Vertigo Makes the World Go Round – A Case of BPPV

Vertigo Makes the World Go Round – A Case of BPPV: Medical Student Clinical Pearl

Johnathan Rose, Med III

Class of 2022

Dalhousie Medical School New Brunswick (DMNB)

Reviewed by Dr. Maria Kovalik

Copyedited by Dr. Mandy Peach


A 73-year-old female presented to the emergency department via EMS with a three-day history of dizziness and associated nausea. On further questioning she stated that the dizziness began suddenly when she awoke three days prior. It felt like her environment was spinning and was made worse with movements. Episodes lasted about 30-60 seconds and would resolve if she stayed still. Her mobility was impaired due to feeling unsteady on her feet. She felt nauseous when dizzy but had no emesis; Gravol provided mild relief. She denied any headaches, vision/hearing changes, chest pain, shortness of breath, bowel/bladder changes, recent infections, muscle weakness, paresthesia, or constitutional symptoms.


She was an otherwise healthy 73-year-old with no past medical or surgical history. She was taking no medications. She did not smoke, drink alcohol, or use any recreational drugs.


Physical Exam:


The patient’s vital signs were all within normal limits and stable. Upon inspection, she appeared her stated age, was well kempt, and was laying very still with her eyes closed. She was alert and oriented x3. Her cranial nerve exam II-XII was normal. She had 5/5 strength in upper and lower limbs bilaterally. Tympanic membranes were normal bilaterally.


Upon sitting up, she had mixed horizontal and torsional nystagmus in her eyes bilaterally, as well as when she laid back down (Figure 1). When performing the Dix-Hallpike manoeuvre, she had mixed horizontal and torsional nystagmus when her head was tilted both left and right.


Figure 1. Types of Nystagmus. Diagram showing the 3 major forms of nystagmus: horizontal, vertical, and rotary.



What is vertigo?


There are four main types of dizziness: vertigo, light-headedness, presyncope, and disequilibrium. Vertigo is the most common, accounting for 54% of presentations1. Vertigo is the sensation of dizziness or illusory movement. Some people may perceive it as the environment moving while others perceive self-motion. It is often caused because of asymmetry in the vestibular system or dysfunction of the labyrinth, vestibular nerve, or central vestibular structures located in the brainstem2. Vertigo is a symptom, not a diagnosis, and the causes can be broken into two broad categories: central and peripheral3.



Does this patient have a central or peripheral cause of vertigo?


The history alone from a patient presenting with vertigo is able to correctly reveal the diagnosis in ¾ patients1. Therefore, it is necessary to ask questions that will help differentiate the causes of vertigo, as further investigations may not be helpful in doing so (Table 1).


Table 1. Distinguishing features between central and peripheral causes of vertigo1, 4.

Peripheral Central
Onset Sudden Gradual
Intensity Severe Mild
Duration Seconds Continuous
Nystagmus Horizontal and torsional; can be inhibited by fixation of gaze Purely vertical, horizontal, or torsional; cannot be inhibited by fixation of gaze
Associated neuro findings Rare Common
Tinnitus Common Rare
Nausea/Vomitting Frequent, severe Infrequent, mild


Physical exam for differentiating between central and peripheral vertigo should include a HINTS exam

Interpretation of the HINTS

“A benign HINTS exam is defined as abnormal HIT + direction-fixed horizontal nystagmus + absent skew.

dangerous HINTS exam is defined as any one of:

  • Normal/untestable HIT
  • or direction-changing horizontal nystagmus present/untestable
  • or skew deviation present/untestable

(Untestable refers to those patients with obvious oculomotor pathology or lethargy in whom the tests were unable to be completed).


The acronym INFARCT can be used to remember what constitutes a dangerous HINTS exam:

Impulse Normal

Fast-phase Alternating

Refixation on Cover Test.”8


Based on her history and physical exam findings, it is likely that our patient has peripheral vertigo.


What is the differential diagnosis for central vertigo1?

  • Multiple sclerosis
  • Migraine
  • Transient ischemic attack or stroke
  • Brain tumor


What is the differential diagnosis for peripheral vertigo1?

  • Benign positional paroxysmal vertigo (BPPV)
  • Ménière’s disease
  • Vestibular neuronitis
  • Acute labyrinthitis
  • Otosclerosis


What type of peripheral vertigo does our patient have?

The most common causes of peripheral vertigo are BPPV, Ménière’s disease, and vestibular neuronitis5. Table 2 illustrates some of the features that can be used to distinguish the causes of peripheral vertigo.

Table 2. Distinguishing features between common causes of peripheral vertigo5.

Ddx Duration Provoking Factors Special features Physical exam findings
Labyrinthitis Seconds – Minutes Change in position Hearing loss and tinnitus Hearing loss
Vestibular neuronitis Seconds – Minutes URTI Imbalance Normal hearing
BPPV Seconds – Minutes Change in position Positional Positive Dix-Hallpike
Ménière’s disease Hours Spontaneous Hearing loss and tinnitus Hearing loss




Taking into account both the history and physical exam, our patient has clear case of BPPV. She had a sudden onset of dizziness that is worse with changes in position and lasts 30-60 seconds before resolving if still. She had associated nausea and no other neurological signs. This, along with a positive Dix-Hallpike, is enough to secure the diagnosis.


