic activity relate to reconfigurations of the low-
5 partly implements this process by regulating thalamic activity through modality-specific thalamic ret
6  are preferred combinations of the number of thalamic afferents and the number of synapses per affere
7 del of visual cortical topography that sorts thalamic afferents by eye input and stimulus polarity al
8 that results from the precise arrangement of thalamic afferents during cortical development.
9 f core (lemniscal) and matrix (nonlemniscal) thalamic afferents to MMN generation.
10 ousal, anxiety, and freezing behavior, while thalamic and basal forebrain projections generate freezi
11 projected to overlapping as well as distinct thalamic and brainstem structures.
12  4 involved the occipital cortex, as well as thalamic and brainstem structures.
13 s at alpha frequencies (8-12 Hz) across both thalamic and cortical areas.
14  investigated propofol-associated changes in thalamic and cortical local power as well as thalamocort
15 al regions, L5 commonly projects to multiple thalamic and extrathalamic sites.
16 wed considerable 5-HT-ir innervation, as did thalamic and hindbrain auditory and lateral line areas a
17 een individual-specific anatomically defined thalamic and hippocampal seeds and all gray matter voxel
18  regarded as cholinergic, including specific thalamic and hypothalamic neurons, the subiculum, the la
19  48 h of SAT to drive synaptic plasticity at thalamic and intracortical inputs onto L2 Pyr neurons.
20 pal atrophy with further reduced mediodorsal thalamic and posteromedial cortical volumes.
21                           We used concurrent thalamic and primary auditory cortical (A1) laminar reco
22                                        While thalamic and subthalamic brain regions play important ro
23  at the population level, individual cortico-thalamic and thalamocortical neurons are sparsely recrui
24                                         This thalamic area directly received anatomical input from th
25                                       In the thalamic area, they ran laterally to the thalamus and po
26  the LH [11, 12], and nearby subthalamic and thalamic areas lack local synaptic connectivity [13, 14]
27 nsory, and motor cortices and interconnected thalamic areas that provide information about potential
28 um, suprachiasmatic nucleus, prethalamic and thalamic areas, posterior tubercle, pretectum, torus sem
29                                              Thalamic arousal network dysfunction may contribute to m
30                            Here, we evaluate thalamic arousal network functional connectivity in TLE
31  The study findings demonstrate that smaller thalamic association nuclei represent a neurodevelopment
32 analysis revealed that FGF15 is generated by thalamic astrocytes and not retino-recipient neurons.
33                                The causes of thalamic atrophy are not fully understood.
34 th multiple sclerosis (MS) and the degree of thalamic atrophy is a strong predictor of disability pro
35                                              Thalamic atrophy is among the earliest brain changes det
36 enerative process as greater contributors to thalamic atrophy than thalamic demyelinating lesions.
37 duced white matter connectivity in a cortico-thalamic auditory pathway between the left auditory moti
38 lamocortical axons and impaired outgrowth of thalamic axons in response to cell-extrinsic factors.
39 ptor-mediated IPSPs in auditory cortical and thalamic brain slices.
40 ontrols, but their pattern of innervation of thalamic cells was not altered.
41 nfirm and extend on previous PET findings of thalamic cholinergic deficits associated with falling hi
42  iron concentration within the basal ganglia-thalamic circuit over 2 years post-SCI.
43  subregions belonging to the cortico-striato-thalamic circuitry (CSTC) play an important role in the
44 anizational changes across the basal ganglia-thalamic circuitry occur early after SCI and progress ov
45 s a model system to study the development of thalamic circuitry.
46                                      The two thalamic circuits also had distinct input patterns, with
47 reased beta bursts in cortical-basal ganglia-thalamic circuits are associated with rigidity and brady
48           Together, our results suggest that thalamic circuits can generate slow oscillatory activity
49 hin dopamine-modulated cortico-basal ganglia-thalamic circuits in schizophrenia.
50 y of I(CAN) and the possible contribution of thalamic circuits to slow rhythmic activity remain uncle
51 t mediate slow forms of rhythmic activity in thalamic circuits.
52 ic connectivity within cortico-basal-ganglia-thalamic circuits.
53  escape or freeze, that involve cortical and thalamic circuits.
54 ves a dynamic interplay between cortical and thalamic circuits.
