Introduction
Vertigo-type balance disorders can result due to a myriad of issues from within either the inner ear or vestibular nuclei of the brain stem. Studies completed by Tacikowska and KubieczkJagielska have shown that 50% of vertigo cases are due to pathology of the inner ear, 15% have psychological and psychiatric causes, 5% are a side-effect of neurological disorders, 5% are caused by orthostatic dizziness and adverse effects of drugs, and the last 25% of vertigo etiology is unknown. Although some of these sources of vertigo are difficult to resolve, the 50% which originate from problems within the inner ear are generally simple to treat. The most frequently diagnosed form of vertigowithin the inner ear category is benign paroxysmal positional vertigo (BPPV), with other common types being acute vestibular neuritis or labyrinthitis, Meniere’s disease, and migraines.


BPPV is most commonly observed within the posterior canal of the vestibular system, although it can result in the superior or lateral canals as well. People of all ages can suffer from this debilitating disorder, but there appears to be a slightly higher demographic in both the elderly and female population for reasons not fully understood. Thankfully, BPPV can be easily diagnosed, isolated, and treated using different maneuvers either under the guidance of a physician or at home with the aid of a family member.


going-crazy-2.jpg
Figure 1: Dizziness



Anatomical Overview

The vestibular system is composed of a collection of structures which work together to provide the individual with a sense of balance and spatial awareness. When working properly, this allows for the coordination of movement and balance. Located within the labyrinth of the inner ear, directly behind the petrous part of the temporal bone, the vestibular system is primarily composed of three semicircular canals and two otolithic organs.

timthumb.jpg
Figure 2: Anatomy of the Vestibular system and supporting structures
















12040055.jpg
Figure 3: Anatomy of the Vestibular system

Utricle and Saccule

The two otolithic organs, known as the Utricle and Saccule, are essentially identical in structure and only differ in their orientation. When the body is in anatomical position, the Saccule is orientated vertically while the Utricle lies horizontal. Both are composed of a gelatinous/semi-fluid membrane known as the otolithic membrane, at the top of which are embedded small crystals called otoconia. Within each is a small 2-3 mm group of hair cell mechanoreceptors called the macula. These hair cells project out hairs called stereocilia which are arranged from shortest to tallest, the tallest of which is known as the kinocilium. The tips of the stereocilia and kinocilium are embedded in the gelatinous otolithic membrane so that whenever your head moves and the membrane shifts, the hairs will also be pulled which will activate the hair cells. If the hairs are bent towards the kinocilium, the mechanoreceptors are excited, but if the hairs are bent away from the kinocilium, they are inhibited. Due to their orientation, the Utricle is activated when vertical head movement occurs and the Saccule is activated when horizontal head movement occurs. Because these organs respond to steady-state head motion, as long as the membrane is displaced the hair cells will be activated and continue firing. Therefore, these organs are involved in sensing linear acceleration, head position, and balance.

Semicircular Canals

The three canals of the inner ear are orientated at 90 degrees to each other:
- The Horizontal (or lateral) canal is in the transverse plane and registers rotation of the head. Example: shaking your head “no”.
- The Anterior (or superior) canal is in the sagittal plane and registers upward and downward motion of the head. Example: nodding your head.
- The Posterior (or inferior) canal is in frontal plane and registers head-to-shoulder movement. Example: wiping your ear on your shoulder

At the base of each canal are hair bundle mechanoreceptors, which project out hairs called stereocilia. These hairs are also arranged from shortest to tallest, the tallest of which being the kinocilium. All these hair bundles are “capped” together with a gelatinous material known as the cupula, and further surrounded by the endolymph fluid of the canal. When the head accelerates in a direction, the canal in that plane experiences retrograde endolymph flow (in the opposite direction of the head movement). This flow of fluid displaces the cupula, pulling on the hairs. If the hairs are bent towards the kinocilium, the mechanoreceptors are excited, but if the hairs are bent away from the kinocilium, they are inhibited. The canals do not respond to steady-state motion but instead only acceleration. Therefore, if your head remains in any prolonged head motion for more than a few seconds the hair cells will return to their tonic firing rate even though the hair cells will remain displaced. Because of this, the canals are involved sensing angular acceleration and balance.

