Medical Concept – Vertigo: The Basics

We recently had a great piece by Dr. Andrew Petrosoniak about the HINTS exam. As a medical student, however, his piece left me with more questions than answers. I decided to go hunting for some foundational concepts surrounding vertigo and bring you along for the ride.

At some point in our medical training, we all encounter the dizzy patient. It can be difficult to determine who has vertigo and who is merely lightheaded.

Pathophysiology

Vertigo is an illusion of movement. It results from a disturbance in the vestibular proprioceptive system. Of patients who present with ‘dizziness’, those who report that ‘the room is spinning when they are not’ or that ‘they are moving when the room is not’ are the most likely to have true vertigo. But keep in mind that not every patient with vestibular pathology describes their dizziness in this way. In one innovative study, patients were asked to describe their dizziness initially and then again ten minutes later; amazingly, half changed their descriptions.

Our vestibular system comprises peripheral (outside the brain) and central (inside the brain and spinal cord) components. The peripheral vestibular system includes the semicircular canals and the utricles. The semicircular canals are tubes containing fluid called endolymph. When we move our head in the three planes of angular motion, the endolymph moves with us, pushing on receptors called hair cells, which transmit information about our location in space to central vestibular system components, which include nuclei in the medulla and pons. The utricles and saccules detect linear movement through similar receptor hair cells. The cerebellum participates as well, sending and receiving signals to and from our eyes and receptors in our muscles and providing additional information about our position in space.

Etiology

Patients who are indeed suffering true vertigo can be divided into two etiologic categories: those suffering central vertigo and those with peripheral causes. Peripheral causes account for the vast majority of vertigo presentations. The goal of evaluation, however, is always to rule out a central cause, which can have more serious consequences and specific management strategies

Peripheral Causes of Vertigo

Benign paroxysmal peripheral vertigo is caused by an otolith (calcium carbonate crystal) from a utricle becoming dislodged and ending up in one of the semicircular canals, usually the posterior. Whenever the head moves in the plane of that semicircular canal, the endolymph – and the patient’s sense of where she is in space – is disturbed, creating the sensation of the room spinning.
Acute labyrinthitis is an inflammation of the labyrinthine organs caused by a viral or bacterial infection that often presents with vertigo and unilateral or bilateral hearing loss.
Acute vestibular neuronitis is an inflammation of the vestibular nerve, usually caused by a viral infection. Unlike labyrinthitis, it does not cause hearing loss.
Meniere’s disease is caused by excessive fluid in the endolymph leading to aural fullness, hearing loss, and tinnitus, in addition to vertigo.
Herpes zoster oticus is a vesicular eruption in the ear caused by reactivation of the varicella zoster virus.

Central Causes of Vertigo

Cerebrovascular disease, causing an arterial occlusion in the posterior circulation can affect the vertebrobasilar system and create vertigo.
Cerebellopontine angle tumour is a neuroma at the angle of the pons and cerebellum that causes a distinct set of cranial nerve findings, as tumour growth progresses and impinges on cranial nerves V, VII, and VIII. Hearing loss, tinnitus and vertigo may present initially, progress to mid-face hypo-esthesia and disequilibrium, and if untreated, death due to brainstem compression.
Migraine headaches may induce vertigo. There may be associated symptoms of aura, nausea, vomiting, and phono- or photophobia.
Multiple sclerosis can cause vertigo through demyelination of white matter in the central nervous system. This is particularly likely if the demyelinating event occurs in the cerebellum or involves cranial nerves.
Drugs, including alcohol, streptomycin, and gentamycin, can cause vertigo through ototoxicity. Other drugs that can produce vertigo include anticonvulsants, antidepressants and caffeine. A careful review of medications is essential, especially in elderly patients, who are more likely to be on multiple medications and are particularly susceptible to the effects of polypharmacy.

Diagnosis

When a patient presents in the emergency department with vertigo, use a step-wise approach to arrive at a diagnosis and plan.

Step 1: Ascertain timing and triggers

Elicit the timing of the dizziness and any factors that provoke it. Was the dizziness abrupt in onset or did it progress gradually? How long have the symptoms lasted? Are they intermittent or constant? Is there anything that aggravates or alleviates the dizziness? Understanding timing and triggers is generally much higher yield than having the patient describe the character of their symptoms.

Acute vestibular syndrome is an abrupt (over seconds to hours) onset of dizziness, nausea, vomiting and gait unsteadiness lasting days to weeks. Vestibular neuritis and posterior circulation stroke are the main causes for this syndrome. If the patient is complaining of chronic dizziness, lasting weeks to months, then one should consider a growing mass in the posterior fossa, or drug side effects as possible causes. Vertigo that is intermittent without any provoking factors can be caused by posterior circulation transient ischemic attacks or vestibular migraines. Finally, brief episodes of vertigo that are triggered by head movement and resolve when movement is stopped, point towards BPPV.

Step 2: Determine whether the vertigo is isolated or associated with other symptoms.

