Three-dimensional vector analysis of the human vestibuloocular reflex in response to high-acceleration head rotations. II. responses in subjects with unilateral vestibular loss and selective semicircular canal occlusion

Abstract

1. We studied the three-dimensional input-output human vestibuloocular reflex (VOR) kinematics after selective loss of semicircular canal (SCC) function either through total unilateral vestibular deafferentation (uVD) or through single posterior SCC occlusion (uPCO), and showed large deficits in magnitude and direction in response to high-acceleration head rotations (head "impulses"). 2. A head impulse is a passive, unpredictable, high-acceleration (3,000-4,000 degrees/s2) head rotation through an amplitude of 10-20 degrees in roll, pitch, or yaw. The subjects were tested while seated in the upright position and focusing on a fixation target. Head and eye rotations were measured with the use of dual search coils, and were expressed as rotation vectors. A three-dimensional vector analysis was performed on the input-output VOR kinematics after uVD, to produce two indexes in the time domain: magnitude and direction. Magnitude is expressed as speed gain (G) and direction as misalignment angle (delta). 3. G. after uVD, was significantly lower than normal in both directions of head rotation during roll, pitch, and yaw impulses, and were much lower during ipsilesional than during contralesional roll and yaw impulses. At 80 ms from the onset of an impulse (i.e., near peak head velocity), G was 0.23 +/- 0.08 (SE) (ipsilesional) and 0.56 +/- 0.08 (contralesional) for roll impulses, 0.61 +/- 0.09 (up) and 0.72 +/- 0.10 (down) for pitch impulses, and 0.36 +/- 0.06 (ipsilesional) and 0.76 +/- 0.09 (contralesional) for yaw impulses (mean +/- 95% confidence intervals). 4. delta, after uVD, was significantly different from normal during ipsilesional roll and yaw impulses and during pitch-up and pitch-down impulses. delta was normal during contralesional roll and yaw impulses. At 80 ms from the onset of the impulse, delta was 30.6 +/- 4.5 (ipsilesional) and 13.4 +/- 5.0 (contralesional) for roll impulses, 23.7 +/- 3.7 (up) and 31.6 +/- 4.4 (down) for pitch impulses, and 68.7 +/- 13.2 (ipsilesional) and 11.0 +/- 3.3 (contralesional) for yaw impulses (mean +/- 95% confidence intervals). 5. VOR gain (gamma), after uVD, were significantly lower than normal for both directions of roll, pitch, and yaw impulses and much lower during ipsilesional than during contralesional roll and yaw impulses. At 80 ms from the onset of the head impulse, the gamma was 0.22 +/- 0.08 (ipsilesional) and 0.54 +/- 0.09 (contralesional) for roll impulses, 0.55 +/- 0.09 (up) and 0.61 +/- 0.09 (down) for pitch impulses, and 0.14 +/- 0.10 (ipsilesional) and 0.74 +/- 0.06 (contralesional) for yaw impulses (mean +/- 95% confidence intervals). Because gamma is equal to [G*cos (delta)], it is significantly different from its corresponding G during ipsilesional roll and yaw, and during all pitch impulses, but not during contralesional roll and yaw impulses. 6. After uPCO, pitch-vertical gamma during pitch-up impulses was reduced to the same extent as after uVD; roll-torsional gamma during ipsilesional roll impulses was significantly lower than normal but significant...

Temporal dynamics of semicircular canal and otolith function following acute unilateral vestibular deafferentation in humans

“…The VOR is composed of two components: the angular VOR derived semicircular canals input, and the linear VOR derived from otolith input. After unilateral vestibular deafferentation (UVD), the canal VOR is known to be deficient during sudden high acceleration rotations toward the side of the lesion (Aw et al 1996;Crane and Demer 1998;Foster et al 1997;Halmagyi et al 1993;Lasker et al 1999Lasker et al , 2000Tabak and Collewijn 1995;Tian et al 2001bTian et al , 2002.…”

The video head impulse test

“…[7][8][9] It quantifies the VOR deficit and shows the associated pattern of overt and covert catch-up saccades in vestibular deficient patients. 6,10 However, search coil measurements require the subject to wear an uncomfortable contact lens, are time intensive, are expensive, and are not practical for acute patients.…”

Deficient high-acceleration vestibular function in patients with polyneuropathy

“…Average ages of patients with predominantly axonal (66 Ϯ 10 y; n ϭ 18, 8 women) and patients with predominantly demyelinating PNP (65 Ϯ 13 y; n ϭ 19, 4 women) were similar. Average duration of symptoms, as recorded in the medical histories, was 6.7 Ϯ 5.5 years (range [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Abnormal clinical findings on patients with PNP included the following: 1) unilaterally (n ϭ 12) or bilaterally (n ϭ 10) abnormal bedside headimpulse tests; 2) stand and gait ataxia (n ϭ 29); 3) sensory deficits (touch: n ϭ 37; pain: n ϭ 33; temperature; n ϭ 33; position: n ϭ 19; vibration: n ϭ 25); and 4) abnormal motor signs (muscle atrophy: n ϭ 20; muscle weakness: n ϭ 19; hyporeflexia or areflexia: n ϭ 33 patients).…”

“…8 To clarify the prevalence of vestibular impairment in unselected patients with predominantly axonal or predominantly demyelinating PNP, we conducted a prospective study using searchcoil head-impulse testing, which assesses vestibular function at natural stimulus frequencies. 9,10 METHODS Participants were selected from patients referred to our academic neurologic center for further evaluation of polyneuropathic symptoms. Detailed history taking and complete neurologic examination were performed.…”