Timothy C. Hain, MD, Most recent update: April 20, 2017
Visual stimulation is often a trigger for dizziness, and sometimes is called "visual vertigo". Patients often complain of disturbances related to
- optic flow (see below)
- visual motion in general
- computer screens
This must be considered in the context that persons with dizziness may have
- nystagmus (involuntary jumping of the eyes)
- a tilt of the eyes (called ocular counterroll)
- asymmetrical or impaired vestibular reflexes
One must also consider that persons with dizziness may have ocular disorders such as:
- latent nystagmus or congenital nystagmus
- Anisometropia (i.e. difference in the optical power between the eyes)
- Abnormal sensory mapping of the eyes (e.g. after retinal detachment, or following correction of strabismus)
- Abnormal movement of the eyes, that may depend on the direction of gaze (i.e. ocular motor palsies, internuclear ophthalmoplegia)
When enumerates all of the possible disturbances, it is amazing that visual vertigo is not more common ! This likely from the amazing power of our nervous systems to adapt to a variety of sensory and motor issues.
Visual dependence is the general term for persons who have increased their weighting of vision. This is usually thought to be due to lack of confidence in vestibular or somatosensory input. Cousins et al (2014) suggested that visual dependence using the Rod/Disk test was associated with high levels of persistent vestibular symptoms after vestibular neuritis.
An alternative name for this is "See sick syndrome", or SSS. This is a term invented by Roderic Gillilan, O.D, an optometrist. The link contains a description of how optometrists view visual vertigo.
How does one measure visual dependence ?
Usually it is with tests that are vulnerable to cognitive bias such as "psychophysics", or posturography. This makes assessment of visual dependence vulnerable to cognitive state, including those who are involved in malingering and makes research studies of visual dependence very vulnerable to bias.
Perhaps because of these problems with measurement, visual dependence and visual vertigo has been mixed up in the literature with psychiatric terms such as "phobic postural vertigo". (e.g. Pollak et al, 2003) While there is no doubt that anxiety or phobia can cause reweighting or upweighting of senses, the lack of a measure for visual dependence that has no psychiatric component, we think, has caused an overemphasis on psychological elements and underemphasis on physiology. Eckhardt-Henn et al (1997) stated that "It becomes obvious that phobic postural vertigo is a generalizing term which encompasses different forms of psychogenic vertigo. The authors plead for a more differentiated diagnosis and subgroup oriented classification of vertigo caused by psychiatric disorders. " We agree.
Visual dependence is a subtype of the general category of "sensory integration disorders". In order to talk about this we have to make a diversion into systems physiology.
(This section is not meant to be a discussion of the "sensory processing disorder", or SPD, which includes a variety of sensory integration disorders, and is felt to be either developmental or related to autism. SPD can include tactile and sound sensitivity, but rarely includes photophobia) (Fernandez-Andres et al, 2015)
Estimation of self and external motion
A mechanism is needed that combines sensory inputs, weights them according to their relevance and reliability, and provides a reasonable estimate of orientation in space, even without any recent sensory input. In engineering terms, we are discussing an “estimator.”
Navigating the space shuttle involves similar problems. The shuttle has dozens of sensors and motors. Some sensors respond quickly, and some slowly. They may differ in accuracy, scaling, coordinate frame, timing, and noise characteristics. No single sensor can provide a complete picture of the shuttle’s state. A mechanism is needed to integrate sensor output and to develop an internal estimate of the state of the system (i.e., position, velocity, acceleration) in order to keep the shuttle on the desired course and heading.
The engineering solution to this problem developed out of work performed by Kalman and is often called a Kalman filter. It is also commonly called an “optimal estimator” or an “internal model.” There is considerable evidence that mechanisms similar to Kalman filters are used for human sensorimotor processing.
The Kalman filter is far more powerful than a simple reflex. Several key concepts must be considered before one can understand how it is superior.
- Internal models of sensors and motor output are used to develop an estimate of the current sensory and motor state. These internal models are adjusted according to experience and must track changes in bodily function. It seems likely that vestibular rehabilitation affects internal models.
- Sensory input is not used to directly compute body state, but rather, the difference between sensor input and predicted sensor input is used to correct the current estimate of body state. This design allows the Kalman filter to easily combine multiple sensor inputs—from eyes, ears, and somatosensors. The Kalman filter continues to work even in the absence of a sensory input, because it uses its estimate when the sensor is missing. Both of these highly desirable features make the Kalman filter far superior to a simple assemblage of reflexes.
- The Kalman gain weights the extent to which a sensory input affects the ongoing state estimate. This weighting provides a method of adjusting for the salience and reliability of sensory streams. It seems highly likely that vestibular rehabilitation adjusts the Kalman gain.
Overall, this sort of mechanism is clearly far superior to vestibular reflexes: Although not as fast, it can be far more accurate, it functions even in the absence of sensory input, and it is modifiable by experience and rehabilitation.
With this background, it is now possible to see why visual dependence is so common. We all use internal estimators that combine sensory information into a best "estimate" as to the self and world motion. These estimators consider several streams of input -- visual, vestibular, body sensation, and internal knowledge. When vestibular sensation is unreliable, our internal estimator adjusts the weighting of other senses.
Usually this is a good idea. Sometimes though, it gets people into trouble. When vision does not correctly reflect self or world motion, visual input can create dizziness. Thus visual dependence is a sensory integration disorder.
Flow field similar to that used in the Microsoft Windows starfield screen saver. Divergence is zero at the center of the field and maximum towards the extremes.