55    Thus, in the healthy state, basal ganglia-thalamic communication during learned movement is more s
56 elopmental mechanisms that lead to the adult thalamic configuration have only been investigated for m
57 tion of ascending brainstem and intralaminar thalamic connections.
58 vide the first evidence that reduced cortico-thalamic connectivity in the auditory modality is a feat
59 dopamine's topographic modulation of cortico-thalamic connectivity within cortico-basal-ganglia-thala
60  recovery of thalamo-occipital and brainstem-thalamic connectivity, with values more closely resembli
61                             To determine the thalamic contribution to non-REM oscillations (sharp-wav
62 lowing: dysfunction within cortical-striatal-thalamic-cortical (CSTC) brain circuits implicated in th
63 gests a dysfunction of the cortical-striatal-thalamic-cortical circuit in OCD, and a previous feasibi
64 anterograde degeneration rather than diffuse thalamic damage in NMOSD.
65 romyelitis optica spectrum disorders (NMOSD) thalamic damage is controversial, but thalamic nuclei we
66 on-refractory ET before and after unilateral thalamic DBS implantation.
67 impairment in essential tremor patients with thalamic DBS.
68  in essential tremor patients with bilateral thalamic deep brain stimulation (DBS).
69 19 participants diagnosed with ET undergoing thalamic deep brain stimulation (DBS; ET(DBS) ) to 19 he
70 ergic balance (i.e., GABA/Glu), may underlie thalamic deficits linked to the risk and development of
71    Here, we investigate the contributions of thalamic demyelinated lesions, thalamic neuronal loss, a
72 reater contributors to thalamic atrophy than thalamic demyelinating lesions.
73              We histologically characterized thalamic demyelination patterns and compared neuronal lo
74  provides a platform for understanding human thalamic development and modeling circuit organizations
75 ng, and lesion volume to better characterize thalamic differences after cortical infarct.
76                             Grossly apparent thalamic discolorations in cm-thick brain slices were T2
77       These results imply that modulation of thalamic driving input to the auditory cortex facilitate
78  that aberrant striatal dopamine and cortico-thalamic dysconnectivity are pathophysiologically relate
79 lthy comparison groups, thus suggesting that thalamic dysfunctions are present even before illness on
80                    Recent studies have shown thalamic engagement in dynamic regulation of cortical ac
81                                 We found the thalamic environment is instructive for TCA navigation a
82 tabolites promoted axon outgrowth from fetal thalamic explants.
83 ions with major cortico-cortical and cortico-thalamic fibers: the corona radiata, corpus callosum, su
84                                          The thalamic filter model suggests that core effects of psyc
85                                   The sparse thalamic firing could promote an incremental integration
86 sequences of transiently disrupting anterior thalamic function were examined, followed by inactivatio
87 riatal gray matter, greater cortico-striatal-thalamic functional connectivity, and lower spontaneous
88                           Hypothesizing that thalamic GABA correlates with ASD symptom severity in ge
89 participants, a positive correlation between thalamic GABA/Water and AQ was found.
90 ts by gender, a negative correlation between thalamic GABA/Water and AQ was observed in male ASD part
91 estigated the interaction between gender and thalamic GABA/Water in predicting Autism-Spectrum Quotie
92 t gender is a significant effect modifier of thalamic GABA/Water's relationship with AQ and RAADS-R s
93 nctional FGF15 in mice led to a reduction in thalamic GABAergic interneurons similar to that observed
94 sy patients to measure the intracortical and thalamic generators of the alpha rhythm during quiet wak
95 hat Pul-T neurons exhibit pretectal, but not thalamic, genoarchitectonical markers, as well as hodolo
96 dy also found promising associations between thalamic glial histological signatures and ensuing relea
97 ons between circulating biomarkers and acute thalamic histopathology in a translational micro pig mod
98                       Thus, a key feature of thalamic ictogenesis is the powerful increase in the inh
99  links topographically with aberrant cortico-thalamic iFC, i.e. aberrant associative striatum dopamin
100 ork for studying convergence of cortical and thalamic information onto the striatum in other sensory
101 d feature selectivity, drastically improving thalamic information transmission.
102 y differentially process distinct classes of thalamic information.
