Battery: It supplies the power to turn the electronic components in a hearing aid on and off.
Bands: This are used to adjust the hearing aid’s amplification as per the hearing aid to the wearer’s loss and preferences. Hearing aids can have a band for each channel or multiple bands per channel. Like channels, the audiologist or hearing specialist can adjust these bands to the wearer’s preference.
Balance – A biological system that enables individuals to know where their bodies are in the environment and to maintain a desired position. Normal balance depends on information from the labyrinth in the inner ear, from other senses such as sight and touch, and from muscle movement.
Balance Disorder – Disruption in the labyrinth, the inner ear organ that controls the balance system, which allows individuals to know where their bodies are in the environment. The labyrinth works with other systems in the body, such as the visual and skeletal systems, to maintain posture.
Barotrauma – Injury to the middle ear caused by a rapid change of air or water pressure. Barotrauma is physical damage to body tissues caused by a difference in pressure between an air space inside or beside the body and the surrounding fluid.
Barotrauma typically occurs to air spaces within a body when that body moves to or from a higher pressure environment, such as when a SCUBA diver, a free-diving diver or an airplane passenger ascends or descends, or during uncontrolled decompression of a pressure vessel. Boyle’s law defines the relationship between the volume of the air space and the ambient pressure.
Damage occurs in the tissues around the body’s air spaces because gases are compressible and the tissues are not. During increases in ambient pressure, the internal air space provides the surrounding tissues with little support to resist the higher external pressure. During decreases in ambient pressure, the higher pressure of the gas inside the air spaces causes damage to the surrounding tissues if that gas becomes trapped. Types of injury
Examples of organs or tissues easily damaged by barotrauma are:
- middle ear(barotitis or aerotitis)
- paranasal sinuses (causing Aerosinusitis)
- eyes(the unsupportive air space is inside the diving mask)
- skin (when wearing a diving suit which creates an air space)
- bone (bone necrosis and temporal lobe injury)
- Teeth (causing Barodontalgia, i.e. barometric pressure related dental pain or dental fractures.
Barotrauma can affect the external, middle, or inner ear. Middle ear barotrauma (MEBT) is the most common being experienced by between 10% and 30% of divers and is due to insufficient equilibration of the middle ear. External ear barotrauma may occur on ascent if high pressure air is trapped in the external auditory canal either by tight fitting SCUBA equipment or ear wax. Inner ear barotrauma (IEBT) though much less common than MEBT shares a similar mechanism. Mechanical trauma to the inner ear can lead to varying degrees of conductive and sensorineural hearing loss as well as vertigo.
The sinuses similar to other air filled cavities are susceptible to barotrauma if their openings become obstructed. This can result in pain as well as epistaxis.
If a diver’s mask is not equalized during descent the relative negative pressure can produce petechial hemorrhages in the area covered by the mask along with subconjunctival hemorrhages.
Pulmonary (lung) pressure damage in scuba divers is usually caused by breath-holding on ascent. The compressed gas in the lungs expands as the ambient pressure decreases causing the lungs to over expand and rupture unless the diver breathes out. The lungs do not sense pain when over-expanded giving the diver little warning to prevent the injury. This does not affect breath-hold skin divers as they bring a lungfull of air with them from the surface, which merely re-expands safely to near its original volume on ascent. The problem only arises if a breath of compressed gas is taken at depth, which will then expand on ascent to more than the lung volume. Pulmonary barotrauma may also be caused by explosive decompression of a pressurised aircraft.
When diving, the pressure differences needed to cause the barotrauma come from two sources:
- descending and ascending in water. There are two components to the surrounding pressure acting on the diver: the atmospheric pressure and the water pressure. A descent of 10 metres (33 feet) in water increases the ambient pressure by approximately the pressure of the atmosphere at sea level. So, a descent from the surface to 10 metres (33 feet) underwater results in a doubling of the pressure on the diver.
- breathing gas at depth from SCUBA equipment results in the lungs containing gas at a higher pressure than atmospheric pressure. So a free-diving diver can dive to 10 metres (33 feet) and safely ascend without exhaling, because the gas in the lungs had been inhaled at atmospheric pressure, whereas a SCUBA diver who breathes at 10 metres and ascends without exhaling has lungs containing gas at twice atmospheric pressure and is very likely to suffer life-threatening lung damage.
