Tricks of Trade: Benign paroxysmal positional vertigo | Beyond the Basics

Benign paroxysmal positional vertigo

Clinical Case

A 63-year old female presents to your ED with positional dizziness since rising out of bed from a nap this afternoon. She says she had a similar episode in the past and reports, “they took the stones out of my ear by making me lay down and move my head a few times.” Based on your assessment of the patient’s history and physical exam you determine she has peripheral vertigo, likely BPPV. However, despite multiple attempts with the Epley Maneuver, the patient is still symptomatic. What next steps could you consider?

Benign paroxysmal positional vertigo: The basics

Benign paroxysmal positional vertigo (BPPV) is a type of peripheral vertigo caused by a cluster of otoconial fragments that are displaced into the involved semicircular canal. The classic presentation is brief episodes of dizziness reported with position changes, commonly with rolling or arising from bed. The condition is more common in females and with advanced age (>40). BPPV should be differentiated from central vertigo and other types of peripheral vertigo including Meniere’s disease, vestibular schwannoma, vestibular neuritis, and labyrinthitis among others. Displaced otoliths are most commonly located in the posterior or horizontal semicircular canals. The strongest positive predictors of BPPV include dizziness lasting <15 seconds and onset with turning over in bed [1]. Episodes occur more frequently in the ear that is habitually dependent while sleeping [2], most commonly the right ear [3]. Regarding canal involvement, a retrospective review of 253 patients demonstrated the following [4]:

  • 83% Unilateral posterior canal
  • 7% Unilateral horizontal canal
  • 6% Bilateral posterior canals
  • 0% Anterior canal

There exist many different diagnostics and therapeutic positional techniques for addressing BPPV. Below we discuss the commonly taught techniques and several viable alternatives to consider when initial evaluation and/or treatment are unsuccessful.

Posterior Canal


1. Diagnostic: Loaded Dix-Hallpike Test

A Dix-Hallpike test is the most commonly taught and used diagnostic technique. However, providers may consider the “loaded” Dix-Hallpike.

Technique: Flex the patient’s head forward 30° in the same plane as the affected posterior canal for 30 seconds before placing supine with traditional technique. The loaded Dix-Hallpike has increased sensitivity, duration of nystagmus, and severity of symptoms compared to the traditional techniques [5]. Consider using pillow/blankets under the thoracic spine to allow adequate cervical extension as an alternative to hanging the patient’s head over the end of the bed (trick of the trade). Elderly patients with severe kyphosis may need to be tested with the head of the bed tilted downward (Trendelenburg).




2. Diagnostic: Sidelying Test

This is an alternative to Dix-Hallpike in patients who cannot lie flat, such as with back pain, limited mobility, obesity, or orthopnea. It can be performed on the edge of the bed (often logistically easier in crowded ED rooms than Dix-Hallpike).

Technique: Rotate the head 45° contralateral to the posterior canal being tested. The patient descends to their side which is ipsilateral to the posterior canal being tested. This position is held for 30 seconds. If the patient experiences vertigo and the provider notices nystagmus, the test is positive. A negative test should prompt testing on the other side.




3. Therapeutic: Epley Maneuver

This is the most commonly taught and performed repositioning maneuver. The American Academy of Neurology and American Academy of Otolaryngology has given this technique a Level A Recommendation and clinical benefit demonstrated in a systematic review [6]. Consider using a “chin tuck”, similar to the loaded Dix-Hallpike, for additional success.

Epley Maneuver vertigo

Epley Maneuver




4. Therapeutic: Semont Maneuver

Much like the Epley Maneuver is a continuation of the Dix-Hallpike Test, this therapeutic maneuver is a continuation of the Sidelying Test. The technique for left-sided posterior canalithiasis involves having a seated patient turn their head 45° to the left. The patient then drops their trunk to the right side, with the head turned 45° to the left (facing “up”). This position is held for 30-60 seconds. The patient then quickly sits up and lies down on the left side without stopping in the seated position. The head should still be kept 45° to the left so that the head now faces “down” and into the bed. This position is held for 30-60 seconds. Return the patient to the upright position.


Semont Maneuver vertigo

Semont Maneuver desired otolith movement

Horizontal Canal


1. Diagnostic: Roll Test

The Roll Test should be considered in patients displaying symptoms consistent with BPPV but posterior canal tests (Dix-Hallpike, Sidelying) are negative or appear to demonstrate horizontal nystagmus.

