戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 Of 109 cranial schwannomas, 106 (97.2%) were vestibular.
2        The feedback model of podokinetic and vestibular adaptive processes had a good fit with the da
3      Contention surrounds whether the evoked vestibular afferent activity encodes a signal of net rot
4 gely explain the main features of GVS-evoked vestibular afferent dynamics.
5 etylcholine receptors (nAChRs) in regulating vestibular afferent gain and activation timing.
6 gical recordings reveal tuning of individual vestibular afferent inputs and their postsynaptic target
7                                   A group of vestibular afferent nerve fibers with irregular-firing r
8          Here we directly investigate single vestibular afferent responses to GVS applied to the mast
9 f vestibulocollic reflexes, we then recorded vestibular afferent responses to the same electrical sti
10 r previous hypotheses about how I (H) shapes vestibular afferent responses.SIGNIFICANCE STATEMENT Ves
11                                              Vestibular afferents also responded to electrical stimul
12 e effect of electrical vestibular stimuli on vestibular afferents and a current model of central vest
13 lated signal of head rotation encoded by the vestibular afferents can cause perceptions of both linea
14 gs and found aberrant central projections of vestibular afferents in both cases.
15 her electrical vestibular stimuli encoded by vestibular afferents induce a net signal of linear accel
16 me that efferent-mediated slow excitation of vestibular afferents is mediated by muscarinic acetylcho
17         Efferent-mediated slow excitation of vestibular afferents is of considerable interest given i
18 by a model combining the influence of EVS on vestibular afferents with known mechanisms of vestibular
19 ing from neurons receiving direct input from vestibular afferents within minutes, as well as a decrea
20 by high-frequency signals encoded by primary vestibular afferents, but undergo low-pass filtering at
21 keys during temporally precise activation of vestibular afferents.
22 aps between the inner ear hair cells and the vestibular and auditory nuclei to allow vestibular and s
23  sensory neurons, to the later appearance of vestibular and cerebellar dysfunction.
24 rizing the vestibulo-ocular reflex (VOR) and vestibular and headache symptom severity.
25 it in which SOM cells are key integrators of vestibular and luminance signals.
26       We propose a dynamic feedback model of vestibular and podokinetic adaptation that can fit rotat
27 t role in determining a cell's PFD, and that vestibular and proprioceptive cues drive these computati
28       Path integration is thought to rely on vestibular and proprioceptive cues yet most studies in h
29 n of multiple sensory inputs such as vision, vestibular and somatosensory systems.
30  the vestibular and auditory nuclei to allow vestibular and sound information processing.
31 aine develop abnormal responsiveness to both vestibular and visual stimuli characterized by heightene
32                However, the potential of the vestibular apparatus for phylogenetic reconstruction amo
33 odel for nonsyndromic deafness with enlarged vestibular aqueduct (EVA; OMIM #600791).
34 ularly if sensory neuronopathy and bilateral vestibular areflexia coexist.
35  the cause of cerebellar ataxia, neuropathy, vestibular areflexia syndrome (CANVAS) and a major cause
36            Cerebellar ataxia, neuropathy and vestibular areflexia syndrome (CANVAS) is a progressive
37 ebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (CANVAS) is a recently rec
38 ebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (CANVAS).
39 s also termed cerebellar ataxia, neuropathy, vestibular areflexia syndrome (CANVAS).
40 mic bilateral sensorineural hearing loss and vestibular areflexia.
41 nized tissue (KT) width (i.e., <2 mm) at the vestibular aspect of 19 implants who underwent soft tiss
42 oved vestibular function; however, no direct vestibular assessment was made.
43              The CAVA (Continuous Ambulatory Vestibular Assessment) device has been developed to prov
44                                              Vestibular balance control is dynamically weighted durin
45 cdh15a transgene-mediated rescue of auditory/vestibular behavior and hair cell morphology and activit
46 tant pan-otic CREs recombine in auditory and vestibular brain nuclei, making it difficult to ascribe
47 iating from its binding site and support our vestibular Ca(2+) sensor-model further.
48                                           In vestibular cerebellum, primary afferents carry signals f
49 ated in responses to fast head movements and vestibular compensation.
50 that combines an inner ring barrier with two vestibular condensates.