Avoidance and treatment
Diving barotrauma can be avoided by eliminating any pressure differences acting on the tissue or organ by equalizing the pressure. There are a variety of techniques:
- The air spaces in the ears, and the sinuses. The risk is burst eardrum. Here, the diver can use a variety of methods, to let air into the middle ears via the Eustachian tubes. Sometimes swallowing will open the Eustachian tubes and equalise the ears.
- The lungs. The risk includes pneumothorax, arterial gas embolism, and mediastinal and subcutanous emphysemas. which are commonly called burst lung or lung overpressure injury by divers. To equalise, all that is necessary is not to hold the breath during ascent. This risk does not arise when snorkel diving from the surface, unless the snorkeller breathes from a high pressure gas source underwater, or from submerged air pockets. Some people have pathologies of the lung which prevent rapid flow of excess air though the passages, which can lead to lung barotrauma even if the breath is not held during rapid depressurisation. These people should not dive as the risk is unacceptably high. Most commercial or military diving medical examinations will look specifically for signs of this pathology.
- The air inside the usual eyes-and-nose diving mask (also known as a half mask). The main risk is bleeding around the eyes from the negative pressure or orbital emphysema from higher pressures. Here, let air into the mask through the nose. Do not dive in eyes-only goggles as sometimes seen on land with industrial breathing sets.
- Air spaces inside a dry suit. The main risk is folds of skin getting pinched inside folds of the drysuit. Most modern drysuits have a tube connection to feed air in from the cylinder. Air must be injected on the descent and vented on the ascent.
Following barotrauma of the ears or lungs from diving the diver should not dive again until thoroughly cleared by a doctor, which can take many months.
Use of a hyperbaric chamber. Patients undergoing hyperbaric oxygen therapy must learn to equalize in order to avoid barotrauma. Some patients may be at greater risk of otic barotrauma than others.
Blast induced barotrauma
An explosive blast and explosive decompression create a pressure wave that can induce barotrauma. The difference in pressure between internal organs and the outer surface of the body causes injuries to internal organs that contain gas, such as the lungs, gastrointestinal tract, and ear.
Lung injuries can also occur during rapid decompression, although the risk of injury is lower than with explosive decompression.
Ventilator induced barotrauma
Mechanical ventilation can lead to barotrauma of the lungs. This can be due to either:
- absolute pressures used in order to ventilate non-compliant lungs.
- shearing forces, particularly associated with rapid changes in gas velocity.
The resultant alveolar rupture can lead to pneumothorax, pulmonary interstitial emphysema (PIE) and pneumomediastinum.
Industry-related barotrauma in animals
Barotrauma in Diving Sea Mammals: Whales and dolphins also suffer severely disabling barotrauma when exposed to excessive pressure changes induced by navy sonar, oil industry airguns, explosives, undersea earthquakes and volcanic eruptions.
Bats suffer fatal barotrauma around wind farms due to their tiny, mammalian lungs and in contrast with Avian lungs.
Brainstem Implant – Auditory prosthesis that bypasses the cochlea and auditory nerve. This type of implant helps people who can’t benefit from a cochlear implant because the auditory nerves are not working. An Auditory Brain Stem Implant (ABI) is a surgically implanted electronic device that provides a sense of sound to a person who is profoundly deaf, due to sensorineural hearing impairment (due to illness or injury damaging the cochlea or auditory nerve, and so precluding the use of a cochlear implant).
The auditory brain stem implant uses similar technology as the cochlear implant, but instead of electrical stimulation being used to stimulate the cochlea, it is instead used to stimulate the brain stem of the recipient.
Only about a thousand recipients have been implanted with an auditory brain stem implant, due to the nature of the surgery required to implant the device (as it requires brain surgery to implant the device) and the reduced effectiveness of the implant (most auditory brain stem implant recipients only have an awareness of sound – recipients won’t be able to hear musical melodies, only the beat).
In the United States ABIs are only approved for adults (18 & over) and only for patients with Neurofibromatosis type II (NF2). In Europe, ABIs have been used in children and adults, and in patients with NF2 as well as other auditory complications, such as auditory nerve aplasia and cochlea ossification . Speech perception in non-NF2 patients on average has been reported to be higher than that of NF2 patients. The auditory brainstem was first implanted in humans in 1979 at the House Ear Institute, CA, USA. This original ABI consisted of two ball electrodes which were implanted near the surface of the cochlear nucleus. A change from a percutaneous connection to a wireless transcutaneous connection, and from ball electrodes to flat electrodes were the only changes to the implant until 1991, where 25 people had received the ABI .
