Benign Paroxysmal Positional Vertigo Clinical Presentation

Updated: Jan 14, 2022
  • Author: John C Li, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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The onset of benign paroxysmal positional vertigo (BPPV) is typically sudden. Many patients wake up with the condition, noticing the vertigo while trying to sit up suddenly. Thereafter, propensity for positional vertigo may extend for days to weeks, occasionally for months or years. In many, the symptoms periodically resolve and then recur.

The severity covers a wide spectrum. In patients with extreme cases, the slightest head movement may be associated with nausea and vomiting. Despite strong nystagmus, other patients seem relatively unfazed.

People who have BPPV do not usually feel dizzy all the time. Severe dizziness occurs as attacks triggered by head movements. At rest between episodes, patients usually have few or no symptoms. However, some patients complain of a continual sensation of a "foggy or cloudy" sensorium.

Classic BPPV is usually triggered by the sudden action of moving from the erect position to the supine position while angling the head 45° toward the side of the affected ear. Merely being in the provocative position is not enough. The head actually must move to the offending pose. After reaching the provocative position, a lag period of a few seconds occurs before the spell strikes. When BPPV is triggered, patients feel as though they are suddenly thrown into a rolling spin, toppling toward the side of the affected ear. Symptoms start very violently and usually dissipate within 20 or 30 seconds. This sensation is triggered again upon sitting erect; however, the direction of the nystagmus is reversed.



See the list below:

  • The physical examination findings in patients affected by BPPV are generally unremarkable. All neurotologic examination findings except those from the Dix-Hallpike maneuver may be normal. However, the presence of neurotologic findings does not preclude the diagnosis of BPPV.

  • The Dix-Hallpike maneuver is the standard clinical test for BPPV. The finding of classic rotatory nystagmus with latency and limited duration is considered pathognomonic. A negative test result is meaningless except to indicate that active canalithiasis is not present at that moment.

    • This test is performed by rapidly moving the patient from a sitting position to the supine position with the head turned 45° to the right. After waiting approximately 20-30 seconds, the patient is returned to the sitting position. If no nystagmus is observed, the procedure is then repeated on the left side.

    • Dix-Hallpike maneuver tips include the following:

      • Do not turn the head 90° since this can produce an illusion of bilateral involvement.

      • Tailor briskness of the Dix-Hallpike test to the individual patient.

      • Consider the Epley modification. From behind the patient, performing the maneuver is easier, since one can pull the outer canthus superolaterally to visualize the eyeball rotation.

      • In typical nystagmus, the axis is near the undermost canthus. Minimize suppression by directing the patient gaze to the anticipated axis of rotation.

  • Classic posterior canal BPPV produces geotropic rotatory nystagmus. The top pole of the eyes rotates toward the undermost (affected) ear.

  • Purely horizontal nystagmus indicates horizontal canal involvement.

  • Sustained or nonfatiguing nystagmus may indicate cupulolithiasis rather than canalithiasis.

A study by Yetiser and Ince indicated that the head-roll maneuver is the most effective positioning test for diagnosing lateral canal BPPV, in a comparison with the head-bending and lying-down positioning tests. The study, which involved 78 patients with lateral canal BPPV, found that using the head-roll maneuver, the affected side was located in 75% of patients with apogeotropic nystagmus and in 95.6% of patients with geotropic nystagmus. [4]



A few factors predispose patients to BPPV. These include inactivity, acute alcoholism, major surgery, and central nervous system (CNS) disease. A complete neurotologic examination is important because many patients have concomitant ear pathology, as follows:

  • Idiopathic pathology - 39%

  • Trauma - 21%

  • Ear diseases - 29%

  • Otitis media - 9%

  • Vestibular neuritis - 7%

  • Ménière disease - 7%

  • Otosclerosis - 4%

  • Sudden sensorineural hearing loss - 2%

  • CNS disease - 11%

  • Vertebral basilar insufficiency - 9%

  • Acoustic neuroma - 2%

  • Cervical vertigo - 2%

The following are some interesting highlights and associations gleaned from various studies.

A study by Chang et al suggested that BPPV can be triggered by dental procedures. The study, which included 768 patients with BPPV and 1536 controls, found that within 1 month before they were diagnosed, 9.2% of the patients with BPPV had undergone dental treatment, compared with 5.5% of controls within a month before they were identified. Adjustments for demographic factors and comorbidities indicated that a positive relationship exists between recent dental procedures and BPPV. [5]

A retrospective study by Faralli et al indicated that in persons with migraine headache and BPPV, the onset of BPPV tends to occur earlier in life than it does in patients with this form of vertigo but no migraine. The investigators found that the mean age at BPPV onset for patients with migraine was 39 years, compared with 53 years for patients without migraine. In addition, highly recurrent BPPV was found in 19.4% of the migraine patients, compared with 7.3% of persons without migraine. Moreover, the frequency of atypical eye movements and Ménière-like vertigo was greater in patients with both migraine and highly recurrent BPPV. Faralli and colleagues stated, however, that it has not yet been determined whether a direct pathophysiologic association exists between migraine and BPPV. [6]

A study by Picciotti et al indicated that the recurrence of BPPV is significantly associated with the employment of antihypertensives in single use, central nervous system agents, proton-pump inhibitors, vitamin D, and thyroid hormones. [7]

A report by Messina et al indicated that hypertension, dyslipidemia, and preexisting cardiovascular comorbidities are risk factors for recurrent episodes of BPPV, with the odds ratios ranging from 1.84 to 2.31. [8]

A study by Teggi et al indicated that in patients in whom BPPV first arises between the ages of 40 and 60 years, the presence of anti-thyroid autoantibodies strongly predicts recurrence. [9]