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Volume 8 Suppl 1 December 2009
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Taking a History From the Dizzy Patients
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Byung-Kun Kim
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Res Vestib Sci. 2009;8(Suppl 1):7-15.
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Abstract
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- Vertigo, defined as an illusion of the movement, always indicates an imbalance within the vestibular system. The same sensation can result from lesions in such diverse locations as the inner ear, the visual-vestibular interaction centers in the brainstem and cerebellum, or the subjective sensation pathways of the thalamus or cortex. Many neuro-otological disease, such as benign paroxysmal positional vertigo, vestibular neuritis, Meniere’s disease, stroke, migraine, phobic postural vertigo etc., can cause vertigo. The peripheral and central causes of vertigo can usually be distinguished based on other features in the history, which are discussed in detail. Research in Vestibular Science 2009;8(2 suppl 1):S7-S15
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Bedside Otologic Examination
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Won-Ho Chung
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Res Vestib Sci. 2009;8(Suppl 1):16-17.
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Bedside Neurologic Examination of Dizzy Patients
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Ji Soo Kim
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Res Vestib Sci. 2009;8(Suppl 1):18-21.
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Abstract
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- Differentiating peripheral from central pathology is most important in clinical practice of dizziness. The bedside examination for dizziness should include a systematic study of spontaneous and evoked nystagmus, head impulse test, evaluation of the ocular motilities including saccades, smooth pursuit, and optokinetic nystagmus. Examination of the balance and coordination function may disclose dysfunction of the cerebellar system. In contrast to the nystagmus of peripheral origin, the central nystagmus may show various patterns. Usually pure vertical and torsional nystagmus, direction-changing nystagmus, and nystagmus not suppressed by fixation indicates a central pathology. In case of positioning/ positional nystagmus which does not follow the characteristic patterns of benign paroxysmal positional vertigo and does not respond to repeated canalith repositioning maneuvers, a possibility of central positional vertigo should be considered. The patterns of head-shaking nystagmus (HSN) from central lesions include an unusually strong HSN elicited by weak head-shaking, initially ipsilesional HSN, strongly biphasic HSN, strong HSN in patients without caloric paresis, HSN in the opposite direction of spontaneous nystagmus and perverted HSN (e.g. downbeat nystagmus after horizontal head-shaking). Head impulse test is mostly negative in the central vestibulopathies, even in the presence of vertigo and spontaneous nystagmus. Disorders of ocular motility and coordination, and severe imbalance also suggest central lesions. Careful bedside evaluation provides valuable information on the underlying pathology of dizziness. Research in Vestibular Science 2009;8(2 suppl 1):S18-S21
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Laboratory Tests for Semicircular Canal Function
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Sung Won Chae
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Res Vestib Sci. 2009;8(Suppl 1):22-30.
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Abstract
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- The semicircular canals sense angular acceleration and are arranged in roughly parallel pairs. The vestibuloocular reflex (VOR) is responsible for maintaining binocular fixation and stabilizing binocular foveal images during head movements. The VORs are divided into two types: angular and linear. Angular reflexes are initiated by activation of the semicircular canals. There are several kinds of test for semicircular canal function such as caloric test, rotation test, and pulse step sine test. Caloric testing remains the most useful laboratory test in determining the responsiveness of a labyrinth. It is one of the few tests that allow one labyrinth to be studied independently of the other. The stimulus can be applied relatively easily with techniques that are commonly available. Caloric testing relies on stimulating or cooling the vestibular system by alternately heating and cooling the external auditory canal with water or air. Rotational tests analyze the responses of both labyrinths together. They require a high-torque motor-driven chair and relatively advanced software to analyze the results. Rotatory chair testing is useful in assessing vestibular function in patients with suspected bilateral vestibular hypofunction and children. Step changes in head velocity can be used instead of sinusoidal rotations to identify vestibular hypofunction. Time constant are determined by the time after onset of the stimulus at which slow phase eye velocity has decreased by 67% of its initial value. The use of a novel “pulse-step-sine” (PSS) rotational stimulus can identify abnormal function of the horizontal semicircular canals in human subjects with unilateral and bilateral vestibular deficits.
Research in Vestibular Science 2009;8(2 suppl 1):S22-S30
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Laboratory Tests for Otolith Function
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Jae Yun Jung, Myung-Whan Suh, Chung-ku Rhee
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Res Vestib Sci. 2009;8(Suppl 1):31-36.