In the US in 1992 an eight electrode implant developed by Cochlear Limited, the House Ear Institute and Huntington Medical Research Institute . An electrode array with 21 electrodes developed by Cochlear Limited was developed for the European market at the same time. The processor for both the eight and 20 electrode implants used Nucleus 22 ABI (Cochlear Limited) external speech processors. Since 1999 a 21 electrode array implant has been used with the Nucleus 24 ABI (Cochlear Limited) speech processor.
A 12 electrode array implant with a speech processor based on the C40+ cochlear implant (Med-El) and a 16 electrode array implant with the Clarion-1.2 cochlear implant (Advanced Bionics) have also been developed.
BiCROS – stands for Bilateral Contralateral Routing of Signal. A hearing aid with two microphones, one at each ear and one receiver. Used for hearing aid wearer who has one aidable ear and one that is not aidable. Contra Lateral Routing of Signal (CROS) is a hearing aid technology for people with unilateral hearing. The technology allows two implementations: CROS and BiCROS. Using this technology, a hearing aid-like device on the user’s deaf side uses its microphone to pick up sound from that side and sends it to another instrument at the better ear. The sound is then inserted into the good ear. The CROS implementation is for a user who has relatively normal hearing in the good side and has hearing that can’t be aided on the bad side. The receiving BTE device on the bad side transmits the sound to a device on the good side. The user hears the amplified sound from the bad side in their good ear. The users hears the sound from the good side naturally in their good ear, without amplification.
The BiCROS implementation is for a user with little or no hearing on one side and with some hearing loss in their better ear. It works just like the CROS implemenation, except that the device on the good side is actually a fully capable hearing aid for hearing sounds from the good side that is also capable of receiving the sound transmitted from the CROS aid on the other side. Transmission in a CROS or BiCROS configuration can be via wire around the back of the neck or wirelessly via radio. The main advantages of CROS technology are: you can hear sounds coming from your deaf side better (even though you’re hearing them in your better ear, and 2) you can get some cues about the location of the sound.
Primary disadvantages are: 1) the extra sound from the bad side may, at times, interfere with your ability to understand what you’re hearing from your good side, and 2) CROS technology certainly can’t restore natural localization and noise reduction, since that requires two ears, and CROS only inserts sound into one ear.
CROS technology may be a help for some people with unilateral hearing. BiCROS may help those whose good ear is also somewhat impaired. See the latest Google search for CROS and BiCROS. People with unilateral hearing may also be interested in checking out the BAHA conductive hearing aid. Finally, people with unilateral or noticeably unbalanced hearing loss may want to check out the information about Acoustic Neuromas.
bluetooth compatibility – uses bluetooth technology to allow digital instruments to communicate wirelessly. Bluetooth is a proprietary open wireless technology standard for exchanging data over short distances (using short-wavelength radio transmissions in the ISM band from 2400–2480 MHz) from fixed and mobile devices, creating personal area networks (PANs) with high levels of security. Created by telecoms vendor Ericsson in 1994, it was originally conceived as a wireless alternative to RS-232 data cables. It can connect several devices, overcoming problems of synchronization.
Bluetooth is managed by the Bluetooth Special Interest Group, which has more than 16,000 member companies in the areas of telecommunication, computing, networking, and consumer electronics. The SIG oversees the development of the specification, manages the qualification program, and protects the trademarks. To be marketed as a Bluetooth device, it must be qualified to standards defined by the SIG. A network of patents is required to implement the technology and are licensed only for those qualifying devices; thus the protocol, whilst open, may be regarded as proprietary.
body hearing aid – a hearing aid with a microphone, amplifier, and battery worn on the chest and connected to an ear-worn receiver with a cord. Body worn aids
This was the first type of hearing aid invented by Harvey Fletcher while working at Bell Laboratories.Body aids consist of a case and an earmold, attached by a wire. The case contains the electronic amplifier components, controls and battery while the earmold typically contains a miniature loudspeaker. The case is typically about the size of a pack of playing cards and is carried in a pocket or on a belt. Without the size constraints of smaller hearing devices body worn aid designs can provide large amplification and long battery life at a lower cost. Body aids are still marketed in emerging markets because of their lower cost.[
BTE – A behind the ear hearing aid system. Also called post-auricular hearing aid. BTE aids consist of a case, an earmold or dome and a connection between them. The case contains the electronics, controls, battery, microphone(s) and often the loudspeaker. Generally, the case sits behind the pinna with the connection from the case coming down the front into the ear. The sound from the instrument can be routed acoustically or electrically to the ear. If the sound is routed electrically, the speaker (receiver) is located in the earmold or an open-fit dome, while acoustically coupled instruments use a plastic tube to deliver the sound from the case’s loudspeaker to the earmold.