51 prove clinical care and our knowledge of the vestibular contributions to balance.
52                 Our results demonstrate that vestibular control of the upper limb maintains reaching
53 n subjects reported that the parieto-insular vestibular cortex (PIVC), a core area of the vestibular
54 ortex modulate activity in core areas of the vestibular cortex during attentive visual processing.SIG
55 vestibular cortex (PIVC), a core area of the vestibular cortex, is inhibited when visual processing i
56  modulate the magnitude of inhibition of the vestibular cortex.
57 vide support for the notion of altered visuo-vestibular cortical interactions in vestibular migraine,
58  symptoms are attributable to impaired visuo-vestibular cortical interactions, which in turn disrupts
59  macaque area MSTd that integrate visual and vestibular cues regarding self-motion.
60 comotor efference copies selectively replace vestibular cues, similar to what was previously observed
61                                   Hearing or vestibular deficits were reported in 18/121 (15%) childr
62 and depending on the species, mild to strong vestibular deficits.
63 are the key RA-synthesis enzymes involved in vestibular development.
64 rrent approaches for diagnosis of hearing or vestibular disorders are mostly based on physical examin
65 s for efficient gene therapy of cochlear and vestibular disorders by showing that even severe dysmorp
66  drug delivery systems to treat auditory and vestibular disorders.
67  low dose of DT caused profound SNHL without vestibular dysfunction and had no effect on wild-type (W
68 the severity rather than the age of onset of vestibular dysfunction differentiates whether hyperactiv
69 ids have been used to treat hearing loss and vestibular dysfunction for many years.
70 reflex (VOR) responses demonstrated that the vestibular dysfunction of the Zpld1 mutant mice is cause
71 tial for using antisense technology to treat vestibular dysfunction.
72 igh rates of post-operative hearing loss and vestibular dysfunction.
73 sociated with profound retinal, auditory and vestibular dysfunction.
74 mproves hearing sensitivity, and ameliorates vestibular dysfunction.
75 ir death leads to permanent hearing loss and vestibular dysfunction.
76                               Stimulation of vestibular efferent neurons excites calyx and dimorphic
77 our genetic evidence indicates that auditory/vestibular end organs and subsets of hair cells therein
78  findings support the notion that peripheral vestibular end organs are not passive transducers of hea
79 naling and plasticity.SIGNIFICANCE STATEMENT Vestibular end organs in the inner ear receive efferent
80  primary afferents carry signals from single vestibular end organs, whereas secondary afferents from
81  barrier (BLB) was investigated in the human vestibular endorgan, the utricular macula, using postmor
82 he deletion of sst1.1 did not impact acousto-vestibular escape responses but led to abnormal explorat
83 test and examinations of ocular and cervical vestibular evoked myogenic potentials and dynamic visual
84                       Mutants have deficient vestibular evoked potential (VsEP) responses to jerk sti
85 ence frame confirms the functional nature of vestibular-evoked arm movement.
86 efore the upper limb plays an active role in vestibular-evoked balance responses.
87                   Furthermore, modulation of vestibular-evoked muscle responses occurred rapidly ( ap
88        These high-frequency contributions to vestibular-evoked neck muscle responses could stabilize
89 ected head transients.SIGNIFICANCE STATEMENT Vestibular-evoked neck muscle responses rely on accurate
90                                              Vestibular excitatory inputs in Group I motoneurons are
91 g different surgical techniques-suturing the vestibular flap margin apically to the base of the recip
92 timulation as a potential therapy to restore vestibular function after bilateral vestibulopathy.
93 ividuals with documented normal auditory and vestibular function and surgical specimens from patients
94 dicated an apparent persistent importance of vestibular function at increasing speeds.
95 ence of an effective treatment of peripheral vestibular function in a mouse model of USH1C and reveal
96    These findings suggest a need to evaluate vestibular function in hearing impaired individuals, esp
97 he deafness progressed with aging, while the vestibular function of Elmod3-/- mice was normal.
98  ear areas; moreover, it rescued hearing and vestibular function of mice in vivo.
99                 Improvements in auditory and vestibular function were sustained well into adulthood.
100 r cell survival, restoration of cochlear and vestibular function, restoration of neural responses in
101  interactions, which in turn disrupts normal vestibular function.
