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ABSTRACT: Vertigo in and around magnetic resonance imaging (MRI) machines has been noted for years [1, 2]. Several mechanisms have been suggested to explain these sensations [3, 4], yet without direct, objective measures, the cause is unknown. We found that all of our healthy human subjects developed a robust nystagmus while simply lying in the static magnetic field of an MRI machine. Patients lacking labyrinthine function did not. We use the pattern of eye movements as a measure of vestibular stimulation to show that the stimulation is static (continuous, proportional to static magnetic field strength, requiring neither head movement nor dynamic change in magnetic field strength) and directional (sensitive to magnetic field polarity and head orientation). Our calculations and geometric model suggest that magnetic vestibular stimulation (MVS) derives from a Lorentz force resulting from interaction between the magnetic field and naturally occurring ionic currents in the labyrinthine endolymph fluid. This force pushes on the semicircular canal cupula, leading to nystagmus. We emphasize that the unique, dual role of endolymph in the delivery of both ionic current and fluid pressure, coupled with the cupula's function as a pressure sensor, makes magnetic-field-induced nystagmus and vertigo possible. Such effects could confound functional MRI studies of brain behavior, including resting-state brain activity.
Current biology: CB 09/2011; 21(19):1635-40. · 10.99 Impact Factor
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Charles Chong-Hwa Hong,
James C Harris,
Godfrey D Pearlson,
Jin-Suh Kim,
Vince D Calhoun,
James H Fallon,
Xavier Golay, Joseph S Gillen,
Daniel J Simmonds,
Peter C M van Zijl,
David S Zee,
James J Pekar
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ABSTRACT: We studied the neural correlates of rapid eye movement during sleep (REM) by timing REMs from video recording and using rapid event-related functional MRI. Consistent with the hypothesis that REMs share the brain systems and mechanisms with waking eye movements and are visually-targeted saccades, we found REM-locked activation in the primary visual cortex, thalamic reticular nucleus (TRN), 'visual claustrum', retrosplenial cortex (RSC, only on the right hemisphere), fusiform gyrus, anterior cingulate cortex, and the oculomotor circuit that controls awake saccadic eye movements (and subserves awake visuospatial attention). Unexpectedly, robust activation also occurred in non-visual sensory cortices, motor cortex, language areas, and the ascending reticular activating system, including basal forebrain, the major source of cholinergic input to the entire cortex. REM-associated activation of these areas, especially non-visual primary sensory cortices, TRN and claustrum, parallels findings from waking studies on the interactions between multiple sensory data, and their 'binding' into a unified percept, suggesting that these mechanisms are also shared in waking and dreaming and that the sharing goes beyond the expected visual scanning mechanisms. Surprisingly, REMs were associated with a decrease in signal in specific periventricular subregions, matching the distribution of the serotonergic supraependymal plexus. REMs might serve as a useful task-free probe into major brain systems for functional brain imaging.
Human Brain Mapping 11/2008; 30(5):1705-22. · 5.88 Impact Factor
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ABSTRACT: To use combined proton (1H) and sodium 23 (23Na) magnetic resonance (MR) imaging to noninvasively quantify total tissue sodium concentration and to determine if concentration is altered in malignant human brain tumors.
Absolute tissue sodium concentration in malignant gliomas was measured on quantitative three-dimensional 23Na MR images with tissue identification from registered 1H MR images. Concentration was determined in gray matter (GM), white matter (WM), cerebrospinal fluid (CSF), and vitreous humor in 20 patients with pathologically proven malignant brain tumors (astrocytoma, n = 17; oligodendroglioma, n = 3) and in nine healthy volunteers. Sodium concentration in tumors and edema was determined from 23Na image signal intensities in regions that were contrast material enhanced on T1-weighted 1H images (tumors) or regions that were only hyperintense on fluid-attenuated inversion recovery (FLAIR) 1H images (edema). Sodium concentrations were measured noninvasively from 23Na images obtained with short echo times (0.4 msec) by using external saline solution phantoms for reference. Differences in mean sodium concentration of all healthy tissue and lesions in patients were tested with a paired t test. Concentration in uninvolved tissues in patients was compared with that in the same tissue types in the volunteers with an independent samples two-tailed t test.
Mean concentration (in millimoles per kilogram wet weight) was 61 +/- 8 (SD) for GM, 69 +/- 10 for WM, 135 +/- 10 for CSF, 113 +/- 14 for vitreous humor, 103 +/- 36 for tumor, 68 +/- 11 for unaffected contralateral tissue, and 98 +/- 12 for FLAIR hyperintense regions surrounding tumors. Significant differences (P <.002) in sodium concentration were demonstrated by using a t test for both tumors and surrounding FLAIR hyperintense tissues versus GM, WM, CSF, and contralateral brain tissue.