BTEs can be used for mild to profound hearing loss. As the electrical components are located outside the ear, the chance of moisture and earwax damaging the components is reduced, which can increase the durability of the instrument. BTEs are also easily connected to assistive listening devices, such as FM systems, to directly integrate sound sources with the instrument. BTE aids are commonly worn by children who need a durable type of hearing aid
Benign Paroxsysmal Positional Vertigo (BPPV): Condition caused due to displacement of certain crystals in the inner ear. An affected individual will feel dizzy only in certain body/ head position. Benign paroxysmal positional vertigo (BPPV) is a disorder caused by problems in the inner ear. Its symptoms are repeated episodes of positional vertigo, that is, of a spinning sensation caused by changes in the position of the head. BPPV is the most common cause of vertigo symptoms. Vertigo, a distinct process some people confuse with dizziness, accounts for about 6 million clinic visits in the U.S. every year, and 17–42% of these patients eventually are diagnosed with BPPV. Other causes of vertigo include:
- Motion sickness/Motion Intolerance: a disjunction between visual stimulation, vestibular stimulation, and/or proprioception
- Visual exposure to nearby moving objects (examples of optokinetic stimuli: passing cars, falling snow)
- Other diseases: (labyrinthitis, Ménière’s disease, migraine. etc.)
Signs and symptoms
- Vertigo: Spinning dizziness, which must have a rotational component.
- Short duration (paroxysmal): Lasts only seconds to minutes
- Positional in onset: Can only be induced by a change in position.
- Nausea is often associated
- Visual disturbance: It may be difficult to read or see during an attack due to the associated nystagmus.
- Pre-syncope (feeling faint) or syncope (fainting) is unusual.
- Emesis (vomiting) is uncommon but possible.
- Rotatory (torsional) nystagmus, where the top of the eye rotates towards the affected ear in a beating or twitching fashion, which has a latency and can be fatigued (if you repeatedly continue placing yourself in the position to cause vertigo the symptoms should lessen each time).
- Nystagmus should only last for 30 seconds to one minute.
Patients do not experience other neurological deficits such as numbness or weakness, and if these symptoms are present, a more serious etiology such as posterior circulation stroke, must be considered.
The spinning sensation experienced from BPPV is usually triggered by movement of the head, will have a sudden onset, and can last anywhere between a few seconds to several minutes. The most common movements patients report triggering a spinning sensation are tilting their head upwards in order to look at something, and rolling over in bed.
Within the labyrinth of the inner ear lie collections of calcium crystals known as otoconia or otoliths. In patients with BPPV, the otoconia are dislodged from their usual position within the utricle and they migrate over time into one of the semicircular canals (the posterior canal is most commonly affected due to its anatomical position). When the head is reoriented relative to gravity, the gravity-dependent movement of the heavier otoconial debris (colloquially “ear rocks“) within the affected semicircular canal causes abnormal (pathological) fluid endolymph displacement and a resultant sensation of vertigo. This more common condition is known as canalithiasis.
In rare cases, the crystals themselves can adhere to a semicircular canal cupula rendering it heavier than the surrounding endolymph. Upon reorientation of the head relative to gravity, the cupula is weighted down by the dense particles thereby inducing an immediate and maintained excitation of semicircular canal afferent nerves. This condition is termed cupulolithiasis.
There is evidence in the dental literature that malleting of an osteotome during closed sinus floor elevation, otherwise known as osteotome sinus elevation or lift, transmits enough percussive and vibratory forces capable of detaching otoliths from their normal location and leading to the symptoms of BPPV.
