Vertigo

Primary Category

Essential Neurology

P-Category

Essential Neurology

Secondary Category

S-Category

Authors:

Bao Quoc Nguyen MD,

Peter Johns MD

Introduction

Vertigo is a false feeling of motion caused by dysfunction of the inner ear or the central vestibular system.

This is a common complaint from patients in a primary care setting and emergency room.

A thorough neurological examination and history taking are crucial to narrow down the diagnosis.

Physicians need to apply the correct bedside testing to the right patient to avoid unnecessary neuroimaging.

Definition

Vertigo is a symptom of vestibular dysfunction, typically described as an illusion of motion.

Patients may find it hard to put their feelings into words. The most common complaint is a spinning sensation. Terms such as "whirling,” "tilting,” or "moving” are usually used.

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Dizziness is an umbrella term for vertigo, pre-syncope, and disequilibrium. Physicians should confirm the symptom of vertigo before evaluating further.

Etiology

Central lesion: caused by central vestibular system (e.g., cerebellum, brainstem, vestibular nuclei) lesions or dysfunction

Cerebrovascular diseases (e.g., transient ischemic attack, ischemic and hemorrhagic stroke)
Cerebellopontine angle tumor
Migraine
Multiple sclerosis

Peripheral lesion: caused by the inner ear or the vestibulocochlear nerve dysfunction

Benign positional paroxysmal vertigo (most common)
Vestibular neuronitis
Acute labyrinthitis
Cholesteatoma
Herpes zoster oticus (Ramsay Hunt syndrome)
Ménière’s disease
Otosclerosis
Perilymphatic fistula

Miscellaneous

Cervical vertigo
Drug-induced vertigo
Psychological

Anatomy Recall

Figure 1: Vestibular nuclei and Vestibular tracts

Primary sensory neurons in the vestibular ganglia send information about angular and linear motion from the semicircular canals and otolith organs (utricle and saccule), respectively, via the vestibular component of CN VIII to the vestibular nuclei.

Vestibular nucleus complex:

Four nuclei on each side of the brainstem.
It lies on the lateral floor of the fourth ventricle in the pons and rostral medulla.

Table 1: Functions and connections of Vestibular nuclei

Vestibular Nuclei	Gives rise to	Connects with
Lateral (Deiter’s)	Lateral vestibulospinal tract	ㅤ
Superior	ㅤ	Medial longitudinal fasciculus
Medial	Medial vestibulospinal tract	Medial longitudinal fasciculus
Inferior	Medial vestibulospinal tract	ㅤ

The lateral and medial vestibulospinal tract descends via the spinal cord to innervate antigravity and head/neck muscle, respectively, maintaining balance and head position.

The connection with the medial longitudinal fasciculus (MLF) creates the crosstalk between the vestibular and the visual system, displayed by the vestibulo-ocular reflex (VOR).

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There are commissural fibers originating from vestibular nuclei passing through the vomiting center, which may explain why patients usually experience nausea during an acute vertiginous attack.

Pathophysiology

An uncomfortable sensation (e.g., disequilibrium, vertigo) happens when the cerebellum detects a mismatch between the external feedback (e.g., spatial orientation information transmitted by the vestibular system) and its internal parameter.

A lesion occurs anywhere along with the vestibular pathway → the cerebellum receives uneven information from both sides → the mismatch occurs → vertigo.

Clinical Evaluation

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When approaching a patient with vertigo, remember the mnemonic “TITRATE”: TIming, TRiggers, And Targeted Examination.

History

Duration of symptoms

Vertigo never continues permanently

Many factors help the vestibular system compensate for the lesion over weeks and months.
Constant “vertigo” lasting for months or years might not be vestibular.

Due to the difficulty in describing vertiginous sensations, the clinical course is better than the quality of symptoms as a starting point for downstream diagnostic reasoning.

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Caution: Some patients may claim they experience a consistent feeling of dizziness, but in fact, they are vulnerable to frequent episodic vertigo.

Trigger factors

Head movement always exacerbates vertigo, and that is why patients avoid moving during a vertiginous attack.

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If head movement does not worsen the attack, then such an episode might be another type of dizziness.

Table 2: Trigger factors of several causes of vertigo

Conditions	Trigger factors	Mechanism
Benign Paroxysmal Positional Vertigo (BPPV)	Positional changes, particularly getting in or out of bed or turning over in bed	Dislodge calcium carbonate structures of the otolith organs into semicircular canals → disrupts the endolymph dynamic → spinning sensation
Vestibular neuritis	Viral infection, especially upper airway infection	Postviral inflammation of the eighth cranial nerve
Vertebral artery dissection	Neck hyperextension	↓ blood supply to the posterior circulation → resembles lateral medullary dysfunction
Perilymphatic fistula or Superior canal dehiscence	Coughing, exertion, or loud noises (Tullio phenomenon)	↑ pressure transmitted from the cerebrospinal fluid (CSF) space to the inner ear via an abnormal anatomical defect
Migrainous vertigo	Any trigger factors of migraine (e.g., flashing lights, sleep disturbance, certain food)	Some authors theorized that the neuropeptide surge causes vertigo, not the headache itself

Associated symptoms

Nausea/vomiting

Very common with an acute vertigo attack.