Types of Hair Cells

Within both of these structures there are two types of nerve-to-hair cell bundle connections:
- Type 1 (Vessel shaped): record phasic and rapid head movement
- Type 2: record static/slow head movement

Mechanoreceptors for equilibrium.jpg
Figure 4: Activation of hair cell receptors within the semicircular canals and Otolithic organs


Input and Output Pathways

Input:


Information from the vestibular system travels to the brain via two nerves. Fibers from the horizontal and anterior canals exit through the superior vestibular nerve, while fibers from the posterior canals exit via the inferior vestibular nerve. The superior and inferior vestibular nerve then fuse together to for the vestibular branch, whose cell body is in the vestibular (Scarpa's) ganglion located at the distal end of the internal auditory meatus. the axons of the vestibular branch travel the course of the internal auditory meatus and integrate into cranial nerve VIII. Cranial nerve VIII enters the brain stem between the pons and medulla at the pontomedullary junction which is where the IVth ventricle is largest. Almost all of cranial nerve VIII's afferents then synapse on one of the four vestibular nuclei in eithe rht rostral medulla or caudal pons. However, a few of the afferents go directly to the cerebellum via the infeior cerebella peduncle.

From the four vestibular nuclei, the 2nd order vestibular afferents travel to various regions of the brain and body.

tmp15F78.jpg
Figure 5: Vestibular input pathways

Ascending Tracts:
- Afferents from the superior, inferior, and medial nuclei ascend in the medial longitudinal fasciculus (MLF) to the three extraocular motor nuclei (III, IV, and VI). This aids in controlling eye movements.
- Afferents from the inferior and medial nuclei travel to the cerebellum. This aids in coordinating postural adjustments.
- Afferents from the superior nuclei travel to the thalamus which then relays the information to the cortex. This aids in conscious perception of movement and gravity

Descending Tracts:
- Afferents from the lateral nuclei descend ipsilaterally via the lateral vestibulospinal tract through the length of the spinal cord to the sacrum
- Afferents from the medial nuclei descend bilaterally in the medial vestibulospinal tract through the spinal cord to thoracic levels in the body
- Both of these tracts help in controlling head and body position so that the person can maintain their balance.
In summary, the main projections from the vestibular nuclei are to the spinal cord, the three extraocular motor nuclei (III, IV, and VI), thalamus which then relays the information to the cortex, and cerebellum.

Output:


The role of the efferent vestibular system has proven difficult to determine and still isn't fully understood. It's known that hair cells and the afferent nerve terminals of the vestibular system are innervated by efferent fibers which travel via the vestibular nerve and originate from the brain stem, but the purpose of this is still up for debate. One hypothesis is that this output from the brain aids in vestibular plasticity, tone, and overall compensation, but this is just one of the many ideas concerning this issue. It may be several more years or decades before a definitive understanding of the efferent vestibular system is established.


Pathogenesis


Overview of BPPV:


Benign Paroxysmal Position Vertigo is by far the most common inner ear disorder related to vertigo. BPPV is a condition that presents itself as a sudden onset of dizziness provoked by changes in head position and rotation. Its characteristic clinical presentation is believed to result from free-floating otoconia in the semicircular canals of the vestibular labyrinth. The term “paroxysmal” describes a critical characteristic of the disorder: that it is an episodic disorder rather than than persistent. The use of the term “position” implies an association between the symptoms a patient experiences and their head position with respect to gravity. Note that these symptoms are associated with a rotational movement of the head, rather than the stagnant position of the head. BPPV is typically easily diagnosed and readily treated through simple office-based maneuvers. Although long since its first recognition, the pathophysiology behind BBPV has only recently been understood and clarified. BBPV is understood to result from cupulothiasis and canalithiasis, and can theoretically have an effect on any of the three semicircular canals. Of the three canals however, BPPV of the superior canal is extremely rare. On the other hand, it is commonly found in the posterior canal.

16FF3.jpg
Figure 6: Overview of endolymph flow and activation of the mechanoreceptor hair cells within the semicircular posterior canal

Posterior canal BPPV


Cases of Benign Paroxysmal Position Vertigo are most commonly found in the posterior canal. It is thought that canalithiasis is the pathophysiology behind most cases of posterior canal BPPV (source 5). Due to its anatomical arrangement, the posterior canal is the most gravity dependent portion of the vestibular labyrinth in both supine and standing positions. It is logical, then, that most free-floating debris in the endolymph tends to gravitate towards the posterior canal. Once this debris enters the canal, the cupula acts as a barrier blocking it from exiting at the shorter end. Due to gravitational constraints, it is much more difficult for the debris to exit from the longer end of the canal on its own.

