If scenes like the picture above bother you, there is a chance you have VVM.


VVM is a common phenomenon we are seeing post-concussion. It is intimately tied to our balance (and its perception), the function of our autonomic nervous system and ultimately our quality of life. It is something almost all of us take for granted as it developed normally in almost all of us from infancy to adolescence.


So, what is it we are discussing here?


Let us back up and talk about dizziness a bit first. Many of our post-concussion patients complain of dizziness and/or imbalance. Ever wonder about the factors that contribute to your balance and/or dizziness? What gives one person the ability to balance on a tight-rope or score an acrobatic goal?


The systems involved are the following:

1. The vestibular system – The vestibular system is discussed in a general way elsewhere on this website. It is the gyroscope of the body that tells your brain how you are oriented relative to gravity. The brain uses this information in the following ways:

  • VOR (vestibulo-ocular reflex): to control eye movement when you move your head so that images remain stable on your retina. This system is intact by 1 year of age and is fully mature by 3 years old.
  • VSR (vestibulospinal reflex): to recruit your musculature to maintain balance while you are moving. The vestibulospinal mechanism, or the effectiveness of the vestibular system in postural control, continues to develop beyond 15 years of age.
  • VCR (vestibulocollic reflex): to stabilize the neck musculature to stabilize the head.

2. The somatosensory system: by 3 years of age, somatosensory effectiveness in postural control emerges. The somatosensory system is a broad system of nerves and pathways that relay information about sensations detected all over your body to your brain. There are different types of sensory nerves that have specialized functions. Some of the things your somatosensory system detects are: heat, pain, touch, chemicals, proprioception (a signal to represent the position of a limb relative to an adjacent limb at any given moment), haptic perception (the ability to judge the way your environment is while you are moving, i.e., like a blind person getting around with a probing cane or white cane), and kinesthesia (sense of movement). Anyone who has fumbled around in a dark room before can appreciate how the somatosensory system was helpful.

3. The visual system: although visual system’s effectiveness in postural control is less mature than that of the somatosensory system before age 7.5 years, it remains the the dominant source of information for postural control in standing in children less than 7.5 years old. The visual system is complex and performs many tasks. Some of these tasks include visual acuity, contrast sensitivity, pattern perception, facial perception, being able to see 2 objects side by side (i.e., overlapping in your field of view) as separate, colour perception, depth perception, motion perception and much more. One can see how visual cues can give you information that would be helpful to maintaining posture, whether you are just standing still or in motion.

4. Your belief system: If you have a strong belief about your balance capabilities in different contexts, this will enhance your balance. Having done an acrobatic feat before will give you confidence that you can do it again even if it took you a while to work up to that point. Training in different postures in different contexts is important for the development of postural abilities. The time period between the ages of 4 and 6 years is a transition period in which mature patterns are emerging. These mature patterns involve integration of all of the above systems. Efficiency in doing this evolves between 7 and 15 years of age.

A disease to any of these systems will affect your ability to balance and/or your sense of stability. Depending on which of the above systems are affected, and where they are affected, the clinical picture will differ. Moreover, even in those without dysfunction in these areas, everyone has their own trained capability in each one of these systems. The capability of these systems in turn can depend on and/or correlate with numerous other factors, e.g., your diet and any possible deficiencies, medication you may take, past medical history, your birth weight!, etc.

VVM is a type of dizziness that results from your vestibular system telling your brain something that is at odds with what your visual system is telling you.


When you are in a train and the neighbouring train starts to depart, how do you know you are not rolling backwards? The visual signal is identical in both scenarios. The answer is because your vestibular system – and your somatosensory system – tells you that you are not moving. The vestibular system is unique in that it is dependent on gravity (which is fixed, doesn’t change) and it is sensitive to any acceleration. It also, by design, has a physiological setup that is redundant in many aspects. That is, the vestibular system has many structures that do the same task, making it more resilient to injury. In the train example above, your vestibular system does not detect any motion so it tells you that the illusion of self-motion is not real. Thus, the visual system operates in the context of the vestibular system. This makes sense for the above reasons but also when you consider that your eyes are in your head, and an accurate assessment of where your head lies is important for providing context to what you see.