102 l in Usher mice, indicating profound loss of vestibular function.
103 inally rescues hearing and partially rescues vestibular function.
104     The findings were suggestive of improved vestibular function; however, no direct vestibular asses
105 ASO-29 treatment at P15 despite the profound vestibular functional deficits that persist with treatme
106 gous S324Tfs*3 mice have normal auditory and vestibular functions but show an abrupt onset of spontan
107 ized coding via temporal whitening for other vestibular functions.
108  Nrp2- and PlxnA1-expressing neurites of the vestibular ganglion away from nonsensory epithelia, thus
109               Previous studies from immature vestibular ganglion neurons (VGNs) identified hyperpolar
110                                              Vestibular ganglion neurons (VGNs) transmit information
111 ally redundant FGF ligands may contribute to vestibular hair cell differentiation and supports a deve
112 ion is a specific and early marker of Type-I vestibular hair cell identity.
113                    Little is known about how vestibular hair cells adopt a Type I or Type II identity
114 used dual patch-clamp recordings from turtle vestibular hair cells and their afferent neurons to show
115                      Both type I and type ll vestibular hair cells express the alpha9 and alpha10 sub
116  and ultrastructure of efferent terminals on vestibular hair cells in alpha9, alpha10, and alpha9/10
117                                              Vestibular hair cells in the inner ear encode head movem
118 fferentially expressed genes in auditory and vestibular hair cells suggests that GFI1 serves differen
119 ou4f3 expression in cochlear hair cells than vestibular hair cells, administration of a low dose of D
120 -rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defe
121 s, a robust model for mammalian auditory and vestibular hair cells, we identified a urea-thiophene ca
122 oad punctate cytoplasmic distribution in the vestibular hair cells, whereas it was detected in the en
123 heading in neurons with congruent visual and vestibular heading preferences, whereas they stabilize t
124 n result from cerebellar, proprioceptive, or vestibular impairment; when in combination, it is also t
125 ouse and human databases of genetic auditory/vestibular impairments confirms the critical role of the
126 y lack acoustic-evoked behavioral responses, vestibular-induced eye movements, and hair-cell activity
127                   These results suggest that vestibular influence on ankle muscle control is adjusted
128           These results demonstrate that the vestibular influence on ankle muscles during locomotion
129                              KEY POINTS: The vestibular influence on human walking is phase-dependent
130   Using a split-belt treadmill, we show that vestibular influence on locomotor activity is modulated
131  circuits that in flies control auditory and vestibular information processing and motor coordination
132 brains, hippocampal cells combine visual and vestibular information to encode head direction.
133 beam tests that are consistent with abnormal vestibular input, but normal vestibulo-ocular reflexes a
134  during rotation to isolate the influence of vestibular input, uncontaminated by inertial factors.
135  part, due to altered temporal processing of vestibular input.
136 might result from a selective suppression of vestibular inputs in favor of a feed-forward balance reg
137 b amputees (LLAs) heavily rely on visual and vestibular inputs, and somatosensory cues from their int
138 eeds has potential as an assessment tool for vestibular interventions.
139 ly, but not only, if cerebellar dysfunction, vestibular involvement and cough coexist.
140 howed cerebellar involvement, and six showed vestibular involvement.
141 oupling between the C-loop and the Cys-loop, vestibular loop, and beta1-beta2 loops.
142                                              Vestibular loss triggers transient increases in postsyna
143 apillaries constituting the BLB in the human vestibular macula utricle from normal and Meniere's dise
144 two eye-head coupling types, associated with vestibular mechanisms.
145                                              Vestibular migraine (VM) is the most common cause of spo
146                   Chronically, patients with vestibular migraine develop abnormal responsiveness to b
147                                              Vestibular migraine is among the commonest causes of epi
148                     Our findings reveal that vestibular migraine patients exhibited abnormally elevat
149 olds were significantly further increased in vestibular migraine patients relative to healthy control
150 ed visuo-vestibular cortical interactions in vestibular migraine, as evidenced by vestibular threshol
151                              The independent vestibular modulation of muscle activity from each limb
152 clades, our results confirm the relevance of vestibular morphology for addressing the controversial p
153 tify the phylogenetic signal embedded in the vestibular morphology of extant anthropoids (monkeys, ap
154          This fin-body synergy was absent in vestibular mutants, suggesting sensed imbalance promotes
155            Behaviorally relevant patterns of vestibular nerve activation generated a rapid and substa
156 his study, the effects of iDC stimulation on vestibular nerve fiber firing rate was investigated usin
157                  To directly manipulate OKAN vestibular-neurectomy was performed in goldfish that sev
158 we measure sensory computations in zebrafish vestibular neurons across multiple axes in vivo.
