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MY APPROACH to Visually Induced Dizziness
Background
Visually induced dizziness (VID) can be defined as the sense of dizziness triggered by visual stimuli, consisting of spatial disorientation without oscillopsia or illusory motion.1 Most VID will be triggered by motion in the visual field, busy surroundings (eg, the grocery store), driving, and relative motion of visual surroundings associated with body movement.1 It is hypothesized that VID occurs primarily in patients with central or peripheral vestibular disorders and develops due to an over-reliance on visual cues due to these vestibular deficiencies.2 Women are affected more frequently by both peripheral and central vestibular disorders at a rate of 7:3 and 2:1, respectively.3 As could be suspected, studies have shown that gonadal hormone fluctuations play a significant role in the prevalence, severity, and fluctuation of symptoms of vestibular disorders and associated VID.3 Testing for VID can be difficult due to fluctuation in symptoms and relatively poor sensitivity of current testing methods.4 However, due to the specificity of symptoms of VID, a simple questionnaire can be given to diagnose and determine severity of the condition.4 The following case is an example of successful treatment of VID in a female patient with peripheral vestibular dysfunction.
History and chief complaint
MR, a 51-year-old female, presented with complaints of dizziness. She stated that over the prior several years she had symptoms of dizziness, imbalance when walking, the feeling that she was going to fall backwards when standing, veering to the left while driving, and general discomfort due to unsteadiness. She also stated that she rated her quality of life as “poor” because of the severity of these symptoms. She worked an office job averaging 8 to 10 hours per day on the computer and struggled with concentrating and meeting deadlines due to her symptoms.
MR’s medical history was positive for hypertension and seasonal allergies. She had a history of Bell’s palsy (10 years prior) on the left side that recovered about 90% with mild persistent droop around her mouth when speaking and smiling. Her ocular history was positive for a cotton wool spot in the left eye diagnosed by her previous eye doctor 1 year prior. Her only medication was losartan, with no known drug allergies. Her family medical and ocular history was unremarkable.
MR went through testing by other providers before presenting to my office. She reportedly was seen by her primary optometrist, ophthalmologist, ENT physician, vestibular therapist, and neurologist. Neuro-imaging was not performed. Extensive vestibular testing was performed by the ENT physician with the only findings being unilateral weakness on the right side during caloric testing. All other exam findings were unremarkable, and there was no known etiology for the dizziness.
Initial clinical findings
A comprehensive neuro-visual evaluation was performed at MR’s initial visit. MR’s baseline dizziness was reported as a 3 on a scale of 1 to 10. Visual acuities with her habitual progressive lenses were 20/20 in each eye and with both eyes together. Ocular motilities were smooth and unrestricted in each eye and pursuits scored 4+ on the 4+ scale for ability; however, she noted her dizziness increased to a 7 out of 10 during this testing. Saccades scored 3-4+ on the 4+ scale for ability with few undershoots, and again she noted a 7 out of 10 dizziness during the testing. Cover test results were orthophoria at distance and 6^ exophoria at near. MR’s near point of convergence (NPC) revealed a repeatable break at 4 inches with a consistent recovery at 15 inches. Prism bar vergence ranges were normal at distance and reduced at near with X/10/6 for base in (BI) and X/12/6 for base out (BO). Vergence facility with 3^BI/12^BO testing revealed mild weakness with a score of 12.5 cycles per minute (cpm). She noted an 8 out of 10 dizziness for all vergence testing. Worth 4-Dot testing revealed fusion at near and intermittent OS suppression at distance. MR’s visual midline was centered for personal and peri-personal space, but shifted 2 inches to the left in her extra-personal space. She noted no change in dizziness with midline testing.
Balance testing was performed on a foam pad. MR was instructed to stand balanced while looking at a target straight ahead, then stand balanced with her eyes closed. MR’s center of gravity was significantly shifted toward her toes and she had a hunched posture with eyes opened. With eyes closed, MR hunched her posture even more and almost fell forward after only 2 seconds. When MR walked down a long hallway, she veered to the left and was continuously trying to correct with an almost limping or hopping motion. Testing was then repeated with the addition of yoked prism lenses. A 3 prism diopter power was used for testing and was presented individually in orientations of base up, base down, base right, and base left. With each trial, MR’s balance was re-evaluated. MR’s center of gravity improved to more central and she adjusted her shoulders back to a less hunched position when standing on the foam pad with both the base down and base left orientations. She also walked more centered in the hallway and had less sway in hips while wearing base left yoked prism lenses. Due to a positive response with both the base down and the base left orientations, a final trial of combination yoked prism of base down and base left was tested. MR noted the most comfort with this combination, and the balance and walking tests were both still improved. If MR were to have any symptoms or if performance was not improved as expected with the 3 prism diopter power, repeat trials with more or less power would have been performed.
All ocular health findings were normal for her age in each eye. MR was diagnosed with the following conditions: visual–vestibular dysfunction, visual spatial disorientation, binocular dysfunction, myopia, astigmatism, and presbyopia. MR was also referred for neuro-imaging (MRI of the brain and internal auditory canals), and results came back unremarkable, with still no known etiology for the dizziness.