103 with absence seizures, the ictal increase in thalamic inhibition is enhanced by the loss-of-function
104 reticular nucleus (TRN), the major source of thalamic inhibition, regulates thalamocortical interacti
105 an AUC of 0.67 (0.60-0.73), basal ganglia or thalamic injury had an AUC of 0.81 (0.75-0.87), and abno
106 hibited an additional surface-in gradient of thalamic injury on the ventricular side, which was alrea
107                                              Thalamic innervation of associative cortex targets sever
108 e exceptions, including a transient stronger thalamic innervation of D2 SPNs and stronger cortical NM
109 nally, a differential effect of cortical and thalamic innervation onto striatal GABAergic neurons out
110  pig's cortical rostrum gyrus receives dense thalamic innervation, has a thin Layer 1 and contains ro
111 as a key developmental mediator of colliculo-thalamic innervation.
112                                 In turn, the thalamic input during hippocampal-cortical communication
113      Chronic monocular deprivation decreased thalamic input from the deprived eye to the binocular vi
114             A recent study demonstrates that thalamic input from the posterior medial (POm) nucleus t
115 hibited by reduced PV activity regardless of thalamic input strength.
116 e inferior pulvinar (PIm), which is the main thalamic input to area MT, shows a retinotopic organizat
117           We observed that cortical, but not thalamic input, enhanced the number of releasable GABAer
118                   Together, FS neurons track thalamic input, mediating feedforward inhibition.
119 on across cortical lamina and receive direct thalamic input.
120 ons are transient preferential recipients of thalamic inputs and undergo activity-dependent migration
121 PVs compensate for reduced SST activity when thalamic inputs are strong with less compensation when t
122 nputs are strong with less compensation when thalamic inputs are weak.
123 tionally arousing stimuli suggest that these thalamic inputs exert a significant influence over BL ac
124                                      We find thalamic inputs make distinct connections in L1, where V
125 chronically impairs binocular integration in thalamic inputs to primary visual cortex.
126 ine thalamus and one of the major sources of thalamic inputs to the hippocampal formation and the med
127 in DA neurons (DANs) as well as cortical and thalamic inputs to the striatum.
128              As predicted by our findings in thalamic inputs, Ca(2+) imaging from V1 neurons revealed
129      In contrast, visual acuity is spared in thalamic inputs.
130 ty in a functional network encompassing left thalamic, insular, and temporal nodes (p < 0.05).
131  significance of direct hippocampal-anterior thalamic interactions for spatial processing.
132 spects of large-scale cortical-basal ganglia-thalamic interactions using dynamic functional MRI measu
133  capacity links topographically with cortico-thalamic intrinsic dysconnectivity in schizophrenia.
134                                              Thalamic involvement did not affect electrographic seizu
135 n each group and determine seizure risk with thalamic involvement.
136 d (p = 0.31), or subependymal (p = 0.44) MRI thalamic lesion volumes correlated with thalamic volume.
137 I) scans of 95 subjects with MS to correlate thalamic lesion volumes with global MRI metrics.
138 teractions within the cortical-basal ganglia-thalamic loop might play a role in the modulation of EEG
139 articipants were implanted with bilateral CM thalamic macroelectrodes and M1 subdural electrodes that
140 emerging view of functional diversity across thalamic microcircuits and its structural basis.
141 to existing knowledge to continue developing thalamic models.
142 n striatal module, and 3) cortico-hippocampo-thalamic module, reminiscent of the three-stage theory.
143                                      Reduced thalamic MPF may reflect inflammation-related tissue swe
144 changes believed to be pathogenic within the thalamic network is non-canonical.
145 nnel function during the critical period for thalamic network stabilization in immature brain remains
146 ets of plasticity (the cortico-basal ganglia-thalamic network), suggesting that feedback signals have
147 ever, little is known about the cortical and thalamic networks within which corticocollicular neurons
148    Transcriptional differences between these thalamic neuronal identities are tied to cellular featur
149 tributions of thalamic demyelinated lesions, thalamic neuronal loss, and cerebral white matter (WM) l
150      Here, we examine connectivity of single thalamic neurons (lateral geniculate nucleus, LGN) onto
151 to be played by a population of lumbar spino-thalamic neurons (LSt), which express galanin and other
152 , the value discrimination activity of these thalamic neurons increased during learning, with the lea
153 input-output connectivity patterns of single thalamic neurons is critical for building functional mod
154 native T-type Ca(2+) current recorded in rat thalamic neurons of the central medial nucleus.