159 dition to projecting to motoneurons, central vestibular neurons also receive direct sensory input fro
160  a genetically defined population of central vestibular neurons in rhombomeres 5-7 of larval zebrafis
161 ing preferred directions converge on central vestibular neurons, conferring more simple or complex tu
162 ischarge rate and sensitivity of first-order vestibular neurons.
163 in mice the deep cerebellar nuclei (DCN) and vestibular nuclei (VN) are two major sources of inhibiti
164                     Importantly however, the vestibular nuclei also comprise other neuronal classes t
165 ularly dense in the dorsal tegmentum, medial vestibular nuclei and lateral parabrachial nucleus, and
166 rs to compare how the brainstem auditory and vestibular nuclei develop in embryonic chicks and mice.
167 exposure results in activation of the caudal vestibular nuclei in pigeons that is independent of ligh
168 ticular formation (RF), pontine and midbrain vestibular nuclei, and medullary raphe.
169 l where vestibular symptoms emanate from the vestibular nuclei, which are sensitized by migraine-rela
170 end organs, whereas secondary afferents from vestibular nucleus carry integrated signals.
171  diverse fast-firing capacities among medial vestibular nucleus neurons of mice, we identify a group
172 tentiation, and reductions in BK currents in vestibular nucleus neurons.
173 ity of fast-spiking cell types in the medial vestibular nucleus of mice of both sexes, we examined th
174 t of the periaqueductal gray, and the medial vestibular nucleus that were also neurotensinergic.
175 of the thalamus, 0.24 ug . g(-1) +/- 0.04 in vestibular nucleus) and significantly greater than that
176 fasciculus (MLF), and neurons in the lateral vestibular nucleus, whose axons project through the asce
177 uals and avestibular patients, could disrupt vestibular ocular reflex and vestibular-perceptual thres
178  benign intracranial tumours, which included vestibular or other benign schwannomas, WHO grade 1 meni
179 and regenerated hair cells in the utricle, a vestibular organ detecting linear acceleration, acquired
180 UBC to specific ganglion cell, hair cell and vestibular organ subtypes in mice.
181           In both the organ of Corti and the vestibular organ, impaired terminal differentiation mani
182 tanding of sensorineural plasticity in adult vestibular organs and further elucidate the roles that s
183                                          The vestibular organs of reptiles, birds, and mammals posses
184  sensory hair cells of both the auditory and vestibular organs on E8-E10 may implicate Sema signaling
185 ermine the reliance of zebrafish hearing and vestibular organs on Tmc proteins.
186 3D expression flanking the sensory tissue in vestibular organs suggests that it may repel Nrp2- and P
187        In sensory hair cells of auditory and vestibular organs, the ribbon synapse is required for th
188     Herein, we investigated PCP of the mouse vestibular organs.
189 ctionally coupled Purkinje cell types in the vestibular part of the caudal vermis (lobules IX and X)
190  weeks old), normal activity in the efferent vestibular pathway is required for function of these irr
191 whereas abducens activation by the pretectum-vestibular pathway was not affected.
192  We investigated the hypothesis that central vestibular pathways are sensitized in VM by measuring se
193  to 300-400 Hz, raising the question whether vestibular pathways contribute to head stabilization at
194 ontext of parallel work focused on how early vestibular pathways encode self-motion.
195 , could disrupt vestibular ocular reflex and vestibular-perceptual thresholds of self-motion during r
196 role in responses to fast head movements and vestibular plasticity.
197 e occipital cortex and found that the visual-vestibular posterior insular cortex area was less activa
198                    Here, we demonstrate that vestibular primary afferents encode high-frequency stimu
199 nformation at the earliest stages of central vestibular processing in a manner that depends on the cu
200 lar afferents and a current model of central vestibular processing.