It can be triggered by any action which stimulates the posterior semi-circular canal which may be:
- Tilting the head
- Rolling over in bed
- Looking up or under
- Sudden head motion
- Post head injury
BPPV may be made worse by any number of modifiers which may vary between individuals:
- Changes in barometric pressure – patients often feel symptoms approximately two days before rain or snow
- Lack of sleep (required amount of sleep may vary widely)
BPPV is one of the most common vestibular disorders in patients presenting with dizziness and migraine is implicated in idiopathic cases. Proposed mechanisms linking the two are genetic factors and vascular damage to the labyrinth.
Although BPPV can occur at any age, it is most often seen in people over the age of 60. Besides aging, there are no major risk factors known for developing BPPV, although previous episodes of trauma to the head or inner ear infections known as labyrinthitis, may predispose individuals to future development of BPPV.
The condition is diagnosed by taking a patient history, and by performing the Dix-Hallpike maneuver and/or the roll test. Patients with BPPV will report a history of vertigo as a result of fast head movements. Many patients are also capable of describing the exact head movements that provokes their vertigo.
The Dix-Hallpike test is a common test performed by examiners to determine whether the posterior semicircular canal is involved. It involves a reorientation of the head to align the posterior semicircular canal (at its entrance to the ampulla) with the direction of gravity. This test will reproduce vertigo and nystagmus characteristic of posterior canal BPPV.
When performing the Dix-Hallpike test, patients are descended quickly to a supine position with the neck extended by the clinician performing the manoeuvre. For some patients, this maneuver may not be indicated and a modification may be needed that also targets the posterior semicircular canal. Such patients include those who are too anxious about eliciting the uncomfortable symptoms of vertigo and those who may not have the range of motion necessary to comfortably be in a supine position. Obesity can also present a challenge when performing this assessment. The modification involves the patient moving from a seated position to side-lying without their head extending off the examination table, such as with Dix-Hallpike. The head is rotated 45 degrees away from the side being tested and the eyes are examined for nystagmus. A positive test is indicated by patient report of a reproduction of vertigo and nystagmus. Both the Dix-Hallpike and the side-lying testing position have yielded similar results and as such the side-lying position can be used if the Dix-Hallpike cannot be performed easily.
The roll test can determine whether the horizontal semicircular canal is involved. The roll test requires the patient to be in a supine position with his/her head in 20° of cervical flexion. Then the examiner quickly rotates the head 90° to the left side, and checks for vertigo and nystagmus. This is followed by gently bringing the head back to the starting position. The examiner then quickly rotates the head 90° to the right side, and checks for vertigo and nystagmus. In this roll test, the patient may experience vertigo and nystagmus on both sides, but rotating towards the affected side will trigger a more intense vertigo. Similarly, when the head is rotated towards the affected side, the nystagmus will beat towards the ground and be more intense.
As mentioned above, both the Dix-Hallpike and roll test provoke the signs and symptoms in subjects suffering from archetypal BPPV. The signs and symptoms patients with BPPV experience are typically a short-lived vertigo, and observed nystagmus. In some patients, though rarely, the vertigo can persist for years. Assessment of BPPV is best done by a health professional skilled in management of dizziness disorders, commonly a physiotherapist, audiologist or other medical physician.
The nystagmus associated with BPPV has several important characteristics which differentiate it from other types of nystagmus.
- Positional: the nystagmus occurs only in certain positions
- Latency of onset: there is a 5-10 second delay prior to onset of nystagmus
- Nystagmus lasts for 5–120 seconds
- Visual fixation suppresses nystagmus due to BPPV
- Rotatory/Torsional component is present or (in the case of lateral canal involvement) the nystagmus beats in either a geotropic (towards the ground) or ageotropic (away from the ground) fashion
- Repeated stimulation, including via Dix-Hallpike maneuvers, cause the nystagmus to fatigue or disappear temporarily.
Although rare, CNS disorders can sometimes present as BPPV. A practitioner should be aware that if a patient whose symptoms are consistent with BPPV, but does not show improvement or resolution after undergoing different particle repositioning maneuvers, which are detailed in the Treatment section below, need to have a detailed neurological assessment and imaging performed to help identify the pathological condition.
Two treatments have been found effective for relieving symptoms of posterior canal BPPV: the canalith repositioning procedure (CRP) or Epley maneuver, and the liberatory or Semont maneuver. The CRP employs gravity to move the calcium build-up that causes the condition.The particle repositioning maneuver can be performed during a clinic visit by health professionals or taught to patients to practice at home. In the Semont maneuver, patients themselves are able to achieve canalith repositioning. Both treatments, when performed by a health professional, appear to be equally effective. When practiced at home, the CRP is more effective than the Semont maneuver. The most effective repositioning treatment for posterior canal BPPV is the therapist-performed CRP combined with home practiced CRP.