The hierarchy of these systems in our internal map develops sequentially as discussed above. In normally developed individuals, vision plays the least dominant role in postural control when compared to the other systems mentioned above.

This means the brain does not have the same quality of reliable information coming from the vestibular system. This means that patients resort to other systems, i.e., visual system, to compensate for this deficit. Both systems are usually involved in postural control in healthy people, but as previously mentioned, the visual system is usually subservient to the vestibular system. But in VVM patients, this hierarchy is reversed, that is, the visual system becomes the new preferred system and the vestibular system is subservient to it. That is, these patients are said to be visually dominant. This is a problem for several reasons:


1. The information we take in visually is rarely stable/fixed/monotonous like gravity is (you will remember, the vestibular system is like a gyroscope that is dependent solely on motion with respect to gravity);

2. The visual system is less efficient at detecting motion of yourself relative to your environment (remember the train example above);

3. Relying on a weaker strategy (i.e., visual compensation for vestibular shortcomings) prevents patients from training better strategies (i.e., restoring the vestibular system to its throne); that is, it limits a patient’s ability to compensate or perform better.


Moreover, this is particularly problematic and frustrating for many post-concussion patients because 2/3 of these patients also have injury affecting the functioning of the visual system. Any effort to rehabilitate post-concussion (focal, more on this distinction later) visual issues before restoring the vestibular system to its throne may just further empower the minister (i.e., the visual system) in this neurological coup d’ état.

Before we get into this, right of the bat we will mention that the following answer is largely academic. For patients who are not interested in superfluous explanations, you can skip to the next section. Just know that the visual and vestibular systems are two sides of the same coin. The idea of (artificially) separating them is only useful for academics but not for rehabilitation.   There is still a lot we don’t know about the neurophysiology of the experience of vision. Without going into detail about Post-traumatic Vision Syndrome (PTVS), this is a diagnosis often given to patients who satisfy the criteria for the same by behavioural optometrists post-head injury or post-neurological injury. Generally, it hinges on the theory that there are two main processes in the visual system: focal and ambient. The focal represents the ability to focus in detail on an object. Most of us know that we can use our peripheral vision to sneakily focus on something, but we also know that it is easier to do so when the eye is pointed at the object of interest (i.e., using our macula). Conversely, our peripheral vision is mostly used to carry out the ambient process. The ambient process gives information we use for balance, coordination and posture. Nerve fibers from the peripheral part of the retina that form the ambient process travel to midbrain where they communicate with other systems involved with motion – somatosensory and vestibular. Furthermore, the focal system operates in the context of the ambient system similar to the way the visual system operates in the context of the vestibular system in VVM theory. PTVS is a syndrome that occurs because there is a new imbalance between the focal vs. ambient visual systems; specifically, there is attenuation of the ambient system. You will remember that it is the ambient system, according to this theory, that depends on the vestibular and somatosensory system for accurate spatial orientation and that one’s focal vision depends on one’s ambient vision. Any way you cut it, whether from an optometric or vestibular perspective, vision operates in the context of spatial orientation which is largely dictated by the vestibular and somatosensory systems.     PTVS contains many characteristics; some of them are spatial disorientation and unstable ambient vision (vs. focal vision) which have many similarities to the symptoms of VVM. One can start to look for similarities in the physiological mechanism of both conditions, but there are many question marks surrounding both. One thing is for sure, similar areas of one’s central nervous system are involved and similar types of injuries (e.g, whiplash, concussion) can cause them.   From a rehabilitative perspective, PTVS and VVM are both attempts to describe an overlapping set of symptoms that occur in the post-concussion population. Both call for similar rehabilitative techniques for restoring spatial orientation, balance and decreasing ‘dizziness’ are the same.

The answer is yes. This shows that neurological damage is not the cause of VVM. It is caused by a faulty compensation to attenuated vestibular signals.