201 es and for our understanding of disorders of vestibular processing.
202 estibular afferents with known mechanisms of vestibular processing.
203                                We focused on vestibular projections to ON and OFF classes of unipolar
204 nner ear function, causes hyperactivity; (2) vestibular rather than auditory failure causes hyperacti
205 ment at P1, P5 or P15 resulted in sufficient vestibular recovery to support normal balance behaviors,
206 ing ASO-29 treatment have normal or elevated vestibular response thresholds when treated during a cri
207                                              Vestibular schwannoma (VS) is the most common tumor of t
208 elf-reported occupational noise exposure and vestibular schwannoma (VS), found in several studies, re
209 ent option for small-sized (Koos I up to II) vestibular schwannoma (VS).
210                 Diagnostic entities included vestibular schwannomas (1011 [20.6%] of 4905 patients),
211 nherited disorder characterized by bilateral vestibular schwannomas (VS) that arise from neoplastic S
212            NF2 is characterized by bilateral vestibular schwannomas (VSs) that cause progressive and
213 urofibromatosis type 2 (NF2) and progressive vestibular schwannomas (VSs).
214 ial schwannoma had an LZTR1 mutation (3 were vestibular schwannomas and 1 was a nonvestibular schwann
215 e evaluations, particularly in patients with vestibular schwannomas and candidates for cochlear impla
216                           Here, we show that vestibular schwannomas from NF2 patients and human, merl
217 w-grade tumors affecting the cranial nerves (vestibular schwannomas), meninges (meningiomas), and spi
218 ate normal anatomic structures, evaluate for vestibular schwannomas, assess for inflammatory and/or i
219 haracterized by the development of bilateral vestibular schwannomas.
220  during embryogenesis; and soon after birth, vestibular SCs in mammals transition to lasting quiescen
221                        Central processing of vestibular self-motion signals occurs through an interna
222                        In central regions of vestibular semicircular canal epithelia, the [K(+) ] in
223 ses present in central regions of the turtle vestibular semicircular canal epithelia.
224 , rewarding effects of physical exercise, or vestibular sensation produced via self-motion.
225 nt of coordinated locomotion is regulated by vestibular sensation.
226 es of bodily experiences, such as tactile or vestibular sensations, were not affected by tDCS, confir
227 ne therapy applications in both cochlear and vestibular sense organs.
228             Together these findings link the vestibular sense to the maturation of coordinated locomo
229 ne delivery systems that target auditory and vestibular sensory cells with high efficiency, we delive
230                                   Visual and vestibular sensory deficits were simulated by having eac
231 g resemblance of Tmc protein reliance in the vestibular sensory epithelia of mammals to the maculae o
232 rmation of highly specialized regions of the vestibular sensory epithelia with specific functions in
233 mation of significantly smaller auditory and vestibular sensory epithelia, while conditional overexpr
234                                         Each vestibular sensory epithelium in the inner ear is divide
235                                       Normal vestibular sensory evoked potential (VsEP) responses and
236 ar afferent responses.SIGNIFICANCE STATEMENT Vestibular sensory information is conveyed on parallel n
237 induces Cyp26b1 expression in the developing vestibular sensory organs, which generates the different
238  otoconial formation and zonal patterning of vestibular sensory organs.
239 Here, by investigating the inhibition of the vestibular sensory system when visual processing is prio
240 way that plays a critical role in peripheral vestibular signaling and plasticity.SIGNIFICANCE STATEME
241 thermore, new findings have established that vestibular signals are selectively combined with extrave
242                        Findings suggest that vestibular signals do not serve to scale the internal re
243                                        Thus, vestibular signals enhance the separability of joint tun
244 tion decoding, we tested the hypothesis that vestibular signals help to dissociate self-motion and ob
245 th single neuron and population levels, that vestibular signals help to dissociate self-motion and ob
246              Behavioral studies suggest that vestibular signals play a role in dissociating object mo
247                                 We show that vestibular signals stabilize tuning for heading in neuro
248 bers determines how the cerebellum processes vestibular signals.
249 (63%) and 17 out of 41 patients showed audio vestibular signs (41%), and 11 showed skin signs (27%).