Technique: Have the patient begin by lying supine with the head flexed forward 30°. The provider then rotates the patient’s head rapidly 90° to one side followed by the other side, after re-centering the head. A positive test will involve bursts of nystagmus beating towards the affected ear which are stronger when the affected ear is dependent.




2. Therapeutic: BBQ or Lempert Roll

This repositioning maneuver can be performed as a continuation of the Roll Test and has shown success rates over 90% [7].

Technique: This involves stepwise rotations of the non-tilted head starting in the supine position and ultimately rolling a full 360°, holding each incremental 90° rotation for 30 seconds, starting from the affected to the unaffected side. This  can be repeated 2-4 times until symptoms improve or nystagmus disappears.




3. Therapeutic: Appiani/Gufoni Maneuver

The Appiani/Gufoni Maneuver repositioning maneuver has shown success rates comparable to other techniques in a meta-analysis [8].

Technique: Have the sitting patient descend to their unaffected side, hold this position for one minute or until symptoms subside. Then turning the head 45° towards the bed, holding this position for 1-2 minutes before sitting back up. Repeat until nystagmus is absent.

Appiani/Gufoni Maneuver vertigo

Appiani/Gufoni Maneuver desired otolith movement

Anterior Canal

The same maneuvers can be used to treat both posterior and anterior BPPV (i.e., Epley, Semont). However, there is a paucity of literature given the rarity of this condition. One small study reports success using a “reverse Epley” in 2 of 4 patients [9].

General Guidelines

  1. If your initial therapeutic approach does not work, consider treating the other side as the side of dysfunction can be easily misidentified at first. Serial examinations are often required to confirm BPPV.
  2. Providers should be aware of any underlying spinal or carotid disorders when performing many of the rapid head movements in these patients.
  3. Patients should be observed for a short time immediately after repositioning for signs of possible worsening symptoms and risk of fall [12].
  4. In cases of bilateral BPPV, consider treating the less involved side initially, followed by the more involved side 10-15 minutes later.
  5. Recurrence is common unfortunately despite successful therapeutic intervention. Up to 44% of patients had recurrent symptoms at 2-year follow-up in one study [6].
  6. Patient education: After successful treatment, sleeping slightly elevated or on the uninvolved side may prevent recurrences [10, 11].

Case Resolution

Realizing that you may have mis-identified the side and location of the dysfunction, you perform maneuvers assuming alternative locations for the provoking otoliths. To test for horizontal canal (instead of the more common posterior canal) dysfunction, you perform the roll test and notice nystagmus and worsening symptoms when facing the right side. Consequently, you have the patient perform the Lempert Roll technique, which causes her symptoms to resolve.

While you observe her for 10 minutes, there is no recurrence of her symptoms and she can ambulate without issues. You advise her to sleep on her left side. Outpatient follow-up with a physical therapist, specializing in vestibular disorders, should be strongly considered, especially if the patient is at risk for falls or if responsiveness to treatment was unclear.


The authors would like to extend a special thanks to Jeff Walter PT, DPT, NCS whose in-depth knowledge, experience, and research in the area of vestibular disorders were essential to this post. He is the creator of a FOAM blog: Vestibular Today on vestibular disorders that include many useful resources, diagrams, and videos.


  1. Noda K, Ikusaka M, Ohira Y, Takada T, Tsukamoto T. Predictors for benign paroxysmal positional vertigo with positive Dix–Hallpike test. Int J Gen Med. 2011;4: 809. PMID 22162937
  2. Çakir BÖ, Ercan İ, Çakir ZA, Civelek Ş, Sayin İ, Turgut S. What is the true incidence of horizontal semicircular canal benign paroxysmal positional vertigo? Otolaryngology. 2006 Mar; 134(3):451-4. PMID 16500443
  3. Von Brevern M, Seelig T, Neuhauser H, Lempert T. Benign paroxysmal positional vertigo predominantly affects the right labyrinth. J Neurol Neurosurg Psych Res. 2004 Oct 1; 75(10):1487-8. PMID 15377705
  4. Walters J. Geisinger Vestibular & Balance Center. Unpublished data. 2011.
  5. Andera L, Azeredo WJ, Greene JS, Sun H, Walter J. Optimizing Testing for BPPV–The Loaded Dix-Hallpike. J Int Adv Otol. 2020 Aug; 16(2):171. PMID 32784153
  6. Helminski JO, Zee DS, Janssen I, Hain TC. Effectiveness of particle repositioning maneuvers in the treatment of benign paroxysmal positional vertigo: a systematic review. Physical therapy. 2010 May 1; 90(5):663-78. PMID 20338918
  7. Li J, Guo P, Tian S, Li K, Zhang H. Quick repositioning maneuver for horizontal semicircular canal benign paroxysmal vertigo. J Otol. 2015 Sep; 10(3): 115–117. PMID 29937793
  8. Fu W, Han J, Chang N, et al. Immediate efficacy of Gufoni maneuver for horizontal canal benign paroxysmal positional vertigo: a meta-analysis. Auris Nasus Larynx. 2020 Feb 1; 47(1): 48-54. PMID 31151785
  9. Honrubia V, Baloh RW, Harris MR, Jacobson KM. Paroxysmal positional vertigo syndrome. Am J Otol 1999; 20: 465. PMID 10431888
  10. Shigeno K, Ogita H, Funabiki K. Benign paroxysmal positional vertigo and head position during sleep. J Vestib Res. 2012 Jan 1; 22(4):197-203. PMID 23142834
  11. Li S, Tian L, Han Z, Wang J. Impact of postmaneuver sleep position on recurrence of benign paroxysmal positional vertigo. PloS one. 2013 Dec 18; 8(12):e83566. PMID 24367602
  12. Uneri A. Falling sensation in patients who undergo the Epley maneuver: a retrospective study. Ear Nose Throat J. 2005 Feb; 84(2):82-5. PMID 15794543
By |2021-02-17T11:14:27-08:00Feb 17, 2021|Neurology, Tricks of the Trade|