Nobody knows. In our program, we notice (anecdotally) that VVM patients tend to be more conscientious-type people who identify themselves as “type-A”. Regardless of pre-injury temperament, in our clinical experience, the patients that succeed faster are those who adopt a spirit of mindfulness and are open-minded to biofeedback-type strategies. There is plenty of evidence for biofeedback training for many conditions, e.g., migraine, tension headaches, IBS, hypertension, temporomandibular joint problems, chronic pain, panic disorder, etc. Many of these conditions present themselves as part of the post-concussion syndrome. From a nonscientific perspective, it makes sense that a mindful attitude would be conducive to training neurological skills like rectifying VVM; When we were children and most active in developing our visual and vestibular systems, our spirit was one of mindfulness. When a child attempts to toddle on a curb and loses her balance, does she chastise herself for not being perfect? Or does she get up with a grin and try again with a spirit of curiosity and joy?
For VVM patients, there are no practical, objective investigations that adequately reveal the mechanism of injury (at a molecular level), the nature of the lesion or the best course of therapy. In patients with concussions, this condition will not be seen in an MRI or CT scan.   VVM is diagnosed clinically. That means an excellent history and physical exams is necessary. The history and physical exams have to be both broad and specific so that other conditions are ruled out or identified so that an effective rehabilitation strategy can be created.
Many VVM patients (concussed or not) withdraw from activities and places they find offensive. This will reduce their quality of life. Many either develop clinical depression/anxiety disorders or appear to have developed these disorders. It should however be clear to the reader by now that VVM is not a psychiatric illness.
Because of diverse lifestyles, varying patient temperaments, different past medical histories and co-existing diagnoses, and that VVM is very unintuitive, it is described and interpreted differently by different patients. Some patients find the visual vestibular mismatch a mild nuisance while other find it completely debilitating. Some afflicted patients complain solely of balance issues, others complain of solely autonomic symptoms – light headed, fatigue, exercise intolerance, sweating a lot or feeling dry, feeling cold or warm, bloating, changes in bowel habits, change in urination, difficulty with vision, nausea, postural changes, tremor, changes in your breathing, numbness/tingling, sleep changes – while most patients have some unique interplay of symptoms in both categories. Some patients have different levels of sensitivity to different triggers. The condition can be caused by many different injuries, most commonly in our practice is obviously concussion and whiplash, but sometimes (rarely) it can occur with no injury at all. To add to the skepticism of people who judge VVM patients, many patients that have had similar injuries (i.e., concussion, whiplash, etc.) don’t suffer from VVM. The heterogeneity of VVM creates a stigma that patients “are making it up” or they are hysterical; Or that they have other possible hormonal, neurological, psychological diagnoses.
Treating VVM effectively hinges on thorough history and physical exams. As this is a functional injury, assessments and rehabilitation is structured in a way to gradually restore the patient’s functional ability. This involves thorough assessments of somatosensory, vestibular and visual capabilities/deficiencies. Neuromuscular therapy, vestibular therapy and judiciously applied vision therapy in an integrated fashion (like in life and normal human development) is the cornerstone treating balance disorders. As mentioned above, these patients tend to have many symptoms so strategies to mitigate the effect of the same while maximizing their involvement in life are also implemented. To withdraw patients entirely from activities can lead to problems with sleep, mood, cognition, worsening VVM and so on. Although VVM is not a psychiatric diagnosis, VVM patients have a higher incidence of psychiatric diagnoses. Strategies to help with symptoms reduction, functional enhancement and mood may include but are not limited to:
  1. CBT for insomnia for those with sleep difficulty
  2. Mindfulness, CBT and/or other psychological therapies
  3. Energy management
  4. School/Work accommodations
  5. Biofeedback modalities
  6. Therapeutic activities
  7. Treating other general medical conditions (e.g., sinusitis, etc.)
  8. Cardiovascular exercise program
  9. Dietetics
  10. Cognitive compensatory strategies and rehabilitation
  11. +/- Pharmacotherapy
  It must be apparent now that this condition can be well treated if all relevant diagnoses are brought to light and treatment is carried out on different fronts in an integrative, coordinated, multi-disciplinary fashion. Many disciplines are involved in the care of VVM patients to enhance successful reintegration to life and all its joys.
In our program, we have seen good outcomes. We attribute this to our multidisciplinary team approach. Success hinges on the ability to address all the issues that are hindering a patient’s function and then having the skillset and technology to rehabilitate them. Those who are able to comply with recommendations have the best outcomes. Those who struggle tend to be the patients who struggle with mood and energy management. That is, it tends to be those who feel trapped in a psychosocial situation that prevents them from engaging in rehab as required.

Research & writing: Dr. Taher Chugh

Last update: August 2018