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ARTICLES: H. -A. Kim, J. -H. Hong, H. Lee, H. -A. Yi, S. -R. Lee, S. -Y. Lee, B. -C. Jang, B. -H. Ahn, and R. W. Baloh Otolith dysfunction in vestibular neuritis: Recovery pattern and a predictor of symptom recovery Neurology 2008; 70: 449-453 [Abstract] [Full text] [PDF]

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Otolith dysfunction in vestibular neuritis: Recovery pattern and a predictor of symptom recovery

Michael Strupp   (8 April 2008)

Reply from the authors

Hyung Lee, Robert W. Baloh UCLA School of Medicine   (8 April 2008)

Otolith dysfunction in vestibular neuritis: Recovery pattern and a predictor of symptom recovery 8 April 2008
Michael Strupp, University of Munich Marchioninistrasse 15, 81377 Munich, Germany Send Correspondence to journal: Re: Otolith dysfunction in vestibular neuritis: Recovery pattern and a predictor of symptom recovery Michael.Strupp{at}med.uni-muenchen.de Michael Strupp	Kim and et al. considered an important question in acute vestibular neuritis. [1] We would like to address a few issues. First, the authors pointed out that such a study had not been previously published. However, a clinical trial was published in Neurology in which the normalization of a displacement of the subjective visual vertical, ocular torsion and postural imbalance was evaluated in 39 patients with acute vestibular neuritis over a period of four weeks. [2] However, in this study, all patients had a persistent peripheral vestibular deficit and the values normalized within this period. Second, it is well known that dynamic deficits of the vestibular ocular reflex, which can be detected by the head impulse test, often persist in vestibular neuritis. However, caloric response may normalize [3] because dynamic deficits are not centrally compensated. This is not true for static deficits, such as a displacement of the subjective visual vertical or ocular torsion. Perhaps the authors can clarify if they examined two different aspects which can—on the basis of the data given—neither be differentiated nor directly correlated (i.e., recovery of peripheral vestibular function versus central vestibular compensation). A post-hoc subgroup analysis of those patients with persistent peripheral vestibular deficit and those without should have been considered. Third, the authors mentioned that their patient did not receive a course of steroids because it is unclear whether the risks outweigh the benefits in terms of symptom recovery. [1] Three studies, in which steroids were very well tolerated, have demonstrated significant benefits in peripheral vestibular function. [4] References 1. Kim HA, Hong JH, Lee H, et al. Otolith dysfunction in vestibular neuritis: recovery pattern and a predictor of symptom recovery. Neurology 2008;70:449-453. 2. Strupp M, Arbusow V, Maag KP, Gall C, Brandt T. Vestibular exercises improve central vestibulospinal com-pensation after vestibular neuritis. Neurology 1998;51:838-844. 3. Schmid-Priscoveanu A, Straumann D, Bohmer A, Obzina H. Vestibulo -ocular responses during static head roll and three-dimensional head impulses after vestibular neuritis. Acta Otolaryngol 1999;119:750-757. 4. Strupp M, Zingler VC, Arbusow V, et al. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med 2004;351:354-361. Disclosure: The author reports no disclosures.
Reply from the authors 8 April 2008
Hyung Lee, Department of Neurology, Keimyung University School of Medicine 194 Dongsan dong, Daegu, 700-712 South Korea, Robert W. Baloh UCLA School of Medicine Send Correspondence to journal: Re: Reply from the authors hlee{at}dsmc.or.kr Hyung Lee, et al.	We appreciate the interest of Dr. Strupp in our paper on the recovery pattern in vestibular neuritis (VN). [1] Dr. Strupp also found that static otolith dysfunction normalized during follow-up of patients with VN. [2] However, as mentioned in our paper, no previous report studied the recovery pattern after VN using a battery of static (subjective visual vertical, ocular torsion, skew deviation, and vestibular evoked potential) and dynamic (head shaking, head thrust, and caloric) vestibular tests. Their second and third points address the issues of central compensation, symptom recovery, and effectiveness of treatment of VN which deserve careful consideration. Central compensation occurs for both static and dynamic vestibular deficits after VN even though some test results remain abnormal (e.g., head thrust and caloric tests). Our study indicates that the head thrust test is a much better indicator of symptom recovery than the caloric test. Dr. Strupp also suggests that three studies have shown that steroids provide a significant benefit with low risk in the treatment of VN. We disagree. Only their study met the rigorous criteria of a prospective, randomized, double blind study. [4] They reported a single outcome measure which was the extent of recovery of caloric symmetry at one year. Patients treated with steroids had normal caloric responses significantly more often than those not treated with steroids. They performed a head thrust test but did not report the results and they did not include a measure of symptom recovery. Our study and the study of Nutti et al. found that the head thrust test is the best predictor of symptom recovery. [5] We found no significant difference in the extent of caloric recovery in patients with or without dizziness at follow-up. Regarding the risk of high dose steroids, only one of the 70 patients who received steroids in their study had a GI bleed and two with normal blood glucose on entry developed hyperglycemia requiring treatment (4% severe complications). Three reported dyspepsia and five reported mood swings but were able to continue treatment (11% minor complications). We reiterate our concern that the risks of high dose steroids for VN may outweigh the benefits in symptom recovery. Reference 5. Nutti D, Mandala M, Broman AT, Zee DS. Acute vestibular neuritis: prognosis based on bedside clinical tests (thrusts and heaves). Ann NY Acad Sci 2005:1039:359-367. Disclosure: The authors report no disclosures.