What is Benign Paroxysmal Positional Vertigo?
Benign paroxysmal positional vertigo (or BPPV) is one of the most common causes of dizziness and vertigo. It can create a sudden sensation of you spinning or falling, or the world spinning around your head. It can create difficulty standing or balancing, make it impossible to walk, and provoke nausea and vomiting. BPPV can range from a mild issue to a severely disabling condition. It can be a source of extreme anxiety and frustration.
How Common is Benign Paroxysmal Positional Vertigo?
Benign paroxysmal positional vertigo is the most common cause of vertigo. It accounts for roughly 30% of diagnoses in dizzy patients (1).
BPPV has been estimated to affect up to 50% of people at some point during their lives. It becomes progressively more common with age (2).
What are the Symptoms of Benign Paroxysmal Positional Vertigo?
The most common symptom of BPPV is a sensation of spinning or falling that occurs after tilting or turning your head. BPPV can also produce a lack of coordination, difficulty with balance and gait, and create issues with sudden movements. It can make people feel light-headed and disoriented as if they are about to pass out. It can lead to nausea and vomiting.
BPPV can make it very challenging to get out of bed without losing your balance and falling. It can create cognitive difficulties and brain fog. In some cases the primary symptom of BPPV can be severe anxiety and panic attacks.
What Causes Benign Paroxysmal Positional Vertigo?
The vestibular system, also known as the inner ear, has two systems of receptors known as the otoliths and the vestibular canals.
Otoliths are specialized receptors that line an area known as the vestibule. The vestibule is a fluid filled compartment with hair cells that are attached to multiple sides of the compartment walls. detect your head’s position relative to gravity, such as when it is tilted or translating (up - down - side to side). The hair cells are embedded with tiny calcium crystals, called otoconia. The otoconia make the hair cells bend down towards gravity. When the hair cells bend, they fire inputs to the vestibular nerve, and impulses are conducted into the brainstem, cerebellum, and brain. Whatever the position of the head, some cluster of hair cells will be bending down, which tells the brain where the head is in relation to gravity at all times.
The inner ear also contains a series of membranous canals encased in bone known as the vestibular labyrinth. The semicircular canals are fluid-filled tubes that contain specialized hair cells. When the head moves, the inertia of the fluid makes it take a moment for the fluid to start to move. This bends the hair cells, which activates the vestibular nerve, and impulses are conducted into the brainstem, cerebellum and brain. These inputs allow the brain to perceive where the head is in relation to the body, as well as what direction the head is moving.
The fluid of the vestibule is continuous with the semicircular canals. For a host of reasons, otoconia crystals can sometimes detach and float around the vestibule. At times they can float into one or more semicircular canals, where they do not belong.
BPPV occurs when the crystals of the otolith are dislodged into the semicircular canal(s) and become trapped there. When otoconia migrate into one or more of the semicircular canals, they make these receptors gravity-dependent. This is a major problem, as the semicircular canals normally only respond to head movement. In BPPV, changes in head position can allow the loose otoconia to start to float down toward the bottom of the canal. This can create fluid movement inside the canal, which bends the receptor hair cells and creates a sensation of movement.
What are the Consequences of Benign Paroxysmal Positional Vertigo?
In most cases, BPPV is a mild issue that goes away on its own. People often experience BPPV after spending time tilted back in a dental chair, or from having their head extended while getting their hair washed. In many cases, people wake up feeling ok, roll onto their side, a crystal starts to float down a canal, and after a few seconds they start to feel spinning or falling.
BPPV can also become a long lasting and even disabling issue. This is frequently the case where more than one canal system is involved.
When BPPV has been present for an extended period of time, the brain will begin to compensate for the inappropriate input from the involved vestibular canal. Vertigo is by definition a sensory mismatch. The vestibular signal from the involved semicircular canal does not match inputs from the eyes or body in BPPV, which creates the sensation of vertigo. Over time the brain will learn to ignore the inappropriate vestibular signal and accept it as a new normal. This does not mean that all symptoms will resolve as the BPPV becomes compensated. It is very common that people with long standing BPPV present with primary complaints of anxiety and panic disorders, cognitive difficulties, headaches, memory problems, and a host of other neurological symptoms.
Unfortunately, when symptoms subside, it is rarely because the disorder has spontaneously fully resolved. Our brains are constantly trying to adapt and change to the demands of the environment, a concept called neuroplasticity. If the receptors our brain uses to get information about the world have changed, the brain will attempt to respond to these changed receptors. While the patient may no longer experience dizziness and vertigo, they may develop secondary symptoms, including neck or back pain, headaches, brain fog, decreased executive function, balance issues or a general sensation of feeling “off.”
