White matter volume loss drives cortical reshaping after thalamic infarcts.

OBJECTIVE: The integration of somatosensory, ocular motor and vestibular signals is necessary for self-location in space and goal-directed action. We aimed to detect remote changes in the cerebral cortex after thalamic infarcts to reveal the thalamo-cortical connections necessary for multisensory processing and ocular motor control. METHODS: Thirteen patients with unilateral ischemic thalamic infarcts presenting with vestibular, somatosensory, and ocular motor symptoms were examined longitudinally in the acute phase and after six months. Voxel- and surface-based morphometry were used to detect changes in vestibular and multisensory cortical areas and known hubs of central ocular motor processing. The results were compared with functional connectivity data in 50 healthy volunteers. RESULTS: Patients with paramedian infarcts showed impaired saccades and vestibular perception, i.e., tilts of the subjective visual vertical (SVV). The most common complaint in these patients was double vision or vertigo / dizziness. Posterolateral thalamic infarcts led to tilts of the SVV and somatosensory deficits without vertigo. Tilts of the SVV were higher in paramedian compared to posterolateral infarcts (median 11.2° vs 3.8°). Vestibular and ocular motor symptoms recovered within six months. Somatosensory deficits persisted. Structural longitudinal imaging showed significant volume reduction in subcortical structures connected to the infarcted thalamic nuclei (vestibular nuclei region, dentate nucleus region, trigeminal root entry zone, medial lemniscus, superior colliculi). Volume loss was evident in connections to the frontal, parietal and cingulate lobes. Changes were larger in the ipsilesional hemisphere but were also detected in homotopical regions contralesionally. The white matter volume reduction led to deformation of the cortical projection zones of the infarcted nuclei. CONCLUSIONS: White matter volume loss after thalamic infarcts reflects sensory input from the brainstem as well the cortical projections of the main affected nuclei for sensory and ocular motor processing. Changes in the cortical geometry seem not to reflect gray matter atrophy but rather reshaping of the cortical surface due to the underlying white matter atrophy.

Cortical alterations in phobic postural vertigo - a multimodal imaging approach.

OBJECTIVE: Functional dizziness syndromes are among the most common diagnoses made in patients with chronic dizziness, but their underlying neural characteristics are largely unknown. The aim of this neuroimaging study was to analyze the disease-specific brain changes in patients with phobic postural vertigo (PPV). METHODS: We measured brain morphology, task response, and functional connectivity in 44 patients with PPV and 44 healthy controls. RESULTS: The analyses revealed a relative structural increase in regions of the prefrontal cortex and the associated thalamic projection zones as well as in the primary motor cortex. Morphological increases in the ventrolateral prefrontal cortex positively correlated with disease duration, whereas increases in dorsolateral, medial, and ventromedial prefrontal areas positively correlated with the Beck depression index. Visual motion stimulation caused an increased task-dependent activity in the subgenual anterior cingulum and a significantly longer duration of the motion aftereffect in the patients. Task-based functional connectivity analyses revealed aberrant involvement of interoceptive, fear generalization, and orbitofrontal networks. INTERPRETATION: Our findings agree with some of the typical characteristics of functional dizziness syndromes, for example, excessive self-awareness, anxious appraisal, and obsessive controlling of posture. This first evidence indicates that the disease-specific mechanisms underlying PPV are related to networks involved in mood regulation, fear generalization, interoception, and cognitive control. They do not seem to be the result of aberrant processing in cortical visual, visual motion, or vestibular regions.