Case Vignette: Emily is a 37-year-old who is following-up at the clinic for dizziness. She doesn’t understand why she feels dizzy despite all her inner ear tests being normal. “Isn’t the inner ear the balance center? So, if my inner ear is normal, why am I still dizzy? And why do so many things seem to affect the dizziness? Will I always be like this?”
These are common and good questions patients have about dizziness. However, the inner ear is just one player in the dizziness experience. Just like members of a school committee, all members work together to plan, organize and execute plans. However, every member of that committee will have their strengths and weaknesses which will be felt by the whole committee and the work it accomplishes.
So, let’s start by reviewing some of the players of the dizziness/sense of stability committee.
The vestibular nuclei are four brainstem regions that accept all input from the inner ear’s vestibule, the region responsible for detecting head position and motion. The vestibular nuclei work cooperatively with networks that span the entire brain to allow us to integrate our sense of where our body is into our conscious and subconscious existence. Definitely you do many activities every day that rely on this system. Have you ever stopped to think how you are able to do the following activities without conscious control?
- Reading and eye control: How do you know to where to move your eyes to read the next word? How does that change if you’re reading while on the move? Or while the object you’re reading is moving?
- Movement and balance: How can you run without falling? What happens if there is an unexpected divot in the field? How come you don’t tumble?
- Coordination: How can you time your tennis swing so that it hits the ball? How is that you can learn to hit the ball with the right force so that your shot clears the net and lands inbounds? How can you run to where you anticipate the ball will be?
- Spatial Orientation: How is it that you can walk a straight line while on the side walk? Or stay in your lane while driving?
- Automatic physiological adjustments: How do you discriminate between when you’re moving or when your environment is moving (e.g., the train next to you is pulling away slowly rather than you slowly rolling backwards)? How do you maintain adequate arousal (of consciousness) and conscious awareness of your body to do the task you want to do? How does your blood pressure stay regulated when you make quick movements? Why is it that you can get symptoms like fear and nausea in certain environments (e.g., heights, elevators) or that certain environments or movements cause certain emotions and memories?
As you can see, the ability to size up our environment requires much more than just our ability to detect the orientation and motion of our head (i.e., inner ear). If you had to design a robot with artificial intelligence (AI) to do some of the tasks outline above, you would need to use the information from the vestibular nuclei and integrate it with information with other sensors to get the job done. It is no different in our bodies. Using the same logic, problems in doing activities (like the ones listed above) would not necessarily only be due to problems with the vestibular nuclei or information coming from the inner ear. An issue with any of the other sensors or the pathways that connect them, or the way they communicate with one another would be sufficient to cause inefficiency.
In the human body, some examples of the many regions of the brain that communicate with the vestibular nuclei are:
- The visual system – see VVM article for more information on how this information is integrated with vestibular input by the brain.
- The somatosensory system – see VVM article for more information on how this information is integrated with vestibular input by the brain.
- Nuclei that control eye movements – when your head moves while walking or jogging, how come what you see remains steady rather than bouncing up and down with you?
- Cerebellum – responsible of adapting postural and eye movement responses based upon prior experience (Jacob et al., 2007). Do you remember the physical exam doctors perform where they have you repeatedly move your fingertip between the tip of your nose and the doctor’s finger?
- Autonomic functions – connections to multiple areas (such as locus coeruleus, nucleus of the solitary tract, area postrema, central nucleus of amygdala, parabrachial nucleus, infralimbic cortex, hypothalamus) that process stress, nausea/vomiting, emotional memory, arousal, fear, emotional regulation, memory, blood pressure, circadian rhythm, etc. (Balaban et al, 1994).
- Spinal cord – controlling posture of the head and body (http://vestibular.wustle.edu/vestibuar6.thml).
- Multiple regions of the cortex – for properly sizing up our environment and how we can navigate within it efficiently (Urbanski et al., 2008).
