Neural correlates of disturbed perception of verticality

Baier, Bernhard; Suchan, J; Karnath, Hans‐Otto; Dieterich, Marianne

doi:10.1212/wnl.0b013e318248e544

Cited by 109 publications

(112 citation statements)

References 39 publications

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“…To our knowledge, this hypothesis has not been investigated. Nevertheless, the perception of gravity seems to contribute to errors when upright, since SVV roll-tilts have been observed in patients with central lesions along the vestibular pathways that left the vestibulo-ocular pathways unaffected (Baier et al , 2012).…”

Section: Discussionmentioning

confidence: 99%

Spatial orientation in patients with chronic unilateral vestibular hypofunction is ipsilesionally distorted

Müller

Bockisch

Tarnutzer

2016

Clinical Neurophysiology

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OBJECTIVE Acute unilateral peripheral-vestibular hypofunction (UVH) shifts the subjective visual vertical (SVV) ipsilesionally, triggering central compensation that usually eliminates shifts when upright. We hypothesized that compensation is worse when roll-tilted. METHODS We quantified SVV errors and variability in different roll-tilted positions (0°, ±45°, ±90°) in patients with chronic UVH affecting the superior branch (SVN; n=4) or the entire (CVN; n=9) vestibular nerve. RESULTS Errors in SVN and CVN were not different. When roll-tilted ipsilesionally 45°(9.6±5.4°vs. -0.2±6.4°, patients vs. controls, p<0.001) and 90°(23.5±5.7°vs. 16.8±8.8°, p=0.003), the patient's SVV was shifted significantly towards the lesioned ear. When upright, only a trend was noted (3.6±2.2°vs. 0.0±1.2°, p=0.099); for contralesional roll-tilts shifts were not different from controls. Variability was larger for CVN than SVN (p=0.046). With increasing disease-duration, adjustment errors decayed for ipsilesional roll-tilt and upright (p0.025). CONCLUSIONS The reason verticality perception was distorted for ipsilesional roll-tilts, may be the insufficient integration of contralesional otolith-input. Similar errors in SVN and CVN suggest a dominant utricular role in verticality perception, albeit the sacculus may improve precision of SVV estimates. SIGNIFICANCE With deficiencies in central compensation being roll-angle dependent, extending SVV-testing to roll-tilted positions may improve identifying patients with chronic UVH. Highlights:• Visual vertical (VV) was measured in 13 patients with chronic unilateral vestibular hypofunction.• VV shifts in the patients were significant only when rolled ipsilesionally.• Thus VV testing in roll-tilted positions is recommended to identify more subtle vestibular deficits. 3 AbstractObjective: Acute unilateral peripheral-vestibular hypofunction (UVH) shifts the subjective visual vertical (SVV) ipsilesionally, triggering central compensation that usually eliminates shifts when upright. We hypothesized that compensation is worse when roll-tilted. Methods

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Section: Discussionmentioning

confidence: 99%

Spatial orientation in patients with chronic unilateral vestibular hypofunction is ipsilesionally distorted

Müller

Bockisch

Tarnutzer

2016

Clinical Neurophysiology

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“…8,[10][11][12][13] Recent studies, however, have also indicated that the complex motor control system can compensate for impairment to one or more elements of the system by placing increased reliance on remaining intact elements.…”

Section: Introductionmentioning

confidence: 99%

“…[4][5][6][7][8][9] More specifically, lesions within the right middle cerebral artery (MCA) territory are particularly disturbing to both the sense of postural verticality and the ability to stabilize the body in the frontal plane. 8,[10][11][12][13] Recent studies, however, have also indicated that the complex motor control system can compensate for impairment to one or more elements of the system by placing increased reliance on remaining intact elements.…”

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confidence: 99%

Infarct hemisphere and noninfarcted brain volumes affect locomotor performance following stroke