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Colocalization of 5-HT1F Receptor and Calcitonin Gene-Related Peptide in Rat Vestibular Nuclei
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Seong-Ki Ahn, Roza Khalmuratova, Sea-Yuong Jeon, Jin-Pyeong Kim, Jung Je Park, Dong Gu Hur
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Res Vestib Sci. 2009;8(Suppl 1):51-57.
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Abstract
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- Background and Objective: The frequent co-occurrence of migraine and balance disorders suggests a pathophysiologic link between the two. 5-HT1F receptor agonists and CGRP receptor antagonists have recently attracted attention as potential treatments for migraine, and CGRP release from trigeminal neurons has been associated with migraine. The aim of this study was to determine whether CGRP colocalizes with 5-HT1F receptor in rat vestibular nuclei using a double immunohistochemical staining procedure.
Materials and Methods: Male S-D rats were used in this study. Double immunofluorescence was employed to identify the colocalization of 5-HT1F receptor and CGRP in vestibular nuclei using alternating brainstem sections. In addition, other sections of rat brain were processed to visualize the cellular localizations of 5-HT1F receptor and CGRP in vestibular nuclei, so as to allow comparisons of the regional distributions of 5-HT1F receptor and CGRP. In order to perform semi-quantitative analysis on doubly labeled and singly labeled neurons, 4 randomly selected areas were chosen. Stained cells were counted in the superior vestibular nucleus, the medial vestibular nucleus, the lateral vestibular nucleus, and the spinal vestibular nucleus.
Results: Immunopositive neurons for 5-HT1F receptor and CGRP were immunopositive neurons were widely distributed throughout the 4 major vestibular nuclei, respectively. 5-HT1F receptor and CGRP co-expression was observed in the 4 major vestibular nuclei.
Conclusions: This study suggests that 5-HT1F receptor regulates the release of CGRP from vestibular nuclei. This finding indicates that 5-HT1F receptor agonists may ameliorate migrainous vertigo by attenuating elevated levels of CGRP release from vestibular nuclei.
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Typical Patterns of Positional Nystagmus in Acute and Subacute Vestibular Neuritis
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Do-Joon Lee, Jae-Yoon Jung, Jung-Ku Lee, Myung-Whan Suh
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Res Vestib Sci. 2009;8(Suppl 1):61-64.
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Abstract
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- Background and Objective: When vestibular neuritis (VN) is suspected, we are generally not interested in the amplitude change of nystagmus according to the positional change. It is because positional nystagmus is not essential in diagnosing VN. But there might be a typical pattern of amplitude change of positional nystagmus also in these patients. If we understand this pattern of nystagmus change, it might be helpful in diagnosing subacute VN when spontaneous nystagmus is not present. Also it may be helpful in distinguishing VN from other diseases that can accompany non-specific positional nystagmus such as migraine associated dizziness. Accordingly, we aimed to find a typical pattern of amplitude change in positional nystagmus in VN patients. We especially aimed to affirm this typical pattern of positional nystagmus in subacute VN as well as in acute VN.
Materials and Methods: From 2002 through 2008, the videonystagmography of 182 patients who were diagnosed as VN were retrospectively reviewed. Only the patients who presented with an acute spinning vertigo lasting for more than several hours and who were confirmed of unilateral vestibular hypofunction though either caloric test or rotation chair test were included. The patients were divided into acute or subacute VN by the presence or absence of spontaneous nystagmus (SN). The amplitude of nystagmus was compared between the ipsilesional head roll test (iHRT) and contralesional HRT (cHRT). In order to exclude the effect of neck proprioception, that of the ipsilesional body roll test (iBRT) and cBRT was also compared.
Results: Among the 182 patients, 135 were classified as acute VN, and 47 as subacute VN. In the acute VN group, a stronger nystagmus was elicited when the head (p<0.01) and body (p<0.01) was turned to the ipsilesional side. The mean amplitude of nystagmus during iHRT (6.3°/sec) and iBRT (6.6°/sec) was significantly greater than that during cHRT (4.7°/sec) and, cBRT (4.5°/sec) respectively (p<0.01, p<0.01). In the subacute VN group, a stronger nystagmus was elicited when the body (p<0.02) was turned to the ipsilesional side but it was not true during HRT (p=0.35). Also, the positional nystagmus during iHRT (1.8°/sec) and iBRT (2.3°/sec) had no significant difference with that during cHRT (1.8°/sec) and, cBRT (1.3°/sec) respectively.
Conclusions: In acute VN, the positional nystagmus becomes stronger when the head or body is turned to the ipsilesional side compared to the contralesional side. But this typical pattern of positional nystagmus is not evident in subacute VN. The typical pattern of positional nystagmus, which can be found in acute VN, may not be helpful in diagnosing subacute VN.