BPPV Pathophysiology

BPPV is caused by canalithiasis, often calcium carbonate crystals, within the semicircular canals (Figure 2). The semicircular canals normally function to detect angular movements of the head. However, these heavy stones can cause inappropriate movement of the endolymph within the canals during times of linear accelerations, such as with gravity. Ultimately, this causes the improper sensation of spinning when the head shifts with respect to gravity6.


Figure 2. Mechanism of BPPV. Calcium crystals normally found within the utricular cavity are displaced and fall into the semicircular canals. Once displaced, they then cause the erroneous sensation of spinning when the head moves6.



 Although episodes of dizziness last seconds to minutes, the symptoms may persist for up to two weeks, and will often resolve spontaneously6. Symptoms may recur after remission5.

Treatment options are limited for those with BPPV. Medications are often not helpful, and treatment with vestibular suppressant medications such as antihistamines and/or benzodiazepines should be avoided7. For those who find the symptoms to be too distressing, the Epley maneuver may be performed to try and dislodge the otoliths from the semicircular canals (Figure 3)6. This maneuver has roughly a 77% success rate in the literature, but anecdotally seems to be less while also making patients more nauseous5.

Figure 3. Epley Maneuver. Steps involved in trying to reposition the calcium debris within the semicircular canals to migrate toward the common crus and exit into the utricular cavity6.


Our Case

Our patient ended up having BPPV that would likely resolve on its own within 2 weeks. No further diagnostic workup was required. Treatment options were limited; she was disappointed when she learned we had no medications that would provide her relief of her spinning world. The Epley maneuver was offered with the premise that it may or may not help relieve symptoms but will likely make her more nauseous, which she declined.


Clinical Pearls


  • Vertigo is a symptom, not a diagnosis.
  • A detailed history is required to elicit features of central or peripheral causes of vertigo.
  • Serious causes of central vertigo need to be considered.
  • Physical examination should include a neurological, cardiovascular, eye, and ear exam.
  • Rule out orthostatic hypotension by seeing if the patient feels dizzy when they sit up as well as when they lay down.
  • Treatment with vestibular suppressant medications such as antihistamines and/or benzodiazepines should be avoided7.
  • The Epley maneuver may be useful in some patients but will likely increase their nausea.



  1. Labuguen RH. Initial Evaluation of Vertigo. Am Fam Physician. 2006;73(2):244-251.
  2. Evaluation of the patient with vertigo.
  3. Baumgartner B, Taylor RS. Peripheral Vertigo. StatPearls. 2020. Available from:
  4. Chang AK. Dizziness and vertigo. In: Mahadevan SV, Garmel GM, editors. An Introduction to Clinical Emergency Medicine. 2nd ed. Cambridge: Cambridge University Press; 2012. p. 289–300.
  5. Dommaraju S, Perea E. An approach to vertigo in general practice. Australian Family Physician. 2016;45(4):190-194.
  6. Benign paroxysmal positional vertigo.
  7. Stanton M, Freeman AM. Vertigo. StatPearls. 2021. Available from:
  8. MacKay, J. HINTS exam in Acute Vestibular Syndrome. 2016. Retrieved Oct 26, 2021 from
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EM Reflections – March 2017

Thanks to Dr Paul Page for his summary

Edited by Dr David Lewis

Top tips from this month’s rounds:


Vertebral Artery Dissection – a tricky diagnosis and potentially catastrophic if missed…


Consider dissection in vertigo patients even without history of significant or mild trauma.

Headache and/or neck pain followed by vertigo or unilateral facial paresthesia is an important warning sign that may precede onset of stroke by several days. Dizziness, vertigo, double vision, ataxia, and dysarthria are common clinical features. Lateral medullary (Wallenberg syndrome) and cerebellar infarctions are the most common types of strokes.

Diagnosis – CT Angiography

Treatment – Antiplatelet or Anticoagulation (unless contraindications – see article below)

Cervical Artery Dissection in Stroke Study (CADISS) trial, RCT – antiplatelets versus anticoagulants in the treatment of extracranial carotid and vertebral artery dissections (VADs) = no difference found in outcomes between groups receiving antiplatelets vs anticoagulants. CADISS

Vertebral Artery Dissection: Natural History, Clinical Features and Therapeutic Considerations – (full text)

Rounds Presentation by Dr Kavish Chandra (R2 iFMEM)

Download (PDF, 755KB)


Limping Kids – inability to weight bear is always significant…

Need for thorough investigation of non traumatic hip pain in child unable to weight bear. Don’t get biased with previous diagnosis even if by specialists.

Don’t miss – Septic Arthritis or SCFE

From – – Hip Septic Arthritis – Pediatric – Author:

See this SJRHEM ED Rounds on Limping Kids

Take home pearls:

  • A limping/NWB child that can crawl is likely to have pathology below the knee
  • Examine least likely source of symptoms first.
  • Flex, Adduct and Int Rot hip most likely manoeuvre to elicit pain in hip pathology
  • Children >8yrs – X-ray hip first
  • If fever (>38°) or > 24hrs then bloods (incl CRP)
  • CRP < 12 is very reassuring (and a high CRP mandates further Ix to rule out septic arthritis)
  • Positive ultrasound is most likely to be irritable hip
  • Negative ultrasound – X-ray leg



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