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Benign Paroxysmal Positional Vertigo (BPPV)

Symptoms – Cause – Diagnosis – Treatment – Prognosis of Benign Paroxysmal Positional Vertigo – Canalith Repositioning Maneuvers

Benign Paroxysmal Positional Vertigo
Benign paroxysmal positional vertigo (BPPV) is a relatively common condition affecting about 2.4% of the population at some point of their lifetimes. Most commonly it starts for no apparent reason. BPPV is a well-known complication of the head injury and it’s occasionally simulated by labyrinth stroke (see below).
Many people think that vertigo is a specific disease. It is not. Vertigo is only a symptom of one of the conditions described in this site section and literally means a “spinning sensation”. Benign positional vertigo is the most common one.
Vertigo is an unnatural and unprovoked spinning sensation. It feels like either the body or the surrounding is rotating in a particular direction.
In this introduction I will describe a classical presentation of positional vertigo related to the posterior canal. What is “posterior canal” will be described below.

Benign paroxysmal positional vertigo is a spinning sensation triggered by a head movement lasting for about 10 to 20 seconds. Any activity in the rest of the body doesn’t cause any vertigo. There should be no vertigo at rest.
Level of distress due to vertigo and nausea is variable. Sometimes people feel so sick that they end up in the Emergency Room. For the reasons I will explain later, vertigo is provoked by the head rotation in a certain direction and in a particular plane.

Typically, vertigo starts in the morning upon getting out of bed. Some people even fall back onto the bed because they get totally lost in space. Such a shocking presentation is often frightening. The second attempt to get out of bed at a slower pace is much less dramatic. Another scenario is when positional vertigo starts while doing some activity involving rapid change of the head position.
The only associated symptom of benign positional vertigo is nausea and sometimes vomiting. Some people have a sense of instability while walking, which is an “overreaction” to the bouts of vertigo. Sudden head turns while walking may cause a loss of balance. There should be no lack of coordination if the head is not rotating in any plane.

Posterior canal positional vertigo is provoked by the head moved down or up, which is called “top shelf” syndrome. A person may literally fall of a ladder while looking up. Another typical trigger is either the process lying down onto the bed on a particular side or the process of getting up from the opposite body side. Once the head position is settled, the vertigo should go away within half a minute.
Turning head side to side is usually OK with this particular canal.

Benign paroxysmal positional vertigo is more common in the advanced age group, but younger people are not excused. In young population positional vertigo is more common following a head injury.

Vestibular System Design
In order to understand the mechanism of BPPV, some brief introduction into the anatomy of the vestibular system is essential.

Vestibular system is designed to detect acceleration only. Resting state and steady motion with a constant speed are invisible to the vestibular system. It detects two types of acceleration. They are rotational and linear accelerations. Since the vestibular system is located inside the head, only the head motion is relevant.

Vestibular system is a pair of small organs imbedded deep inside temporal bones. The organ is called labyrinth because it is made of a system of three mutually perpendicular semicircular canals. These canals open into a tiny shared cistern on both ends. Each of these canals is plugged on one side with a jelly-like membrane, or cupula. The whole labyrinth system is filled up with a fluid called endolymph.

This portion of the labyrinth is responsible for the sensation of rotation. Whenever the head is rotated in the corresponding plane, the canal detects the direction and the speed of rotation. The mechanism of detection is simple. Due to inertia, the fluid inside the canal lags the wall motion. The inertia generates a tiny force, which pushes the membrane (cupula) that plugs the end of the canal. Cupula contains receptors that sense the speed and the amplitude of the membrane deflection. The information is sent to the brain for processing.

I have already mentioned that labyrinth is a paired organ, which means that identically oriented canals send the same information to the brain in response to the head rotation. Abnormal sensation of rotation, or vertigo, is produced under the conditions when there is a mismatch of the reported rotation characteristics between the two labyrinths. The most common reason for the mismatch is described in the chapter below.

Now about the second function of the vestibular system, or the detection of gravity and linear acceleration. The tiny cistern, where the free ends of all tree canals are open into, contain two bulges in the wall. They are called utricle and saccule. They contain membranes with embedded receptors just like in cupula. The difference is that the membrane moves sideways by inertia generated by “free weights” attached to the surface of the membranes. The free weights are tiny crystals of calcite called otoliths, or otoconia. As long as otoconia stay where they belong, the system is working well. Now, let’s see what happens when they get detached from the membranes of the utriculosaccular device.

Cause of Benign Paroxysmal Positional Vertigo
The most common reason for benign positional vertigo is a mismatch between reported speeds of rotation from the two matching semicircular canals. In the vast majority of cases it is caused by alteration of the flow freedom within one of the canals by displaced otoliths.
Once the otoliths get detached from the membrane they become “waterborne”. They are now free to go wherever the gravity force and the fluid flow are pleased to send them to. As a result, they may end up lodged inside one of the semicircular canals and alter the speed of the endolymph flow within the canal. This, in turn, leads to mismatch in reported speeds of rotation between the sides and presents with the symptom of positional vertigo. Once the otoliths are positioned within the semicircular canals they are called canaliths and the phenomenon has a name of canalithiasis.

Free floating otoconia may travel all the way through the canal and up being attached to the cupula. This is called cupulolithiasis. Naturally gravity and linear acceleration insensitive cupula, becomes sensitive to a broader range of head movements and to the change of the gravity force direction. As a result, positional vertigo is less dependent on the specific head movement and becomes more universal and more disturbing.

Causes of otoconia displacement from the membranes of the utriculosaccular system are not known in the vast majority of cases.  Head trauma is a relatively common cause of BPPV in young people. Strokes may occasionally produce it as well.