Treating Blood Pressure in Intracranial Hemorrhage

hemorrhagic stroke equal podcast

Blood pressure control in the setting of ischemic stroke has a clearly recognized benefit in patient outcomes. The impact of blood pressure control in hemorrhagic stroke is not as well understood. The ACEP E-QUAL Network podcast, a partnership with ALiEM to promote clinical practice improvements, reviewed this topic with Dr. Latha Ganti (University of Central Florida College of Medicine). Dr. Ganti addressed the evidence behind recommended blood pressure targets and the available medications to achieve control. We present highlights from this discussion with Dr. Jason Woods.


What is the goal of blood pressure control in hemorrhagic stroke?

Management of blood pressure in intracranial hemorrhage (ICH) raises questions about the benefit of limiting hematoma expansion while maintaining cerebral perfusion. While it seems intuitive that hypertension should be controlled to limit hematoma expansion, patients with hemorrhagic stroke may be dependent on higher blood pressures for adequate perfusion.

Does lowering blood pressure lead to perihematomal ischemia?

ICH Adapt studies did not show evidence of decreased cerebral blood flow in perihematomal tissue and demonstrated that there is likely preservation of autoregulation which prevents ischemia [1].

Does lowering BP help prevent hematoma expansion and improve outcomes?

The risk of hematoma expansion is highest within the first couple of hours following initial bleeding. Hematoma expansion is clearly associated with worse outcomes. Scoring tools exist to estimate the risk of hematoma expansion. The “spot sign,” seen on source images from a computed tomography angiogram of the brain, suggests an area of dynamic bleeding.

  • ICH ADAPT: no difference in hematoma expansion or clinical outcome with acute blood pressure lowering [2].
  • INTERACT 2: intensive lowering of blood pressure did not result in a significant reduction in mortality or severe disability [3].
  • ATACH 2: intensive lowering of blood pressure did not improve functional outcomes but was associated with increased renal dysfunction [4].

What is the optimal systolic blood pressure (SBP) target?

AHA Guidelines 2015

  • ICH patients with SBP 150-220 mmHg, lower to 14 mmHg is safe
  • ICH patients with SBP > 220 mmHg, aggressive reduction with continuous infusion may be reasonable

So what’s the right thing to do? If data suggests that lowering may not be as beneficial, what should the target blood pressure be?

  • Target SBP 140-160 mmHg is a reasonable target

What medications are preferred for blood pressure control in ICH?

The ideal agent for blood pressure management in ICH would have a quick onset, but short duration, to allow titration.

Recommended first-line:

  • Labetalol
    • Onset < 5 min
    • Duration of effect 2-4 hr
    • IV bolus dose: 20 mg, followed by 20-80 mg every 10 min to a total dose of 300 mg.
    • Infusion dose: 0.5 mg-2 mg/min
    • Avoid in: asthma, COPD, heart failure, AV block
  • Nicardipine
    • Onset 1-2 min
    • Half-life ~ 40 min
    • Infusion dose: 0.5-1 mcg/kg/min, max 3 mcg/kg/min
  • Clevidipine
    • Onset 1-4 min
    • Duration of effect 5-15 min
    • Infusion dose: 1 mg/hr, up to 21 mg/hr, titrate by 2.5 mg/hr every 5-10 min
    • Avoid in: severe aortic stenosis, and lipid metabolism dysfunction or known allergy to eggs or soy (delivered as lipid emulsion)

Available second-line (mostly off-label, not preferred)

  • Esmolol
  • Fenoldopam
  • Hydralazine
  • Enalaprilat


When it comes to blood pressure: keep it simple.

