Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography.
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.
Department of Neurology, University of Munich, Munich, Germany.|German Center for Vertigo and Balance Disorders-IFB, University of Munich, Munich, Germany.
Sandra
S
Becker-Bense
Department of Nuclear Medicine, Johannes Gutenberg-University, Mainz, Germany.
Hans-Georg
HG
Buchholz
Department of Neurology, Johannes Gutenberg-University, Mainz, Germany.
Bernhard
B
Baier
Department of Nuclear Medicine, Johannes Gutenberg-University, Mainz, Germany.
Mathias
M
Schreckenberger
German Center for Vertigo and Balance Disorders-IFB, University of Munich, Munich, Germany.|Department of Nuclear Medicine, University of Munich, Munich, Germany.|Munich Cluster of Systems Neurology (SyNergy), University of Munich, Munich, Germany.
Peter
P
Bartenstein
Department of Neurology, University of Munich, Munich, Germany.|German Center for Vertigo and Balance Disorders-IFB, University of Munich, Munich, Germany.
Andreas
A
Zwergal
German Center for Vertigo and Balance Disorders-IFB, University of Munich, Munich, Germany.|Institute for Clinical Neuroscience, University of Munich, Munich, Germany.
Thomas
T
Brandt
Department of Neurology, University of Munich, Munich, Germany.|German Center for Vertigo and Balance Disorders-IFB, University of Munich, Munich, Germany.|Munich Cluster of Systems Neurology (SyNergy), University of Munich, Munich, Germany.
Marianne
M
Dieterich
D000368:Aged; D020526:Brain Stem Infarctions / Q000000981:diagnostic imaging* / Q000503:physiopathology; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008636:Mesencephalon / Q000000981:diagnostic imaging / Q000503:physiopathology; D009473:Neuronal Plasticity; D049268:Positron-Emission Tomography; D004856:Postural Balance / Q000502:physiology; D015837:Vestibular Diseases / Q000503:physiopathology