Benign Paroxysmal Positional Vertigo (BPPV) for ophthalmologists

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Benign paroxysmal positional vertigo (BPPV) is a common form of acute vertigo characterized by brief (< 1 minute) episodes of vertigo provoked by positional changes (e.g., rolling over in bed, lying down and sitting up from a supine position)[1]. BPPV is commonly attributed to calcium debris within the semicircular canals (SCC), which normally detect angular head accelerations. Debris in the SCC causes inappropriate endolymph movement with changes in position, and therefore causes the sensation of vertigo with positional movement. The posterior SCC is most commonly affected[1]. Recurrent episodes of vertigo may be accompanied by nausea and vomiting and can recur periodically for weeks to months. Patients typically have no hearing loss or other neurologic complaints.

Whilst vertigo typically does not present to ophthalmologists, the symptoms of the sensation of motion (i.e., oscillopia), blurred vision and the presence of nystagmus make it important for ophthalmologists to have some understanding of vertigo including BPPV. Observing nystagmus during a provoking maneuver helps ascertain the diagnosis of BPPV in patients with a typical history and can identify the laterality and specific canal affected[1].


Two theories exist for the mechanism of action of BPPV[2][3]. They differ with respect to how the debris influences cupular dynamics:

  1. Canalithiasis – proposes that free-floating particles, otoconia, have moved from the utricle and collect near the cupula of the affected SCC. Gravity pulls the otoconia through the endolymph canal, creating a plunger-like effect which causes ipsidirectional cupular displacement[2][3].
  2. Cupulolithiasis – proposes that the otoconial debris is attached to the cupula of the affected SCC instead of free-floating in the endolymph. Resulting alterations in cupular deflection lead to pathological perceptions of motion[2][3].

Clinical Presentation

Patients with BPPV present with recurrent episodes of vertigo that last less than 1 minute and are provoked by changes in head movements relative to gravity[4]. These vertigo spells may be associated with nausea and vomiting but patients do not complain of hearing loss or other neurologic symptoms. Nystagmus must be observed during a provoking maneuver as described below to confirm BPPV[5].

Nystagmus features

Posterior semicircular BPPV

Posterior SCC BPPV is the most common type of BPPV and can be tested by the Dix-Hallpike test[1][2]. Activation of both the ipsilateral inferior oblique and contralateral superior rectus leads to an upbeat-torsional nystagmus during the maneuver where the patient is brought from the upright to supine position with the head turned 45° towards the affected ear. The latency of onset between the start of Dix-Hallpike and the start of vertigo or nystagmus can vary between 2-20 seconds, and the nystagmus intensity typically increases and then resolves within 1 minute from the onset of the nystagmus. The nystagmus can reverse directions when the patient is returned to the upright position. Upon repeated testing, the nystagmus is likely fatigue, although repeating the maneuver multiple times is not recommended due to patient discomfort[1][2][4].

Horizontal/Lateral semicircular canal BPPV

Horizontal or lateral semicircular canal BPPV should be considered when the patient has a history compatible with BPPV and the Dix-Hallpike test elicits horizontal or no nystagmus. Horizontal BPPV can be evaluated using the supine roll test (also called the Pagnini-McClure maneuver)[2][3].

Compared to posterior semicircular BPPV, horizontal semicircular BPPV may have no latency, responses do not fatigue and the duration may be greater than 60 seconds[1][6]. The 2 types of lateral semicircular canal BPPV have different nystagmus findings:

  • Geotropic – elicits horizontal nystagmus that beats toward the earth when the patient head is rolled to the pathologic side. When the patient head is rolled to the healthy side, again elicits horizontal nystagmus beating toward the earth (undermost ear), but the direction of nystagmus has changed[2].
  • Apogeotropic – elicits horizontal nystagmus that beats toward the uppermost ear. When the patient head is rolled to the other side, again elicits horizontal nystagmus beating toward the uppermost ear, but the direction of nystagmus has changed[2].

Subjective BPPV

Subjective BPPV is the sensation of vertigo during provocative maneuvers without nystagmus. This may be due to subclinical nystagmus, fatigued response, or less severe BPPV that activates sensation of vertigo but not the vestibule-ocular reflex[3][7].

