RTG 2175 Perception in Context and its neural Basis

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New TP Dieterich/Brandt "Spatial orientation and postural control in unilateral vestibular upper brainstem and thalamus lesions"

Marianne Dieterich, MD1,2, Ahmed Ahmadi, PhD2, Thomas Brandt, MD2,3
1 Department of Neurology, 2 German Center for Vertigo and Balance Disorders, 3 Hertie Professorship, LMU Munich, Germany

It is a recent observation that unilateral central vestibular lesions of the vestibular nuclei, cerebellum, and lower brainstem manifest with rotational vertigo and spontaneous nystagmus, whereas lesions of upper brainstem and thalamus do not but manifest with swaying vertigo, postural imbalance, and spatial disorientation (Brandt & Dieterich 2017; Dieterich et al., 2018). Unilateral vestibular cortex lesions mostly manifest without vertigo (Dieterich & Brandt, 2015). There are two possible explanations for this diversity of perceptual and postural vestibular syndromes: one is based on the intra- and interhemispheric visual-vestibular interaction; the other is based on the differential coding of vestibular input en route from the endorgan via the vestibular nuclei and the thalamus to the cortex, i.e., the transition from the angular head-velocity cell system (located in the lower brainstem) to the head direction cell system (midbrain, thalamus, cortex) as found in rodents (Dumont & Taube 2015).

This transition reflects a mathematical integration of head movements from velocity to direction which is necessary for a continuous updating of the internal spatial representation of the individuum in the 3D- environment (Brandt & Dieterich 2017). Neuronal network-based mathematical modeling of the head direction cell system predicted and confirmed the above described different clinical findings in vestibular lesions of the lower versus the upper brainstem (Dieterich et al., 2018; Glasauer et al., 2018).

This work now requires 3D perceptual and postural investigations of the subjective visual straight ahead, the visual zenith in supine postion, and adjustment of the longitudinal body axis in a space curl. The experiments have to be performed in normal subjects over the entire life span and in patients with acute unilateral central vestibular lesions (from medulla to thalamus and cortex) along the course of the recovery, compensation, or substitution by other senses. The interdisciplinary aspect of the project is the explanation of clinical neurological brainstem and thalamus syndromes by the interaction of specialized vestibular neuronal subsystems. This requires the cooperation of clinicians and basic scientists (engineers, physicists) to further develop current mathematical vestibular models in 3D spatial coordinates. Orientation during locomotion of healthy subjects or patients is based on an continuous update of the internal model of the surrounding space and the location of the individuum within this space.

Figure from Dieterich et al., 2018:

Dieterich et al, 2018


text figure dieterich et al, 2018



  • Brandt T, Dieterich M. The dizzy patient: don’t forget disorders of the central vestibular system. Nat Rev Neurol 2017; 13:352-362.
  • Dieterich M, Brandt T. Why acute unilateral vestibular cortex lesions mostly manifest without vertigo. Neurology 2015; 84:1680-1684.
  • Dieterich M, Glasauer S, Brandt T. Why acute unilateral vestibular midbrain lesions rarely manifest with rotational vertigo: a clinical and modelling approach to head direction cell function. J Neurol 2018; doi.org/10.1007/s00415-018-8828-5.
  • Dumont JR, Taube JS. The neural correlates of navigation beyond the hippocampus. Prog Brain Res 2015; 219:83-102.
  • Glasauer S, Dieterich M, Brandt T. Neuronal network-based mathematical modeling of percieved verticality in acute unilateral vestibular lesions: from nerve to thalamus and cortex. J Neurol 2018; doi:10.1007/s00415-018-8909-5.