Concussed patients with chronic symptoms commonly report dizziness during exposure to environments with complex visual stimuli (e.g. supermarket aisles, busy crossroads). Such visual induced dizziness is well-known in patients with vestibular deficits, in whom it indicates an overreliance on visual cues in sensory integration. Considering that optokinetic after-nystagmus (OKAN) reflects the response of the central network integrating visual and vestibular self-motion signals (velocity storage network), we investigated OKAN in 71 patients [17 (23.9%) females, 30.36 ± 9.05 years old] who suffered from persistent symptoms after a concussion and presented clinical signs suggesting visual dependence. Data were retrospectively compared with 21 healthy individuals [13 (61.9%) females, 26.29 ± 10.00 years old]. The median values of the slow cumulative eye position and of the time constant of OKAN were significantly higher in patients than in healthy individuals (slow cumulative eye position: 124.15 ± 55.61° in patients and 77.87 ± 45.63° in healthy individuals—p = 0.012; time constant: 25.17 ± 10.27 s in patients and 13.95 ± 4.92 s in healthy individuals—p = 0.003). The receiving operating curve (ROC) estimated on the time constant had an overall area under the curve of 0.73. Analysis of the ROC suggests that a test measuring the OKAN time constant could obtain a sensitivity of 0.73 and specificity of 0.72 in determining the origin of the visual-related disturbances in those patients (threshold 16.6 s). In a subset of 43 patients who also performed the Sensory Organization Test (SOT), the proposed OKAN test was twice as sensitive as the SOT. This study suggests that concussed patients with persisting visual symptoms may have an underlying impairment of the velocity storage mechanism and that measuring the OKAN time constant can objectify such impairment.
1 Key points2 The cerebellum is the core structure controlling gaze stability. Chronic 3 cerebellar diseases and acute alcohol intoxication affect cerebellar function, 4 inducing, among others, gaze instability as Gaze-evoked nystagmus. 5 Gaze-evoked nystagmus is characterized by increased centripetal eye-drift. It is 6 used as an important diagnostic sign for patients with cerebellar degeneration 7 and to assess the "driving while intoxicated" condition. 8 We quantified the effect of alcohol on gaze-holding using an approach allowing, 9for the first time, the comparison of deficits induced by alcohol intoxication and 10 cerebellar degeneration. 11 Our results showed that alcohol intoxication induces a two-fold increase of 12 centripetal eye-drift. 13 We establish analysis techniques for using controlled alcohol-intake as a model 14 to help the study of cerebellar deficits. We recorded gaze-holding at varying horizontal eye positions in 15 healthy participants 26 before and 30min after alcohol intake required to reach 0.6‰ blood alcohol content 27 (BAC). Changes in ocular-motor behavior were quantified measuring eye-drift velocity 28 3 as a continuous function of gaze eccentricity over a large range (±40°) of horizontal 29 gaze angles and characterized using a 2-parameters tangent model. 30The effect of alcohol on gaze stability was assessed analyzing: 1) overall effects on the 31 gaze-holding system, 2) specific effects on each eye, 3) differences between gaze angles 32 in the temporal and nasal hemifields. 33For all subjects, alcohol consumption induced gaze instability, causing a two-fold
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