This has to do with how things "stream" past. When one is walking through the aisles of a grocery store, there is a "flow field" of visual motion which can be visualized like water going past the prow of a ship. In other words, there is divergence. Objects to the left side are projected as moving leftward on the periphery of the eye, and objects on the right are projected as moving rightward on the periphery of the eye. Ordinarily, the two flow fields cancel out so that there is no net sensation of rotation. When flow processing is asymmetrical or tilted such as in the utricular syndrome, movement through such environments may induce vertigo.
|Visual environment one patient found to be destabilizing.||A New York subway station escalator.|
Also, persons with impaired vestibular input may weight visual sensation greater than normal persons and become unsteady due to the visual impact. Many times persons with this symptom become faint and have to leave the environment. There is often a panic component. Another example of a flow field is the "starfield" screen saver distributed with Microsoft Window's software.
Patients with vestibular disorders often exhibit increased sway during optic flow. (Redfern et al. 1994).
The flow situation is actually quite a bit more complex than suggested above-- flow fields can be described in terms of four components: translation, expansion, rotation, and shear. Mathematically they can be described using the terms divergence, curl, and deformation of flow with respect to the position of the eye.
These sorts of symptoms can usually be managed by avoidance, conditioning, and dark glasses.
One would expect that anisometropia (difference in optical power between two eyes, often accompanied by spectacles for correction that result in a difference in the size of objects) would cause considerable dizziness, as when the head is moved, there is a potential for the speed of the world movement to vary across eyes. However, the literature is not very supportive of this idea, perhaps because most people can suppress vision in one or the other eye, which they often call "looking out of one eye". Ordinarily people will naturally use the eye with the best vision. One would think that this adaptation would degrade depth perception.
This is a very obscure condition, originally described by Halpern in 1964. Halpern described induction of disturbed balance and vision, associated with inner ear disturbances, which was alleviated by looking with the other eye (Halpern 1964). This syndrome was thought by Halpern to be due to a permanent disturbance of integration of visual, vestibular and cerebellar function. While reasonable, this explanation seems rather vague to us. Halpern also indicated that thresholds for hearing discomfort as well as somatic sensation changed, according to the viewing eye. These findings are bizzare and presently lack an organic explanation.
Bental and Hammond Tooke (1979) reported a case in which the symptoms were again provoked by monocular viewing, and also worsened by applying red filters to the eyes and improved with blue filters. It seems to us that this is simply a single unusual case presentation. The improvement with colored glasses, seems to us, to be pointing towards a psychological source of symptoms. In other words, we find this dubious.
More reasonably, some patients with congenital strabismus have latent nystagmus, a type of congenital nystagmus, that is eliminated by binocular viewing. This sort of patient might have a simlar presentation to "Halpern's syndrome", and should have nystagmus that changes direction accompanying their clinical exam. Similarly, patients with congential strabismus sometimes have anomalous retinal correspondance, and might develop spacial uncertainty with both eyes viewing, relieved by monocular viewing. This is not "Halpern's syndrome", of course, as it is improved by monocular viewing.
The brain must separate out visual motion related to self movement from environmental motion in order to remain well oriented in space and to determine whether other sensory inputs such as the ear and legs are accurate. Persons who have impaired vestibular inputs may inappropriately depend on visual input, and confuse environmental movement with self motion. Most people who drive have experienced the illusion of movement when they are stopped at an intersection, and another car starts to slowly creep forward. This is an example of environmental motion being confused with self motion.
Visual stimulation can also result in postural sway. Normal persons adapt over about 30 seconds to visual input and stop swaying, while persons with vestibular deficits do not adapt. (Loughlin et al. 1996; Loughlin et al. 2001)
While these sorts of symptoms are well understood, and are often treated by vestibular rehabilition, it is not entirely clear how effective this treatment is.
Some people with vestibular disorders become unable to work on computer screens. The precise reason for this is not entirely clear, but some have speculated that it relates to flicker (refresh rate -- see the VEDA newsletter, Vol 16, #4, 1999). According the authors of the VEDA newsletter (optometrists), one should use faster refresh rates, dim and small displays (such as laptop displays), and make sure that your vision is otherwise normal. We have found that some people do better using projection systems -- the combination of a large "screen" and a LED type projector can be useful.
Some people just can't tolerate bright light. This is called photosensitivity in general, but the terminology varies a bit according to the supposed cause. Discomfort from bright light is most commonly complained of in migraine sufferers, where the condition is called "photophobia". Migraine patients are wired differently (DaSilva et al, 2007) and often have central sensitivity to a wide array of sensory inputs. Other sensory amplifications which are common in persons with migraine include allodynia, sensitivity to weather changes, hyperacusis (sensitivity to loud noises -- called phonophobia in migraine patients), motion sensitivity, and medication sensitivity. Migraine patients are also more sensitive to visual motion (which is something different -- a variant of motion sensitivity). The treatment in migraine is avoidance, migraine medications, and dark glasses.
Sometimes photosensitivity/photophobia also is found in people with dizziness, especially after head injuries. Light sensitivity can get mixed up with sensitivity to visual motion, e.g. visual dependence, which can be upregulated in persons with unreliable vestibular systems.
Photophobia is not at all specific to migraine however, and can also accompany migraine imitators such as meningitis, and vertigo imitators such as Cogan's syndrome. Dry eyes is another common cause of photosensitivity (Digre et al, 2012). This is different than visual dependence, and of course different from the discomfort that migraine sufferers excperience from bright lights.
Photophobia is rarely reported in persons with "sensory processing disorder". This term is vague and we think it just translates into "I have no idea what is wrong with you".
This is a mainly theoretical discussion about treatment. There are many potential avenues