Chen

Novak

Manor³

2014

Neurology

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Objective: Brain damage within the right middle cerebral artery (MCA) territory is particularly disruptive to mediolateral postural stabilization. The objective of this cross-sectional study was to test the hypothesis that chronic right MCA infarcts (as compared to left) are associated with slower and more bilaterally asymmetrical gait. We further hypothesized that in those with chronic right MCA infarct, locomotor performance is more dependent on gray matter (GM) volumes within noninfarcted regions of the brain that are involved in motor control yet lie outside of the MCA territory.Methods: Gait speed was assessed in 19 subjects with right MCA infarct, 20 with left MCA infarct, and 108 controls. Bilateral plantar pressure and temporal symmetry ratios were calculated in a subset of the cohort. GM volumes within 5 regions outside of the MCA territory (superior parietal lobe, precuneus, caudate, putamen, and cerebellum) were quantified from anatomic MRIs.Results: Right and left infarct groups had similar poststroke duration (7.6 6 6.0 years), infarct size, and functional independence. The right infarct group demonstrated slower gait speed and greater asymmetry compared to the left infarct group and controls (p , 0.05). In the right infarct group only, those with larger GM volumes within the cerebellum (r 2 5 0.32, p 5 0.02) and caudate (r 2 5 0.56, p , 0.001) exhibited faster gait speed.Conclusion: Individuals with chronic lesions within the right MCA territory, as compared to the left MCA territory, exhibit slower, more asymmetrical gait. For these individuals, larger GM volumes within regions outside of the infarcted vascular territory may help preserve locomotor control. Although approximately two-thirds of stroke survivors regain the ability to walk, 1 many present with diminished locomotor performance characterized by slow walking speed and bilaterally asymmetrical walking patterns. 2,3 Lesions within the right hemisphere of the brain, as compared to the left, appear to be more disruptive to both gait and postural control.4-9 More specifically, lesions within the right middle cerebral artery (MCA) territory are particularly disturbing to both the sense of postural verticality and the ability to stabilize the body in the frontal plane. 8,[10][11][12][13] Recent studies, however, have also indicated that the complex motor control system can compensate for impairment to one or more elements of the system by placing increased reliance on remaining intact elements.14 As such, the extent of residual gait abnormality following an infarct may be dependent on not only infarct hemisphere but also on the integrity of noninfarcted brain regions.The objectives of the study were to investigate the effects of infarct hemisphere, as well as gray matter (GM) volumes within regions outside of the infarcted vascular territory, on locomotor performance in individuals with chronic MCA infarcts. We hypothesized that individuals with

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“…[1][2][3][4][5] However, it seems that small lesions exclusively affecting the IC might not be sufficient to cause vestibular otolith deficits, such as tilt of subjective visual vertical (SVV). 2 Presumably, because of the rareness of isolated insular infarctions, there are no data reporting about vestibular parameters in patients with isolated infarctions of the IC. The approach of this study focused on a strong hypothesis on the exclusive role of the IC in vestibular otolith processing.…”

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confidence: 99%

Insular Strokes Cause No Vestibular Deficits

Baier

Conrad²,

Eulenburg³

et al. 2013

Stroke

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Background and Purpose— In previous imaging studies, the posterior insular cortex (IC) was identified as an essential part for vestibular otolith perception and considered as a core region of a human vestibular cortical network. However, it is still unknown whether lesions exclusively restricted to the posterior IC suffice to provoke signs of vestibular otolith dysfunction. Thus, present data aimed to test whether patients with lesions restricted to the IC showed vestibular otolith dysfunction. Methods— We studied 10 acute unilateral stroke patients with lesions restricted to the IC which were tested for signs of vestibular otolith dysfunction, such as tilts of subjective visual vertical, out of 475 stroke patients. Results— None of the patients was with stroke exclusively affecting the IC-specified vertigo as a symptom. In addition, neither showed a deficit in the perception of verticality (subjective visual vertical tilts) nor showed any further vestibular otolith deficits, such as ocular torsion or skew deviation. Conclusions— It seems that lesions of the posterior IC might have to be combined with lesions of adjacent regions of the cortical and subcortical vestibular network to cause vestibular otolith deficits.

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Neural correlates of disturbed perception of verticality

Abstract: Damage to these regions might lead to an imbalance within the vestibular network of one hemisphere due to a deficit in multimodal signal processing.

Cited by 109 publications

References 39 publications

Spatial orientation in patients with chronic unilateral vestibular hypofunction is ipsilesionally distorted

Spatial orientation in patients with chronic unilateral vestibular hypofunction is ipsilesionally distorted

Infarct hemisphere and noninfarcted brain volumes affect locomotor performance following stroke

Insular Strokes Cause No Vestibular Deficits

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