23Na MR imaging with short echo times can be used to quantify absolute tissue sodium concentration in patients with brain tumors and shows increased sodium concentration in tumors relative to that in normal brain structures.
Radiology 05/2003; 227(2):529-37. · 5.73 Impact Factor
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ABSTRACT: PURPOSE: To use combined proton (1H) and sodium 23 (23Na) magnetic resonance (MR) imaging to noninvasively quantify total tissue sodium concentration and to determine if concentration is altered in malignant human brain tumors. MATERIALS AND METHODS: Absolute tissue sodium concentration in malignant gliomas was measured on quantitative three-dimensional 23Na MR images with tissue identification from registered 1H MR images. Concentration was determined in gray matter (GM), white matter (WM), cerebrospinal fluid (CSF), and vitreous humor in 20 patients with pathologically proven malignant brain tumors (astrocytoma, n = 17; oligodendroglioma, n = 3) and in nine healthy volunteers. Sodium concentration in tumors and edema was determined from 23Na image signal intensities in regions that were contrast material enhanced on T1-weighted 1H images (tumors) or regions that were only hyperintense on fluid-attenuated inversion recovery (FLAIR) 1H images (edema). Sodium concentrations were measured noninvasively from 23Na images obtained with short echo times (0.4 msec) by using external saline solution phantoms for reference. Differences in mean sodium concentration of all healthy tissue and lesions in patients were tested with a paired t test. Concentration in uninvolved tissues in patients was compared with that in the same tissue types in the volunteers with an independent samples two-tailed t test. RESULTS: Mean concentration (in millimoles per kilogram wet weight) was 61 {+/-} 8 (SD) for GM, 69 {+/-} 10 for WM, 135 {+/-} 10 for CSF, 113 {+/-} 14 for vitreous humor, 103 {+/-} 36 for tumor, 68 {+/-} 11 for unaffected contralateral tissue, and 98 {+/-} 12 for FLAIR hyperintense regions surrounding tumors. Significant differences (P < .002) in sodium concentration were demonstrated by using a t test for both tumors and surrounding FLAIR hyperintense tissues versus GM, WM, CSF, and contralateral brain tissue. CONCLUSION: 23Na MR imaging with short echo times can be used to quantify absolute tissue sodium concentration in patients with brain tumors and shows increased sodium concentration in tumors relative to that in normal brain structures. (C) RSNA, 2003
Radiology. 227:529-537.
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ABSTRACT: PURPOSE: To use combined proton (1H) and sodium 23 (23Na) magnetic resonance (MR) imaging to noninvasively quantify total tissue sodium concentration and to determine if concentration is altered in malignant human brain tumors. MATERIALS AND METHODS: Absolute tissue sodium concentration in malignant gliomas was measured on quantitative three-dimensional 23Na MR images with tissue identification from registered 1H MR images. Concentration was determined in gray matter (GM), white matter (WM), cerebrospinal fluid (CSF), and vitreous humor in 20 patients with pathologically proven malignant brain tumors (astrocytoma, n = 17; oligodendroglioma, n = 3) and in nine healthy volunteers. Sodium concentration in tumors and edema was determined from 23Na image signal intensities in regions that were contrast material enhanced on T1-weighted 1H images (tumors) or regions that were only hyperintense on fluid-attenuated inversion recovery (FLAIR) 1H images (edema). Sodium concentrations were measured noninvasively from 23Na images obtained with short echo times (0.4 msec) by using external saline solution phantoms for reference. Differences in mean sodium concentration of all healthy tissue and lesions in patients were tested with a paired t test. Concentration in uninvolved tissues in patients was compared with that in the same tissue types in the volunteers with an independent samples two-tailed t test. RESULTS: Mean concentration (in millimoles per kilogram wet weight) was 61 {+/-} 8 (SD) for GM, 69 {+/-} 10 for WM, 135 {+/-} 10 for CSF, 113 {+/-} 14 for vitreous humor, 103 {+/-} 36 for tumor, 68 {+/-} 11 for unaffected contralateral tissue, and 98 {+/-} 12 for FLAIR hyperintense regions surrounding tumors. Significant differences (P < .002) in sodium concentration were demonstrated by using a t test for both tumors and surrounding FLAIR hyperintense tissues versus GM, WM, CSF, and contralateral brain tissue. CONCLUSION: 23Na MR imaging with short echo times can be used to quantify absolute tissue sodium concentration in patients with brain tumors and shows increased sodium concentration in tumors relative to that in normal brain structures. (C) RSNA, 2003
Radiology. 227:529-537.
