VCR and VOR responses to increasing current amplitudes.

<p><i>A</i>, Pathways connecting the vestibular nerve to neck or extraocular motoneurons. <i>B</i>-<i>D</i>, Average head (blue) and eye (red) movement traces, in monkey J and B, evoked using current amplitudes of 50 (B), 75 (C), and 100% (D) of the maximum for pulse trains delivered at 300pps lasting 100ms. Gray bars indicate stimulus duration and shading represents standard error. Note that for some velocity traces the standard error is smaller than the line thickness. Movements away from implanted side are upwards. Arrows show rebound effect due to the release of inhibition. Insets show peak head and eye velocities for the corresponding traces. <i>EOM</i>, extraocular motoneuron; <i>INC</i>, interstitial nucleus of Cajal; <i>MRST</i>, medial reticulospinal tract; <i>MN</i>, motoneuron; <i>VST</i>, vestibulospinal tract; <i>VN</i>, vestibular nuclei.</p

Interaction of vestibular-driven head and eye movements.

<p><i>A</i>, Average gaze, eye and head position (top panels) and velocity (bottom panels) traces during stimulations when the head was restrained and free. Gray bars indicate stimulus duration and shading represents standard error. <i>B</i>, Plots of average gaze movement amplitude during pulse trains delivered at 50, 100, 200 and 300pps when head-restrained versus free. <i>D</i>, Plots of average eye movement amplitude during pulse trains delivered at 50, 100, 200 and 300pps when head-restrained versus free.</p

Average VCR and VOR responses to increasing pulse rates.

<p><i>A</i>-<i>D</i>, Average head (blue) and eye (red) movement traces, in monkey J and B, evoked using increasing pulse rates of 50 (A), 100 (B), 200 (C) and 300pps (D) at maximum current amplitude. <i>E</i>-<i>G</i>, Plots of peak head and eye velocities as a function of pulse rate for current amplitudes of 50 (E), 75 (F), 100% (G) of the maximum.</p

VCR and VOR response latency and relative contribution to gaze.

<p><i>A</i>-<i>B</i>, Latency of evoked eye or head movements using a 2 standard deviation (A) or slope intercept measurement (B). <i>C</i>, Plots of eye versus head movement amplitude during pulse trains delivered at 50, 100, 200 and 300pps. <i>D</i>, Top panels show the contribution of head and eye to instantaneous gaze velocity during pulse trains delivered at the maximum current amplitude and 300pps. Bottom traces show the contribution of head and eye to cumulative gaze position. The average gaze velocity (top panels) and position (bottoms panels) traces are also plotted for comparison.</p

Factors affecting hearing deterioration in vestibular schwannoma patients treated with gamma knife radiosurgery: the Asan Medical Center experience

<p><b>Objectives:</b> To investigate the changes in hearing and to determine factors predicting hearing deterioration in patients with vestibular schwannoma (VS) who undergo gamma knife radiosurgery (GKRS).</p> <p><b>Design:</b> A retrospective review of medical records in patients diagnosed with VS and initially treated with GKRS at a tertiary care medical center between 1995 and 2015 was performed. Tumor factors (location, volume), parameters related to irradiation to the tumor and cochlea, and distance between the tumor and cochlea were reviewed.</p> <p><b>Results:</b> Fifty-six patients were included in the final analysis with a mean observation period following GKRS as 24.4 ± 27.8 months. Prior to GKRS, the average pure tone threshold at 500, 1k, 2k, and 4k Hz (PTA₄) was 51.0 ± 29.7 dB HL. After GKRS, the mean PTA₄ was 71.6 ± 33.3 dB HL. Significant independent odds ratios for hearing deterioration were 8.5 for extracanalicular tumors, 18.8 for more than 10 shots in GKRS, and 12.2 for a distance between the tumor center and cochlea modiolus less than 20 mm.</p> <p><b>Conclusions:</b> A significant hearing deterioration was shown in 2 years after GKRS. Tumor location, number of radiation shots, and distance between the tumor and cochlea affected hearing level after GKRS.</p