Benign paroxysmal positional vertigo

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

BPPV was first dicribed by Adler and Barany, who described it as a problem in the otolith organs. In 1952, Margaret Dix and Charles Hallpike named it positional nystagmus of the benign positional type and noticed nystagmus and vertigo with different headmovements. It is understood that BPPV is the result of free floating calcium carbonate crystal formation (canalolithiasis) inside the semicircular canals and Movement of these otoconia with head movement will result in inappropriate stimulation of hair cells following movement of the endolymph. According to which semicircular canal the otoconia have migrated to into 3 subtypes including posterior semicircular canal BPPV, lateral semicircular canal BPPV, and superior (anterior) semicircular canal BPPV. Common causes of BPPV may include age related degeneration of the vestibular system, and head trauma. The diagnostic study of choice for BPPV is patient history and observing nystagmus on Dix-Hall pike maneuver and in most of the cases treatment is Epley maneuver.

BPPV was first dicribed by Adler and Barany, who described it as a problem in the otolith organs. In 1952, Margaret Dix and Charles Hallpike named it positional nystagmus of the benign positional type. They noted nystagmus and vertigo with different headmovements. Hallpike also defined it as a peripheral problem rather than central (brain) problem. In 1962 Harold Schuknecht described theory of detached utricular otoconia (cupulolithiasis). Hall et al and Epley described the theory of free floating particle (canalithiasis). The first treatment strategy suggested for BPPV treatment was cawthorne’s exercise (repeatitive head movement which cause vertigo in order to reach central adaption). The newest treatment strategy is to perform Dix Hallpike test to diagnos and induce the vertigo and then performing CRP (Epley) maneuver.

Benign paroxysmal positional vertigo may be classified according to which semicircular canal the otoconia have migrated to into 3 subtypes including posterior semicircular canal BPPV, lateral semicircular canal BPPV, and superior (anterior) semicircular canal BPPV.

It is understood that BPPV is the result of free floating calcium carbonate crystal formation (canalolithiasis) inside the semicircular canals. Movement of these otoconia with head movement will result in inappropriate stimulation of hair cells following movement of the endolymph. In some studies it was demonstrated that people with BPPV in their first degree family are at more risk of development of the disease themselves. One of the theories behind the familial aspect of BPPV is that these families might have less adhesive gelatinous matrix of the utricular macula which predisposed them to BPPV. On microscopic histopathological analysis, crystals with combination of a gelatinous matrix and calcium carbonate are characteristic findings of otoconia in BPPV.

Common causes of BPPV may include age related degeneration of the vestibular system, and head trauma. Less common causes of BPPV include ear surgery, and prolong positioning on the back (in dentist chair).

BPPV must be differentiated from other diseases that cause vertigo, nystagmus, and hearing problems, such as vestibular neuritis, HSV oticus, Meniere disease, labyrinrhine concussion, perilymphatic fistula, semicircular canal dehiscence syndrome, vestibular paroxysmia, Cogan syndrome, vestibular schwannoma, otitis media, aminoglycoside toxicity, recurrent vestibulopathy, vestibular migraine, epileptic vertigo, multiple sclerosis, brain tumors, cerebellar infarction/hemorrhage, brain stem ischemia, chiari malformation, and Parkinson.

The incidence of BPPV is approximately 107 cases per 100,000 individuals worldwide. The prevalence of BPPV is approximately 65 per 100,000 individuals worldwide. Idiopathic BPPV commonly affects individuals older than 50 years of age. BPPV following head trauma can happen in younger ages. women are more commonly affected by BPPV than men. The women to men ratio is approximately 2 to 1.

Common risk factors in the development of BPPV include hyperlipidemia, hypertension, smoking, diabetes mellitus, thyroid dysfunction, general anesthesia, advanced age, female gender, and yoga.

There is insufficient evidence to recommend routine screening for BPPV.

If left untreated, almost 100% of patients with BPPV may experience spontaneous recovery. Common complications of BPPV include nausea, vomiting, fainting, canal conversion, and cervical spine and neurological complications following Dix Hallpike or Epley maneuvers. Prognosis is generally excellent, and almost always BPPV will resolve over days to weeks on its own even without maneuvers or medications.