Mechanism


Epley was the first to describe the mechanism by which canalithiasis causes nystagmus in the posterior canal (source 10). As particles enter the dependent portion of the posterior canal, they will accumulate to a “critical mass” (source 5). In a position where the head is hanging, this mass would move away from the cupula and produce a ampullofugal flow. Ampullofugal deflection of the cupula in the posterior canal produces an excitatory response. This would result in a sudden onset of vertigo and the typical “torsional nystagmus” in the anterior-posterior plane of the canal. In a position where the head is hanging left (stimulation of the left posterior canal) a clockwise nystagmus (as viewed by the examiner) will occur. Conversely, right head tilt will produce a counterclockwise nystagmus. When the otolithic mass reaches its decent and the drag on the endolymph ceases, the cupula returns to its neutral position. This explains the limited duration characteristic of a nystagmus. A “reversal nystagmus” accompanies movement back into the upright position. The mass is displaced in the opposite direction, resulting in a nystagmus in the same plane, but opposite direction. This is a fatigable response due to the tendency of the particles to disperse along the canal overtime. This lesser mass is less effective at creating endolymph drag and deflecting the cupula.

Horizontal canal BPPV

Figure 7: Cupulolithiasis vs. Canalithiasis
Figure 7: Cupulolithiasis vs. Canalithiasis

Although it is known that BPPV typically affects the posterior canal, one report suggest that up to 30% of BPPV may also be in the horizontal canal (source 11). Unlike the posterior canal which has its cupular barrier in its shorter more dependent end, the horizontal canal is slanted up and contains its cupula in the upper end. As a result, free-floating debris in this canal tend to float back out into the utricle during normal head movements.

In horizontal canal canalithiasis, debris is typically found farther along the canal away from the ampulla. If a lateral head turn is performed toward the affected ear, the debris will cause an ampullopetal flow, which is excitatory in the horizontal canal. As a result, a geotropic nystagmus (a very fast phase of nystagmus toward the ground) will be present. Head rotation away from the affected side will produce an inhibitory ampullofugal flow, though in the opposite direction, the nystagmus will still be characteristic of a geotropic nystagmus. It is seen that excitation of a canal creates a greater response than its inhibition; therefore, the direction of head turn that produces the greatest response represents the side that is affected by geotropic nystagmus. (Source 5)

It is apparent that cupulolithiasis plays a larger role in horizontal canal BPPV than in the posterior canal. Rather than freely floating in the canal, the particles directly adhere to the cupula. The vertigo experienced is often intense and persists while the head is in the provoking position. A patient’s head rotation toward the affected side will produce an inhibitory ampullofugal deflection of the cupula. This causes an apogeotropic nystagmus. A head rotation to the opposite side will produce an excitatory ampullopetal deflecting, resulting in a greater apogeotropic nystagmus. Thus, rotation away from affected side will create the strongest response.



Epidemiology


Benign paroxysmal positional vertigo is known to be the most commonly recognized vestibular disorder.
  • Women comprised 66.2% of the patient population with vertigo (source 9)
  • Vertigo was most common in winter (27.1%) and spring (26.3%). The month with the highest occurrence rate (12.9%) was January. (source 9)
  • Higher occurrence of vertigo is found in elderly patients, the age of onset being between the fifth and seventh decades of life. (source 9)
  • There is a slightly higher report of left ear disorders compared to the right (source 9)


seasons.gif
Figure 8 Seasonal variation in the occurrence of vertigo.

gender.gif
Figure 9 Age and sex distributions of vertigo.



History


Although its existence has long been recognized, the underlying pathophysiology for BPPV has only recently been substantiated. Bárány first described the condition in 1921:

“The attacks only appeared when she lay on her side. When she did this, there appeared a strong rotatory nystagmus to the right. The attacked lasted about thirty seconds and was accompanied by violent vertigo and nausea. If, immediately after the cessation of these symptoms, the head was again turned to the right, no attack occurred, and in order to evoke a new attack in this way, the patient had to lie for some time on her back or on her left side.” (Source 12)
Our understanding of the pathogenesis behind BPPV has improved drastically due to intraoperative observations of agglomerated, free-floating particulate matter in the endolymph of the posterior semicircular canal. (Source 5) These observations were enough to support and conform what was only hypothesized, that the movement of otoconia into the semicircular canals underlie most cases of the condition.

