Online supplementary material: hBPPV second episode
Eight months after the first event, the patient was readmitted to emergency department after 48 hours of positional vertigo. A right geotropic hBPPV was diagnosed. He was again successfully treated with a 360º body rotation around the longitudinal axis to the left. Before, as well as after this rehabilitation maneuver, a mild asymmetry between sides was recorded both with vHIT (0,81 vs 1,04) and cVEMP testing (IA=0.30) (Supplemental Digital Content, Figure 1). oVEMP testing was normal. At day 30, clinical examination, vHIT and VEMP testing were all normal.
Since day 30 after the first event, right cVEMP latencies were persistently slightly increased (p13/n23 average of 6 recordings: 15.9/24.3 ms on the right side and 15.2/23.3 ms on the left side; p<0.05, paired T Test) but not oVEMP latencies.
The second hBPPV event is in accordance with the published BPPV recurrence rates (50 % within 10 years and 80% within the first year).(1) In this episode only a mild asymmetry was noted with the vHIT, both before and after the repositioning
maneuver, matching the vHIT first event results registered after the liberatory
maneuver. One hypothetical explanation could be the presence of sub-clinical residual debris, which would later be cleared at day 30.
During this event no major changes were observed in VEMP responses. The persistence of cVEMP latencies asymmetry in BPPV patients has been proposed to reflect irreversible neuronal degenerative changes.(2) Gacek also reported vestibular
ganglion cell loss in five temporal bones from patients with BPPV.(3) This ipsilateral latency shift is however within normal limits(4) , and was not observed in the oVEMP responses, and so doesn’t suggest any pathologic significance.
SUPPLEMENTAL DIGITAL CONTENT, FIGURE LEGEND
Supplemental Digital Content, FIGURE 1.Video head-impulse test (vHIT), cVEMP and oVEMP recordings during the second hBPPV event (right geotropic hBPPV), 8 months after the first event.
Day 1. vHIT: although both eye velocity curves show normal trajectories,
there is a lower VOR gain to the right (0.76, 0.72 and 0.85 to the right and 0.90, 0.99 and 1.16 at 40, 60 and 80 ms, respectively) with an asymmetry of 12% between sides in the regression velocity diagram. VEMPs: There’s a cVEMP light asymmetry between sides (IA= 0.30) but within normal limits;
oVEMPs are normal (IA=0,17)
Day 30. vHIT: The eye velocity curve regained its normal symmetry, both
dynamically from 40 to 80 ms and from regression data (asymmetry of 1%).
VEMPs: cVEMPs and oVEMPs are symmetrical with IA of 0.03 and 0.14, respectively.
Reference List
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2. Yang WS, Kim SH, Lee JD, Lee W-S. Clinical significance of vestibular evoked myogenic potentials in benign paroxysmal positional vertigo. Otol Neurotol
2008;29:1162–1166.
3. Gacek RR. Pathology of benign paroxysmal positional vertigo revisited. Ann Otol Rhinol Laryngol 2003;112:574–582.
4. Basta D, Todt I, Ernst A. Normative data for P1/N1-latencies of vestibular evoked myogenic potentials induced by air- or bone-conducted tone bursts.
Clin Neurophysiol. 2005;116:2216–9.