155 ignificantly lower in Foxp2(+/R552H) cortico-thalamic neurons than in control Foxp2(+/+) neurons.
156 halic excitatory projection neurons, but not thalamic neurons, recapitulated choice abnormalities of
157 d tactile acuity through tonic inhibition of thalamic neurons.
158 ar retrosplenial cortex (RSCg), and anterior thalamic nuclei (ATN) interact to mediate diverse cognit
159 vity from connected basal ganglia output and thalamic nuclei (globus pallidus-internus [GPi] and vent
160                         Identifying specific thalamic nuclei abnormalities in psychosis has implicati
161 y developed, validated method for segmenting thalamic nuclei and complementary voxel-based morphometr
162 e show the step-wise optical fiber targeting thalamic nuclei and map the region-specific functional c
163 om the hippocampal formation to the anterior thalamic nuclei and vice versa impaired performance on t
164 (iFC) between distinct cortical networks and thalamic nuclei are among the most consistent large-scal
165                                  Most dorsal thalamic nuclei contained subunits alpha1, alpha2, alpha
166        Together, our findings reveal how two thalamic nuclei differentially communicate with the PFC
167 ctions to the anteromedial and anteroventral thalamic nuclei for the processing of allocentric inform
168  multiple laboratories researching different thalamic nuclei has contradicted this idea of the thalam
169         We aimed at assessing volume loss of thalamic nuclei in NMOSD.
170 imulation suppresses activity in both visual thalamic nuclei in vivo, moderate-frequency (10 Hz) stim
171                                Thus, rostral thalamic nuclei may participate in spatial representatio
172                                 The anterior thalamic nuclei may represent one vital partner.
173  has long been conjectured that the anterior thalamic nuclei might be key partners with the hippocamp
174 dorsal subiculum projections to the anterior thalamic nuclei produced the severest spatial working me
175                           In addition, motor thalamic nuclei such as anterior and ventromedial, midli
176 onally distinct first-order and higher-order thalamic nuclei to form molecularly defined TRN-thalamus
177 ay, the direct projections from the anterior thalamic nuclei to the dorsal hippocampal formation were
178   For this purpose, we measured RFC in seven thalamic nuclei using fMRI and brain glucose metabolism
179                                              Thalamic nuclei volumes were tested in a cross-sectional
180 n V4 upon stimulus onset, variability in the thalamic nuclei was largely unaffected by visual stimula
181 tromedial, midline, reticular, and posterior thalamic nuclei were also activated.
182 NMOSD) thalamic damage is controversial, but thalamic nuclei were never studied separately.
183 notype seen in humans with lesions of medial thalamic nuclei(1-3).
184 t also a route through specific higher-order thalamic nuclei, creating a parallel feedforward trans-t
185     The lateral geniculate nucleus, like all thalamic nuclei, has two classically defined categories
186 to misrouting of interneurons into nonvisual thalamic nuclei.
187 nverse correlation with frontally projecting thalamic nuclei.
188 minative pain, such as ventral posteromedial thalamic nuclei.
189 formation, receiving input from two distinct thalamic nuclei.
190 nvolvement of visual cortex and higher order thalamic nuclei.
191 end on distinct inputs from sensory-specific thalamic nuclei.
192  neuropeptides, helped the identification of thalamic nuclei.
193 dorsal subiculum projections to the anterior thalamic nuclei.
194 connections in the ipsilateral medial-dorsal thalamic nuclei.
195 lium, and medial portion of the dorsolateral thalamic nucleus (DLM).
196  the pulvinar in mice, the lateral posterior thalamic nucleus (LP).
197          The connectivity of the mediodorsal thalamic nucleus (MD) with extrahippocampal regions and
198  barrels, whereas the higher-order posterior thalamic nucleus (medial part, POm) most densely innerva
199                       One hub, the reticular thalamic nucleus (of the ventral thalamus), was found in
200 fection, we investigated the mouse Posterior thalamic nucleus (Po) cell axons that simultaneously inn
201 ith ascending projections into the submedius thalamic nucleus (SubM) and ventrolateral orbital cortex
202 osensory cortex, and secondary somatosensory thalamic nucleus (the posterior medial nucleus, POm).
