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![An order of visual stimuli for the gaze stability test. (i) Checkerboard pattern stimulus comprising 8 rows × 12 columns of squares reversed in contrast (100%) at 12 Hz. (ii) Optokinetic stimulus with 12 black-and-white vertical stripes sweeping across a screen at 6 s. (iii) Radial optic flow stimulus with moving white dots (size: 0.1∼1.1 degrees of visual angle, speed: 3 s with a flat speed gradient) on a black background expanding from the center of the screen. (A,B) A stationary gazing black dot (5 mm diameter fixation target subtending approximately 0.4 of visual angle) in the center of the light gray screen [RGB (211, 211, 211)].](publication/365748365/figure/fig1/AS:11431281102471043@1669470699871/An-order-of-visual-stimuli-for-the-gaze-stability-test-i-Checkerboard-pattern-stimulus.png)
An order of visual stimuli for the gaze stability test. (i) Checkerboard pattern stimulus comprising 8 rows × 12 columns of squares reversed in contrast (100%) at 12 Hz. (ii) Optokinetic stimulus with 12 black-and-white vertical stripes sweeping across a screen at 6 s. (iii) Radial optic flow stimulus with moving white dots (size: 0.1∼1.1 degrees of visual angle, speed: 3 s with a flat speed gradient) on a black background expanding from the center of the screen. (A,B) A stationary gazing black dot (5 mm diameter fixation target subtending approximately 0.4 of visual angle) in the center of the light gray screen [RGB (211, 211, 211)].
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Introduction
Persistent postural-perceptual dizziness (PPPD) is a chronic vestibular syndrome lasting more than 3 months. The core vestibular symptoms are dizziness, unsteadiness, and non-spinning vertigo, which are exacerbated by upright posture or walking, active or passive motion, and exposure to moving or complex visual stimuli. Among these, vi...
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Context 1
... order of the stimuli in the gaze stability test is shown in Figure 1. Moving visual stimuli, which consisted of (i) a checkerboard pattern stimulus comprising 8 rows × 12 columns of squares reversed in contrast (100%) at 12 Hz, (ii) optokinetic stimulus by 12 black-and-white vertical stripes sweeping across a screen at 6 s, and (iii) radial optic flow stimulus with moving white dots (size: 0.1∼1.1 degrees of visual angle, speed: 3 s with a flat speed gradient) on a black background expanding from the center of the screen, were continuously presented on a PC screen for 30 s each. ...
Context 2
... < 0.0001) (BCEA; F = 10.8, p < 0.01) (Supplementary Table 3). Supplementary Figure 1 shows the results of the post-hoc Tukey test comparing the SD horizontal gaze position and BCEA during exposure to moving visual stimuli among the three moving visual stimuli. The SD horizontal gaze position was significantly higher during optokinetic stimulus by vertical stripes than during checkerboard and optic flow stimuli in all three groups. ...
Citations
... A current model hypothesizes that PPPD may involve functional disruptions at the cortical network level, affecting systems related to motion perception, postural control, locomotion, and spatial orientation [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]. Such disruptions could potentially contribute to the characteristic dizziness observed in PPPD [5], and may also manifest as heightened attention to motion [9], misperception of movement [25], altered posture [24], increased effort in postural control [26], heightened dependence on visual input [27], and compromised spatial navigation [12], among others [5]. ...
(1) Background: Persistent postural-perceptual dizziness (PPPD) is a common chronic dizziness disorder with an unclear pathophysiology. It is hypothesized that PPPD may involve disrupted spatial cognition processes as a core feature. (2) Methods: A cohort of 19 PPPD patients underwent psycho-cognitive testing, including assessments for anxiety, depression, memory, attention, planning, and executive functions, with an emphasis on spatial navigation via a virtual Morris water maze. These patients were compared with 12 healthy controls and 20 individuals with other vestibular disorders but without PPPD. Vestibular function was evaluated using video head impulse testing and vestibular evoked myogenic potentials, while brain magnetic resonance imaging was used to exclude confounding pathology. (3) Results: PPPD patients demonstrated unique impairments in allocentric spatial navigation (as evidenced by the virtual Morris water maze) and in other high-demand visuospatial cognitive tasks that involve executive functions and planning, such as the Towers of London and Trail Making B tests. A factor analysis highlighted spatial navigation and advanced visuospatial functions as being central to PPPD, with a strong correlation to symptom severity. (4) Conclusions: PPPD may broadly impair higher cognitive functions, especially in spatial cognition. We discuss a disruption in the creation of enriched cognitive spatial maps as a possible pathophysiology for PPPD.
Persistent Postural-Perceptual Dizziness (PPPD) is often secondary to vestibular disorders such as Benign Paroxysmal Positional Vertigo (BPPV) and Meniere's disease. However, PPPD secondary to vestibular disorders is often not correctly diagnosed.
The Niigata PPPD Questionnaire (NPQ) was created for to screen for PPPD, but its usefulness for evaluating the symptoms of PPPD has not yet been clearly elucidated.
A 49-year-old man with paroxysmal vertigo had been treated medically for 20 years as a case of Meniere's disease. He had had persistent dizziness 3 years before even in the intermittent periods [not sure what this means?] and he took long? leave of absence from his job one year prior to his first visit to us. As his score on the NPQ was 43 (cutoff score, 27), we suspected of PPPD secondary to Meniere's disease. Because the scores on the Hospital Anxiety and Depression Scale (HADS) were high, he was prescribed serotonin and noradrenaline reuptake inhibitors (SNRIs). In response to this treatment, his symptoms improved and his score on the NPQ dropped to 20. However, 3 months after he returned to work, the paroxysmal vertigo episodes reappeared. As the score on the NPQ remained as low as 26, we considered that the PPPD was well controlled and the paroxysmal vertigo represented flare-up of only Meniere's disease. Subsequently, the Meniere's attacks improved with lifestyle guidance alone.
In summary, we report a case of PPPD secondary to Meniere's disease in which the vertigo episodes were diagnosed as a manifestation of Meniere's disease for a long period of time, despite the presence of typical symptoms of PPPD. NPQ was useful for diagnosing PPPD and evaluating the cause of the vertigo in this patient, which remained stable even in the presence of frequent attacks of Meniere's disease.
