Objective: To evaluate the clinical pathophysiology of oculomotor changes in a patient presenting with a spontaneous semicircular horizontal canal plug.
Patient: A 42-year-old man with acute spontaneous vertigo with spinning and persistent left-horizontal nystagmus, intensity but not direction dependent on head orientation with respect to gravity, indicating a benign paroxysmal positional vertigo due to otoconia causing a plug in the horizontal semicircular canal.
Intervention: Electrophysiological and video-oculographic testing; vestibular rehabilitation.
Main Outcome Measures: Cervical and ocular vestibular evoked myogenic potentials (VEMPs); video head impulse testing.
Results: The video head-impulse test revealed an eye velocity cutoff at 80°/s in the time interval from 40 to 90 ms after initiation of head impulses to the right. This normalized within 2 days after liberatory maneuvers, documenting for the first time a reversible deficiency of the cupular-endolymph high-frequency system dynamics. Cervical and ocular vestibular myogenic potentials were absent during stimulation of the affected side before the liberatory maneuvers but normalized within 30 to 80 days.
Conclusion: This case is special in 4 respects: 1) nystagmus intensity, but not direction, was dependent on head orientation with respect to gravity, indicating a horizontal canal plug; 2) VEMPs were asymmetrical before liberatory maneuvers; 3) VEMPs recovered after Day 30; and 4) video head-impulse test asymmetry recovered. These observations challenge the common belief that VEMPs are evoked by otolith stimulation only. Instead, the assumption of a reversible canal dysfunction by a plug offers a more plausible explanation for all effects.
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http://dx.doi.org/10.1097/MAO.0b013e318287f343 | DOI Listing |
Clin Exp Optom
January 2025
Department of Optometry, School of Paramedical and Rehabilitation Sciences, Mashhad University of Medical Sciences, Mashhad, Iran.
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Biomater Adv
January 2025
Institute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan.
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Department of Pharmacy, Daegu Catholic University, 13-13 Hayang-ro, Hayang-eup, Gyeongsan-Si, Gyeongbuk 38430 Republic of Korea.
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Dizziness Center, Clinical Neuroscience Center, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
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Department of Biochemistry, Dongguk University College of Medicine, 123 Dongdae-ro, Gyeongju 38066, Republic of Korea.
Cortactin (CTTN) is an actin-binding protein regulating actin polymerization and stabilization, which are vital processes for maintaining skeletal muscle homeostasis. Despite the established function of CTTN in actin cytoskeletal dynamics, its role in the myogenic differentiation of progenitor cells remains largely unexplored. In this study, we investigated the role of CTTN in the myogenic differentiation of C2C12 myoblasts by analyzing its effects on actin cytoskeletal remodeling, myocardin-related transcription factor A (MRTFA) nuclear translocation, serum response factor (SRF) activation, expression of myogenic transcription factors, and myotube formation.
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