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Initiation of Smooth Pursuit in Acute Cerebellar Infarction: A Preliminary Study
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Tae Ho Yang, Sun Young Oh
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Res Vestib Sci. 2013;12(2):47-53.
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 Abstract
- Background and Objectives: The cerebellar lesion causes an initiation deficit of smooth-pursuit eye movement depending on the location of the lesion. We investigated the initiation of smooth pursuit in patients with cerebellar infarction and in healthy subjects, using step-ramp stimuli. Materials and Methods: Ten patients with cerebellar infarction documented by brain magnetic resonance imaging and fifty healthy subjects are recruited. To estimate the initiation of smooth pursuit, the onset latency and initial acceleration during the first 100ms of the horizontal smooth pursuit were estimated using the step-ramp target stimuli (5°/sec, 10°/sec, and 20°/sec). Results: In healthy subjects, onset latency of pursuit was shortened and initial acceleration was increased as target velocity was increasing. In patients with unilateral cerebellar infarction, the onset latency of ipsilesional smooth pursuit was significantly delayed at the target velocities of 10°/sec and 20°/sec. For the fast target velocity of 20°/sec, there was significant decrease of the initial acceleration of contralesional pursuit. Conclusion: In comparison with the healthy subjects, the patients with unilateral cerebellar lesions showed significant delay of pursuit onset and decrease of initial eye acceleration in the fast target velocity. These results support that the cerebellar lesions affect not only steady-state smooth pursuit gain but also the processing time required to initiate smooth pursuit, i.e., onset latency and initial acceleration. More extensive study is needed to confirm the role of cerebellum for parametric adjustment of each component of smooth pursuit.
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Ocular Vestibular Evoked Myogenic Potentials Produced by Stimulation With Bone-conducted Vibration in Healthy Subjects
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Tae Ho Yang, Sun Young Oh, Tae Woo Kim, Byoung Soo Shin, Jun Young Lee, Seul Ki Jeong, Man Wook Seo
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Res Vestib Sci. 2012;11(3):97-104.
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Abstract
- Background and Objectives: To provide the empirical basis for using ocular vestibular evoked myogenic potentials (oVEMPs) in response to bone-conducted vibration (BCV) stimulation to indicate vestibular function in normal subjects. Materials and Methods: In response to bone-conducted tone burst (90 dB nHL and 100 dB nHL with frequencies 500 Hz and 1,000 Hz, the oVEMPs were measured in 45 healthy controls. The early negative component (n10) of the oVEMP to brief BCV of the forehead and at each mastoid process is recorded by surface electromyography electrodes just beneath the eyes. We used a hand-held vibrator (Bruel and Kjaer 4810 Mini-Shaker) placed on the forehead, in the midline at the hairline (Fz) and at each mastoid process and quantified the individual differences in n10 magnitude, latency and symmetry to Fz and mastoid BCV at each frequency. Results: In normal subjects, n10 responses were symmetrical in the two eyes during Fz and both mastoid stimuli and the latencies of the onset were consistent among subjects. Response rate is similar between Fz and mastoid stimuli. However, at each stimulation site, response rate is higher on 500 Hz than on 1,000 Hz stimulation. During the mastoid stimuli, the onset latency is slightly shorter and amplitude is larger than the Fz stimuli. The average amplitudes decreased with age and average latency (to peak) increased slightly with increasing age. Conclusion: Clear oVEMP responses to bone-conducted Fz and mastoid stimuli were evoked from normal subjects. It is concluded that bone-conducted stimuli as well as air conduction can evoke myogenic potentials from the ocular muscles.
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Pathophysiology of Vestibular Migr
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Sun Young Oh, Tae Ho Yang
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Res Vestib Sci. 2012;11(3):81-87.
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Abstract
- Vestibular migraine (VM) is an increasingly recognized cause of episodic recurrent vertigo. However, the pathophysiology of VM is still a matter of speculation. An understanding of the relationship between migraine and the vestibular system increases knowledge of the pathogenesis of both migraine and vertigo. The pathophysiology of VM has been known to be related to cortical spreading depression, neurotransmitters (i.e., serotonin, noradrenaline, dopamine, calcitonin gene-related peptide) and calcium ion channel disorder. Moreover, VM is related with Meniere's disease, benign paroxysmal positional vertigo, motion sickness, cerebellar dysfunction, or comorbid psychotic disorder. This review refines recently proposed pathophysiological concept for VM and relationships between migraine and other related disorders.
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