It may cause dehydration and electrolyte imbalance in severe cases.

Can present with both central and peripheral lesions.

Postural and gait instability

The vestibular nuclei send signals to antigravity muscles via the vestibulospinal tract → uneven descending stimulations cause posture instability.

Central lesions have a greater effect on balance probably because other pathways controlling posture are involved as well.

Drop attacks

A sensation of being pulled to the ground while walking or standing without losing consciousness.

Can be of cardiac, psychological, or vestibular origin.

If patients present with vestibular dysfunction and a drop attack, they are very likely to have Ménière's disease.

Prior medical history

Necessary to narrow down possible causes and save time in the diagnostic process.

Risk factors such as hypertension, diabetes mellitus, smoking, and a history of vascular disease increase the suspicion of stroke.

Past head trauma may cause perilymphatic fistula or BPPV.

Prior cancer treatment with certain medications (e.g., cisplatin, aminoglycosides) suggests vestibular toxicity.

Physical Examination

Head impulse, nystagmus, and test of skew (HINTS) plus test

Indication: Patients with continuous vertigo (lasting for hours/days), ongoing vertigo, and spontaneous nystagmus.

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Misuse of the HINTS exam may lead to false-negative (e.g., stroke) or false-positive results (e.g., BPPV, vestibular migraine).

Table 3: HINTS plus test summary

VOR: Vestibulo-ocular reflex; HIT: Head Impulse Test; AICA: Anterior inferior cerebellar artery

ㅤ	Goal	Maneuver	Results	Interpretation	Note
Head Impulse Test	Evaluate the VOR	1. Ask a patient to fixate on a stationary object in front of them (e.g., a physician’s nose, a mask)	Normal: The patient maintains the eyes fixation during head rotation	Normal HIT suggests a central lesion (most likely stroke)	Remember to ask for a neck injury before performing the maneuver
ㅤ	ㅤ	2. Move the head off-center ~20-30 degrees	Abnormal: The patient cannot maintain the eyes fixation during head rotation, followed by a corrective shift of the eyes back to the stationary target (correction saccade)	Abnormal HIT mostly suggests a peripheral lesion (most likely vestibular neuritis)	Rotate the head from off-center toward the center, instead of doing the opposite, to avoid neck injury
ㅤ	ㅤ	3. Rapidly rotate the patient's head toward the center and assess their ability to maintain eyes fixation	ㅤ	ㅤ	ㅤ
ㅤ	ㅤ	4. For more details, watch the video: t.ly/dV-I	ㅤ	ㅤ	ㅤ
Nystagmus	Evaluate spontaneous (primary) and gaze-evoked nystagmus	Look for the direction (left vs. right) of spontaneous horizontal nystagmus	Unidirectional nystagmus: The direction of nystagmus does not change with gaze change	The fast phase beats away from the lesion	If the patient doesn’t have spontaneous nystagmus, then skip the HINTS plus test
ㅤ	ㅤ	Look for gaze-evoked nystagmus while examining the extraocular muscles	Bidirectional nystagmus: The direction of nystagmus changes with gaze change	Bidirectional nystagmus indicates a central lesion	If the nystagmus is vertical, then skip the HINTS plus test and rapidly investigate for a central lesion
ㅤ	ㅤ	For more details, watch the video: t.ly/zu6J	ㅤ	Unidirectional nystagmus indicates a peripheral lesion	ㅤ
ㅤ	ㅤ	ㅤ	ㅤ	Alexander’s law: Nystagmus intensity ↑ when the patient looks toward the fast phase and ↓ when looking toward the slow phase	ㅤ
Test of Skew	Evaluate the vertical ocular alignment	Alternate cover test: 1. The patient maintains a fixed central gaze and opened eyes during the examination	Absent: The eyes remain in a fixed central gaze when uncovered	Vertical ocular misalignment (Skew deviation) suggests damage at the otolithic vestibular nuclei → central lesion, most likely located in the posterior fossa	Do not touch the patient’s face during the maneuver, which triggers eye blinking → error evaluation
ㅤ	ㅤ	2. Repeatedly cover one eye, and then the other eye while looking for a vertical deviation from the central gaze upon uncovering the eye	Presented: The eyes A refixation saccade occurs upon uncovering the eyes → vertical ocular misalignment	ㅤ	ㅤ
ㅤ	ㅤ	For more details, watch the video: t.ly/YGQ	Note: horizontal movement is not skew	ㅤ	ㅤ
Finger Rub Test	The “plus” component of the traditional HINTS test	1. The examiner rubs their fingers together and asks if there is a decrease in hearing	Normal: No hearing change from the patient’s baseline	AICA supplies blood to the labyrinth of the inner ear, unlike other cerebellar arteries infarction, complete AICA infarction compromises VOR and causes hearing loss, resulting in abnormal HIT, and abnormal finger rub test [15]	ㅤ
ㅤ	To screen for Anterior inferior cerebellar artery (AICA) infarct in patients who have abnormal head impulse test	2. Compare both sides	Abnormal: a new and unequal hearing ability between two sides	ㅤ	ㅤ
ㅤ	ㅤ	For more details, watch the video: t.ly/9Sdz	ㅤ	ㅤ	ㅤ