  • Target SBP 140-160 mmHg
  • Top three drugs: Labetalol, Nicardipine, Clevidipine

Although labetalol has common contraindications, it is available as a bolus dose. In a clinical setting where drips may not be readily available, Labetalol can be easier to get.

Interested in more ACEP-EQUAL podcasts?

Listen to the other ACEP E-QUAL podcasts on our Soundcloud account.


  1. Butcher K, Jeerakathil T, Emery D, et al. The Intracerebral Haemorrhage Acutely Decreasing Arterial Pressure Trial: ICH ADAPT. Int J Stroke. 2010;5(3):227-233. PMID: 20536619
  2. Butcher KS, Jeerakathil T, Hill M, et al. The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial. Stroke. 2013;44(3):620-626. PMID: 23391776
  3. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013;368(25):2355-2365. PMID: 23713578
  4. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016;375(11):1033-1043. PMID: 27276234
By |2020-10-09T09:47:57-07:00Oct 23, 2020|Academic, Emergency Medicine, Neurology|

Anticoagulant Reversal in Hemorrhagic Stroke

anticoagulant equal podcast

Acute management of cerebrovascular accidents can be challenging enough, but questions about anticoagulant reversal in the setting of hemorrhagic stroke add another layer of complexity. The ACEP E-QUAL Network podcast, a partnership with ALiEM to promote clinical practice improvements, reviewed this topic with Dr. Joshua Goldstein (Massachusetts General Hospital, Harvard Medical School). Dr. Goldstein addressed common anticoagulants and their reversal agents, summarizing available literature to inform clinical practice. We present highlights from this discussion with Dr. Jason Woods.


What is the goal of anticoagulant reversal?

Since it is impossible to go back in time to prevent intracranial hemorrhage (ICH), the focus of management for hemorrhagic stroke should be to prevent further bleeding and allow brain tissue an opportunity to recover. The goal of anticoagulant reversal in patients with ICH is to decrease ongoing bleeding.


Warfarin is a vitamin K antagonist. Since vitamin K is required for the processing of coagulation factors II, VII, IX, and X, patients on warfarin have decreased amounts of these factors in circulation. To increase the availability of these factors, countering the effect of warfarin therapy can be two-fold:

  1. Replenish vitamin K to allow the production of new factors.
  2. Provide replacement of these factors directly.

Vitamin K supplementation will not provide immediate effect, and it may take up to 24 hours for the production of new coagulation factors. While it should be given early, patients also require factor replacement acutely.

Fresh frozen plasma (FFP) or prothrombin complex concentrate (PCC) can be given to supplement coagulation factors.

  • FFP carries each of the 4 needed factors in addition to other clotting factors.
    • The cost of FFP is low.
    • Transfusion will take some time as it will require ~ 1 L volume.
  • PCC, marketed as Kaycentra in the US, consists of concentrated Factor II, VII, IX, X, and proteins C and S.
    • The cost of PCC is higher.
    • Transfusion is quick, ~70 mL, and leads to rapid correction of INR.

Studies have shown PCC to be associated with faster INR reversal, less ICH expansion, and a non-statistical trend toward decreased mortality [1]. PCC does carry a theoretical risk of thromboembolism given the rapid correction, but no evidence exists to suggest that this is the case.

Direct Oral Anticoagulants (DOACs)

There are 2 categories of DOACs:

  1. Factor II inhibitors (e.g., dabigatran)
  2. Factor Xa inhibitors (e.g., rivaroxaban, apixaban, edoxaban)

Approach to reversal: remove the inhibitor to allow normal function of already existent Factor II or Xa

  • Time
    • Time can be thought of as a reversal agent. Most DOACs have a half-life ~12 hours. If the timing of the last dose is known and it was hours ago, there may not be much medication left to reverse.
  • Monoclonal antibodies
    • Reversal of dabigatran can be achieved with the use of a monoclonal antibody, idarucizumab, to bind up circulating inhibitor.
    • Reversal of Factor Xa inhibitors can similarly be attempted with the use of monoclonal antibody andexanet. Andexanet is notably more expensive than idarucizumab.
  • PCC
    • PCC can be used off-label to outcompete circulating inhibitor with extra coagulation factors and increase the number of functional factors.