250 the extent to which body-based cues, such as vestibular, somatosensory, and motoric cues, are necessa
251                                   Electrical vestibular stimulation (EVS) is an increasingly popular
252                                     Galvanic vestibular stimulation (GVS) uses the external applicati
253 ects the differential impact of a stochastic vestibular stimulation (SVS) on body sway (center-of-pre
254  peripheral spike rate relationships for iDC vestibular stimulation and validate an ex-vivo model for
255                    Here, we applied galvanic vestibular stimulation concurrently with real body movem
256                                      Caloric vestibular stimulation did not alter perceived size of o
257 ties of first person biometric avatars under vestibular stimulation did not support this assumption.
258   Here, we first established that electrical vestibular stimulation modulates human neck motor unit (
259        During the earth-fixed task, galvanic vestibular stimulation produced large polarity-dependent
260                                     Galvanic vestibular stimulation was applied concurrently during r
261 ir velocity was altered without any galvanic vestibular stimulation, indicating a compensatory arm re
262 very of behavioral responses to auditory and vestibular stimulation.
263  the neural mechanisms underlying electrical vestibular stimulation.
264 based on its ability to associate light with vestibular stimulation.
265             We show that, even if electrical vestibular stimuli are encoded as a net signal of head r
266 e debate exists regarding whether electrical vestibular stimuli encoded by vestibular afferents induc
267 ponses by modelling the effect of electrical vestibular stimuli on vestibular afferents and a current
268 t 0.8 m s(-1) while exposed to an electrical vestibular stimulus.
269 encies afferents tended to phase-lock to the vestibular stimulus.
270 ilt thresholds were considered together with vestibular symptom severity or VOR dynamics, VM patients
271 ive to healthy controls, migraineurs without vestibular symptoms and patients with episodic vertigo d
272 ese results support a pathogenic model where vestibular symptoms emanate from the vestibular nuclei,
273 kinje cells to deep cerebellar nuclei and at vestibular synapses in mice.
274 Cs are thought to align with the axes of the vestibular system and provide sensitivity at rotational
275                                          The vestibular system broadcasts head-movement-related signa
276                       In contrast, the adult vestibular system can produce new hair cells in response
277 ced could guide a more reliable screening of vestibular system deterioration.
278    Recent experiments have revealed that the vestibular system encodes this information during everyd
279  suggest that asymmetric connectivity in the vestibular system facilitates representation of ethologi
280 electrical current to selectively target the vestibular system in humans.
281  ionic direct current (iDC) can modulate the vestibular system in-vivo, with potential benefits over
282               It has been suggested that the vestibular system not only plays a role for our sense of
283                                          The vestibular system of the inner ear detects head position
284 tly how this non-invasive tool activates the vestibular system remains an open question.
285          This head stabilization enables the vestibular system to sense the direction of gravity.
286  involved in the sensation of gravity in the vestibular system, is essential for sour sensing in the
287               Hair cells of the auditory and vestibular systems are capable of detecting sounds that
288          Hair cells in both the auditory and vestibular systems receive efferent innervation.
289 ls, the mechanoreceptors of the auditory and vestibular systems, harbor two specialized elaborations
290 epithelia, such as those of the auditory and vestibular systems, results in the precise orientation o
291           Six-month M2 PPD improved at disto-vestibular (T0-5.2/T1-3.0 mm) and disto-lingual (T0-5.4/
292 ability was not associated with the clinical vestibular tests.
293  expression did not parallel the established vestibular-then-auditory sequence.
294 ions in vestibular migraine, as evidenced by vestibular threshold elevation following visual motion e
295 abnormally elevated reflexive and perceptual vestibular thresholds at baseline.
296 eas of the subordinate sensory system (e.g., vestibular), thus reducing potential conflict with ongoi
297                                  KEY POINTS: Vestibular type I and type II hair cells and their affer
298 iophysical properties of IK,L in adult mouse vestibular type I hair cells.
299  orientation and its expression in the mouse vestibular utricle is restricted, resulting in two regio
300 es (HR, 10.0; 95% CI, 7.0 to 15.3); auditory-vestibular-visual sensory deficits (HR, 2.3; 95% CI, 1.3

 
Page Top