The diagnostic study of choice for BPPV is patient history and observing nystagmus on Dix-Hall pike maneuver.

The hallmark of BPPV is recurrent brief positional vertigo. A positive history of hyperlipidemia, hypertension, smoking, diabetes mellitus, thyroid dysfunction, general anesthesia, advanced age, female gender, and yoga is suggestive of BPPV. The most common symptoms of BPPV include positional vertigo, imbalance, nausea and vomiting.

Physical examination of patients with BPPV is usually remarkable for balance problems and nystagmus on Dix-Hall pike maneuver.

There are no diagnostic laboratory findings associated with BPPV.

There are no ECG findings associated with BPPV.

There are no x-ray findings associated with BPPV.

There are no echocardiography/ultrasound findings associated with BPPV.

There are no CT scan findings associated with BPPV, but If patients doesn’t respond to treatment or doesn’t show the typical nystagmus on Dix-Hall pike maneuver, we may use CT scan in order to rule out other abnormalities.

There are no MRI findings associated with BPPV, but If patients doesn’t respond to treatment or doesn’t show the typical nystagmus on Dix-Hall pike maneuver, we may use MRI in order to rule out other abnormalities.

There are no other imaging findings associated with BPPV.

There are no other diagnostic studies associated with BPPV, but If patients doesn’t respond to treatment or doesn’t show the typical nystagmus on Dix-Hall pike maneuver, in order to rule out other abnormalities we may perform some additional test such as electronystagmography (ENG) or video nystagmography (VNG) and audiometry.

Pharmacologic medical therapy is recommended among BPPV patients who does not answer well to Epley maneuver and continue to have multiple vertigo attacks which reduces their quality of life. Preferred regimen Betahistine 24 mg PO q12h for 7 days.

The mainstay of treatment for BPPV is office maneuvers. For posterior canal BPPV we perform Epley maneuver or Semon maneuver. For horizental canal BPPV we perform Lempert roll maneuver. For superior canal BPPV we perform Epley maneuver.

Surgery is not the first-line treatment option for patients with BPPV. Surgery is usually reserved for patients with refractory BPPV. The surgery options include transection of the posterior ampullary nerve, argon laser (inducing ossification of the posterior canal) and surgical occlusion of the posterior canal with bony plugs. Since hearing loss is one of the most important complications of these procedures, hearing problem in the other ear is contraindication for surgery.

Effective measures for the primary prevention of BPPV is preventing the modifiable risk factors from happening such as hyperlipidemia, hypertension, smoking, diabetes mellitus, general anesthesia, and yoga.

There are no established measures for the secondary prevention of BPPV.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

BPPV was first dicribed by Adler and Barany, who described it as a problem in the otolith organs. In 1952, Margaret Dix and Charles Hallpike named it positional nystagmus of the benign positional type. They noted nystagmus and vertigo with different head movements. Hallpike also defined it as a peripheral problem rather than central (brain) problem. In 1962 Harold Schuknecht described theory of detached utricular otoconia (cupulolithiasis). Hall et al and Epley described the theory of free floating particle (canalithiasis). The first treatment strategy suggested for BPPV treatment was cawthorne’s exercise (repeatitive head movement which cause vertigo in order to reach central adaption). The newest treatment strategy is to perform Dix Hallpike test to diagnos and induce the vertigo and then performing CRP (Epley) maneuver.

• BPPV was first dicribed by Adler and Barany, who described it as a problem in the otolith organs.^[1][2][3][4]

• In 1952, Margaret Dix and Charles Hallpike named it positional nystagmus of the benign positional type.
• They noted nystagmus and vertigo with different head movements.
• Hallpike also defined it as a peripheral problem rather than central (brain) problem.
• In 1824 Marie-Jean Flourens concluded that semicircular canals are not a hearing organ but a balance-related organ.
• In 1962 Harold Schuknecht described theory of detached utricular otoconia (cupulolithiasis).
• Hall et al and Epley described the theory of free floating particle (canalithiasis).

