Visual vertigo

By Marcello Cherchi, MD PhD

For patients

Visual vertigo (VV) refers to the sensation of disequilibrium a person can feel when seeing certain patterns (such as a carpet) or doing visual tasks (such as reading or driving).  The idea that visual input can make a person feel disequilibrium is controversial; not all doctors agree that this can happen.  VV is usually diagnosed and managed by neuro-optometrists.  VV is often treated with vision therapy (visual exercises), and sometimes with special glasses lenses, prisms or tints.  VV can happen in isolation (“by itself”), but it can also happen at the same time as another “dizzy disease,” such as inner ear problems, so your doctor may want to check some tests of inner ear function before referring you to a neuro-optometrist. 

For clinicians

Overview

Visual vertigo (Bronstein 1995) refers to a perceived disturbance of equilibrium in response to visual stimuli. A broad range of visual experiences can trigger visual vertigo, including moving visual stimuli (such as movie screens), visual stimuli that are stationary but detailed or complex (such as a patterned carpet) or visual stimuli that conflict with other sensory input (such as when riding an escalator).

The brain relies heavily on visual input in order to calculate one’s position in, and movement through, space. The influence of visual stimuli is such that simply showing someone videos or even stationary pictures can induce the patient to adjust his or her posture (Lestienne, Soechting et al. 1977, Kuno, Kawakita et al. 1999, Guerraz, Yardley et al. 2001, Guerraz and Bronstein 2008). In some people the brain appears to “pay more attention” to visual stimuli than is appropriate (which is sometimes called “visual dependence”), with the result being that these individuals experience sensitivity to visual stimuli that can manifest with a sensation of disturbed balance (Bronstein 2004, Bronstein, Golding et al. 2013).

In some cases, an individual with another balance disorder (such as from an inner ear problem) can additionally have a component of visual vertigo (Bronstein 2004) due to visual dependence (Cousins, Cutfield et al. 2014). In such cases it is especially important to recognize that there are multiple sources of the impaired balance. It is for this reason that a thorough assessment (Pavlou, Davies et al. 2006) is warranted before embarking on a treatment plan. Such assessment may include some vestibular (“inner ear”) tests, balance tests (such as computerized dynamic posturography) (Bronstein 1995) and a neuro-optometric examination — in other words, a multi-disciplinary approach is often required.

A neuro-optometry examination evaluates specific ocular motor and visual functions, such as accommodation, convergence/divergence, phorias, fixation, binocularity, fusion, depth perception and other aspects of visual processing, as well as the ways in which these phenomena interact with the vestibular system. A neuro-optometry examination may include refraction, a retinal examination, a slit lamp examination, and a Lancaster test.

Patients with neuro-optometric deficits may experience eye strain, double vision, visual fatigue, headaches, and visual vertigo. Such patients may have difficulty with specific visual tasks, such as reading, looking at computer screens or traveling in vehicles.

There is controversy in the medical community regarding treatment for visual vertigo. Visual rehabilitation (“vision therapy”) appears promising (Cohen 2013). The evidence supporting this approach is modest, but since it appears to pose no medical risk, we offer it to patients for whom other treatment options are unavailable or impractical. A neuro-optometrist oversees this aspect of a patient’s care. The goals of treatment may include decreasing sensitivity to visual motion, increasing visual comfort, and improving visual-vestibular integration.

In patients who have visual vertigo in addition to some other source of imbalance, a combination of treatments may be appropriate, including vision therapy, physical therapy and medical therapy.

Discussion

Approximately 50% of all of the brain’s pathways are related in some way to vision (Patil, Grossman et al. 2023), so it is unsurprising that many non-visual neurological functions interface in some way with visual functions.  The maintenance of equilibrium is among these.

Visual vertigo (VV) remains a controversial topic, and one about which neuro-ophthalmologists and neuro-optometrists often disagree, both on the existence of the diagnosis and its treatment (Subramanian, Barton et al. 2022).

