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Objective<p>Vestibular signals are involved in higher cortical functions like spatial orientation and its disorders. Vestibular dysfunction contributes, for example, to spatial neglect which can be transiently improved by caloric stimulation. The exact roles and mechanisms of the vestibular and visual systems for the recovery of neglect are not yet known.</p>Methods<p>Resting-state functional connectivity (fc) magnetic resonance imaging was recorded in a patient with hemispatial neglect during the acute phase and after recovery 6 months later following a right middle cerebral artery infarction before and after caloric vestibular stimulation. Seeds in the vestibular [parietal operculum (OP2)], the parietal [posterior parietal cortex (PPC); 7A, hIP3], and the visual cortex (VC) were used for the analysis.</p>Results<p>During the acute stage after caloric stimulation the fc of the right OP2 to the left OP2, the anterior cingulum, and the para/hippocampus was increased bilaterally (i.e., the vestibular network), while the interhemispheric fc was reduced between homologous regions in the VC. After 6 months, similar fc increases in the vestibular network were found without stimulation. In addition, fc increases of the OP2 to the PPC and the VC were seen; interhemispherically this was true for both PPCs and for the right PPC to both VCs.</p>Conclusion<p>Improvement of neglect after caloric stimulation in the acute phase was associated with increased fc of vestibular cortex areas in both hemispheres to the para-hippocampus and the dorsal anterior cingulum, but simultaneously with reduced interhemispheric VC connectivity. This disclosed a, to some extent, similar but also distinct short-term mechanism (vestibular stimulation) of an improvement of spatial orientation compared to the long-term recovery of neglect.</p

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Objective<p>Vestibular signals are involved in higher cortical functions like spatial orientation and its disorders. Vestibular dysfunction contributes, for example, to spatial neglect which can be transiently improved by caloric stimulation. The exact roles and mechanisms of the vestibular and visual systems for the recovery of neglect are not yet known.</p>Methods<p>Resting-state functional connectivity (fc) magnetic resonance imaging was recorded in a patient with hemispatial neglect during the acute phase and after recovery 6 months later following a right middle cerebral artery infarction before and after caloric vestibular stimulation. Seeds in the vestibular [parietal operculum (OP2)], the parietal [posterior parietal cortex (PPC); 7A, hIP3], and the visual cortex (VC) were used for the analysis.</p>Results<p>During the acute stage after caloric stimulation the fc of the right OP2 to the left OP2, the anterior cingulum, and the para/hippocampus was increased bilaterally (i.e., the vestibular network), while the interhemispheric fc was reduced between homologous regions in the VC. After 6 months, similar fc increases in the vestibular network were found without stimulation. In addition, fc increases of the OP2 to the PPC and the VC were seen; interhemispherically this was true for both PPCs and for the right PPC to both VCs.</p>Conclusion<p>Improvement of neglect after caloric stimulation in the acute phase was associated with increased fc of vestibular cortex areas in both hemispheres to the para-hippocampus and the dorsal anterior cingulum, but simultaneously with reduced interhemispheric VC connectivity. This disclosed a, to some extent, similar but also distinct short-term mechanism (vestibular stimulation) of an improvement of spatial orientation compared to the long-term recovery of neglect.</p

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Objective<p>Vestibular signals are involved in higher cortical functions like spatial orientation and its disorders. Vestibular dysfunction contributes, for example, to spatial neglect which can be transiently improved by caloric stimulation. The exact roles and mechanisms of the vestibular and visual systems for the recovery of neglect are not yet known.</p>Methods<p>Resting-state functional connectivity (fc) magnetic resonance imaging was recorded in a patient with hemispatial neglect during the acute phase and after recovery 6 months later following a right middle cerebral artery infarction before and after caloric vestibular stimulation. Seeds in the vestibular [parietal operculum (OP2)], the parietal [posterior parietal cortex (PPC); 7A, hIP3], and the visual cortex (VC) were used for the analysis.</p>Results<p>During the acute stage after caloric stimulation the fc of the right OP2 to the left OP2, the anterior cingulum, and the para/hippocampus was increased bilaterally (i.e., the vestibular network), while the interhemispheric fc was reduced between homologous regions in the VC. After 6 months, similar fc increases in the vestibular network were found without stimulation. In addition, fc increases of the OP2 to the PPC and the VC were seen; interhemispherically this was true for both PPCs and for the right PPC to both VCs.</p>Conclusion<p>Improvement of neglect after caloric stimulation in the acute phase was associated with increased fc of vestibular cortex areas in both hemispheres to the para-hippocampus and the dorsal anterior cingulum, but simultaneously with reduced interhemispheric VC connectivity. This disclosed a, to some extent, similar but also distinct short-term mechanism (vestibular stimulation) of an improvement of spatial orientation compared to the long-term recovery of neglect.</p

Feedback related negativity.

<p>Grand average waveforms of feedback-related visual evoked potentials for the maximum loss (red), maximum gain (black), minimum loss (green) and minimum gain (blue) condition showing the FRN effect with larger FRN amplitudes in response to loss feedback compared to gain feedback (onset of feedback stimuli at 0 ms). The scalp topography (derived from the peak amplitude of the difference waveform of maximum loss and maximum gain condition observed 270 ms after presentation of the feedback stimulus) shows a frontocentral maximum over Fz.</p

Paradigm.

<p>Schematic diagram showing the design of a trial of the gambling task used in this study.</p

Time frequency analysis.

<p>The comparison (difference) of the results of the time-frequency analysis of maximum loss and maximum gain conditions revealed theta, alpha and low-beta activity to be more pronounced in the maximum loss condition and delta and high-beta activity to be more pronounced in the maximum gain condition (onset of feedback stimuli at 0 ms). For all frequencies, we found frontocentral maxima of differences between conditions. The scalp topographies are derived from the peak amplitudes of the difference waveforms (maximum loss minus maximum gain condition) of the extracted frequency-specific wavelet layers (latencies: delta 150 ms; theta 340 ms; alpha 550 ms; low-beta 630 ms; high-beta 360 ms). The dotted lines indicate the frequencies of interest (from the bottom up: delta, theta, alpha, low-beta and high-beta).</p

Mean values of electrophysiological measures per condition and ANOVA results.

<p>Amplitudes are reported in µV; latencies are reported in milliseconds. n.s.  =  not significant.</p

Characteristics of the participant group.

<p>Characteristics of the participant group.</p