It should be noted that there are no reliable tests for measuring DOAC activity.

Dual Antiplatelet Therapy (DAPT)

The most common agents are aspirin and Plavix (clopidogrel). The issue with patients on these antiplatelet agents is not a lack of platelets, but the presence of medication that suppresses normal platelet function. Theoretically, if one could provide extra platelets, the inhibiting agent could be saturated and the remaining platelets provide some functional activity.

The PATCH trial demonstrated, however, that platelet transfusion led to significantly worse outcomes [2]. While there is no readily available reversal agent for DAPT, platelet transfusion should be avoided. In fact, observational data suggest that patients on single antiplatelet therapy don’t fare worse and may not need reversal like those with DAPT [3].


Warfarin reversal

  • IV vitamin K + PCC (or FFP)

Dabigatran reversal

  • Specific agent: Idarucizumab
  • Non-specific agent: PCC

Factor Xa inhibitor reversal

  • Specific agent: Andexanet
  • Non-specific agent: PCC

Antiplatelet reversal

  • No available agent
  • Transfusion of platelets associated with worse outcomes.

Interested in more ACEP-EQUAL podcasts?

Listen to the other ACEP E-QUAL podcasts on our Soundcloud account.


  1. Steiner T, Poli S, Griebe M, et al. Fresh frozen plasma versus prothrombin complex concentrate in patients with intracranial haemorrhage related to vitamin K antagonists (INCH): a randomised trial. Lancet Neurol. 2016;15(6):566-573. [PMID: 27302126]
  2. Baharoglu MI, Cordonnier C, Al-Shahi Salman R, et al. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial. Lancet. 2016;387(10038):2605-2613. [PMID:27178479]
  3. Khan NI, Siddiqui FM, Goldstein JN, et al. Association Between Previous Use of Antiplatelet Therapy and Intracerebral Hemorrhage Outcomes. Stroke. 2017;48(7):1810-1817. [PMID:28596454]
By |2020-10-09T09:33:43-07:00Oct 16, 2020|Academic, Emergency Medicine, Neurology|

IDEA Series: 3D-printed pediatric lumbar puncture trainer

Pediatric lumbar puncture trainers are less available than adult trainers; most are the newborn size and quite expensive. Due to age-based practice patterns for fever diagnostic testing, most pediatric lumbar punctures are performed on young infants, and residents have fewer opportunities to perform lumbar punctures on older children.1 Adult lumbar puncture trainers have been created using a 3D-printed spine and ballistics gel, which allows for ultrasound guidance.2 No previous model has been described for pediatric lumbar puncture.


SAEM Clinical Image Series: Found Down with Altered Mental Status

non-contrast head CT

A forty-nine-year-old male with a history of polysubstance abuse, including methamphetamine and intravenous (IV) drug use, rectal cancer, and human immunodeficiency virus (HIV) was brought into the emergency department by emergency medical services (EMS) after he was found down at the bottom of a flight of stairs by his roommate. In the emergency room, he was found to have a Glasgow Coma Scale (GCS) score of 7 and was intubated for airway protection. Non-contrast head CT was performed. Per the roommate, the patient had been “not himself,” exhibiting strange behavior and weight loss. History and review of systems (ROS) were otherwise unobtainable due to the acuity of illness.


SAEM Clinical Image Series: Double Vision

cranial nerve palsy CN3

Chief complaint: Double vision

History of Present Illness: 61 year old female with history of HTN, DM, hyperlipidemia, and chronic low back pain presenting with double vision. She received an epidural spinal injection yesterday for the 4th time for low back pain. She was sedated for the procedure and woke up with headache, neck stiffness, and left eye “jumping around,” which progressed to double vision 1 hour later.

There was no blurry or double vision with either eye closed. She had 1 episode of emesis. She presented to the ED 24 hours later with continued headache and double vision.


By |2019-10-30T21:13:07-07:00Oct 14, 2019|Neurology, Ophthalmology, SAEM Clinical Images|

SAEM Clinical Image Series: Young Woman with a Headache


[Click for larger view]

Chief complaint: Headaches for 1 year

History of Present Illness: A 31-year-old woman with no significant past history presents with a dull headache.

She notes the headache is generalized, has been almost daily for a year and is worsened by bending over. She denies nausea, vomiting, photophobia, trauma, seizures, focal weakness, numbness, or vision change. Acetaminophen and ibuprofen provide only mild, short-acting relief. She takes oral birth control and her periods have been normal.


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