Insofar as visual vertigo is construed as a “visual processing” problem, candidate mechanisms include neurological disease such as migraine, which in itself can cause a variety of visual abnormalities, as well as photophobia and other types of visual hypersensitivity. Visual vertigo is probably distinct from misokinesia (Jaswal, De Bleser et al. 2021, Webb 2022).

It also seems likely that visual vertigo can arise from primary ophthalmologic processes (see ophthalmologic visual deficits and disequilibrium). Visual vertigo is often suspected in patients with unilateral (or asymmetrical) cataracts or macular degeneration, or strabismus. Common to these disease processes are inter-ocular disparities which interfere with the brain’s ability to fuse the images from each eye into a single coherent percept, and thus have the potential to impair the stereopsis required for depth perception. This type of visual impairment will limit the reliability/utility of visual input when the brain attempts to arrive at conclusions regarding a person’s orientation and movement. Of particular relevance are diseases such as:

• Anisometropia (significantly different refractive needs between the two eyes). Although it is possible to provide each eye with a lens of different refractive power, one of the results of this is that the size of the image projected on each retina will be different (which is called aniseikonia), and the larger that difference, the more likely it is that the brain will fail to fuse those images, and thus depth perception will be impaired.
• Intra-ocular lens implants following cataract surgery. These implants cannot change shape (and therefore cannot adjust refraction for different viewing distances) the way that a native lens does, and thus have a fixed distance of best acuity.
• Status post LASIK surgery, particularly when configured for monovision (one eye used for near viewing, the other eye for far viewing).
• Strabismus (ocular misalignment) of any type. There are several possible consequences of ocular misalignment.
  1. First, a patient will (maladaptively) continue to attempt using both eyes (even though they are mis-aligned), and thus will perceive two images (called diplopia), which is disorienting.
  2. Second, a patient may simply suppress (ignore) the visual input from one eye (usually the non-dominant eye). This strategy achieves haplopia (perception of a single object) at the expense of sacrificing stereopsis, and thus impairs depth perception.
  3. Third, a patient may develop anomalous retinal correspondence (ARC) (more on this below).
• Orbitopathies in which the globe (eyeball) itself is vertically displaced, such as hypoglobus from silent sinus syndrome (Pula and Mehta 2014). This situation creates a misalignment of the visual axes due to an anatomical abnormality, one that cannot be overcome by extra-ocular muscle adaptation.

Retinal correspondence merits further discussion as it is often overlooked in this context.

In normal retinal correspondence (NRC), correctly functioning ocular motility directs the eyes such that light emitted from a point source will fall on the same location of each retina, and the viewer will experience this perception as “seeing a single object” (haplopia). In other words, normal retinal correspondence is needed in order for the brain to fuse the images from the two eyes successfully into a single percept.

Anomalous retinal correspondence (ARC) was first described in 1826 by Johannes Peter Müller (Simonsz 2010). ARC occurs when malfunctioning ocular motility results in a situation in which light emitted from a point source falls on different (non-congruent, non-corresponding) locations in each retina. This means that when an individual tries to focus on a point of interest, that point will fall on the fovea (area of highest acuity) of one eye, but will fall on some extra-foveal location (of lower acuity) of the other eye. This attempts to fuse the images of the two eyes (in order to achieve haplopia), but one image will be of poorer acuity than the other — in other words, the attempt at fusion is only partially successful. For further details the reader is referred to the excellent discussion at https://entokey.com/binocular-vision-3/ (accessed 11/24/22).

A neuro-optometrist or neuro-ophthalmologist may diagnose ARC using a synoptophore (Rutstein, Daum et al. 1989), Bagolini striated glasses (Bagolini 1976, Bagolini 1999), the Worth 4-dot test (Worth 1903) or the after-image test (Hansen 1954), although these tests sometimes give discrepant results (Garg, Jain et al. 1969, Rutstein, Daum et al. 1989).

References