Functional brain imaging of peripheral and central vestibular disorders

Authors: 

Marianne Dieterich 1 and Thomas Brandt 2

1 Department of Neurology, Johannes Gutenberg-University of Mainz, Mainz and

2 Department of Neurology, Ludwig-Maximilians University of Munich, Munich,Germany

Correspondence to: Prof. Marianne Dieterich, MD, Department of Neurology, Johannes Gutenberg-University of Mainz, Langenbeckstrasse1, 55131Mainz,Germany

E-mail: dieterich@neurologie.klinik.uni-mainz.de

This review summarizes our current knowledge of multisensory vestibular structures and their functions in

humans. 

Most of it derives from brain activation studies with PET and fMRI conducted over the last decade.

The patterns of activations and deactivations during caloric and galvanic vestibular stimulations in healthy

subjects have been compared with those in patients with acute and chronic peripheral and central vestibular

disorders. 

Major findings are the following: 

(1) In patients with vestibular neuritis the central vestibular system exhibits a spontaneous visual-vestibular activation^deactivation pattern similar to that described in healthy volunteers during unilateral vestibular stimulation. 

In the acute stage of the disease regional cerebral glucose metabolism (rCGM) increases in the multisensory vestibular cortical and subcortical areas, but simultaneously it significantly decreases in the visual and somatosensory cortex areas. 

(2) In patients with bilateral vestibular failure the activation^deactivation pattern during vestibular caloric stimulation shows a decrease of activations and deactivations. 

(3) Patients with lesions of the vestibular nuclei due to Wallenberg’s syndrome show no activation or significantly reduced activation in the contralateral hemisphere during caloric irrigation of the ear ipsilateral to the lesioned side, but the activation pattern in the ipsilateral hemisphere appears ‘normal’.

These findings indicate that there are bilateral ascending vestibular pathways from the vestibular nuclei to the

vestibular cortex areas, and the contralateral tract crossing them is predominantly affected. 

(4) Patients with posterolateral thalamic infarctions exhibit significantly reduced activation of the multisensory vestibular cortex in the ipsilateral hemisphere, if the ear ipsilateral to the thalamic lesion is stimulated. 

Activation of similar areas in the contralateral hemisphere is also diminished but to a lesser extent.

These data demonstrate the functional importance of the posterolateral thalamus as a vestibular gatekeeper. 

(5) In patients with vestibulocerebellar lesions due to a bilateral floccular deficiency, which causes downbeat nystagmus (DBN), PET scans reveal that rCGM is reduced in the region of the cerebellar tonsil and flocculus/paraflocculus bilaterally. 

Treatment with 4-aminopyridine lessens this hypometabolism and significantly improves DBN. 

These findings support the hypothesis that the (para-) flocculus and tonsil play a crucial role in DBN. 

Although we can now for the first time attribute particular activations and deactivations to functional deficits in distinct vestibular disorders, the complex puzzle of the various multisensory and sensorimotor functions of the phylogenetically ancient vestibular system is only slowly being unraveled.

 Keywords: vestibular system; vestibular disorder; functional imaging; fMRI; PET

Abbreviations: fMRI=functional magnetic resonance imaging; PET=positron emission tomography; BC=brachium

conjunctivum; PIVC=parieto-insular vestibular cortex; VOR=vestibulo-ocular reflex; CVTT=central ventral tegmental tract; INC = interstitial nucleus of Cajal; MLF; medial longitudinal fasciculus; NPH = nucleus prepositus hypoglossi; PPRF = paramedian pontine reticular formation; Vce = nucleus ventrocaudalis externus; Vim = nucleus ventro-oralis intermedius; Dc=nucleus dorsocaudalis; Vci=nucleus ventrocaudalis internus; VPLo=nucleus ventroposterior lateralis oralis; PMT = nucleus of the paramedian tract; DBN = downbeat nystagmus; rCGM = regional cerebral glucose metabolism.

doi:10.1093/brain/awn042

Fuente :Brain (2008),131 ,2538^2552

http://brain.oxfordjournals.org/