• The first treatment strategy suggested for BPPV treatment was cawthorne’s exercise (repeatitive head movement which cause vertigo in order to reach central adaption).^[5][6][7][8]
• Brandt and Daroff suggested a maneuver consisting of laying down on each side for 30 seconds.
• Semont and Sterkes described liberatory maneuver (semont maneuver). In this maneuver patient lays down to the provocative side looking downward. When nystagmus stops the doctor should rapidly moved the patient head 90 degree on the other side.
• The newest treatment strategy is to perform Dix Hallpike test to diagnose and induce the vertigo and then performing CRP (Epley) maneuver.

For more information about Dix Hallpike maneuvers, click here.

For more information about Epley maneuvers, click here.

The following are a few famous cases of BPPV:

• Arthur Black, writer and former CBC radio host
• Lebron James, NBA
• Crown Princess Mette-Marit of Norway

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Benign paroxysmal positional vertigo may be classified according to which semicircular canal the otoconia have migrated to into 3 subtypes including posterior semicircular canal BPPV, lateral semicircular canal BPPV, and superior (anterior) semicircular canal BPPV.

Benign paroxysmal positional vertigo may be classified according to which semicircular canal the otoconia have migrated to into 3 subtypes:^[1]

• Posterior semicircular canal BPPV
• Lateral semicircular canal BPPV
• Superior (anterior) semicircular canal BPPV

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

It is understood that BPPV is the result of free floating calcium carbonate crystal formation (canalolithiasis) inside the semicircular canals. Movement of these otoconia with head movement will result in inappropriate stimulation of hair cells following movement of the endolymph. In some studies it was demonstrated that people with BPPV in their first degree family are at more risk of development of the disease themselves. One of the theories behind the familial aspect of BPPV is that these families might have less adhesive gelatinous matrix of the utricular macula which predisposed them to BPPV. On microscopic histopathological analysis, crystals with combination of a gelatinous matrix and calcium carbonate are characteristic findings of otoconia in BPPV.

The normal physiology of semicircular canals can be understood as follows:^[1]

• One of the most important inner ear structures are horizontal, superior (anterior) and posterior semicircular canals.
• There is an osseous ampullae at the end of each semicircular canal which consist of ampulla crest, the crista ampullaris, and hair cells.
• Semicircular canals are hollow structures with endolymph inside them.
• The movement of endolymph following changing head position will stimulate hair cells to send an impulse to the brain, determining the head position.
• The horizontal semicircular canal detects the head movement in the transverse plane (head turning to right and left).
• The superior (anterior) semicircular canal detects head rotational movement in the sagittal plane (head nodding).
• The posterior semicircular canal detects head rotational movement in the coronal plane (head touching the shoulders)

• It is understood that BPPV is the result of free floating calcium carbonate crystal formation (canalolithiasis) inside the semicircular canals.^[2]
• These debris are normally attached to the membrane of utriculus, a gravity-sensitive structures in the inner ear.
• Movement of these otoconia with head movement will result in inappropriate stimulation of hair cells following movement of the endolymph.
• The inappropriate impulses to the brain will result in false sensation of spinning.

• The development of idiopathic BPPV may be the result of multiple genetic mutations.^[3][4]
• In some studies it was demonstrated that people with BPPV in their first degree family are at more risk of development of the disease themselves.
• One of the theories behind the familial aspect of BPPV is that these families might have less adhesive gelatinous matrix of the utricular macula which predisposed them to BPPV.

Conditions associated with BPPV include:^[5][6]

• Migraine headache
• Diabetes mellitus
• Meniere disease

• there is no gross pathology findings with BPPV.

• On microscopic histopathological analysis, crystals with combination of a gelatinous matrix and calcium carbonate are characteristic findings of otoconia in BPPV.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Common causes of BPPV may include age related degeneration of the vestibular system, and head trauma. Less common causes of BPPV include ear surgery, and prolong positioning on the back (in dentist chair).

• There are no life-threatening causes of BPPV.

