Abstract
Background: We examined whether, after onset of acute unilateral vestibular neuritis (aUVN), initial disease effects, subsequent peripheral recovery and central compensation cause similar changes in vestibular ocular reflex (VOR) gains in all 3 semi-circular canal planes.Methods: 20 patients, mean age 56.5 years, with pathological lateral canal video head impulse test (vHIT) VOR gains due to aUVN, were subsequently examined with vHIT in all 3 canal planes on average 4.3 and 36.7 days (“5 weeks”) after aUVN onset.Results: Lateral and anterior deficit side (DS) average gains equaled 0.41 at aUVN onset. Non-deficit, normal, side (NS) gains were 0.88 and 0.81, respectively. Mean posterior DS gain was similar at onset, 0.43, provided only gains lower than 0.6 (lower limit of healthy controls) were considered. NS posterior mean gain at onset (0.68) was less (p ≤ 0.0006) than lateral and anterior NS gains. After 5 weeks, DS lateral, anterior and posterior canal gains increased (p ≤ 0.05), on average, to 0.65, 0.59, and 0.58, respectively. NS gains increased to 0.91, 0.87, and 0.76 (p = 0.007), respectively. At 5 weeks deficit-lateral/normal-lateral canal plane gain asymmetries were significantly (p < 0.0008) reduced from 36.9 to 19.4%, deficit-anterior/normal-posterior asymmetry decreased from 28.6 to 18.1%, while deficit-posterior/normal-anterior asymmetry changed from 29.7 to 21.4%, all to circa 20%. Roll plane asymmetries decreased slightly over 5 weeks (28.6–18.1%) but pitch plane asymmetries remained significantly less (p = 0.001), not different from 0% regardless of initial DS posterior canal vHIT gain. Yaw plane asymmetry changes are identical to those of the lateral canals (36.7–19.4%).Conclusions: These results indicate that, at onset, aUVN of the superior vestibular nerve has a similar effect on lateral and anterior deficit DS VOR gains, and on posterior DS canal VOR gains if the inferior nerve was also affected at onset. The significant improvements to equal 5 week levels of DS gains and slightly greater posterior NS gain improvements, compared to lateral and anterior NS gains, yielding a common canal plane gain asymmetry of 20% at 5 weeks, suggest similar neural compensation mechanisms were active along VOR pathways. Unexpectantly, canal plane improvement was not replicated in pitch plane asymmetries.
Highlights
With the introduction of the video Head Impulse Test (vHIT) technique for testing vertical semi-circular canal function (1), it became possible to investigate whether weaknesses in any of the 6 directions of canal gains cause corresponding weaknesses in balance control for one or more of the 3 directions of body plane angular motion—pitch, roll, and yaw—representing movements in the sagittal, frontal, and transverse planes, respectively (2)
At unilateral vestibular neuritis (UVN) onset all lateral and 18 of 20 anterior canal deficit side gains were less than the lower limit of healthy control gains reported by Pogson et al (19) which have been copied into Table 1
The lateral canal deficit was confirmed by the canal paresis (CP) values, all of which were higher than 64%
Summary
With the introduction of the vHIT technique for testing vertical semi-circular canal function (1), it became possible to investigate whether weaknesses in any of the 6 directions of canal gains cause corresponding weaknesses in balance control for one or more of the 3 directions of body plane angular motion—pitch, roll, and yaw—representing movements in the sagittal, frontal, and transverse planes, respectively (2). The fundamental first step measuring the effect of a peripheral vestibular disease such as unilateral vestibular neuritis (UVN) on weakened superior and inferior vestibular nerve afferent gains from the lateral, anterior, and posterior canals could be quantified (2, 3). Similar gain values were obtained within 5 days of acute UVN onset by Allum and Honegger (2) (mean gains 0.4, 0.44, and 0.69 for lateral, anterior, and posterior deficit side gains). In contrasting viewpoints based on vHIT tests, Büki et al (7) argued that there was slower recovery and Lee et al (8) faster recovery for posterior compared to lateral and anterior deficit canal gains. After onset of acute unilateral vestibular neuritis (aUVN), initial disease effects, subsequent peripheral recovery and central compensation cause similar changes in vestibular ocular reflex (VOR) gains in all 3 semi-circular canal planes
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