Do steroids stop the spins?
A 58-year-old woman is admitted for observation after acute onset of sustained vertigo with associated nausea, vomiting, and difficulty walking because of a tendency to fall to the right. She reports an antecedent viral illness but denies ear fullness, headache, hearing or vision loss, tinnitus, ear pain, numbness or weakness of face or body, or limb incoordination. On exam, she is afebrile and has horizontal nystagmus with a torsional component with the quick component to the left that improves with vision fixation. The Dix-Hallpike maneuver doesn't exacerbate her symptoms. You suspect she has a peripheral rather than a central lesion and could have vestibular neuritis. You consult an online reference, which suggests that no therapies have been proven to be effective for vestibular neuritis.
In patients with suspected vestibular neuritis, do any pharmacotherapies speed symptom resolution compared with watchful waiting?
Using PubMed (www.PubMed.gov), enter "vestibular neuritis AND pharmacotherapy" in the query box. You limit to "randomized controlled trial" and find one article.
This innovative study provides a new therapeutic approach for patients with this disabling illness. Outcomes were assessed only at baseline and 12 months; interval assessments would have been helpful. The investigators used the surrogate outcome of extent of unilateral vestibular deficit, which may not correlate with clinical symptoms. The analysis included only the 81% of patients who completed follow-up; it would have been helpful to see the reasons for loss to follow-up, since they may be related to prognosis (i.e, people feeling the worst or best drop out). This patient population is highly selected, and some concern may be raised regarding prolonged steroid administration for patients in whom there may be some doubt about the diagnosis (benign positional vertigo vs. vestibular neuritis). Would a shorter course of steroids be equally effective?
Patient Preferences & Clinical Decision
Apart from the intervention tested in the present trial, you have little to offer to her. She agrees to start a 3-week course of methylprednisolone because she is "willing to try anything." You start a [H.sub.2]-receptor antagonist for cytoprotection.
RELATED ARTICLE: M. Strupp et al.
Methylprednisolone, Valacyclovir, or the Combination for Vestibular Neuritis (N. Engl. J. Med. 351:354-61, 2004).
* Design: Randomized, blinded, placebo-controlled clinical trial. The two-by-two factorial design allows for evaluation of the interaction between methylprednisolone and valacyclovir.
* Setting: Emergency departments in two hospitals in Germany (Munich and Mainz).
* Subjects: Patients aged 18-80 years were eligible for enrollment if they had acute or subacute onset of severe, prolonged rotatory vertigo, nausea, and postural imbalance; horizontal nystagmus with a rotational component toward the unaffected ear and the head-thrust maneuver showed an ipsilateral deficit of the horizontal semicircular canal; caloric irrigation showed a lack of or hyporesponsiveness of the horizontal canal in the affected ear; and perceived displacement of verticality of the eyes rotated toward the affected ear without vertical divergence of one eye above the other. Patients underwent neurologic, neuro-ophthalmologic, neuro-otologic exams; electronystagmography, calorics, and eye movement testing; and MRI.
* Intervention: Patients were randomized to one of four treatment groups: placebo, methylprednisolone, valacyclovir, and methylprednisolone-valacyclovir. Methylprednisolone was administered as a single daily dose of 100 mg (days 1-3), 80 mg (days 4-6), 60 mg (days 7-9), 40 mg (days 10-12), 20 mg (days 13-15), 10 mg (days 16-18), and 10 mg (days 20-22). Valacyclovir was given as two 500-mg tablets three times daily for 7 days. Patients received a gastric antisecretory agent.
* Outcomes: Primary efficacy was extent of unilateral peripheral vestibular paresis at 12 months.
* Results: Of the 141 participants, 38 received placebo, 35 received methylprednisolone, 33 received valacyclovir, and 35 received methylprednisolone-valacyclovir. Groups were similar at baseline and patients who were noncompliant, had severe adverse effects, or were lost to follow-up were excluded from the final analysis. At 12 months, improvement in vestibular paresis was 40% in the placebo group, 62% in the methylprednisolone group, 36% in the valacyclovir group, and 59% in the methylprednisolone-valacyclovir group. A significant effect of methylprednisolone but not valacyclovir was observed, and the addition of valacyclovir did not affect the efficacy of methylprednisolone. Complete recovery of peripheral vestibular function by calorics was achieved by 27%, 76%, 37%, and 79% of patients in the placebo, methylprednisolone, valacyclovir, and methylprednisolone-valacyclovir groups, respectively. One patient in the steroid group had bleeding from a gastric ulcer and discontinued treatment.
BY JON O. EBBERT, M.D., AND ERIC G. TANGALOS, M.D.
DR. JON O. EBBERT and DR. ERIC G. TANGALOS are with the Mayo Clinic in Rochester, Minn. To respond to this column or suggest topics for consideration, write to Dr. Ebbert and Dr. Tangalos at our editorial offices or email@example.com.
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|Title Annotation:||Mindful Practice|
|Author:||Ebbert, Jon O.; Tangalos, Eric G.|
|Publication:||Internal Medicine News|
|Date:||Sep 15, 2004|
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