Head impulse gain and saccade analysis in pontine-cerebellar stroke and vestibular neuritis

Abstract

Objective: We sought to quantify and compare angular vestibulo-ocular reflex (aVOR) gain and compensatory saccade properties elicited by the head impulse test (HIT) in pontine-cerebellar stroke (PCS) and vestibular neuritis (VN).Methods: Horizontal HIT was recorded #7 days from vertigo onset with dual-search coils in 33 PCS involving the anterior inferior, posterior inferior, and superior cerebellar arteries (13 AICA, 17 PICA, 3 SCA) confirmed by MRI and 20 VN. We determined the aVOR gain and asymmetry, and compensatory overt saccade properties including amplitude asymmetry and cumulative amplitude (ipsilesional trials [I]; contralesional trials [C]). Results:The aVOR gain (normal: 0.96; asymmetry 5 2%) was bilaterally reduced, greater in AICA (I 5 0.39, C 5 0.57; asymmetry 5 20%) than in PICA/SCA strokes (I 5 0.75, C 5 0.74; asymmetry 5 7%), in contrast to the unilateral deficit in VN (I 5 0.22, C 5 0.76; asymmetry 5 54%). Cumulative amplitude (normal: 1.1°) was smaller in AICA (I 5 4.2°, C 5 3.0°) and PICA/SCA strokes (I 5 2.1°, C 5 3.0°) compared with VN (I 5 8.5°, C 5 1.3°). Amplitude asymmetry in AICA and PICA/SCA strokes was comparable, but favored the contralesional side in PICA/SCA strokes and the ipsilesional side in VN. Saccade asymmetry ,61% was found in 97% of PCS and none of VN. Gain asymmetry ,40% was found in 94% of PCS and 10% of VN.Conclusion: HIT gains and compensatory saccades differ between PCS and VN. VN was characterized by unilateral gain deficits with asymmetric large saccades, AICA stroke by more symmetric bilateral gain reduction with smaller saccades, and PICA stroke by contralesional gain bias with the smallest saccades. Saccade and gain asymmetry should be investigated further in future diagnostic accuracy studies. Classification of evidence:This study provides Class II evidence that aVOR testing accurately distinguishes patients with PCS from VN (sensitivity 94%-97%, specificity 90%-100%). Acute vestibular syndrome (AVS), characterized by prolonged spontaneous vertigo, 1 is frequently due to vestibular neuritis (VN) but may be caused by pontine-cerebellar stroke (PCS).2-4 A negative clinical head impulse test (HIT), or absence of compensatory saccade, plus assessment for skew deviation and direction-changing nystagmus predict PCS in the context of AVS 5-8 better than the reference standard, diffusion-weighted imaging (DWI), which may be falsely negative. 8,9 Because clinical HIT is subjective, 10 quantitative assessment is desirable. A small videooculographic (VOG) study has compared the angular vestibulo-ocular reflex (aVOR) gain, the ratio of eye velocity to head velocity, in a contemporaneous group of patients with AVS consisting of PCS and VN.11 However, the quantitative aspect of the pivotal sign of clinical

Acute Unilateral Vestibulopathy

“…24,25 In terms of a 3-dimensional analysis, superior division, inferior division, and total unilateral vestibulopathy patterns can thus be diagnosed and differentiated; in superior division forms, the function of the posterior canal is spared; in inferior vestibular neuritis, the function of the horizontal and anterior canal is spared.…”

Acute Diagnosis and Management of Stroke Presenting Dizziness or Vertigo

“…34 In this respect, the recently developed video-based equipment for HIT would be helpful for objective measurements of head impulse VOR gains. 35,36 Laboratory Tests…”

The video head impulse test during post-rotatory nystagmus: physiology and clinical implications

“…Furthermore, the suppression of SN quick phases during a HIT might actually help the interpretation of responses recorded using video goggles since automated VOR gain calculations using slow-phase velocities are more accurate if there are no intervening corrective saccades or nystagmus (Mantokoudis et al 2015a). In addition, a period of suppression of quick phases during fast head movements might influence the analysis of corrective saccade latencies and cumulative saccade amplitudes, which differ in patients with central and peripheral causes of vertigo (Chen et al 2014).…”

“…One then looks for the telltale sign of a hypoactive labyrinth; a corrective saccade that follows and is in the direction of the inadequate slow-phase response (Halmagyi and Curthoys 1988). Using high-resolution measuring techniques that can be easily applied at the bedside, such as the video head impulse test (vHIT) (MacDougall et al 2009), one can quantify the vestibular response, both measuring the gain (slow-phase eye movement/head movement) of the VOR and the amplitude and timing of any corrective saccades (Bartl et al 2009;MacDougall et al 2009;Chen et al 2014). One potential problem, however, is that patients with acute vertigo often have a spontaneous nystagmus (SN), which may make it Abstract The aim of this study was to test the effects of a sustained nystagmus on the head impulse response of the vestibulo-ocular reflex (VOR) in healthy subjects.…”