Abstract
Objectives: To reveal the neural basis of Wernicke's encephalopathy (WE) with impaired vestibulo-ocular reflex (VOR), we evaluated resting-state functional connectivity (rs-fc) in the vestibular processing brain regions.Methods: Rs-fc between the vestibular regions and the rest of the brain were compared with neurotological features including the head-impulse tests (vHIT) and caloric responses in patients with WE (n = 5, mean age 53.4 ± 10 years) and healthy controls (n = 20, mean age 55.0 ± 9.2 years). Rs-fc analyses employed a region of interest (ROI)-based approach using regions selected a priori that participate in vestibular processing including the cerebellar vermis, insula, parietal operculum, and calcarine cortex.Results: The main neurologic findings for patients with WE were mental changes; gait ataxia; spontaneous and gaze-evoked nystagmus (GEN); and bilaterally positive HIT for the horizontal canals. Video HIT documented bilateral horizontal canal dysfunction with decreased gain and corrective saccades. Caloric irrigation and rotation chair testing revealed prominent bilateral horizontal canal paresis. Patients with WE also had decreased spatial memory, which substantially recovered after treatments. Functional connections at the predefined seed regions, including the insular cortex and parietal operculum, were attenuated in the WE group compared to healthy controls.Conclusions: WE is related to impaired VOR and visuospatial dysfunction, and fMRI documented changes in the rs-fc of multisensory vestibular processing regions including the insula, parietal operculum, and superior temporal gyrus, which participate in integration of vestibular perception.
Highlights
Wernicke’s encephalopathy (WE) is an acute neuropsychiatric syndrome resulting from thiamine deficiency associated with many clinical conditions that impair thiamine absorption, including chronic alcohol abuse, gastrointestinal surgery, prolonged vomiting, chemotherapy, and systemic infectious and non-infectious diseases [1]
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The aim of this study was to evaluate the functional connectivity of vestibular processing areas related to WE in the presence of vestibular paresis by using a well-established, data-driven neuroimaging analysis method
Summary
Wernicke’s encephalopathy (WE) is an acute neuropsychiatric syndrome resulting from thiamine (vitamin B1) deficiency associated with many clinical conditions that impair thiamine absorption, including chronic alcohol abuse, gastrointestinal surgery, prolonged vomiting, chemotherapy, and systemic infectious and non-infectious diseases [1]. Findings of ocular abnormality include nystagmus, unilateral or bilateral palsy of any extraocular muscles and conjugate-gaze palsies, optic disc edema and retinal hemorrhages have been reported in patients with WE [2]. Vestibular dysfunction with an impaired horizontal vestibulo-ocular reflex (VOR) is another important feature of WE [1]. Rs-fc among different regions and between established networks can be atypical in patients with certain brain diseases [8]. Few studies have investigated actual temporal changes in the functional connectivity of specific brain regions in patients with WE and impaired vestibular function. We hypothesized that atypical rs-fc in vestibular processing brain regions may be associated with vestibular dysfunction in WE. The aim of this study was to evaluate the functional connectivity of vestibular processing areas related to WE in the presence of vestibular paresis by using a well-established, data-driven neuroimaging analysis method
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