Early writings from Schuknecht postulated that the debris which adhered to the cupula, rather than floating freely in the canals, were typically more responsible for BPPV. On the contrary, the action of free-floating debris is currently the accepted pathophysiological mechanism for typical BPPV.


Symptoms



The key feature of benign paroxysmal positional vertigo is the sensation of spinning, tilting or falling, without any actual movement occurring. This sensation is known as vertigo. Many patients consult their doctors about vertigo after experiencing dizziness or poor balance. It is important to note that dizziness is nonspecific and can result from disorders in a variety of organ systems. Understanding the difference between dizziness and vertigo is an important distinction. (source 1)

• Patients describe sudden attacks of either horizontal or vertical vertigo, elicited by certain head positions and movements

• Although dizziness alone is not a definitive sign of vertigo, it is a common symptom

• Nausea and vomiting can accompany vertigo

• Most common movements include: extending the neck to look up, rolling over in bed, and bending forward.

• The attacks typically last less than 30 seconds

• Vertigo is often episodic and patients may experience several attacks a week or along the course of one day (source 1)



Causes of BPPV


The most common cause of benign paroxysmal positional vertigo is primary BPPV. This is BPPV found in isolation and is also termed “idiopathic” BPPV. This type of BPPV reports for 50-70% of cases. (Source 5) Commonly recognized conditions associated with secondary BPPV include: vestibular neurolabrynthitis, Meniere’s disease, head trauma, and migraines.

Head trauma: This is the most common association to BPPV, representing 7-17% of all cases (source 13). This is logical when considering the anatomy of the vestibular system. A blow to the head may cause the otoconia to dislodge from the macula and become displaced.

Viral neurolabyrinthitis: Also called “vestibular neuronitis” is an inflammation of the inner ear and has been seen to occur in up to 15% of BPPV cases. (source 13).

Meniere’s disease: Although the disease isn't fully understood, it's believed that it causes an excess of or change in the consistency of the endolymphic fluid of the canals. There is no cure, therefore it's considered a chronic condition. The underlying mechanism behind the association between Meniere’s disease and BPPV is not well understood, but a correlation clearly exists between the two.

Migraines: A recurrent throbbing headache of varying intensity that often only affects one side of the head. Often accompanied by nausea, disturbed vision, and sensitivity to light and sound.

8c2a3afda183a7dc295be24e06feedee--vertigo-occupational-therapy.jpg
Table 1: Overview of causes of Vertigo

Treatment


Maneuvers

- Dix-Hallpike maneuver is a well-established diagnostic maneuver for determining BPPV. The patient is initially in a seated and then lowered into a supine position. The patient’s eyes are carefully observed for nystagmus. There typically is a latency in the onset of the nystagmus after the head is lowered (most likely due to the build up of mass from the otoconia causing a lag). For posterior BPPV, a positive test is defined by the presence of slight vertical component (upbeating) and torsional nystagmus with the superior portion rotating toward the affected side (source 2). For horizontal canal BPPV, the supine role maneuver, completed by laying the patient in a supine position followed immediately by turning the patients head toward the side of interest. If positive, in a majority of cases a geotropic nystagmus will occur (source 11). Some cases (about 27% of cases [source 11]) will result in a apogeotropic nystagmus. After both sides are tested, the direction of the roll that produces the greatest nystagmus intensity is deemed that affected side.

- Epley maneuver: The first reports published by Epley on the “canalith repositioning procedure” (CRP) did not come until the 1990’s. This is also termed the “Epley maneuver” and has gained much success for high efficacy. Mechanical vibrations of the skull are routinely used and the head is moved through five different positions. Many modern day clinicians perform a modified version of CRP, one being particle re-positioning maneuver (PRM).





- Particle repositioning maneuver: PRM is a 3-position maneuver that disregards the need for skull vibration. The procedure should typically take less than 5 minutes to complete and follows a period of 24-48 hours were the patient should remain upright to allow the otoliths to settle.

- Prolonged position maneuver: Of the several techniques used to treat lateral canal BPPV, this seems to be the simplest. It involves the patient lying on their side with the affected ear facing up for 12 hours. This can sometimes result in a conversion to posterior canal BPPV, which can then be treated with standard reposition maneuvers.