Figure 2: Head Impulse Test

A: The left ear’s peripheral vestibular function is intact. With the head turned to the left, the vestibulo-ocular reflex helps the eyes maintain visual fixation.
B: The left ear’s peripheral vestibular function is impaired. With the head turned to the left, the eyes shift with it, failing to maintain visual fixation; the patient then saccades back to the object. This indicates a peripheral vestibular disorder on the left side. — A: The left ear’s peripheral vestibular function is intact. With the head turned to the left, the vestibulo-ocular reflex helps the eyes maintain visual fixation. B: The left ear’s peripheral vestibular function is impaired. With the head turned to the left, the eyes shift with it, failing to maintain visual fixation; the patient then saccades back to the object. This indicates a peripheral vestibular disorder on the left side.

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In lateral medullary stroke (or Wallenberg Syndrome), the ischemic lesion spares the superior and most part of the medial vestibular nuclei (main sources of the MLF) → intact vestibulo-ocular reflex (VOR) → normal head impulse test.

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One study in a stroke center showed that the HINTS plus test had a higher sensitivity in detecting stroke than the ABCD² score.

Dix-Hallpike maneuver

To confirm the diagnosis of Benign Paroxysmal Positional Vertigo (BPPV).

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Although Dix-Hallpike is a simple and reliable bedside test, emergency physicians often overlook or misuse it.

We will discuss Dix-Hallpike and similar maneuvers in more detail in our BPPV chapter.

To learn how to perform the test, we suggest this video:

Hearing test

To further investigate the cause of vertigo.

The examiner can check the hearing ability quickly with several methods (eg, whisper to the ear, finger rub).

The Weber and Rinne tests are used to distinguish conductive and sensorineural hearing loss. We suggest this video to learn how to perform and interpret Weber and Rinne test.

Additional neurologic signs

A careful neurologic examination is a must in any patient presenting with vertigo. Physicians should assess all cranial nerves, muscle strength, sensory function, coordination, gait, and deep tendon reflexes.

Focal neck pain after trauma or spontaneously appearing may suggest vertebral artery dissection.

Lateral medullary signs (e.g., diplopia, dysarthria, dysphagia, focal weakness, or paresthesias) suggests brainstem infarction.

Signs of local demyelination in patients with multiple sclerosis.

Some patients experience a sensation of aural fullness during an attack of Meniere’s disease.

Patients may experience headache, photophobia, and sonophobia in vestibular migraine, but not in all attacks.

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The Five Dangerous D's: Dysphagia, Dysarthria, Diplopia, Dysmetria, and Dysphonia strongly suggest a central cause of vertigo.

Diagnostic Tests

Neuroimaging

Indicated when suspecting vertigo secondary to a central lesion.

The procedure of choice in most cases is magnetic resonance imaging (MRI) of the brain with or without a magnetic resonance angiogram (MRA).

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MRI yields a better diagnostic value than computed tomography (CT) scan in evaluating the posterior fossa lesion and acute ischemic changes.

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MRA shows specificity and sensitivity of over 95 percent in detecting stenosis or occlusion of the posterior circulation.

Additional studies

Laboratory tests: considered based on history and clinical presentation

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Laboratory tests only detect the cause of vertigo in <1% of patients with all kinds of dizziness.

Electrocardiogram (ECG): to look for evidence of cardiogenic syncope or arrhythmia.

Audiometry

More sensitive than office testing (e.g., Weber and Rinne test, finger rub test) to identify hearing loss.
Quantify the hearing loss at high and low frequencies → to identify low-frequency sensorineural hearing loss → necessary to confirm Meniere’s disease.
Can detect unilateral hearing loss in almost all cases of vestibular schwannoma and may be a powerful screening test for this tumor.

Caloric testing: to assess isolated peripheral vestibulopathy

Less accurate than the head impulse test in acute settings.
However, the caloric test does not require head movement → favorable in patients with limited cervical mobility or coma.
To further understand and learn how to perform the test, watch the video: t.ly/_WQa

Approach

The differential diagnosis from a complaint of vertigo is massive; therefore, a diagnostic workup for a patient should be individualized.

However, in patients with an acute onset of vertigo, we should initially rule out stroke, especially in the emergency room environment.

Figure 3: Approach to Vertigo in the Emergency Room

Source: Flow chart of the initial approach to the diagnosis of acute vertigo. From Tintinalli's Emergency Medicine: AComprehensive Study Guide (9th ed., p. 1148), by Judith E. Tintinalli, 2019, McGraw Hill. Reprinted with permission

To understand the above approach in more detail, we suggest watching this video from Dr. Johns - the author of the flow chart:

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