- Areas deeper down in the cortex – the thalamus serves as a relay center between the vestibular cortex and the reticular formation, which is responsible for arousal (of consciousness) and conscious awareness of body (Dieterich et al., 2008).
Case Vignette: Emily was educated about the above: all the different parts of the brain that are involved in processing and executing perception of stability and postural control. These represent many areas that can be trained to improve balance. So, if treatment only focuses on inner ear issues (which she does not have), the results will be equally ethereal.
Case Vignette: Emily finds her dizziness is much worse around her menses, when she’s stressed and when she’s tired. She admits to having struggled with anxiety her whole life and she finds it’s worse now because she finds her recovery is slower than she was expecting and doubts as to whether she will ever be getting better keep resurfacing.
Examples of conditions that can cause non-inner ear dizziness, even in a non-concussion population, are:
- Migraine – it is estimated that about 25% of migraineurs will experience vertigo stemming from their migraines, possibly not at the same time as their headaches, making it amongst the top causes of dizziness (Teixido et al., 2014). Migraine is a process that affects the entire brain, including many of the areas that are involved in perception of balance and postural control, as discussed in the answer to Question A, above.
- TBI – listen to our podcast episodes 13 & 14 for more information about dizziness in this context. It is estimated that about 15% of concussion patients will go on to develop chronic dizziness that will require treatment.
- Anxiety – it is estimated that about 60% of dizziness patients have anxiety; 50-85% have panic disorder and 45% have depression (Brandt, 1996; Holmberg et al., 2007; Holmberg et al., 2005; Aronson et al., 1988; Jacob, 1988). From the answer to Question A of this article, above, you can see how anxiety can occur in dizziness patients as areas of the brain that process anxiety are involved in networks that process postural control and sense of stability.
- Disuse disequilibrium – (i.e., deconditioning) less exercise can cause reduced muscle bulk, joint range-of-motion and reaction time which can make one feel more unstable and dizzier; the propensity to developing this increases with advancing age. (Herdman et al., 2000)
So, the question then becomes how does one know what is causing the patient’s symptoms?
Admittedly, there is a lot of overlap between the symptoms of these conditions and a patient can have more than one of these conditions at the same time. The history and physical exam become very important in teasing out what has the highest probability of accounting for the patient’s symptoms. In patients with more than one reasons for non-inner ear dizziness (e.g., anxiety and disuse disequilibrium) it may not ultimately be very important to delineate which condition is responsible for how much of the clinical picture. The name of the game is to enhance performance and function and this can always be trained; having a high index of suspicion of what the mechanisms of dizziness are in any given patient will make the treatment plan more efficient.
Case Vignette: Emily has anxiety and post-concussion syndrome. Both conditions affect the neural circuits discussed in the answer of Question A at the top of this article. Therefore, treatment will need to target both of these areas. Some patients can feel brushed off when they are told that anxiety is contributing to their “physical” symptoms. This requires a fair amount of education so that the patient understands that parts of the brain that process anxiety are also involved in one’s perception of stability. In Emily’s case, she was educated that dizziness is an experience rather than a concrete thing. For example, an avocado is a thing but its flavour is an experience; surely, we can agree that most of us will have a slightly different experience of the way avocado tastes. Like that, all of us will have a different experience of the way dizziness is experienced, and each one of our experiences are valid and real. Less efficient brain function can occur when we are tired and brainwaves are slower, or when we are stressed and some regions of the brain are more active, disturbing the ideal balance of the brain. Emily was then able to understand her dizziness experience better and open her mind to how possible treatment strategies fit into her care (see section E, below).
Case Vignette: Emily was initially noted to have BPPV which was treated and then went away. However, her dizziness persisted, albeit differently than it was before she had her BPPV treated. She wonders if the two are related; and how to know if the treatment of BPPV was successful?
Yes, this is very common. For example, we have had many patients with BPPV (Benign Paroxysmal Positional Vertigo, an inner ear condition) who went on to develop a second reason for their dizziness, a non-inner ear-related cause for their dizziness, above and beyond BPPV. About 18% of BPPV is said to be due to concussions (Baloh et al., 1987).