203 ysiological signals in the centromedian (CM) thalamic nucleus and primary motor (M1) cortex that diff
204  synapses of Po versus ventral posteromedial thalamic nucleus axons in the whisker sensory cortex.
205    (2020) find evidence that central lateral thalamic nucleus electrical stimulation reactivates the
206              Similarly, the secondary visual thalamic nucleus in mice (the lateral posterior nucleus,
207 ventral posterior medial (VPM) somatosensory thalamic nucleus most densely innervates layer 4 (L4) ba
208  prefrontal cortex, the hippocampus, and the thalamic nucleus reuniens constitute a typical example o
209             Recordings collected from the CM thalamic nucleus revealed a low-frequency power (3-10 Hz
210 , than those between Po and ventro-posterior thalamic nucleus synapses in S1.
211 a topographically and functionally organized thalamic nucleus that is largely dedicated to visual pro
212           Synapses from the posterior medial thalamic nucleus to edge TRN cells evoke slower, less de
213 of the TRN-synapse with the posterior medial thalamic nucleus, a higher-order structure that carries
214 rom PV-positive neurons in the medial dorsal thalamic nucleus, and from SOM-positive neurons in the v
215 ain, such as parabrachial nucleus and medial thalamic nucleus, as well as sensory-discriminative pain
216  conveys this information to the mediodorsal thalamic nucleus, magnocellular part (MDmc).
217 d nucleus, ventral posterior division of the thalamic nucleus, paraventricular hypothalamic nucleus,
218 ional subnetworks in a primary somatosensory thalamic nucleus.
219 ntiate human embryonic stem cells (hESCs) to thalamic organoids (hThOs) that specifically recapitulat
220  mechanisms regulating slow (<1 Hz) forms of thalamic oscillations are not well understood.
221 hat GluD1 is preferentially colocalized with thalamic over cortical terminals in both the striosome a
222  analyses demonstrated significantly reduced thalamic (p = 0.0016) VAChT expression in fallers compar
223 alpha, complicating prevailing theories of a thalamic pacemaker.
224                              The presence of thalamic pathology in a number of neurological condition
225 rtices to determine whether there is a trans-thalamic pathway parallel to the established primary som
226 uclei, creating a parallel feedforward trans-thalamic pathway.
227 ore reveals covariation in the properties of thalamic pathways serving all major input modalities and
228  conjoint importance of hippocampal-anterior thalamic pathways, these findings help explain why patho
229              To test the generality of trans-thalamic pathways, we sought to establish its presence b
230 rallel cortico-thalamo-cortical (i.e., trans-thalamic) pathways.
231  each auditory structure, but collicular and thalamic populations showed better performance than cort
232        As well as being of shorter duration, thalamic post-stimulatory activity emerged following a l
233 uggest the degeneration of efferent/afferent thalamic projections and/or a neurodegenerative process
234 (2)-weighted, and diffusion-weighted MRI and thalamic proton MRS 4-14 days after birth.
235 e matter tracts including the left and right thalamic radiation (TR), superior longitudinal fasciculu
236                Corticospinal tracts, and the thalamic radiation and callosal fibers involving motor f
237 , but negatively with FA values in posterior thalamic radiation and left corpus callosum in patients
238  white matter microstructure in the anterior thalamic radiation demonstrated significant associations
239 tructure of the cingulum bundle and anterior thalamic radiation was associated with improving symptom
240 e gyrus part of the cingulum, left posterior thalamic radiation, and bilateral superior thalamic radi
241  right medial lemniscus, bilateral posterior thalamic radiation, and bilateral superior thalamic radi
242  superior longitudinal fasciculus, posterior thalamic radiation, and corona radiata (all p < 0.05).
243 r thalamic radiation, and bilateral superior thalamic radiation, and increased mean diffusivity in th
244 r thalamic radiation, and bilateral superior thalamic radiation.
245  superior longitudinal fasciculus, posterior thalamic radiations, and sagittal stratum (Cohen's d's r
246 s in corpus callosum, anterior and posterior thalamic radiations, inferior fronto-occipital fasciculu
247 rs-fMRI time series of cortical networks and thalamic regions of interest were used to measure iFC.
248 n frontal, parietal, occipital, accumbal and thalamic regions.
249 within the thalamus, and the location of the thalamic relay for those signals.SIGNIFICANCE STATEMENT
250 ularly for comparison of the location of the thalamic relay in monkeys and in humans.
