Patients with vestibular migraine are susceptible to motion sickness. This study aimed to determine whether the severity of posture instability is related to the susceptibility to motion sickness. We used a visual motion paradigm with two conditions of the stimulated retinal field and the head posture to quantify postural stability while maintaining a static stance in 18 patients with vestibular migraine and in 13 age-matched healthy subjects. Three parameters of postural stability showed differences between VM patients and controls: RMS velocity (0.34 ± 0.02 cm/s vs. 0.28 ± 0.02 cm/s), RMS acceleration (8.94 ± 0.74 cm/s2 vs. 6.69 ± 0.87 cm/s2), and sway area (1.77 ± 0.22 cm2 vs. 1.04 ± 0.25 cm2). Patients with vestibular migraine showed marked postural instability of the head and neck when visual stimuli were presented in the retinal periphery. The pseudo-Coriolis effect induced by head roll tilt was not responsible for the main differences in postural instability between patients and controls. Patients with vestibular migraine showed a higher visual dependency and low stability of the postural control system when maintaining quiet standing, which may be related to susceptibility to motion sickness.
We investigated gait performance utilizing a quantitative gait analysis for 2 groups: (1) idiopathic normal-pressure hydrocephalus (INPH) patients who had a positive response to the cerebrospinal fluid tap test (CSFTT) and (2) healthy controls. The aims of the study were (1) to analyze the characteristics of gait features, (2) to characterize changes in gait parameters before and after the CSFTT, and (3) to determine whether there was any relationship between stride time and stride length variability and Frontal Assessment Battery (FAB) scores in INPH patients. Twenty-three INPH patients and 17 healthy controls were included in this study. Compared with healthy controls, the gait of INPH patients was characterized by lower velocity, shorter stride length, and more broad-based gait. Patients with INPH had a longer stance phase with increased double-limb support. Variability in stride time and stride length was increased in INPH patients. Stride time and stride length variability were correlated with FAB score. After the CSFTT, gait velocity, stride length, and step width significantly improved. There were significant decreases in stride time and stride length variability. These results suggest that the CSFTT for INPH patients might improve the so-called balance-related gait parameter (ie, step width) as well. Stride time and stride length variability also responded to the CSFTT. Association between FAB scores and both stride time and stride length variability suggests involvement of similar circuits producing gait variability and frontal lobe functions in INPH patients.
Purpose: Patients with benign paroxysmal positional vertigo (BPPV) experience gait unsteadiness not only during the attacks but also between the spells. This study aimed to measure gait changes in BPPV and determine whether these changes are associated with the involved canal or lesion side.Methods: We recruited 33 patients with a diagnosis of unilateral BPPV. Patients with other vestibular or central nervous system disorders were excluded. Gait was assessed using the GAITRite™ system before and after canalith repositioning treatment (CRT).Results: After CRT, improvements were observed in various gait parameters including velocity (p < 0.001), cadence (p < 0.001), functional ambulation profile (p = 0.011), and the coefficient of variation of stride time (p = 0.004). Exploration of the center of pressure (COP) distribution also revealed improved stabilization during locomotion after CRT. The spatiotemporal gait variables did not differ between the patients with horizontal- and posterior-canal BPPV, or between the ipsilesional and contralesional sides before CRT.Conclusions: The gait parameters reflecting velocity and rhythmicity along with stability of COP distribution improved after the resolution of BPPV. Episodic overexcitation of semicircular canal may impair the vestibular information that is integrated with the other reference afferent systems and lead to impaired gait performance.
We investigated differences in cortical thickness between idiopathic normal-pressure hydrocephalus (INPH) patients and healthy controls. We also explored whether a relationship exists between cortical thinning and gait disturbance in INPH patients. Forty-nine INPH patients and 26 healthy controls were imaged with MRI, including 3-dimensional volumetric images, for automated surface-based cortical thickness analysis across the entire brain. Compared with age- and gender-matched healthy controls, unexpectedly, INPH patients showed statistically significant cortical thickening mainly in areas located in the high convexity of the frontal, parietal, and occipital regions. Additionally, cortical thinning mainly in temporal and orbitofrontal regions was observed in the INPH group relative to the control group. The Gait Status Scale (GSS) scores were negatively correlated with cortical thickness in the medial orbital part of the superior frontal gyrus, gyrus rectus, superior temporal gyrus, temporal pole, and insula. A distinctive pattern of cortical thickness changes was found in INPH patients. We cautiously suggest that cortical thickening in INPH can result from reactive gliosis. Further, our results support the hypothesis that cortical thinning in INPH can result from neuronal degeneration. In addition, cortical thinning can play an important role in gait disturbances in INPH patients.
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