The differential effects of acute right- vs. left-sided vestibular failure on brain metabolism

Abstract

The human vestibular system is represented in the brain bilaterally, but it has functional asymmetries, i.e., a dominance of ipsilateral pathways and of the right hemisphere in right-handers. To determine if acute right- or left-sided unilateral vestibular neuritis (VN) is associated with differential patterns of brain metabolism in areas representing the vestibular network and the visual-vestibular interaction, patients with acute VN (right n = 9; left n = 13) underwent resting state (18)F-FDG PET once in the acute phase and once 3 months later after central vestibular compensation. The contrast acute vs. chronic phase showed signal differences in contralateral vestibular areas and the inverse contrast in visual cortex areas, both more pronounced in VN right. In VN left additional regions were found in the cerebellar hemispheres and vermis bilaterally, accentuated in severe cases. In general, signal changes appeared more pronounced in patients with more severe vestibular deficits. Acute phase PET data of patients compared to that of age-matched healthy controls disclosed similarities to these patterns, thus permitting the interpretation that the signal changes in vestibular temporo-parietal areas reflect signal increases, and in visual areas, signal decreases. These data imply that brain activity in the acute phase of right- and left-sided VN exhibits different compensatory patterns, i.e., the dominant ascending input is shifted from the ipsilateral to the contralateral pathways, presumably due to the missing ipsilateral vestibular input. The visual-vestibular interaction patterns were preserved, but were of different prominence in each hemisphere and more pronounced in patients with right-sided failure and more severe vestibular deficits.

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

“…The patients with vestibular lesion signs, i.e., pathological SVV tilts, underwent two resting state PET scans following injection of 150 ± 20MBq FDG in a standardized manner [27] in an ECAT Exact PET Scanner (Siemens/CTI, Knoxville) while they lay supine in a quiet, darkened room with eyes closed and without any artificial stimulation: (A) during the acute stage of brainstem infarction (mean on day 4.4 after symptom onset, range: day 2 to 7) and (B) 6 months later after clinical recovery, corresponding to that in earlier studies on peripheral vestibular (mean day 6.6, respectively 6.8) [17,19] and medullary lesions (mean day 8) [22]. The interval between symptom onset and first PET scan varied between the patients for logistical reasons (e.g., availability of the tracer or scanning time, transport logistics).…”

“…The interval between symptom onset and first PET scan varied between the patients for logistical reasons (e.g., availability of the tracer or scanning time, transport logistics). The time frame of 6 months was chosen for the second PET scan, since the clinical vestibular deficit had recovered by that time, and this time frame closely corresponds to that used in earlier studies on peripheral and medullary vestibular lesions [14,19,22]. …”

“…A statistical threshold of p<0.001 (uncorrected) and a minimal cluster size > 10 voxels were always applied. These methods of standardized PET data acquisition, image reconstruction, and statistical analyses was chosen for optimal comparability of the data to those of earlier FDG-PET studies on vestibular syndromes [14,19,22,27]. …”

Vestibular compensation: the neuro-otologist’s best friend

“…In humans, follow-up brain metabolism studies (FDG-PET) comparing patients in the acute and chronic stages of peripheral vestibular imbalance due to incomplete lesions in vestibular neuritis revealed both cortical and sub-cortical activation patterns in the acute phase, which resemble those of peripheral vestibular stimulation on the contralateral side in healthy subjects [ 64 , 65 ]: a contralesional increase in rCGM in posterolateral thalamus and retroinsular vestibular cortex was observed. This asymmetry reversed within 3 months with peripheral vestibular nerve recovery and behavioural restitution.…”

Hippocampal gray matter volume in bilateral vestibular failure

“…Vestibular deafferentation induces several plastic functional [Bense et al, 2004a;Becker-Bense et al, 2013;Helmchen et al, 2014] and structural [Helmchen et al, 2009[Helmchen et al, , 2011zu Eulenburg et al, 2010] changes in the brain. It is a matter of debate whether these changes are clinically beneficial, subserve vestibular compensation, or purely reflect the consequence of a lack of vestibular input.…”