- Barrel roll maneuver: This was also described by Epley and consist of rolling the patient around 360 degrees, while keeping the lateral semicircular canal perpendicular to the ground. By rolling the patient away from the affect ear in 90 degree increments, it is believed that the particles will relocate out of the involved canal into the utricle.

- Liberatory maneuver: Based on the cupulolithiasis theory, the liberatory maneuver was described in 1988 by Sermont and colleagues. This maneuver involved a series of rapid changes of head position that is believed to free deposits attached to the cupula.

Surgical treatment
Due to the nature of BPPV being a benign disorder, surgery should typically be avoided unless noted otherwise or the disorder persist after bedside maneuvers have been applied.

- Singular neurectomy: A procedure that involves the sectioning of the posterior ampullary nerve. Although early reports have shown this procedure to be highly effective, notable difficulties have been found to accompany it. Most notable are cases of hearing loss, as well as the procedure itself being technically demanding.

- Posterior semicircular canal occlusion: This provided an alternative procedure from singular neurectomy that demonstrated negligible effects on hearing (source 14). It is performed by making fenestration in the bony posterior canal. The canal is then occluded with a plug. The occlusion does in fact impair normal inner ear physiology initially, causing a postoperative imbalance. This however is resolved by the brain within a few weeks.


Glossary

- Cupulolithiasis: Otoconia crystals stick to the cupula within a semicircular canal. This results in a change in the density of the cupula, making it nearly impossible for the cupula to remain in its neutral position for even the slightest movement majorly displaces it.
- Canalithiasis: Otoconia crystals in a semicircular canal cause the endolymph flow to either slow down or reverse in direction with normal movement.
- Nystagmus: A repetitive, involuntary rapid eye movement that occurs either side-to-side, up-and-down, or in a circle. May slightly blue vision, result in a reduced depth of perception, or affect balance and coordination.
- Geotropic Nystagmus: Refers to nystagmus beating toward the ground
- Apogeotropic Nystagmus: Refers to nystagmus beating away from the ground.
- BPPV: One of the most common causes of vertigo. Results when one or several otoconia crystals become dislodged from the top of the otolithic membrane and fall into one of the semicircular canals (generally posterior). This messes with the endolymph flow of the canal, resulting in vertigo and/or other symptoms.
- Acute vestibular neuritis or labyrinthitis: A viral infection of the inner ear which results in inflammation of the vestibular nerve. This disrupts the transmission of information from the inner ear to the brain, resulting in dizziness, vertigo, balance issues, nausea, and in extreme cases loss of hearing.
- Meniere’s disease: The exact cause of Meniere’s disease isn’t fully understood, but it appears to result in an abnormal amount or consistency of endolymph in the semicircular canals. This excessive or abnormal fluid causes the semicircular canals to function abnormally, resulting in feelings of pressure, episodes of vertigo, hearing loss, and tinnitus. Considered a chronic condition for which there is no cure.
- Epley Maneuver: Also known as the canalith repositioning procedure. A maneuver by which any loose otoconia in the posterior semicircular canal which are causing vertigo are rolled out of the canal in order to diminish or resolve the symptoms.
- Otoconia: Miniscule crystals of calcium carbonate that are embedded in the top of the gelatinous membranes of the Utricle and Saccule.
- Stereocilia: Hair projections originating from the hair cells of the Utricle, Saccule, and three semicircular canals. The ones located in the Utricle and Saccule are embedded in the gelatinous membranes of these organs, and the ones located in the canals are capped with a gelatinous cupula. When head movement occurs the various gelatinous materials are shifted, causing these hair cells to be displaced which further results in activation of the mechanoreceptor hair cells. They are about 10-50 micrometers in length and are organized by height from shortest to tallest.
- Kinocilium: The tallest of the stereocilia; there is only one per group of stereocilia (1 to 40-70). The hair cell is depolarized (excited) if the stereocilia are pushed towards the kinocilium, and the hair cell is hyperpolarized (inhibited) if the stereocilia are pulled away from the kinocilium.



