Citation: Guerraz, M., Yardley, L., et al. Visual vertigo: symptom assessment, spatial orientation and postural control. Oxford University Press 2001; 124: 1646-1656
Summarized by: Amy M. Bartal, O.D. Resident, Vision Therapy and Rehabilitation EyeCare Professionals, PC Hamilton, NJ
(A Southern College of Optometry,Private Practice Residency)
Summary: The purpose of this article is to determine the cause of visual vertigo by assessing symptoms, spatial orientation, and postural control.
Methods: Twenty one individuals were identified with visual vertigo (VV) after reporting worsening of symptoms including vertigo, dizziness, unsteadiness or spatial disorientation by certain visual surroundings. These patients were compared with visually dependent individuals with a bilateral labyrinthine-defective (LDS) disorder, and normal subjects using questionnaires and experimental stimuli. All subjects answered several surveys including the Situational Vertigo Questionnaire, Vertigo Symptom Scale, Childhood Motion Sickness Questionnaire, Spielberger Trait Anxiety Inventory, and Vertigo Handicap Questionnaire. These surveys measured patient symptoms, level of anxiety, and experiences with motion sickness for all groups. The experimental stimuli required the subjects to orient a linear rod vertically while in three settings: darkness, within a tilted frame, and within a rotating disc. Body sway was also measured in four visual conditions. Subjects were instructed to stand bare-foot on a force platform and fixate on a luminescent dot with their eyes opened, eyes closed, while the target was located within a tilted frame or a rotating disc. The data measured formed two computed quotients. The Romberg quotient (RQ = eyes closed sway/eyes opened sway) reflects the amount of postural instability with stationary visual surroundings. The visual-kinetic quotient (V-KQ = rotating disc sway/eyes open sway) quantifies the destabilizing effect of moving stimuli. Statistical analysis was based on a multi-way analysis of variance and co-variance for the questionnaire data and the visual vertical and postural data, respectively.
Results: The data collected through the subject questionnaires revealed significantly higher levels of visually induced anxiety symptoms in the VV and LDS patients compared to the normal controls. The VV subjects also had significantly higher levels of vertigo. There were no statistical differences found correlating childhood motion sickness or levels of handicaps felt with the different experimental groups. In the subjective visual vertical and postural tests, both the VV and LDS patients demonstrated an increase in tilt of the vertical rod both with the static tilted frame and the rotating disc. Postural deviation when facing the titled frame and rotating disc was also increased in both of these groups. When comparing the stabilizing effect of vision there was a statistical increase in the LDS subjects but not the VV when compared to the controls. In contrast, the destabilizing effect of a moving visual stimulus had a greater impact on the VV subjects and not the LDS patients.
In conclusion, VV patients have an abnormally large perceptual and postural response to disorienting visual environments. VV develops in individuals who are visually dependent and rely on visual cues more than vestibulo-proprioceptive inputs. Treatment is aimed at increasing subjective and postural tolerance to disorienting visual stimuli and increasing the patients’ use of vestibulo-proprioceptive cues. Repetitive optokinetic stimulation has shown improvement in postural stability and patient symptoms.
Case in Point: A 43 year old woman presented to our office 2.5 years ago with symptoms of headaches and vertigo that was exacerbated by certain visual environments such as shopping malls, supermarkets with tall aisles, and in general all fluorescent lighting. Her history included several minor traumatic brain injuries (auto accident, hitting her head on a shelf, etc) non of which caused loss of consciousness, or required hospitalization.
Examination revealed a diagnosis of mild convergence excess. The rest of the ocular health and visual examination was unremarkable with the notable exception that viewing an Optokinetic drum caused tremendous increase in symptomatology. This occured whether the OKN drum was spinning or not and even occured when the drum was diplaced from the patient’s line of sight (left side placement was the worst). Critical Flicker Frequency was atypically high (her threshold was about 50Hz, average patients are in the 43-45Hz range). This means that her sensitivity to flicker was very high.
Our treatment plan revolved around prescribing a therapeutic tint (she responded positively to a BPI Omega tint-purplish hue). Upon eyeglass dispensing she reported that the glasses allowed her the first headache-free, non-vertigo day in over 2 years.
Vision therapy centered around restoring fusional vergence to normal levels and gradually introducing eye movement procedures for fixation, pursuit, and saccades that required greater speed, visual motor integration, and cognitve distractors. The vision therapy (along with the tinted spectacles) proved to reduce her symptoms dramatically. Other intervention that the patient felt was helpful was Logan chiropractic treatment, B complex vitamins, and increasing sleep to 8 hours per evening.
We recently saw her one year after post vision therapy and she maintains that she is almost symptom free virtually every day.