The Epley maneuver (particle repositioning) does not address the actual presence of the particles (otoconia), rather it changes their location. The maneuver aims to move these particles from some locations in the inner ear which cause symptoms such as vertigo, and reposition them to where they do not cause these problems.
The Brandt-Daroff exercises may be prescribed by the clinician as a home treatment method usually in conjunction with particle repositioning maneuvers or in lieu of the particle repositioning maneuver. The exercise is a form of habituation exercise, designed to allow the patient to become accustomed to the position which causes the vertigo symptoms. The Brandt-Daroff exercises are performed in a similar fashion to the Semont maneuver; however, as the patient rolls onto the unaffected side, the head is rotated toward the affected side. The exercise is typically performed 3 times a day with 5-10 repetitions each time, until symptoms of vertigo have resolved for at least 2 days.
For the Lateral (Horizontal) canal, a separate maneuver has been used for productive results. It is unusual for the lateral canal to respond to the canalith repositioning procedure used for the posterior canal BPPV. Treatment is therefore geared towards moving the canalith from the lateral canal into the vestibule. The roll maneuver or its variations are used and involves rolling the patient 360 degrees in a series of steps to reposition the particles. This maneuver is generally performed by a trained clinician who begins seated at the head of the examination table with the patient supine There are four stages, each a minute apart and at the third position the horizontal canal is oriented in a vertical position with the patient’s neck flexed and on forearm and elbows. When all four stages are completed, the head roll test is repeated and if negative treatment ceases.
Medical treatment with anti-vertigo medications may be considered in acute, severe exacerbation of BPPV, but in most cases are not indicated. These primarily include drugs of the anti-histamine and anti-cholinergic class, such as meclizine and scopolamine respectively. The medical management of vestibular syndromes has become increasingly popular over the last decade, and numerous novel drug therapies (including existing drugs with new indications), have emerged for the treatment of vertigo/dizziness syndromes. These drugs vary considerably in their mechanisms of action, with many of them being receptor or ion channel-specific. Among them, include betahistine or dexamethasone/gentamicin for the treatment of Ménière’s disease, carbamazepine/oxcarbazepine for the treatment of paroxysmal dysarthria and ataxia in multiple sclerosis, metoprolol/topiramate or valproic acid/tricyclic antidepressant for the treatment of vestibular migraine, and 4-aminopyridine for the treatment of episodic ataxia type 2 and downbeat and upbeat nystagmus. These drug therapies offer symptomatic treatment, and do not affect the disease process or resolution rate. Medications may be used to suppress symptoms during the positioning manoeuvres if the patient’s symptoms are severe and intolerable. More dose-specific studies are required however, in order to determine the most effective drug(s) for both acute symptom relief and long term remission of the condition. For a complete list of these novel therapies and their associated target symptoms, follow the link below to the Informahealthcare website.
Surgical treatments, such as a semi-circular canal occlusion, do exist for BPPV but carry the same risk as any neurosurgical procedure. Surgery is reserved as a last resort option for severe and persistent cases which fail vestibular rehabilitation (including particle repositioning and habituation therapy).
Devices such as a head over heels “rotational chair” are available at some tertiary care centers Home devices, like the DizzyFIX, are also available for the treatment of BPPV and vertigo.
The Semont maneuver has a cure rate of 90.3%. It is performed as follows:
- The patient is seated on a treatment table with their legs hanging off the side of the table. The therapist then turns the patient’s head towards the unaffected side 45 degrees.
- The therapist then quickly tilts the patient so they are lying on the affected side. The head position is maintained, so their head is turned up 45 degrees. This position is maintained for 3 minutes. The purpose is to allow the debris to move to the apex of the ear canal.
- The patient is then quickly moved so they are lying on the unaffected side with their head in the same position (now facing downwards 45 degrees). This position is also held for 3 minutes. The purpose of this position is to allow the debris to move toward the exit of the ear canal.
- Finally, the patient is slowly brought back to an upright seated position. The debris should than fall into the utricle of the canal and their symptoms of vertigo should decrease or end completely. Some patients will only need one treatment, but others may need multiple treatments depending on the severity of their BPPV.