Common causes of BPPV may include:^[1][2]

• Age related degeneration of the vestibular system
• Head trauma

Less common causes of BPPV include:^[3]

• Ear surgery
• Prolong positioning on the back (in dentist chair)

• The development of idiopathic BPPV may be the result of multiple genetic mutations which leads to less adhesive gelatinous matrix of the utricular macula which predisposed them to BPPV.

Cardiovascular	No underlying causes
Chemical/Poisoning	No underlying causes
Dental	Prolong positioning on the back (in dentist chair)
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	Ear surgery/ vestibular abnormalities
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	Familial predisposition to BPPV
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	No underlying causes
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	Head trauma
Urologic	No underlying causes
Miscellaneous	No underlying causes

List the causes of the disease in alphabetical order:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

BPPV must be differentiated from other diseases that cause vertigo, nystagmus, and hearing problems, such as vestibular neuritis, HSV oticus, Meniere disease, labyrinrhine concussion, perilymphatic fistula, semicircular canal dehiscence syndrome, vestibular paroxysmia, Cogan syndrome, vestibular schwannoma, otitis media, aminoglycoside toxicity, recurrent vestibulopathy, vestibular migraine, epileptic vertigo, multiple sclerosis, brain tumors, cerebellar infarction/hemorrhage, brain stem ischemia, chiari malformation, and Parkinson.

BPPV must be differentiated from other diseases that cause vertigo, nystagmus, and hearing problems, such as vestibular neuritis, HSV oticus, Meniere disease, labyrinrhine concussion, perilymphatic fistula, semicircular canal dehiscence syndrome, vestibular paroxysmia, Cogan syndrome, vestibular schwannoma, otitis media, aminoglycoside toxicity, recurrent vestibulopathy, vestibular migraine, epileptic vertigo, multiple sclerosis, brain tumors, cerebellar infarction/hemorrhage, brain stem ischemia, chiari malformation, and Parkinson.

On the basis of vertigo, nystagmus, and hearing problems, BPPV must be differentiated from vestibular neuritis, HSV oticus, Meniere disease, labyrinrhine concussion, perilymphatic fistula, semicircular canal dehiscence syndrome, vestibular paroxysmia, Cogan syndrome, vestibular schwannoma, otitis media, aminoglycoside toxicity, recurrent vestibulopathy, vestibular migraine, epileptic vertigo, multiple sclerosis, brain tumors, cerebellar infarction/hemorrhage, brain stem ischemia, chiari malformation, and Parkinson.

