Vestibular thalamus

Baier, Bernhard; Conrad, Julian; Stephan, Thomas; Kirsch, V.; Vogt, Thomas; Wilting, Janine; Müller‐Forell, Wibke; Dieterich, Marianne

doi:10.1212/wnl.0000000000002238

Cited by 42 publications

(22 citation statements)

References 39 publications

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“…However, a case report showed that thalamic astasia and SVV tilt also occurred in a patient with paramedian/centromedian thalamic stroke [57]. This was confirmed by a recent voxel-based behavioral mapping analysis that attributed SVV tilts to lacunar strokes of both posterolateral and central paramedian thalamic subnuclei [24]. Here two distinct systems of graviceptive processing within the thalamus were described: contraversive tilts of SVV were associated with lesions of the central and posterolateral nuclei, whereas ipsiversive SVV tilts were associated with regions located more inferior, involving nuclei endymalis thalami and inferior parts of the nuclei parafascicularis thalami.…”

Section: Discussionmentioning

confidence: 77%

“…Of the latter, two patients showed ipsiversive tilts of the SVV; here the infarction partly affected inferior thalamic nuclei such as the nuclei endymalis thalami or parafascicularis thalami. These inferior parts of the thalamus convey parts of the vestibular graviceptive pathways [24]. …”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, it was used to check if the lesion site in our patients fits that of larger patient samples reported in the literature [23,24]. This procedure ensured a homogeneous sample of patients with typical midbrain lesions that cause unilateral vestibular dysfunction.…”

Section: Methodsmentioning

confidence: 99%

“…We performed group subtraction analyses and in addition compared the patients’ imaging data with those of age- and gender-matched healthy controls. Voxelwise lesion-behavior mapping (LBM) was performed on the structural MRI data of the patients in order to determine the exact extent of the acute lesion site and to check whether vestibular structures are affected on analogy to the data of larger sample sizes [23,24]. …”

Section: Introductionmentioning

confidence: 99%

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Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography

et al. 2016

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The aim of the study was to uncover mechanisms of central compensation of vestibular function at brainstem, cerebellar, and cortical levels in patients with acute unilateral midbrain infarctions presenting with an acute vestibular tone imbalance. Eight out of 17 patients with unilateral midbrain infarctions were selected on the basis of signs of a vestibular tone imbalance, e.g., graviceptive (tilts of perceived verticality) and oculomotor dysfunction (skew deviation, ocular torsion) in F18-fluordeoxyglucose (FDG)-PET at two time points: A) in the acute stage, and B) after recovery 6 months later. Lesion-behavior mapping analyses with MRI verified the exact structural lesion sites. Group subtraction analyses and comparisons with healthy controls were performed with Statistic Parametric Mapping for the PET data. A comparison of PET A of acute-stage patients with that of healthy controls showed increases in glucose metabolism in the cerebellum, motion-sensitive visual cortex areas, and inferior temporal lobe, but none in vestibular cortex areas. At the supratentorial level bilateral signal decreases dominated in the thalamus, frontal eye fields, and anterior cingulum. These decreases persisted after clinical recovery in contrast to the increases. The transient activations can be attributed to ocular motor and postural recovery (cerebellum) and sensory substitution of vestibular function for motion perception (visual cortex). The persisting deactivation in the thalamic nuclei and frontal eye fields allows alternative functional interpretations of the thalamic nuclei: either a disconnection of ascending sensory input occurs or there is a functional mismatch between expected and actual vestibular activity. Our data support the view that both thalami operate separately for each hemisphere but receive vestibular input from ipsilateral and contralateral midbrain integration centers. Normally they have gatekeeper functions for multisensory input to the cortex and automatic motor output to subserve balance and locomotion, as well as sensorimotor integration.

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Section: Discussionmentioning

confidence: 77%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography

et al. 2016

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“…This finding is important as it suggests that, in addition to involving the TPJ, the electrical stimulation “activates” a network of brain regions accounting for the complex phenomenal experience of OBEs. Both the TPJ and posterolateral thalamus have been involved in the sense of self-orientation and uprightness (Kheradmand et al, 2015 ; Baier et al, 2016 ; Kirsch et al, 2017 ) and the medial occipital cortex has been involved in autoscopic hallucinations (Jonas et al, 2014 ). A PET study during OBEs evoked by cortical electrical stimulation revealed activation beyond the TPJ, in the precuneus and the posterior thalamus (De Ridder et al, 2007 ).…”

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confidence: 99%

Commentary: Out-of-Body Experience during Awake Craniotomy

Nakul

Lopez

2017

Front. Hum. Neurosci.

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Global multisensory reorganization after vestibular brain stem stroke

Conrad

Boegle

Ertl

et al. 2020

Ann Clin Transl Neurol

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Objective: Patients with acute central vestibular syndrome suffer from vertigo, spontaneous nystagmus, postural instability with lateral falls, and tilts of visual vertical. Usually, these symptoms compensate within months. The mechanisms of compensation in vestibular infarcts are yet unclear. This study focused on structural changes in gray and white matter volume that accompany clinical compensation. Methods: We studied patients with acute unilateral brain stem infarcts prospectively over 6 months. Structural changes were compared between the acute phase and follow-up with a group of healthy controls using voxel-based morphometry. Results: Restitution of vestibular function following brain stem infarcts was accompanied by downstream structural changes in multisensory cortical areas. The changes depended on the location of the infarct along the vestibular pathways in patients with pathological tilts of the SVV and on the quality of the vestibular percept (rotatory vs graviceptive) in patients with pontomedullary infarcts. Patients with pontomedullary infarcts with vertigo or spontaneous nystagmus showed volumetric increases in vestibular parietal opercular multisensory and (retro-) insular areas with right-sided preference. Compensation of graviceptive deficits was accompanied by adaptive changes in multiple multisensory vestibular areas in both hemispheres in lower brain stem infarcts and by additional changes in the motor system in upper brain stem infarcts. Interpretation: This study demonstrates multisensory neuroplasticity in both hemispheres along with the clinical compensation of vestibular deficits following unilateral brain stem infarcts. The data further solidify the concept of a right-hemispheric specialization for core vestibular processing. The identification of cortical structures involved in central compensation could serve as a platform to launch novel rehabilitative treatments such as transcranial stimulations.

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Vestibular thalamus

Abstract: Our data indicate that there are 2 anatomically distinct graviceptive signal processing mechanisms within the vestibular network in humans that lead, when damaged, to a vestibular tone imbalance either to the contraversive or to the ipsiversive side.

Cited by 42 publications

References 39 publications

Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography

Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography

Commentary: Out-of-Body Experience during Awake Craniotomy

Global multisensory reorganization after vestibular brain stem stroke

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