Measuring optokinetic after-nystagmus: potential for detecting patients with signs of visual dependence following concussion

Abstract

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.

Patterns of vestibular dysfunction in chronic traumatic brain injury

“…Consistent with our findings, abnormality rates on either test are often < 25% with few reports of bilateral involvement ( 4 , 12 , 13 , 29 – 31 ). Three studies which included vertical canal vHIT showed increased detection rates with reports of abnormal function of at least one semicircular canal in 21.2–52% of patients ( 12 , 32 , 33 ). Otolith function has been mainly studied using cVEMPs with rates of saccular dysfunction ranging between 0 and 52% ( 7 , 12 , 13 , 29 , 31 , 33 – 35 ).…”

“…Only recently have studies begun to investigate the central vestibular pathways which might be involved in post-traumatic dizziness and imbalance. Dysfunction of the brainstem/cerebellar velocity storage mechanism was demonstrated in one study ( 32 ); patients with chronic TBI and visually induced dizziness had prolonged time constants and increased slow cumulative eye position on recordings of optokinetic after nystagmus ( 32 ). In another study involving provocative visual motion stimuli, subacute TBI patients with these symptoms showed increased activation in several brain regions including area OP2 of the posterior peri-sylvian region and retro-insular cortex ( 59 ), a cortical region implicated in motion perception and integration of visual and vestibular information ( 60 , 61 ).…”

Concussion Rehabilitation

“…It is currently believed this reflex is generated through the central processing network integrating visual, vestibular, and proprioceptive information. Symptoms related to optokinetic dysfunction could be related to the best known "visual vertigo" or "visually induced dizziness," dizziness that appears during exposure to environments with complex visual stimuli (e.g., supermarket aisles) [74].…”

Concussed patients with visually induced dizziness exhibit increased ocular torsion and vertical vergence during optokinetic gaze-stabilization

“…Visual motion hypersensitivity represents one of the most common sequalae, affecting 70–80% of those affected by blunt head injuries 2 . The condition, also known as Visually Induced Dizziness (VID), is believed to be caused by a reweighing of sensory inputs after which the patient becomes more visually dependant 3 . VID patients have traditionally been viewed as vestibular, due largely to the nature of their symptoms being described as dizziness.…”