The most worrisome causes of vertigo are central, including cerebrovascular accidents and intracranial masses. Because these causes have serious consequences and specific treatments, it is important to ascertain the likelihood of a central cause.
The cerebellum and brainstem are small structures; it is unusual to find an ischemic lesion or mass that affects only the vestibulocochlear nerve’s nucleus. The presence of other neurological signs and symptoms (resulting from compromise of other central structures) point toward a central cause. A quick mnemonic for associated neurological symptoms is the 5 Ds: dizziness (vertigo), diplopia, dysarthria, dysphagia and dysmetria (cerebellar ataxia). Sensorimotor deficits in the extremities and loss of consciousness also support a central cause of vertigo. Even so, other aspects of the history and physical exam must be integrated into the decision-making process, since they will affect pre-test probability; central causes of vertigo may still be associated with an otherwise normal neurologic examination.

Step 3: Rule out a central process.

If the patient presents with acute vestibular syndrome, apply the HINTS bedside examination.

Briefly, the HINTS exam includes:

Head Impulse Test: This test measures the integrity of the vestibulo-ocular reflex. If the Head Impulse Test is abnormal it implies that the vestibular nerve is impaired. A normal HIT implies that the lesion is central, and should be considered an abnormal finding on the HINTS exam. The most important point however is that the head impulse test can ONLY be performed when the patient is experiencing vertigo symptoms.
Nystagmus: Unidirectional, horizontal nystagmus suggests a peripheral lesion. All other nystagmus (direction-changing, bilateral, purely vertical) should raise the suspicion for a central etiology.
Skew Test: This test reveals vertical strabismus caused by a supranuclear lesion in the posterior fossa, a central cause of vertigo.

If any one of the above is abnormal, the sensitivity for a central cause is about 100% and stroke management should be initiated. If the HINTS test in inapplicable, but the patient’s history and exam raise suspicion for stroke, stroke management should again be initiated.

If suspicion for central lesion remains low, try to rule-in a peripheral process.

Step 4: Identify the peripheral cause.

Acute severe dizziness lasting 24 hours or longer that presents with no other neurological findings, a unidirectional horizontal nystagmus, and a positive head impulse test indicates acute vestibular neuritis or labrynthitis (if hearing is also affected). Consult ENT, consider corticosteroids, and manage nausea and vomiting.

Recurrent positional vertigo that is elicited by changes in head position, lasts less than one minute, and resolves during rest are key features of benign paroxysmal positional vertigo (BPPV). The Dix-Hallpike maneuver is used to elicit nystagmus, which can indicate which canal is affected. A posterior canal defect causes vertical torsional nystagmus when the head is extended and hung over the edge of the bed. For a visual explanation of the Dix-Hallpike, click here. Posterior or anterior canal BPPV can be managed with the Epley maneuver, which aims to reposition the displaced canalith. A similar maneuver to replace a horizontal canalith involves lying supine and turning the head towards the unaffected side in 90 degree increments. These maneuvers can be attempted in the emergency department, but patients can also use them to manage vertigo symptoms at home. Some physiotherapists have expertise in the Epley maneuver, and may be helpful for patients who have difficulty mastering this challenging routine at home.

Recurrent spontaneous attacks of dizziness are typical of Meniere’s disease, and are usually accompanied by unilateral ear fullness, hearing loss, and roaring tinnitus. Episodes may last for hours. The HIT test, however, may be normal as the peripheral vestibular system is intact. Always be mindful that such recurring attacks may represent TIAs and impending basilar ischemia, especially if they appear with an accelerated frequency.

Conclusion

In summary, when a patient presents with vertigo, the most useful tool at your disposal is a detailed history and relevant physical exam. The timing, triggers and associated symptoms should all help you narrow the differential diagnosis for your patient’s vertigo. The physical examination can further help establish the pre-test probability for those important-to-catch central causes, so that you can pursue appropriate investigations and management.

Peer reviewed by Dr. Sarah Luckett-Gatopoulos (@SLuckettG) and staff reviewed by Dr. Andrew Petrosoniak(@petrosoniak).
[bg_faq_start]

References

Edlow, J. A. (2013). Diagnosing dizziness: we are teaching the wrong paradigm! Academic Emergency Medicine, 20(10): 1064-1066.
Kerber, K. A. (2009). Vertigo and dizziness in the emergency department. Emergency Medicine Clinics of North America, 27(1): 39-viii
Labuguen, R. H. (2006). Initial evaluation of vertigo. American Family Physician, 73(2): 244-251.
Lin, M. (2011). Acute vestibular syndrome and HINTS exam.
Swadron, S. P. (2011). A simplified approach to vertigo.
Video for diagnosing posterior stroke.

[bg_faq_end] [bg_faq_start]

Reviewing with the Staff (Dr. Andrew Petrosoniak)

Remember, ALL vertigo gets worse with movement – both central and peripheral. In BPPV, movement causes the symptoms. Spend your time during the history deciding the timing and triggers of vertigo and not the quality of symptoms. Studies have confirmed that the symptom quality is not a reliable predictor of the underlying etiology. Continuous vertigo has a different set of causes than does intermittent vertigo. Spend your time differentiating between the two. If vertigo is continuous, think of it as acute vestibular syndrome and use the HINTS exam.
[bg_faq_end]