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Volume 10 Suppl 1 June 2011
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Vestibular Neuritis: Current Principles of the Assessment and the Diagnosis
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Jae Ho Ban1, Yong-Hwi An2
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Res Vestib Sci. 2011;10(Suppl 1):3-8.
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Abstract
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- Vestibular neuritis presents as a sudden onset of rotary vertigo with associated nausea, vomiting, and generalized imbalance. In general, the dizziness lasts from a few hours to several days with gradual, definite improvement throughout the course. Vestibular neuritis is now considered to be the more accurate term for cases that do not involve hearing loss. The diagnosis of vestibular neuritis depends on the history of spontaneous, prolonged vertigo, physical findings that are consistent with a unilateral peripheral vestibular paralysis, and the absence of other neurological symptoms and signs. History and physical examination alone are usually adequate for diagnosis, although one must ensure that a central insult is not at fault. Relevant differential diagnoses are pseudo-vestibular neuritis due to acute pontomedullary brainstem lesions or cerebellar nodular infarctions, vestibular migraine, sudden sensorineural hearing loss accompanies vertigo with a vestibular neuritis-like pattern and monosymptomatically beginning Meniere's disease. Vestibular function tests including caloric test, vestibular evoked myogenic potential are useful to identify the side of involvement and to localize the pathology to the inferior or superior vestibular nerve.
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Pseudo-vestibular Neuritis
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Jae-Hwan Choi, Kwang-Dong Choi
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Res Vestib Sci. 2011;10(Suppl 1):9-12.
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Abstract
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- Acute vestibular syndrome is the rapid onset of vertigo, nausea, and vomiting (with nystagmus, unsteady gait, and head motion intolerance) over seconds-hours, lasting days-weeks. This presumed-viral, peripheral vestibular disorder is known as vestibular neuritis (without auditory symptoms), labyrinthitis (with auditory symptoms), generically acute peripheral vestibulopathy (APV). Most acute vestibular patients have APV, but some have an acute central vestibular syndrome resulting from lesions affecting the pons (the root entry zone of the vestibular nerve, vestibular fascicle, vestibular nucleus), inferior cerebellum (uvula and nodulus), or vestibular cortex (insula). Clinically, it is important to differentiate central vestibular syndrome from APV, because it can produce cerebellar swelling that can lead to brainstem compression and death unless there is neurosurgical intervention. The type of nystagmus evident on examination had been said to differentiate APV from central vestibulopathy, but assessment of nystagmus alone cannot distinguish all cases, and perhaps half of patients with pseudo-vestibular neuritis have unidirectional nystagmus mimicking APV. Therefore, in patients with acute vestibular syndrome, no improvement within 48 hours, abnormal neurological signs, severe headache, profound postural imbalance, unilateral hearing loss, normal head impulse test, and central patterns on vestibular function tests suggest a pseudo-vestibular neuritis.
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Diagnosis of Benign Paroxysmal Positional Vertigo
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Jong Dae Lee
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Res Vestib Sci. 2011;10(Suppl 1):13-18.
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Abstract
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- Benign paroxysmal positional vertigo (BPPV) is the most common cause of recurrent vertigo and is a clinical disorder characterized by brief recurrent spells of vertigo often brought about by certain head position changes as may occur with looking up, turning over in bed, or straightening up after bending over. The diagnosis of BPPV can be made based upon the history and examinations such as Dix– Hallpike test and supine roll test.
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Central Positional Vertigo
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Tae-Kyeong Lee
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Res Vestib Sci. 2011;10(Suppl 1):19-23.
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Abstract
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- Positional and positioning vertigo and nystagmus syndromes are usually caused by benign paroxysmal positional vertigo (BPPV). However, it has been recognized sinister central disorders can also lead to positional vertigo and nystagmus in rare occasions. Central positional vertigo (CPV) and nystagmus (CPN) can be caused by cerebellar dorsal vermis lesion, tumors or hemorrhage on the dorsolateral region of the fourth ventricle, degenerative disorders involving cerebellum, and sometimes in migraine. Therefore, the differentiation of benign positional vertigo from sinister central one is important in clinical practice. In the presence of accompanying signs and symptoms suggesting cerebellar or brainstem involvement, the differentiation is straightforward. However, some cases of CPV show only positional vertigo syndrome without accompanying signs or with subtle abnormalities. Efforts have been made to distinguish central from peripheral positional vertigo by clinical features, but only the direction of nystagmus during an attack could allow differentiation. The mechanism of CPN from case-series and animal studies has been postulated the interruption of cerebellar modulation of gravitational pathways by the lesions in dorsal vermis or near the vestibular nucleus. This paper reviewed the clinical characteristics of CPV mainly focused on the differentiation from BPPV.
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Management of Benign Paroxysmal Positional Vertigo
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Yun-Hoon Choung, DDS, Hye Jin Lim
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Res Vestib Sci. 2011;10(Suppl 1):27-31.
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Rehabilitation of Vestibular Hypofunction
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Do-Joon Lee, Chung-Ku Rhee, Myung-Whan Suh
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Res Vestib Sci. 2011;10(Suppl 1):32-37.