251       These characteristics show that the MD thalamic relay is not passive but instead assembles inpu
252 endent transcription of the receptor Fn14 in thalamic relay neurons and the induction of its ligand T
253 ich networks are engaged through specialized thalamic reticular neurons, including antagonistic subpo
254                                          The thalamic reticular nucleus (TRN) is implicated in schizo
255                 During sleep, neurons in the thalamic reticular nucleus (TRN) participate in distinct
256  thalamic activity through modality-specific thalamic reticular nucleus (TRN) subnetworks.
257  to the cortex and inhibitory neurons of the thalamic reticular nucleus (TRN) that regulate the flow
258                                          The thalamic reticular nucleus (TRN), the major source of th
259  circuits formed by GABAergic neurons in the thalamic reticular nucleus and glutamatergic relay neuro
260 y-linked gene Cacna1h in iKOp/q mice reduces thalamic reticular nucleus burst firing and promotes rat
261 cortico-pulvinar projections that engage the thalamic reticular nucleus enable the pulvinar to estima
262                                 Moreover, in thalamic reticular nucleus neurons, burst firing is impa
263 hich was accompanied by persistent firing in thalamic reticular nucleus neurons.
264 , we report a Brn3c(+) RGC projection to the thalamic reticular nucleus, a visual nucleus that was no
265 ain, especially in the hypothalamus, septum, thalamic reticular nucleus, certain cortices and other l
266            Interestingly, inborn deletion of thalamic reticular nucleus-enriched, human childhood abs
267 least from two sources, substantia nigra and thalamic reticular nucleus.
268 ts from the retina, visual cortices, and the thalamic reticular nucleus.
269 tical mechanisms, rather than an exclusively thalamic rhythmogenesis, are key in driving seizure icto
270                                        Using thalamic slices derived from adult mice of either sex, w
271                                     In vivo, thalamic slow oscillations are regulated by strong bidir
272 y (10 Hz) stimulation powerfully facilitates thalamic spiking.
273 low oscillations and their coordination with thalamic spindles, an interregional dialog that is neces
274                   However, during repetitive thalamic stimulation, the typical shift of the excitator
275           The authors sought to characterize thalamic structural abnormalities in psychosis and a neu
276 lar nucleus of the thalamus (PVT), a midline thalamic structure that is increasingly being recognized
277 SS females had lower volumes in striatal and thalamic subdivisions.
278  as multiple cortical cell-type-specific and thalamic subnucleus-specific recurrent loops, with both
279                                As in sensory thalamic systems, large amygdalar terminals innervated e
280                           In sauropsids, the thalamic target of the tecto-fugal pathway is the nucleu
281                              In rodents, the thalamic target of these TGCs afferents is the caudal di
282  midbrain, and all areas innervated multiple thalamic targets, including those with core and matrix c
283 ese findings demonstrate that stimulation of thalamic terminals in the DMS is sufficient to reinforce
284 us, which is consistent with observations of thalamic tremor cells in ET patients.
285                                              Thalamic units were phase-locked to delta and spindles i
286 PFC, and fired at consistent lags with other thalamic units within spindles, while CA1 units that wer
287 WRs with sparse but consistent activation of thalamic units.
288 xisting ataxia and diminishes cerebellar and thalamic vacuolation and Purkinje cell dendritic atrophy
289 pared with the 14 subjects with the greatest thalamic volume (p = 0.03).
290 ations were reflected in lower putaminal and thalamic volume bilaterally.
291 alamic connectivity, and smaller ipsilateral thalamic volume compared with controls (p < 0.05 for eac
292                                              Thalamic volume correlated with cerebral T2 lesion volum
293               The 12 subjects with the least thalamic volume had a 17.6% reduction of median neuronal
294                                      Reduced thalamic volume over time was associated with increased
295                                              Thalamic volume trajectories were assessed in a prospect
296 d with improving symptoms while reduction of thalamic volume was found in those with stable symptoms.
297 s, and cerebral white matter (WM) lesions to thalamic volume.
298  MRI thalamic lesion volumes correlated with thalamic volume.
299 ness (p = 0.02), whole brain (p = 0.002) and thalamic volumes (p < 0.001).
300  layer (GCIPL), whole-brain, gray matter and thalamic volumes in patients with and without focal infl

 
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