Other common conditions that can trigger non-inner ear-related dizziness are (Staab et al., 2007; Staab et al., 2009):
- Vestibular neuritis (~7-10%);
- Migraine (~15%);
- mTBI (~15%);
- Panic disorder (~15%);
- Generalized anxiety disorder (~15%);
- Autonomic dysfunction (~ 7%);
- Dysrhythmias (i.e., cardiovascular causes) ;
- Other general medical conditions or an adverse drug reaction (~ 2%).
Inner ear conditions like, BPPV, tend to be felt more like vertigo. Vertigo is the illusion of movement of oneself or the environment upon moving one’s head, due to an abnormality somewhere between the inner ear and the cortex, where vertigo is perceived.
There are several diagnoses for types of dizziness that come from areas other than the inner. This is discussed at length in our podcast episodes on dizziness, episodes 13 & 14. One of the most common of these diagnoses is Chronic Subjective Dizziness (CSD). There are many other synonyms for CSD, and many other terms to describe specific features of CSD. CSD is described as a vague, daily, unsteadiness (i.e., swaying or rocking) that is always there but can wax and wane depending on many factors (i.e., stress, fatigue, position). It is called CSD when it has been there for at least 3 months. CSD can:
- Occur when the patient moves or their surroundings move, it does not relate to a specific movement direction or position like for inner ear-related causes of vertigo, however, it tends to be worse in standing/walking than it is in sitting, which in turn, tends to be worse than when lying down.
- Be aggravated by exposure to large-field moving visual stimuli (e.g., like the commotion in a train station) or complex visual patterns (like busy tiling/décor in hotel lobbies or museums like the Royal Ontario Museum).
- Be aggravated by exposure to small-field, precision, visual activities (e.g., reading, using a computer, fine motor tasks with the hands – like cutting hair, sewing, machine repair, etc.).
Vestibular tests for CSD are usually found to be normal; most of the abnormalities seen are functional deficits that tally with reports by the patient of what they can or cannot do. Normal vestibular tests may cause patients to feel brushed off, or that the cause for their dizziness was “missed” by those tests. Patients tend to feel more validated when an objective abnormality is found. However, the way to validate patients is to educate them about their experiences as we are doing in this article. Once they appreciate the nature of their problem, patients are then more receptive to the factors that influence it and how to improve it.
Case Vignette: Emily was educated about what BPPV is and how common it is in the post-concussion population. Although the name implies that it is benign, it did not feel “benign” to her as it triggered persistent dizziness of a different nature. She was explained that they were in fact different causes of dizziness: BPPV is treated with repositioning maneuvers and the symptoms are sort of there or not-at-all (i.e., situation is more ‘black-and-white’); her other dizziness needed to be treated differently and would be there in varying levels of severity depending on many other factors like fatigue and stress (i.e., ‘shades of grey’). As is the case with post-concussion patients, BPPV crystals tend to be more recurrent and involve multiple canals and be a little more resistant to treatment (Katsarkas 1999). So, when Emily had a recurrence of BPPV, she was able to take it in stride and not fear that both her conditions were getting worse, and that all her treatment for the second cause of dizziness was not all for naught. She would come into the clinic and have the specific canal that was affected identified with our video frenzels. Being able to see the abnormality on video made her feel validated. The crystal was then repositioned, knowing full well that she may need to have this done a few times before it takes. She also knew that this process of recurrent BPPV would eventually peter out and that the worst thing she could do is worry about it. Being able to see the resolution of her telling eye movements using the video frenzel system after successfully repositioning the crystal also made her feel validated. And it was easier for her to understand now that her CSD is actually getting much better by helping focus her on objective markers of improvement like the fact that she was back at work and back to exercising, both of which she found enjoyable.