Otoconia may get into any of the three canals. In about 80 to 90 percent, so called, posterior canal is the victim. The reason for more common involvement of the posterior canal is due to the fact that rotation in bed while asleep occurs the plane of this canal. Since we always turn side to side during sleep any free floating otoconia are most likely to get into this canal. This is also an explanation for the most common onset of symptoms in the morning upon awakening.

Horizontal canal is the second in line for catching the otoconia. It relatively infrequently develops spontaneously. Treatment of benign paroxysmal positional vertigo involves a set of head rotations in a specific plane and in a particular direction. Incorrectly performed canalith repositioning by a medical professional or a “vestibular exercise” performed by patients may cause horizontal canal canalithiasis. It happens because canaliths that are being repositioned end up inside the horizontal canal rather than where they belong.

Horizontal canal positional vertigo is very disturbing. These patients are often unable to lie down neither to the back, nor to either side.

Anterior canal canalithiasis is very rare. Even if does occur occurs, it commonly resolves on its own without any treatment.

Diagnosis of BPPV
The diagnosis of BPPV is based exclusively on the basis of the reported complaints and neurological examination. Diagnostic tests play a minor role. Videonystagmography (VNG) might be handy in some cases but it is usually not essential.

Head movements in a suspected victim of BPPV predictably produce a specific type of nystagmus. Nystagmus is an eye movement phenomenon, which in this case consists of repetitive jerky eye movements in one direction. A normal version of nystagmus is called an optokinetic  nystagmus is when a person looks at a passing by train or another similar object.

Hallpike maneuver will diagnose a posterior canal BPPV. The person tested lies down onto the back while having head turned to either side. The affected side is the one that produces a vertical nystagmus with a rotatory component. Rotatory means that the eyeballs besides jerking vertically have an additional visible rotational component.

Horizontal canal is diagnosed by turning head to one side than to the other one while laying supine on a small pillow. The nystagmus is horizontal in this case. Unlike posterior canal BPPV, the nystagmus  is always present while the head is rotated to either direction but is worse on one of the sides. Diagnosing the involved side in horizontal canal BPPV is tricky. If the fast component of the nystagmus is towards the ground, then the bad side is the one that has stronger nystagmus. If the fast nystagmus component is towards the sky, then the bad side is the opposite. This conclusion is somewhat controversial because I have read different opinions. Based on my own experience, this approach to the side diagnosis is pretty accurate.

Treatment of Benign Paroxysmal Positional Vertigo
Once the canal-offender is spotted, the treatment is simple and logical.

The head has to be turned 360 degrees, usually in 90 degree increments. Patient’s head is positioned the way that canaliths inside the affected canal start moving towards the exit under the gravity force. After about 30 seconds the head is turned 90 degrees in the plane of the canal. Each subsequent 90-degree head turn is expected to propel the canaliths closer to the open end of the canal. By the time 360 degrees are done, the canaliths should be out.

Each side and each particular canal requires the correct direction and the right plane of rotation. Otherwise, it simply won’t work.

It is obvious that human neck can’t be turned 360 degrees, so the body is also rotated in between the head rotations.

How efficient is approach? Providing it is performed correctly, it works in majority of patients with BPPV. Some patients get very nauseous in the process. Some even vomit multiple times.

Two possible approaches may help. The first is trying finish canalith repositioning maneuvers correctly on the very first attempt. The more times this procedure is repeated the more likely the patient will feel sick. Another approach is giving Meclizine a couple of hours prior to the manipulation.

Meclizine is otherwise useless for the management of this type of vertigo, even though it is used all the time by medical professionals.

Another limitation is inability to perform canalith repositioning the right way just because the patient’s neck is not flexible enough, which happens all the time in people of advanced age. Since people of advanced age have positional vertigo much more frequently, this limitation is encountered on a regular basis. Unfortunately, if canalith repositioning cannot be performed, waiting and praying for the spontaneous resolution is the only approach that is left in this case.

Positional vertigo does resolve spontaneously but it might take weeks or even months.

Some doctors advocate special “vestibular exercise” for people with positional vertigo, which entails repetitive head movements in different directions. I am not a supporter of this type of approach. It is probably as efficient a hitting a TV stand with a fist and hoping that something will get fixed after all. Moreover, these exercises may covert posterior canal canalithiasis into the horizontal one. I have seen these transformations after vestibilar exercises and following self-treatment with canalith repositioning maneuvers.

Prognosis of BPPV
Benign Paroxysmal Positional Vertigo is a benign condition with a good response to specific canalith repositioning maneuvers. Cupulolithiasis (otoliths stuck to the cupula) is not so easy to manage. Canalith repositioning maneuvers might not work well.

Symptoms produced by other reasons, like narrowing of the semicircular canals, will not respond to such treatment at all.

Positional Vertigo Caused by Strokes and Tumors
Positional vertigo is occasionally caused by reasons other than migration of otoconia. Gradually developing vertigo is usually caused by tumors or abnormal blood vessels in the lower part of the brain (brainstem and cerebellum).

Abruptly developed vertigo is caused by strokes.

On the contrary to BPPV, vertigo in these conditions is associated with other signs of brain damage. Vomiting without significant nausea, weakness as well as numbness in some part of the body, lack of balance while walking or shaking in the hands with difficulty controlling precise movements are always the signs of some trouble.

Any comments about this page will be greatly appreciated at doctorstrizhak@gmail.com Content copyright 2017. DOCTORSTRIZHAK.COM. All rights reserved.
Disclosure: This Web Site is intended for education purpose only. The information provided on this site must not be perceived as a guide for self-diagnosis or self-treatment. Every effort is made to keep the information current, but there are absolutely no guarantees of timely updates. By Andre Strizhak