Conclusion

Patients dealing with brief, episodic, positioned-provoked vertigo will likely find characteristic signs of BPPV when undergoing Dix-Hallpike testing. Although a variety maneuvers are tested and described, PRM is found to be the simplest and more effective treatment for patients with BPPV. Current evidence does not support the use of routine skull vibration with repositioning. Although it is recommended by clinicians to remain upright for at most 48 hours post repositioning, recent evidence has suggested that this is unnecessary. No factors to date have shown to indicate an increased risk of BPPV recurrence after successful repositioning. Still, the correlation between BPPV recurrence and migraine suggests further research should be done on the topic. For those who do not respond to repositioning maneuvers, posterior canal occlusion is a effective alternative.



Links

- https://www.dizziness-and-balance.com/disorders/bppv/lcanalbppv.htm
(Supplemental materials and videos on varying BPPV maneuvers)

- http://vestibular.org/migraine-associated-vertigo-mav
(Article done on the correlation of Migraines to BPPV)

- http://www.childneurologyfoundation.org/disorders/vertigo
(Research done on vertigo experienced in early childhood)



Quiz Questions

Multiple Choice:

1. The most common source of peripheral vertigo is
a) Migraines
b) BPPV
c) Vestibular neuritis or labyrinthitis
d) Meniere’s disease
e) Unknown

2. The two otolithic organs are associated with
a) Linear acceleration
b) Balance
c) Head position
d) Angular acceleration
e) A, B, & C
f) B, C, & D

3. Which of the following is not a known secondary cause of BPPV?
a) Migraines
b) Head trauma
c) Meiniere’s disease
d) PTSD

4. Which of the following is not a maneuver used to treat BPPV
a) Dix-hallpike maneuver
b) Epley maneuver
c) Barrel-roll maneuver
d) Liberatory maneuver

5. Afferents from which areas of the vestibular system travels along the inferior vestibular nerve?
a) Anterior canal
b) Horizontal canal
c) Utricle
d) Saccule

True/False:


1. The Utricle is orientated horizontally, while the Saccule is orientated vertically.

2. BPPV is most commonly caused by otoconia in anterior semicircular canal

3. Cupulolithiasis is when otoconia accumulate in a critical mass in a semicircular canal (generally posterior) causing the endolymph to either slow down or reverse in direction.

4. It is apparent that cupulolithiasis plays a larger role in posterior canal BPPV than in the horizontal canal.

5. When performing the Dix-Hallpike maneuver, a nystagmus should be seen immediately following lowering of the head.

Short Answer/Essay:


1. Watch the video and describe the Epley maneuver in detail.

2. Name the three canals (including their alternative name), and describe which plane each one is orientated in and what type of movement activates it.

3. Describe the symptoms, pathogeneses, and causes of BPPV in detail.

4. Thoroughly describe the pathway of sensory information from the vestibular system to the cerebral cortex.

5. Explain the process by which an action potential is generated in the semicircular canals.



Answers

Multiple Choice:

1. B
2. E
3. D
4. A
5. D

True/False:

1. T
2. F
3. F
4. F
5. F

Short Answer/Essay:

1. Begin by having the patient sit straight up and look straight ahead. Then, help the patient lay back and tilt their head 45 degrees towards the affected side and 20-30 degrees backwards (extension). If BPPV is present nystagmus will occur. In this case, continue the maneuver by keeping the patient in this position for 30-60 seconds. Then, turn the patient's head 45 degrees towards the other side and hold for 30-60 seconds. Have the patient then roll onto this side of their body (head should be orientated 45 degrees from the horizontal) and hold that position for 30-60 seconds. The maneuver is then completed by having the patient sit up and remain still for a few minutes.

2. The Horizontal (Lateral) canal is orientated in the transverse plane and registers side-to-side rotation of the head (shaking your head “no”). The Anterior (Superior) canal is orientated in the sagittal plane and registers upward and downward motion of the head (nodding your head). The Posterior (Inferior) canal is orientated in frontal plane and registers head-to-shoulder movement (wiping your ear on your shoulder).

3. The main symptom associated with BPPV is vertigo. However, there are several other symptoms which are often seen such as dizziness, nausea, and vomiting. If of the posterior semicircular canal, the main cause of BPPV is generally the accumulation of loose otoconia in the canal. They bond together, forming a critical mass that interferes with the endolymph flow, either slowing it down or causing it to reverse entirely. This in turn results in vertigo and nystagmus. If of the horizontal semicircular canal, the main cause of BPPV is generally the accumulation of loose otoconia on the cupula. This causes a change in the density of the cupula (making it heavier) which in turn causes it to be more sensitive to head movement. This causes the the mechanoreceptors of the canal to fire excessively, resulting in vertigo and nystagmus. Both of these can be the result of a head trauma which dislodged some of the otolithic organ otoconia, causing them to fall into the canal. However, viral neurolabyrinthitis, meniere's disease, and migraines affecting any of the canals can also result in BPPV.