Case Vignette: Emily wanted to know why not everyone who gets BPPV develops CSD? She also wanted to know why and how anxiety made her dizziness worse?
Certain behaviours have been identified to contribute to the development of CSD (Staab et al., 2007):
- Anxious, introverted temperament or pre-existing anxiety disorders.
- High level of anxiety and hypervigilance about vestibular symptoms; and excessive worrying about potentially adverse outcomes from one of the potential triggers mentioned above in section C.
- Development of an anxiety or depressive disorder during the course of CSD.
Case Vignette: It was explained to Emily that anxiety can be seen as increased frequency of electric activity in the circuits of the brain that process fear, attention and sensory regulation.
- These areas of the brain communicate with the same parts of the brain that process feelings of dizziness, and so, in this case, anxiety will actually increase the ‘volume’ of the dizziness directly experienced by her brain.
- Secondly, the more she focused on what was wrong, the more she unintentionally ‘trained’ the propensity to get more of what’s wrong.
- Thirdly, because anxiety creates desperation, she pushed her system into a fight-or-flight situation, and the brain does what it’s designed to do – adapt. That is, her brain makes an attempt to make up for what was lost (e.g., accurate vestibular signal because of BPPV) by changing the master formula it applies to spatial awareness, postural control and the sensation of stability. Our article on Visual Vestibular Mismatch goes into this in greater detail but in summary, Emily unwittingly, in one fell swoop, changed the recipe for balance that took her 37-years to develop. Even though the ‘ingredients’ (vestibular input, visual input, somatosensory input) were all of normal quality, the ratio of the ingredients was all changed, for the worse. She had developed more primitive postural control strategies, like the ones she would have had around 2 years old. So, her body replaced her vestibular system’s input with her visual system’s; a much more primitive strategy for postural control and perception of stability, and she felt it by having dizziness. Logically speaking, this is a perfectly reasonable thing for the brain to do, when one what part of the system is not carrying its load, then another part usurps its duties; however, in this case, there is a ‘false alarm’ and every part is actually able to carry its own load. We just have to prove it to her.
Managing anxiety is a big topic and one that has been touched on throughout our podcast “Concussions 101”. However, certain ways of thinking, or cognitions, are maladaptive and add ‘fuel to the fire’; they kind of set one up to perpetuate this ‘false alarm.’ For example, Emily kept thinking that she would never get better despite the facts showing the contrary.
She displayed examples of several cognitive distortions:
- Emotional reasoning: I feel like all hope is lost; therefore, all hope is lost. Are you sure, maybe you feel like all hope is lost; but all hope is not lost?
- Fortune-telling: I know I’ll never get better. How do you know? Is it possible that you will get better especially since you are doing so much better now? Look at all the things that have improved? And we know BPPV is the cause for your setback which will be better in a day or two with treatment.
- Overgeneralizing: I haven’t been able to get back to my goal of swimming, so I’ll never swim again. As we explained, we want you to rebalance your system on dry land first. You have progressed so much but once you progress a bit more, your system will be resilient enough to deal with the different sensations involved in swimming, e.g., head is horizontal, no feeling of the ground pushing back up against your feet, visual system is not under optimal conditions. With some more progress, you will get back to swimming.
- Mind-reading: I know my boss thinks that I’m faking and that my symptoms are not real. How do you know? Perhaps she believes you but she has deadlines too and she is thinking of how she can make them with you not functioning at your peak ability?
- Polarizing: I’m always dizzy and so everything sucks. Perhaps things are not so black-and-white. Perhaps things are not as bad you feel. Let’s look at the facts…
Correcting misunderstandings of her condition and her cognitive distortions like the above made a big difference in the way Emily experienced her dizziness, almost overnight; it reduced the dizziness’s ‘volume’ if you will. In many ways, it would be advantageous, if possible, to embrace the dizziness as a novel and temporary experience that can be enjoyed like when one is tipsy after a drink too many. This level of acceptance is the best springboard to improvement.