Treatment protocol
Based on the clinical findings and subjective responses during testing, MR was prescribed an updated progressive lens glasses prescription with a combination of base down and base left yoked prism. MR was seen for a 1- month follow-up evaluation, during which she noted a significant improvement in her symptoms. Binocular findings were still reduced at this visit, and MR was still not fully functional during activities of daily living (ADL); therefore, vision therapy was initiated. During her vision therapy program, the following visual skill areas were emphasized: peripheral awareness, visual–vestibular integration, and binocular fusion. As MR progressed through the program, activities were introduced that worked on balance and visual skills simultaneously to ensure that her visual system was stable during movement and daily vestibular activities. She completed 15 sessions of weekly vision therapy. Below is a summary of MR’s testing at the end of vision therapy compared with baseline and 1-month follow-up evaluation.
|
Baseline |
1-Month Follow-Up |
Post Vision Therapy |
Progressive Glasses Prescription |
OD: -1.25 DS OS: -1.00-0.75x135 Add: +1.75 |
OD: -0.75-0.50x090 OS: -0.75-0.75x130 Add: +2.00 2^BD and 2^BL OD, OS |
OD: -0.75-0.50x090 OS: -0.75-0.75x130 Add: +2.00 2^BD and 2^BL OD, OS |
Distance Acuity |
20/20 OD, OS, OU |
20/20 OD, OS, OU |
20/20 OD, OS, OU |
Near Acuity |
20/20 OD, OS, OU |
20/20 OD, OS, OU |
20/20 OD, OS, OU |
EOMS |
Full and unrestricted 7/10 dizziness |
Full and unrestricted |
Full and unrestricted No dizziness |
Pursuits |
4+ 7/10 dizziness |
4+ No dizziness |
4+ No dizziness |
Saccades |
3-4+ 7/10 dizziness |
3-4+ No dizziness |
4+ No dizziness |
Cover Test |
D: Orthophoria N: 6 exophora |
D: Orthophoria N: 6 exophora |
D: Orthophoria N: 6 exophora |
NPC |
4” / 15” 7/10 dizziness |
4” / 8” 5/10 dizziness |
1-2” No dizziness |
Distance Vergence |
BI: x/6/4 BO: x/8/6 8/10 dizziness |
BI: x/6/4 BO: x/8/6 5/10 dizziness |
BI: x/6/4 BO: x/10/6 No dizziness |
Near Vergence |
BI: x/10/6 BO: x/12/6 8/10 dizziness |
BI: x/12/6 BO: x/12/8 5/10 dizziness |
BI: x/16/12 BO: x/35/25 No dizziness |
Vergence Facility |
12.5 cpm 8/10 dizziness |
12 cpm 6/10 dizziness |
17 cpm No dizziness |
Worth 4 Dot |
D: Intermittent OS suppression N: Fusion |
D: Fusion N: Fusion |
D: Fusion N: Fusion |
Visual Midline |
Personal: centered Peri-personal: centered Extra-personal: 2” left |
Personal: centered Peri-personal: centered Extra-personal: 2” left |
Personal: centered Peri-personal: centered Extra-personal: 2” left |
Balance on Foam |
Weight in toes, hunched posture |
Centered weight with sway, slight hunch |
Stable centered weight and upright posture |
Walk in Hallway |
Veer to left, hip sway |
Mild veer to left, no hip sway |
Centered, no hip sway |
Treatment outcomes
At completion of the vision therapy program, MR reported that her quality of life was better than it had been in years. She no longer experienced dizziness, had no imbalance when walking, and was back to driving safely without veering to one side. She reported that she confidently completed tasks at work and was now able to exercise again without symptoms. MR continued to wear the yoked prism lenses until 1 year despite complete resolution in symptoms at the 9-month follow-up. She noted that she was nervous to discontinue the lenses prior to this time since she was concerned about a regression in symptoms. Once she fully discontinued the yoked prism lenses and returned to standard progressive lenses only, no regression in objective findings or subjective symptoms was noted.
With patients with VID, a complete neurological, cardiac, and vestibular evaluation are necessary in order to determine any possible cause of the symptoms. Vestibular therapy can be helpful for some patients, but this therapy often fails to address visual aspects of the condition. Although studies report that VID is caused by an underlying vestibular dysfunction and treatment should be aimed at addressing the vestibular issue, this case proves that the imbalance in visual–vestibular connection and associated visual deficiencies are worth treating and can thereby dramatically improve a patient’s quality of life.
Additional Info
- Steenerson KK, Hoskin J, Fife TD. Visually induced dizziness. Curr Opin Neurol. 2022;35(1):113-117.
- Van Ombergen A, Heine L, Jillings S, et al. Altered functional brain connectivity in patients with visually induced dizziness. Neuroimage Clin. 2017;14:538-545.
- Mucci V, Hamid M, Jacquemyn Y, et al. Influence of sex hormones on vestibular disorders. Current Opin Neurol. 2022;35(1):135-141.
- Pavlou M, Davies RA, Bronstein AM. The assessment of increased sensitivity to visual stimuli in patients with chronic dizziness. J Vestib Res. 2006;16(4-5):223-231.
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