4. Information from the vestibular system travels to the brain via two nerves. Fibers from the horizontal and anterior canals exit through the superior vestibular nerve, while fibers from the posterior canals exit via the inferior vestibular nerve. The superior and inferior vestibular nerve then fuse together to for the vestibular branch, whose cell body is in the vestibular (Scarpa's) ganglion located at the distal end of the internal auditory meatus. the axons of the vestibular branch travel the course of the internal auditory meatus and integrate into cranial nerve VIII. Cranial nerve VIII enters the brain stem between the pons and medulla at the pontomedullary junction which is where the IVth ventricle is largest. Cranial nerve VIII's afferents then synapse on the superior nuclei. The superior nuclei afferents then travel to the thalamus, which relays this information to the cortex.

5. When the head accelerates in one direction, the endolymph drags in the opposite direction due to its high density and reflects that cupula. There are hair cells sticking up in the cupula. A bundle of hair cells is called the stereocilia, and the tallest one is the kinocilia. These all are connected through a mechanical linkage, a spring system called tip-links. As hair cells bend towards the kinocilia, this pulls the mechanically gated tip-links and allows for an influx of potassium. This changes the membrane potential (depolarization) and allows for the influx of calcium that creates an action potential.



References

1. MacGill, M. (2017, November 24). Vertigo: Causes, symptoms, and treatments. Retrieved December 07, 2017, from https://www.medicalnewstoday.com/knowledge/160900/vertigo-causes-symptoms-treatments
2. Furman, J. (2006). Benign Paroxysmal Positional Vertigo. Geriatric Otolaryngology,155-164. doi:10.3109/9780849374487-143. Heide, W. (2007). Faculty of 1000 evaluation for Epidemiology of benign paroxysmal positional vertigo: a population based study. F1000 - Post-publication peer review of the biomedical literature. doi:10.3410/f.1058974.5109314. Neuhauser, H. K. (2013). The Epidemiology of Vertigo and Imbalance. Oxford Textbook of Vertigo and Imbalance,197-206. doi:10.1093/med/9780199608997.003.00185. Parnes, L. (2014). Chapter-10 Benign Paroxysmal Positional Vertigo. Textbook of Vertigo: Diagnosis and Management,128-144. doi:10.5005/jp/books/11995_106. Riga, M., Bibas, A., Xenellis, J., & Korres, S. (2011). Inner Ear Disease and Benign Paroxysmal Positional Vertigo: A Critical Review of Incidence, Clinical Characteristics, and Management. International Journal of Otolaryngology,2011, 1-7. doi:10.1155/2011/7094697. Shan, X., Wang, A., & Wang, E. (2017). Comments on an Update of Clinical Practice Guideline: Benign Paroxysmal Positional Vertigo. Otolaryngology,07(03). doi:10.4172/2161-119x.10003058. Teixido, M., Baker, A., & Isildak, H. (2017). Migraine and benign paroxysmal positional vertigo: a single-institution review. The Journal of Laryngology & Otology,131(06), 508-513. doi:10.1017/s00222151170005369. Yetiser, D., & Ince, D. (2015). Demographic analysis of benign paroxysmal positional vertigo as a common public health problem. Annals of Medical and Health Sciences Research,5(1), 50. doi:10.4103/2141-9248.149788
10. Epley JM. The canalith repositioning procedure: for treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1992;107:399-404.
11. Uno A, Moriwaki K, Kato T, Nagai M, Sakata Y. [Clinical features of benign paroxysmal positional vertigo]. Nippon Jibiinkoka Gakkai Kaiho 2001;104:9-16.
12. Bárány R. Diagnose von Krankheitserschernungen in Bereiche des Otolithenapparates. Acta Otolaryngol (Stockh) 1921;2:434-7.
13. Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases. Neurology 1987;37:371-8
14. Parnes LS, McClure JA. Effect on brainstem auditory evoked responses of posterior semicircular canal occlusion in guinea pigs. J Otolaryngol 1985; 14:145-50