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Abstract
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- Vestibular rehabilitation therapy is an exercised-based approach to treat individuals with vestibular hypofunction. Vestibular hypofunction may not restore fully, but central compensation in combination with sensory substitution is thought to reduce impairment and vertiginous symptom. Vestibular rehabilitation therapy can improve the functional balance, stabilize the ocular reaction and decrease the disequilibrium. The m ajor m echanism of vestibular rehabilitation therapy is thought to be compensation, adaptation, and substitution. In this article we aimed to answer several questions related to vestibular rehabilitation therapy. The questions are; what is the evidence of vestibular rehabilitation therapy, what is the indication of vestibular rehabilitation therapy, otolithic dysfunction and vestibular rehabilitation therapy, how to rehabilitate the vesibulospinal reflex, the role of virtual reality in vestibular rehabilitation therapy, the role of medication in vestibular rehabilitation therapy, difference between self directed home exercise and supervised directed exercise, optimal duration of vestibular rehabilitation therapy, and the role of vestibular therapeutist in vestibular rehabilitation therapy.
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Managements for Vestibular Migraine
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Byung-Kun Kim
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Res Vestib Sci. 2011;10(Suppl 1):38-43.
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Abstract
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- Although vestibular migraine is the most common cause of non-positional recurrent vertigo, well designed clinical trials are not yet available. Treatment for vestibular migraine generally follows the recommended treatment of migraine. Management includes dietary and lifestyle modifications and medications. In this review, preventive treatment with beta blockers, calcium channel blockers, antiepileptic drugs and antidepressants, as well as acute treatment with non-steroidal anti-inflammatory drugs and triptans are described.
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Therapy for Nystagmus
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Sun-Young Oh1,2, Tae-Woo Kim2
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Res Vestib Sci. 2011;10(Suppl 1):44-49.
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Abstract
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- Nystagmus often causes decreased visual acuity as a direct result of the inability to maintain stable foveal vision. The eye movements themselves do not require treatment if the patient is asymptomatic. However, therapy is necessary if visual disability is present. Treatments are included pharmacologic treatment, optical devices, and operation. There are few controlled treatment trials for therapeutic efficacy. Recently, treatment with 3, 4-diaminopyridine and 4-aminopyridine have been shown to be effective for downbeat and upbeat nystagmus. Gabapentin, baclofen, and clonazepam also are useful in patients with downbeat nystagmus. Baclofen is the therapy of choice for periodic alternating nystagmus. Gabapentin often is effective for acquired pendular nystagmus. Clonazepam and valproate also may be effective for acquired pendular nystagmus. Memantine is promising in the treatment of pendular nystagmus. Optical devices that negate the negative effects of nystagmus continue to undergo development research. These and other medical, surgical, and optical devices are potentially useful alone or in combination with other therapies.
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Management for Psychogenic Vertigo
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Eun-Ho Kang
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Res Vestib Sci. 2011;10(Suppl 1):50-54.
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A Practical Approach to Dizziness
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Bronstein AM, FRCP
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Res Vestib Sci. 2011;10(Suppl 1):61-61.
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Benign Paroxysmal Positional Vertigo
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Sung Huhn Kim
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Res Vestib Sci. 2011;10(Suppl 1):75-79.
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Treatment for Menière's disease: Evidence Based Medicine
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Dong Hyun Kim, Sung Kwang Hong
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Res Vestib Sci. 2011;10(Suppl 1):81-84.
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Diagnosis and Treatment of Vascular Vertigo
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Sun-Young Oh
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Res Vestib Sci. 2011;10(Suppl 1):85-92.
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Abstract
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- Acute vestibular syndrome is often due to vestibular neuritis but can result from vertebrobasilar strokes. Misdiagnosis of posterior fossa infarcts in emergency care settings is frequent. As many as 25% of patients with risk factors for stroke who present to an emergency medical setting with isolated, severe vertigo, nystagmus, and postural instability have an infarction of the brainstem or cerebellum. Bedside oculomotor findings may reliably identify stroke in acute vestibular syndrome. The presence of normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation (vertical ocular misalignment) was very sensitive for diagnosis of stroke. This article was included about the clinical symptoms and neurological examinations of vascular vertigo, especially focusing on differential diagnosis of ischemic stroke of the vertebrobasilar territory from the acute peripheral vestibular syndrome, and therapeutic aspect for vascular vertigo.
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The Pathophysiology of Meniere’s Disease
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Sung-Il Nam
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Res Vestib Sci. 2011;10(Suppl 1):95-98.
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Abstract
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- Meniere’s disease is a disorder of the inner ear characterized by intermittent episodic vertigo, fluctuating hearing loss, ear fullness and tinnitus. The pathophysiology is commonly explained by a distension of membranous labyrinth by the endolymph, equally called endolymphatic hydrops. Endolymphatic hydrops, found on post-mortem examination, is the histologic hallmark. The cause of Meniere’s disease remains unclear. Numerous factors play a role in the development of hydrops related cochleovestibular dysfunction. Currently, there is no universally accepted theory on the underlying pathophysiology of this disease. On the basis of hisopathologic studies, it is assumed that endolymphatic hydrops is the pathologic feature most descriptive of Meniere’s disease. This review highlights some of the recent advances in the understanding of the possible pathophysiology of endolymphatic hydrops and Meniere’s disease.
KBS
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