For example, many don’t know this, but quicksand is only about 3 feet deep, and it is denser than humans, so nobody should drown in it. However, if panic sets in, desperation may cause you to force a situation, even though the ideal solution was on its way. Just a little patience, sound reasoning and a calm and collected approach is required.
- Education. Knowledge is power; and it also checks anxiety as seen in the vignette above. When it’s dark out and you see something squiggly on the ground, and panic sets in as you think it’s a snake, symptoms of sweating, muscle tension, palpitations and butterflies in the stomach, are very real. However, once some light is shed on the situation (by your phone) you realize it’s just a rope and all those symptoms vanish very quickly. Like that, once the patient no longer fears the unknown, the power it had over them goes. Education also helps patients learn what they can expect so that they can plan for the road ahead. It also is an opportunity to discuss the treatment plan and to garner enthusiasm and confidence for the same.
- Anxiety. There are many techniques to treat this and that information can fill a text book. But generally, effective strategies for Emily were Cognitive Behavioural Therapy (CBT) – especially since she had pre-existing anxiety; relaxation techniques – guided mindfulness meditation, muscle tension awareness training, resonance frequency breathing; therapeutic activities and managing her schedule better to check her ‘time poverty’. Rest breaks should not only be realized at night when it’s time to go to bed. How well would are children perform in school if that’s the way it was? For optimal neurological performance, a balanced lifestyle, including play time and downtime, is important.
- Autonomic nervous system regulation. HRV training and a progressively demanding cardiovascular exercise regimen helps strengthen the autonomic nervous system and makes it functioning more efficient.
- Mindfulness of sensory reweighting. We can train the patient to become aware of what all the senses bring to their current experience of stability. Then we can train them to use more efficient strategies. In a sense, if a patient can re-adopt the mindset they would have had as children learning this the first time around, it will be equally likely the success would be had. It’s not like as developing children we had to go to therapy to learn how to feel stable (at least for the vast majority), so if we can set up the conditions under which you were initially exposed to balance challenges, it is commonly seen that the right solution comes naturally. In that context, it is very important to monitor for fight-or-flight reactions, or panic symptoms, as those are counterproductive. It’s not like little Johnny would get panicky when he tripped and tumbled; he would grin and get up and do it again without even a thought as to whether he would tumble again. This requires a great deal of mindfulness and is a theme that permeates rehabilitation in general. Basically, we are helping patients retrace their steps in normal human development with an eye of identify any deficiencies and plugging them up with rehabilitation.
- Core stabilization and efficiency. Rehearsing postural control strategies in different contexts is a natural extension of ‘mindfulness of sensory reweighting’, discussed above. People have to learn how meet the expected and unexpected with ideal movement strategies. At first, things need to be programmed consciously and then it becomes subconscious, like riding a bike. Eventually, we need to lessen safety behaviours – i.e., stop touching furniture/walls, get your head up while walking, avoid using trekking poles, try using the treadmill without holding on, sit on stability ball, experimenting with doing things with your eyes closed and see if you can get the sense of stability to tally with what that movement feels like with eyes open.
- Habituation to motion intolerance. This employs the same principle of an allergy shot. If there is something that you’re allergic to, we will give you a little bit of it, not enough to cause a significant reaction but enough for your body to get used to it so that when it does encounter the allergen, it won’t “overreact”. This is basically saying that we need to get used to the discomfort that motion causes. You don’t have to love it, but try not to hate it. Most enjoyable things in life started out a bit uncomfortable, i.e., leaving your mom to go to school was once a terror but when you graduate and secured a profession and income you like, you are happy you did it. Like that, embracing the dizziness will set you free. It can be your sensei. If the discomfort of motion seems to be tugging you in a direction you don’t want to be going, it’s important to become aware of any fight-or-flight response and quell it. There are many strategies to do so as discussed in point 2 (“Anxiety”) above in addition to consciously emphasizing to yourself the experience of feeling grounded, connected to the ground by gravity. Get in touch with the weight of your in a spirit of mindfulness. This needs to be done often enough. The name of the game here is to do it while minimizing any effects on symptoms.
