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Institute
Eyeseecam: an eye movement-driven head camera for the examination of natural visual exploration
(2009)
Functional mri of galvanic vestibular stimulation with alternating currents at different frequencies
(2005)
A third eye for the surgeon
(2006)
Eye movements and balance
(2003)
Unilateral peripheral vestibular lesions not only lead to vertigo, nystagmus and imbalance, but also to a bias in the perception of verticality, which can be measured as tilt of the subjective visual vertical (SVV). Previously, this tilt has been assumed to be caused by a residual otolith bias, for example, because unequal numbers of active haircells on both sides of the utricular striola might result in an imbalance of the firing rates of central otolith neurons. Here we propose that a tilt of the subjective visual vertical might as well be caused by a vertical semicircular canal bias in the roll axis after unilateral peripheral lesions. The canal bias, acting similar to angular velocity stimuli, influences the SVV via the central gravity estimator, which under normal circumstances resolves a perceptual tilt-translation ambiguity. To illustrate our hypothesis, we compare model predictions to data on SVV measurements in patients with unilateral vestibular lesions while being tilted or being rotated eccentrically. We further embed the model of peripheral processing in a neural network that implements the idiotropic bias and represents the direction of gravity as population code in a three dimensional spherical topography.
Objective To investigate long-term recovery of allocentric and egocentric spatial orientation as a sensitive marker for hippocampal and extrahippocampal network function in transient global amnesia (TGA).
Methods A group of 18 patients with TGA performed an established real-space navigation paradigm, requiring allo- and egocentric spatial orientation abilities, 3 days (postacute stage) and 3 months (follow-up) after symptom onset. Visual exploration behavior and navigation strategy were documented by a gaze-controlled, head-fixed camera. Allo- and egocentric spatial orientation performance was compared to that of 12 age-matched healthy controls. Navigation-induced brain activations were measured using [18F]-fluorodeoxyglucose-PET in a subgroup of 8 patients in the postacute stage and compared to those of the controls.
Results In the postacute stage, the patients navigated worse and had higher error rates than controls in allocentric (p = 0.002), but not in egocentric, route planning (p = 0.30), despite complete recovery of verbal (p = 0.58) and figural memory (p = 0.11). Until follow-up, allocentric navigation deficits improved, but higher error rates and reduced use of shortcuts persisted (p < 0.0001). Patients still exhibited relatively more fixations of unique landmarks during follow-up (p = 0.05). PET measurements during the postacute stage showed increased navigation-induced brain activations in the right hippocampus, bilateral retrosplenial, parietal, and mesiofrontal cortices, and cerebellar dentate nucleus in patients compared to controls (p < 0.005).
Conclusions Patients with TGA show selective and prolonged deficits of allocentric spatial orientation. Activations in right hippocampal and extrahippocampal hubs of the cerebral navigation network functionally substitute for the deficit in creating and updating the internal cognitive map in TGA.