TRFII-1

Multimodal brain imaging of vestibular syndromes

 

Principle Investigator(s):

Marianne Dieterich, MD, FANA, FEAN
Peter Bartenstein, MD
Sandra Becker-Bense, MD

 

Objectives:

The objective of the project is to use a multimodal imaging approach combining imaging techniques in MRI (e.g., DTI, VBM, VLBM, FcMRI) and PET (FDG and neurotransmitter GABAA) to explore central adaptive changes in patients with well-defined vestibular syndromes due to strategic lesions along vestibular pathways.

 

Project description(s):

Subproject 1:  Neurotransmitter imaging of vestibulo-cerebellar syndromes (FDG-, GABAA-PET)

 

Bild1

Fig.1:     FDG-PET in (A) Acute vestibular neuritis right and (B) acute medullary infarctions right. Different compensation strategies seem apparent: after peripheral lesions (A), compensation occurs at the cortical level; after vestibular nucleus lesions (B), it occurs preferably in brainstem-cerebellar loops [Bense et al. 2004; Becker-Bense et al. 2013; Becker-Bense and Dieterich 2013].

 

Our earlier results in patients with medullary infarctions indicate that FDG-uptake as a surrogate marker of synaptic activity is increased in the contralateral brainstem and cerebellum [Fig.1], indicating the crucial role of this structures in central compensation of infratentorial vestibular lesions. Since the GABAA system is highly present in the cerebellum, we will now investigate the cerebral GABAA-receptor availability using the benzodiazepine antagonist C-11 Flumazenil in patients with acute strategic vestibulo-cerebellar lesions (e.g. acute medullary stroke, pure peripheral loss) and ongoing vestibulo-cerebellar impairment, e.g. downbeat nystagmus syndrome.

 

Subproject 2: Structural and functional connectivity via vestibular pathways (MRI)

Structural and functional interconnections of the areas of the bilateral central vestibular network have not yet been completely delineated. This includes both ipsilateral and contralateral pathways and crossing sites on the way from the vestibular nuclei via the thalamic relay stations to multiple “vestibular cortex” areas. Previous and recent lesion studies provided evidence that at cortical level vestibular information is represented prominently in the hemisphere ipsilateral to the stimulated ear and in the right hemisphere in right-handers and in the left hemisphere in left-handers. Therefore, our aim is to identify the physiological pathways in healthy right- and left-handers using structural and functional connectivity analyses by DTI and FcMRI (Fig.2).

In a second step, we plan to analyze how lesions within the pathways affect the network and determine which compensatory mechanisms take place.

 

           Bild2

 Fig. 2: Schematic overview of the vestibular rope ladder system. The basic network of the vestibular system is best visualized as a rope ladder. We focused on the core region of the parieto-insular vestibular cortex (PIVC) in the opercular–insular region and identified 5 separate and distinct vestibular brainstem pathways. Our study revealed 3 brainstem crossings of the bilaterally organized vestibular circuitry. These are located (1) at the level of the vestibular nuclei (VN), (2) at the pontine level above the vestibular nuclei, and (3) at the mesencephalic level with the interstitial nucleus of Cajal (INC) as the crucial structure. The fourth crossing travels transcallosally between the vestibular cortex areas of both hemispheres (according to Kirsch et al. 2015) 

Methods:

Subproject 1:

- FDG- and GABAA-PET (MCM-I, MCM-M; MCM-T)

- MRI (voxel-based morphometry, behavioral lesion mapping)
  (MCM-I, -M; -T)

- correlation analyses with neurophysiological and behavioral
  parameters (MCM-M)

Subproject 2:

- structural and functional MRI (DTI, FcMRI; VBM, VLBM) (MCM-I, -M; -T)

 

Relevant publications:

Baier B, Bense S, Birklein F, Buchholz HG, Mischke A, Schreckenberger M, Dieterich M (2010) Evidence for modulation of opioidergic activity in central vestibular processing: A [(18)F] diprenorphine PET study. Hum Brain Mapp 31(4): 550-5.

Becker-Bense S, Buchholz H-G, Best C, Schreckenberger M, Bartenstein P, Dieterich M (2013) Vestibular compensation in acute unilateral medullary infarction. FDG-PET study. Neurology 80: 1103-1109.

Becker-Bense S, Dieterich M, Buchholz HG, Bartenstein P, Schreckenberger M Brandt T (2013) The differential effects of acute right- vs. left-sided vestibular failure on brain metabolism. Brain Structure and Function May 18;DOI: 10.1007/s00429-013-0573-z.

Dieterich M, Bense S, Lutz S, et al. (2003) Dominance for vestibular cortical function in the non-dominant hemisphere. Cerebral Cortex 13: 994-1007

Kienast T, Hariri AR, Schlagenhauf F, Wrase J, Sterzer P, Buchholz HG, Smolka MN, Gründer G, Cumming P, Yoshitaka Kumakura Y, Bartenstein P, Dolan RJ, Heinz A (2008) Dopamine storage capacity in the amygdala gates processing of aversive stimuli in amygdala and anterior cingulate cortex: a combined PET – fMRI study. Nat Neurosci 11:1381-1382

Kirsch V, Keeser D, Hergenroeder T, Erat O, Ertl-Wagner B, Brandt T, Dieterich M (2015) Structural and functional connectivity mapping of the vestibular circuitry from human brainstem to cortex. Brain Struct Funct. 2015 Jan 1. [Epub ahead of print]

 

Team: 

 

Bense Sandra Bartenstein_klein Dietrich_1_Img103076 Stephan Thomas
Sandra Becker-Bense Peter Bartenstein Marianne Dieterich Valerie Kirsch Thomas Stephan

 

Contact:

Sandra Becker-Bense

Address: Marchioninistr. 15, 81377 Munich, Germany

Tel: + 49 (0) 89 4400 7 6968

Fax: + 49 (0) 89 4400 7 8881