The unresolved sensory mismatches that exist in people with incompletely resolved BPPV can lead to significant decreases in quality of life, particularly as we age (5).
How Else Can I Get BPPV?
Benign paroxysmal positional vertigo is very common following a traumatic brain injury or whiplash injury. Head impact on a car’s headrest during a motor vehicle collision can forcefully dislodge a cloud of otoconia that will float through the vestibule. People may think they are fine after such an injury, go home to bed, and wake up spinning after the otoconia settle into a canal. The involved canal begins to provide the wrong information about where your head is in space and creates a vertigo-producing sensory mismatch with rapid changes in head movement. Provocative head movements occur when lying down, tipping the head up or down, sitting up from laying down or turning over in bed after waking, tilting the head back or bending down, such as to tie a shoelace.
The incidence of dizziness, vertigo and balance disorders following a mild traumatic brain injury (mTBI) is estimated to range from 15-78% in the general population and approximately 14% in hospitalized patients. BPPV is the common source of dizziness in the post-concussion population, and commonly involves more than one canal. It is more likely to recur than spontaneous BPPV, and more difficult to resolve (5).
How is Benign Paroxysmal Positional Vertigo Treated?
BPPV is typically treated with repositioning maneuvers, which involves moving the head through a sequence of positions that facilitate the crystals to float back to where they belong. The most common form of BPPV involves otoconia in the posterior canal. Historically BPPV was considered incurable and would be treated with surgical destruction of the vestibular nerve. The late, great Portland neurotologist John Epley developed the Epley Maneuver for repositioning posterior canal otoconia. This involves holding the patient’s head in a series of sustained positions that allow the otoconia to float back where it belongs. This revolutionary maneuver has resolved vertigo for millions of people (4).
Dr. Epley was a close friend to our practice. Our Dr. Zielinski had the honor of performing in our clinic the last repositioning maneuver Dr. Epley saw before his passing.
Simple cases of BPPV may require as little as one Epley maneuver. More complicated cases may require multiple maneuvers. When the lateral or superior semicircular canals are involved, other types of repositioning maneuvers become necessary. Severe cases may involve more than one canal being affected, which is common after sustaining a head injury.
How is the NeuroRescue Program Different?
There are many different forms of BPPV, and complicated cases may involve more than one canal mechanism. The mechanism of onset is also important, as post-traumatic BPPV is frequently much more complicated to treat and highly prone to recurrence (6). Most primary care providers are trained to recognize and at times treat single posterior canal BPPV, often with good results. More complicated variants are more difficult to properly diagnose, and it is common that we see individuals suffering with complicated polycanal BPPV that have been misdiagnosed, often with anxiety disorders.
Severe and complicated cases of BPPV can be challenging to diagnose and properly treat without appropriate technology. An accurate BPPV canal diagnosis requires the ability to see different patterns of spontaneous eye movements that occur in the dark when the head is placed in positions that activate various canals. The involved canal or canals are determined by specific patterns of spontaneous eye movements (known as nystagmus) that develop in response to particular head positions. These can only be properly seen when vision is denied, as we all use visual fixation on targets to override nystagmus. This analysis is impossible without infrared recording of eye movements with technology known as videonystagmography (7).
In more complicated cases of BPPV, additional technology may be needed to properly assess which canals are involved and require repositioning maneuvers. Video head impulse testing has been shown to be very effective in detecting specific canal involvement in BPPV where other forms of assessment may be ineffective (8).
As part of your NeuroRescue Program, we have all the tools needed to properly assess and address complicated variants of BPPV. We are highly skilled in BPPV treatment, and successfully resolve challenging cases on a regular basis.
It is also very important to understand the difference between peripheral and central vestibular disorders. Peripheral vertigo involves problems with the vestibular receptors themselves, with BPPV existing as the most common type of peripheral vertigo. Central vestibular disorders involve the vestibular circuitry within the brainstem and brain. The symptoms and findings of central vestibular disorders can mimic peripheral vertigo (9). Over time, incompletely resolved BPPV can lead to inappropriate central vestibular adaptation as your brain attempts to determine a “new normal'' input from your vestibular canals and calibrate eye movements to compensate for this. These changes create compensations that are in effect central vestibular dysfunction, and can create as many problems as they solve.