Diseases	Clinical manifestations					Para-clinical findings		Gold standard	Additional findings
	Symptoms				Physical examination
						Lab Findings	Imaging
	Acute onset	Recurrency	Nystagmus	Hearing problems
Peripheral
BPPV [1][2][3]	+	+	+/−	−	+ Dix-Hallpike maneuver	−	−	Dix-Hallpike maneuver	May be associated with nausea, vomiting, and gait instability
Vestibular neuritis [4]	+	+/−	+ /− (unilateral)	−	+ Head thrust test	−	−	History/ Physical exam	May be associated with nausea, vomiting, gait instability and previous upper respiratory infection
HSV oticus [5][6][7][8]	+	+/−	−	+/−	Taste loss in the front two-thirds of the tongue Acute facial nerve paralysis Vesicles in the ear canal, the tongue, and/or hard palate	+ VZV antibody titres	In MRI with gadolinium dye we may have enhancement of the facial nerve and cranial nerve VIII	History/ Physical exam	May be associated with otalgia, dry mouth, and dry eyes
Meniere disease [9][10]	+/−	+	+/−	+ (Progressive)	Sensorineural hearing loss	−	In CT scan we may see small or invisible vestibular aqueduct	History/ Physical exam/ Rulling out other diagnoses	May be associated with nausea, vomiting, and tinnitus
Labyrinthine concussion [11][12]	+	−	−	+	high frequency hearing loss	−	We may see other evidences of head trauma or temporal bone fracture	History/ Physical exam	It happens following blunt head trauma May be associated with dizziness or tinnitus
Perilymphatic fistula [13][14][15]	+/−	+	−	+	Tullio phenomenon	−	CT scan may show fluid around the round window recess	History/ Physical exam/Imaging	Can be a complication of a stapedectomy, head injury, or heavy lifting It may be provoked by sneezing, lifting, straining, coughing, and loud sounds
Semicircular canal dehiscence syndrome [16][17]	+/−	+	−	+ (air-bone gaps on audiometry)	Tullio phenomenon	−	CT scan may show defect in the arcuate eminence of the superior semicircular canal	History/ Physical exam/Imaging	It may be provoked by Valsalva maneuver, coughing, and sneezing
Vestibular paroxysmia [18][19][20]	+	+	+/− (Induced by hyperventilation)	−	Impaired caloric testing	−	We may see evidence of vestibulocochlear nerve compression on MRI	History/ Physical exam/Imaging	It may be provoked by head turn or other action They respond well to treatment with carbamazepine or oxcarbazepine
Cogan syndrome [21][22][23]	−	+	+/−	+	Interstitial keratitis Oscillopsia Absent vestibular function on caloric test Systemic vasculitis (Aortitis)	Increased ESR and cryoglobulins	In CT scan we may see calcification or soft tissue attenuation obliterating the intralabyrinthine fluid spaces	History/ Physical exam	It may cause Ménière-like attacks
Vestibular schwannoma [24][25]	−	+	+/−	+	Sensorineural hearing loss + Rinne test Lateralization of Weber test to the normal ear	−	In CT scan we may see erosion, and widening of the internal acoustic meatus Hypointense mass on T1-weighted MRI, and hyperintense mass on T2-weighted MRI	Imaging	Gadolinium-enhanced MRI scan is definitive diagnostic test of acoutic neuroma
Otitis media [26][27]	+	−	−	+/−	Fever Presence of effusion in the middle ear	Increased acute phase reactants	Opacification of the middle ear	History/ Physical exam	Patient may show other signs and symptoms of upper respiratory infection such az cough, nasal discharge, and fever
Aminoglycoside toxicity [28]	+	−	−	+	Oscillopsia	−	−	History/ Physical exam	May be associated with nausea, vomiting, and ataxia It may be irreversible Gentamicin is the most common one
Recurrent vestibulopathy [29][30]	+	−	−	−	−	−	−	History/ Physical exam	The underlying pathophysiology is unknown It may happen infrequently, every one to two years It may be associated with nausea and vomiting It may overlap with vestibular migraine
Central
Vestibular migrain [31][32]	–	+	+/−	+/−	History of migraine headaches	−	They may have white-matter hyperintensities (WMHs) on MRI	ICHD-3 criteria	It may be associated with anxiety and depression
Epileptic vertigo [33]	−	+	+/−	−	They may experience loss of consciousness and motor/sensory problems	−	−	EEG	They response well to anti-seizure drugs
Multiple sclerosis [34][35][36]	−	+	+/−	−	Lhermitte’s sign Spasticity Increased reflexes Internuclear ophthalmoplegia Optic neuritis Gait disturbance	Elevated concentration of CSF oligoclonal bands	Brain atrophy and some contrast enhancing plaques on CT scan Cerebral plaques disseminating in space and time on MRI	History and physical examination Imaging CSF analysis	MS is at least two times more common among women than men The onset of symptoms is mostly between the age of fifteen to forty years, rarely before age fifteen or after age sixty
Brain tumors [37]	+/−	+	+	+	Papilledema Focal neurological deficits	Cerebral spinal fluid (CSF) may show cancerous cells	On CT scan most of the brain tumors appears as a hypodense mass lesions On MRI most of the brain tumors appears as a hypointense or isointense on T1-weighted scans, or hyperintense on T2-weighted MRI.	Imaging Biopsy	Patieny may experience headache, seizures, visual changes and changes in personality, mood and concentration
Cerebellar infarction/hemorrhage	+	−	++/−	−	Limb ataxia Gait disturbance Dysarthria	−	Based on the time interval between stroke and imaging we may have different presentations	Imaging	Posterior inferior cerebellar artery is the most common artery that causes vertigo
Brain stem ischemia	+	−	+/−	−	Contralateral body weakness Visual field deficits Oculomotor abnormalities Bulbar findings	−	Based on the time interval between stroke and imaging we may have different presentations For more information click here	Imaging	It may be associated with subclavian steal syndrome
Chiari malformation [38][39]	−	+	+	−	Tachycardia Pupillary dilatation Impaired gag reflex Impaired coordination	−	In CT scan we may see hydrocephalus, herniated cerebellar tonsils, and a flattened spinal cord In MRI we may see cerebellar tonsillar herniation, wedge shaped tonsils, syringohydromyelia, small posterior fossa, obstructive hydrocephalus, and brainstem anomalies	Imaging	Patient may experience ringing in the ears
Parkinson [40][41][42]	−	+	−	−	Hypomimia Cogwheel rigidity Resting tremor Gait problems Bradykinesia	−	On brain CT scan, Parkinson disease is characterized by cortical and subcortical atrophy MRI findings in Parkinson disease are reduction in T2 relaxation time and reduced iron content in putamen and GPe	History and physical examination	Patients may present with slowness of movement (bradykinesia), shaking hands while they are at rest (resting tremor) and muscle stiffness (rigidity).

