Abstract Body

Imaging and neurophysiological work has advanced our understanding of cortical vestibular topography. Here, we will concentrate on one of the final frontiers in neuro-otology – the cause of “presbyvestibulopathy” or, more correctly, unexplained dizziness of the elderly (UDE). Retrospective imaging assessment suggested that UDE patients had increased small vessel disease (SVD) in brain scans compared to patients with vestibular causes of dizziness (Ahmad et al 2015-doi:10.1016/j.jns.2015.09.006). The current prospective study recruited 38 patients with UDE, normal vestibular assessment (video-head impulse test), no orthostatic hypotension, and an age-matched control group. Structural and DW-MRI were obtained, as well as simultaneous co-registration of postural sway and EEG. UDE patients had higher vascular risk factors and poorer gait and cognitive performance than controls. MRI showed lower fractional anisotropy in the genu of the corpus callosum and the right inferior longitudinal fasciculus and higher hyperintensity in frontal white matter than controls. UDE patients had greater instability-driven changes in EEG power than controls, that is, greater delta, lower theta/alpha/beta power during unsteadiness periods. In contrast to controls, SVD load correlated negatively with delta-power during periods of instability in patients. Thus, clinical, MRI and EEG findings indicate that SVD is a significant factor in the development of dizziness in the elderly, likely disrupting brain networks involved in the cortical control of postural balance (with thanks to Dunhill Medical Trust for funding and Richard Ibitoye and Patricia Castro the two leading workers in this project).

Abstract Body

Current knowledge of multisensory vestibular structures and their functions in the human cortex will be presented as revealed from brain activation studies of the last two decades with PET and MRI. These tools confirmed that humans have several separate cortical areas that tracer and electrophysiological studies in animals, especially in monkeys, had identified earlier.

First, the pathways from the vestibular nuclei in the brainstem to vestibular cortical areas are described in normals, followed by the typical cortical activation pattern of unilateral vestibular stimulation.

Interestingly, this cortical network is not activated symmetrically in the two hemispheres, but is determined by three factors: (1) the subject’s handedness, (2) the side of the stimulated ear, and (3) the direction of the induced vestibular nystagmus. Activation was found to be stronger in the non-dominant hemisphere (right hemisphere in right-handers) and in the hemisphere ipsilateral to the stimulated ear. Second, the importance of structural MRI imaging for the clinical routine of patients with an acute vestibular syndrome and additional central neurological signs will be discussed. Acute central vestibular syndromes of the brainstem and cerebellum are much more frequent than those caused by cortical vertigo due to acute lesions of the insular-opercular region or the inferior parietal lobe.

Lesions at the cortical level are more often associated with balance disorders and disorientation as well as deficits in navigation. They are related to a dysfunction of the vestibular-hippocampal axis, which is the basis of both the central vestibular system and the memory system (working memory, attention).

Abstract Body

Behaviour in the environment requires continuous updating of the internal representation of the body and the surroundings of the body. Altered perceptions of the self or the environment include depersonalization/derealization (DD) symptoms, which occur on a continuum from healthy to pathological states. A sensory mismatch may elicit erroneous perceptions of the body in the physical space. Consistently, sensory deficiencies can provoke discrepancies between the multi-sensory frame given by experience and the actual perception, accompanied by dizziness, unsteadiness and distress. Conversely, DD symptoms have also been related to Impairment of the capacity to regulate emotions, with an increased risk of cognitive and psychiatric comorbidity in patients with vestibular disease.

Vestibular signals contribute to the perception of the body and its interactions with the environment. In healthy subjects, artificial vestibular stimulation of the semicircular canals or the otoliths can induce DD symptoms. In vestibular patients, DD symptoms are more frequent and more severe when the clinical recovery is deficient, and they correlate with erroneous updating orientation in space. Furthermore, DD symptoms reported by patients with phantom limb pain may decrease after asymmetric vestibular stimulation (either of the horizontal semicircular canals or the utricles), which may provide an update of the immediate experience of the body. These effects can be accompanied by symptoms related to the sensory conflict and may modulate higher neural processes, with influence from individual factors. Further studies are needed to comprehend the vestibular contribution to cognitive and emotional processes.