Central vestibular disorders are an entirely different set of conditions, and require the advanced neurodiagnostic testing technology we use in the NeuroRescue Program to properly diagnose. The strategies for rehabilitation of central disorders are also uniquely different for each patient. We work with central vestibular disorders daily, as there is a component of central vestibular dysfunction in a wide range of neurological conditions. We are usually very successful at resolving central vestibular disorders.
We use a wide variety of therapies for treating BPPV and the central vestibular consequences of this condition. These may involve various types of canalith repositioning maneuvers for BPPV (10), or specific exercises to retrain the integration of your eyes and inner ear during head movement (11). It may involve specific forms of eye exercises to enhance your stability (12), or transcutaneous electrical stimulation to stimulate your vestibular system (13). It may involve specific types of visual stimulation exercises (14), or visual stimulation coupled with specific head movements (15). It may involve the use of transcranial magnetic stimulation to decrease your dizziness (16), or even the use of exercises performed in a virtual reality environment (17).
All of our therapies are tailored to the specific realities of your case. Taking a cookie-cutter approach to a condition this complicated will be doomed to fail. No two presentations of BPPV are alike, and the same is true of the NeuroRescue Program.
How does the NeuroRescue Program work?
We design your unique NeuroRescue Program to be among the most comprehensive diagnostic and therapeutic protocols available today. We create individual NeuroRescue Programs based on a comprehensive analysis of every relevant neurological system and pathway, using gold-standard, cutting edge neurodiagnostic technologies and examination procedures and state-of-the-art therapies.
We begin with your Discovery Day, wherein we perform a comprehensive history of not only your condition, but your life on a timeline. This allows us to dive deeply into your case and see all of the factors that led to where you are now. It helps us uncover hidden problems and associated conditions that may be making it difficult for you to move your recovery forward.
Our examination allows us to identify the areas and pathways of your brain and vestibular system that are involved in not only in your BPPV, but also in any associated secondary symptoms. We do this by precisely quantifying the function of your visual, vestibular, and proprioceptive systems through computerized analysis of your eye movements, your inner ear reflexes, and your balance in a host of different sensory conditions.
We employ technologies including Videooculography and Saccadometry to measure several classes of eye movements. We use Video Head Impulse Testing to measure the function of your inner ear, and Computerized Dynamic Posturography to assess your balance in different sensory conditions.
We use NeuroSensoryMotor Integration testing to evaluate hand-eye coordination and cognition, and Virtualis testing to assess dynamic eye tracking and perception of vertical in a virtual reality environment.
We combine all of this with a comprehensive physical and neurological examination of your sensory, motor, autonomic, and cognitive systems. We review any relevant laboratory testing, radiological imaging, and prior neurodiagnostic testing, and integrate that information with our findings.
We use this information to identify which parts of your nervous system are working properly, which systems are struggling, and the precise point at which your systems fatigue.
We can then design a NeuroRescue Program that is unique and specific to your brain, and yours alone. Your NeuroRescue Program works to rejuvenate and reintegrate the damaged neurons and pathways in your central and peripheral nervous systems, and restore normal function to your semicircular canals. It works to improve energy, endurance, and functional capacity within your involved fragile systems.
We use our technologies and procedures to not only see what we need to address, but also when it is time to stop and let you rest. We address your impaired neurological function from multiple angles of therapy, and provide metabolic support to improve neurological recovery.
While we cannot bring back neurons that have been lost, your NeuroRescue Program allows us to take the pathways that remain and maximize their efficiency and endurance. And by focusing on the integration of systems, we can do more than just get pathways working better, we can get them working together again. This gives us our best opportunity to return you to living a healthy, vibrant, and fulfilling life.
Your Next Best Step:
Living with benign paroxysmal positional vertigo can be challenging, but there is hope for recovery and remission. To see if the NeuroRescue Program is right for you, contact one of our patient care coordinators to schedule your Discovery Day.
And remember, it’s never too late to start getting better.
References:
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117684/
2. https://www.menieres.org.uk/information-and-support/symptoms-and-conditions/bppv
3. www.advances.umed.wroc.pl/pdf/2018/27/10/1355.pdf
4. https://pubmed.ncbi.nlm.nih.gov/25485940/
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8058011/
6. https://pubmed.ncbi.nlm.nih.gov/15477514/
7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609213/
8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7593380/
9. https://pubmed.ncbi.nlm.nih.gov/28429801/
10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3438743/
11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057116/
12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5308452/
13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7050666/
14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4851359/
15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097942/