- Visual motion desensitization +/- vision therapy. This is similar to point 6 above except it rather than getting used to your own movement, you are gradually getting used to the motion of the world around you as seen through your eyes. Sometimes vision therapy helps here
- Fatigue/Energy management. This has been discussed at length elsewhere but is very important to check the “time poverty” many of us find ourselves in nowadays as we are pulled in so many different directions.
- Fostering confidence. Ultimately, like a bird leaving the next, the ability to perform rehab in real-life settings that you will encounter in daily life is what will foster confidence and in turn, enjoyment. This will also help integrate rehab into the daily routine so that it gets done often. We have often given people strategic exercises that involved grocery stores and libraries.
Aronson, T. A. & Logue, C. M. (1988) Phenomenology of panic attacks: a descriptive study of panic disorder patient’s selfreports.Journal of Clinical Psychiatry, 49, 8–13.
Balaban CD, Beryozkin G. Vestibular nucleus projections to nucleus tractus solitarius and the dorsal motor nucleus of the vagus nerve: potential substrates for vestibulo-autonomic interactions. Experimental Brain Research. 98: 200-12. PMID 8050507 DOI: 10.1007/BF00228409
Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases. Neurology 1987; 37: 371–8
Brandt, Thomas. (2003). Phobic postural vertigo. 10.1007/978-1-4757-3801-8_32.
Dieterich M, Brandt T., Functional brain imaging of peripheral and central vestibular disorders, Brain, Volume 131, Issue 10, October 2008, Pages 2538–2552, https://doi.org/10.1093/brain/awn042
Herdman S., Clendaniel R., Vestibular rehabilitation, 4nd ed. Philadelphia: Davis, 2014
Holmberg, Johan & Karlberg, Mikael & Harlacher, Uwe & Magnusson, Måns. (2007). One-year follow-up of cognitive behavioral therapy for phobic postural vertigo. Journal of neurology. 254. 1189-92.10.1007/s00415-007-0499-6.
Holmberg, Johan & Karlberg, Mikael & Harlacher, Uwe & Magnusson, Måns. (2005). Experience of handicap and anxiety in phobic postural vertigo. Acta oto-laryngologica. 125. 270-5. 10.1080/00016480410023001.
Jacob RG. Panic disorder and the vestibular system. Psychiatr Clin N Am 1988; 11: 361-374.
Jacobs, Jesse & Horak, Fay. (2007). Cortical control of postural responses. Journal of neural transmission (Vienna, Austria : 1996). 114. 1339-48. 10.1007/s00702-007-0657-0.
Katsarkas A. Benign paroxysmal positional vertigo (BPPV): idiopathic versus post-traumatic. Acta Otolaryngol. 1999;119(7):745-9.
Staab, Jeffrey & Eggers, S & Neff, B. (2010). Validation of a clinical syndrome of persistent dizziness and unsteadiness. J Vest Res. 20. 172-173.
Staab, Jeffrey & J Ruckenstein, Michael. (2007). Expanding the Differential Diagnosis of Chronic Dizziness. Archives of otolaryngology–head & neck surgery. 133. 170-6. 10.1001/archotol.133.2.170.
Teixido M, Carey J. Migraine – More than a headache.
Urbanski, Marika & Thiebaut de Schotten, Michel & Rodrigo, Sebastian & Catani, Marco & Oppenheim, Catherine & Touze, Emmanuel & Chokron, Sylvie & Meder, Jean & Levy, Richard & Dubois, Bruno & Bartolomeo, Paolo. (2008). Brain networks of spatial awareness: Evidence from diffusion tensor imaging tractography. Journal of neurology, neurosurgery, and psychiatry. 79. 10.1136/jnnp.2007.126276.
Research & writing: Dr. Taher Chugh
Last update: August 2019