ABBREVIATIONS

VZV= Varicella zoster virus, MRI= Magnetic resonance imaging, ESR= Erythrocyte sedimentation rate, EEG= Electroencephalogram, CSF= Cerebrospinal fluid, GPe= Globus pallidus externa, ICHD= International Classification of Headache Disorders

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

The incidence of BPPV is approximately 107 cases per 100,000 individuals worldwide. The prevalence of BPPV is approximately 65 per 100,000 individuals worldwide. Idiopathic BPPV commonly affects individuals older than 50 years of age. BPPV following head trauma can happen in younger ages. women are more commonly affected by BPPV than men. The women to men ratio is approximately 2 to 1.

• The incidence of BPPV is approximately 107 cases per 100,000 individuals worldwide.^[1]

• The prevalence of BPPV is approximately 65 per 100,000 individuals worldwide.

• Idiopathic BPPV commonly affects individuals older than 50 years of age.^[2]
• BPPV following head trauma can happen in younger ages.

• There is no racial predilection to BPPV.

• women are more commonly affected by BPPV than men. The women to men ratio is approximately 2 to 1.^[3]

• There is no region predilection to BPPV.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Common risk factors in the development of BPPV include hyperlipidemia, hypertension, smoking, diabetes mellitus, thyroid dysfunction, general anesthesia, advanced age, female gender, and yoga.

Common risk factors in the development of BPPV include:^[1][2][3][4]

• Hyperlipidemia
• Hypertension
• Smoking
• Diabetes mellitus
• Thyroid dysfunction
• General anesthesia
• Advanced age
• Female gender
• Yoga

Less common risk factors in the development of BPPV include:

• Ceiling painting
• Mechanics who spend a lot of time under cars
• Running on treadmill

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

There is insufficient evidence to recommend routine screening for BPPV.

• There is insufficient evidence to recommend routine screening for BPPV.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

If left untreated, almost 100% of patients with BPPV may experience spontaneous recovery. Common complications of BPPV include nausea, vomiting, fainting, canal conversion, and cervical spine and neurological complications following Dix Hallpike or Epley maneuvers. Prognosis is generally excellent, and almost always BPPV will resolve over days to weeks on its own even without maneuvers or medications.

• The symptoms of BPPV usually develop after 40-50 years of life start with vertigo that last less than one minute and starts after specific head movements.^[1]
• If left untreated, almost 100% of patients with BPPV may experience spontaneous recovery.^[2]

• Common complications of BPPV include:^[3][4]
  • Nausea
  • Vomiting
  • Fainting
  • Canal conversion
  • Cervical spine and neurological complications following Dix Hallpike or Epley maneuvers

• Prognosis is generally excellent, and almost always BPPV will resolve over days to weeks on its own even without maneuvers or medications.^[2]
• Resolving of the BPPV which is the result of head trauma or structural abnormalities might take a little more time.
• Recurrence is common and happens in more than 30% of patients.
• Patients older than 40 years of age, with horizontal BPPV or post traumatic BPPV are more susceptible to recurrence.

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