Differential Diagnosis

Otologic disorders:

  • Meniere’s disease – characterized by spontaneous vertigo lasting minutes to hours. Unlike BPPV, fluctuating aural symptoms include tinnitus, low-frequency hearing loss and fullness are present[2][8].
  • Vestibular neuritis or labyrinthitis – usually preceded by a viral prodrome, and the vertigo has a gradual onset, followed by a sustained level of vertigo lasting days to weeks. The vertigo is present at rest and does not necessarily require positional changes for its onset; vertigo may also be accompanied by sustained, severe levels of nausea, vomiting, sweating, and pallor[2].
  • Vestibular paroxysmia – recurrent, spontaneous attacks of vertigo lasting seconds to minutes due to vascular compression of the vestibular nerve. The positional triggers are distinct from BPPV and a crescendo-decrescendo pattern of nystagmus is not seen. A positive response to treatment with carbamazepine or oxcarbazepine is diagnostic[8][9].
  • Superior canal dehiscence syndrome – attacks of vertigo and oscillopsia (the sensation that objects are wavering back and forth) after a trigger of loud sounds, Valsalva maneuvers, or pressure changes of the external auditory canals. Unlike BPPV, vertigo in this syndrome is induced by pressure changes, not positional changes relative to gravity[2].

Neurologic disorders

Findings of down beating nystagmus on the Dix-Hallpike maneuver or direction-changing nystagmus occurring without changes in head position suggests a neurologic/central cause of vertigo and not peripheral, such as BPPV[2].

  • Vestibular migraine –in contrast to BPPV, episodes tend to be of shorter duration with frequent recurrences, and a migraine headache usually accompanies or follows the vertigo spell[5][10].
  • Central positional vertigo – may occur with lesions of the cerebellum. The downbeat nystagmus is static and persists as long as the provocative position, in contrast to BPPV which has a transient nystagmus. Lack of a torsional component to the nystagmus differentiates central positional nystagmus from that with anterior canal BPPV[2][8].


  • Postural/orthostatic hypotension – can present as episodic vertigo or dizziness, but symptoms only occur upon arising from a lying or sitting position and not due to changes in head position relative to gravity. Diagnosis can be made based on blood pressure measurements while the patient is supine and standing[2][8].
  • Persistent postural-perceptual dizziness (PPPD) – one or more symptoms of dizziness, unsteadiness or non-spinning vertigo on most days for at least 3 months, last for hours at a time, and usually wax and wane in intensity. Visual hypersensitivity from looking at complex or moving stimuli (eg, looking at traffic) is a characteristic feature of PPPD. BPPV may trigger or coexist with PPPD, but BPPV has distinct bouts of vestibular symptoms and nystagmus associated with positional changes, while PPPD is not associated with head motion-provoked vertigo, and has chronic waxing and waning dizziness, unsteadiness and non-spinning vertigo[11][12]. This is also known as visual variant vertigo.

Treatment of BPPV

BPPV can usually be treated using particle repositioning maneuvers. Posterior canal BPPV commonly uses the Epley and Semont maneuvers[1], and the Epley maneuver may be more effective than the Semont maneuver[13]. Horizontal canal BPPV uses the Lempert roll and Gufoni maneuvers[14][15].


BPPV has an overall favorable prognosis for recovery because untreated episodes of BPPV usually resolve spontaneously[2][13]. Patients with BPPV due to vestibular neuronitis and trauma may have a prolonged course than those with idiopathic BPPV. However, recurrence of BPPV episodes are common in the next one to five years. Patients with horizontal canal BPPV have a higher recurrence rate[2].


Ophthalmologists should be aware of BPPV. The roles of the ophthalmologist are to ensure that there are no ophthalmologic signs of central (rather than peripheral) vestibulopathy (e.g., purely rotary or purely vertical (upbeat or downbeat) nystagmus); to look for other ocular motor findings (e.g., ophthalmoplegia, skew deviation) or papilledema that might suggest central rather than peripheral etiologies for the vestibular symptoms; and to recognize the distinctive history of visual environmental hypersensitivity triggers in the persistent perceptual positional disorder (PPPD) which sometimes follows BPPV.

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