Table of Contents
- Anatomy Recall
- Figure 1: Vestibular nuclei and Vestibular tracts
- Table 1: Functions and connections of Vestibular nuclei
- Clinical Evaluation
- Duration of symptoms
- Trigger factors
- Table 2: Trigger factors of several causes of vertigo
- Associated symptoms
- Prior medical history
- Physical Examination
- Head impulse, nystagmus, and test of skew (HINTS) plus test
- Table 3: HINTS plus test summary
- Figure 2: Head Impulse Test
- Dix-Hallpike maneuver
- Hearing test
- Additional neurologic signs
- Diagnostic Tests
- Additional studies
- Figure 3: Approach to Vertigo in the Emergency Room
- Further Reading
- 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.
- 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.
Dizziness is an umbrella term for vertigo, pre-syncope, and disequilibrium. Physicians should confirm the symptom of vertigo before evaluating further.
- 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
- Multiple sclerosis
- Peripheral lesion: caused by the inner ear or the vestibulocochlear nerve dysfunction
- Benign positional paroxysmal vertigo (most common)
- Vestibular neuronitis
- Acute labyrinthitis
- Herpes zoster oticus (Ramsay Hunt syndrome)
- Ménière’s disease
- Perilymphatic fistula
- Cervical vertigo
- Drug-induced vertigo
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
Gives rise to
Lateral vestibulospinal tract
Medial longitudinal fasciculus
Medial vestibulospinal tract
Medial longitudinal fasciculus
Medial vestibulospinal tract
- 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).
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.
- 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.
When approaching a patient with vertigo, remember the mnemonic “TITRATE”: TIming, TRiggers, And Targeted Examination.
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.
Caution: Some patients may claim they experience a consistent feeling of dizziness, but in fact, they are vulnerable to frequent episodic vertigo.
- Head movement always exacerbates vertigo, and that is why patients avoid moving during a vertiginous attack.
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
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
Viral infection, especially upper airway infection
Postviral inflammation of the eighth cranial nerve
Vertebral artery dissection
↓ 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
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
- 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.
- 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.
Head impulse, nystagmus, and test of skew (HINTS) plus test
- Indication: Patients with continuous vertigo (lasting for hours/days), ongoing vertigo, and spontaneous nystagmus.
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
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
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
3. Rapidly rotate the patient's head toward the center and assess their ability to maintain eyes fixation
4. For more details, watch the video: t.ly/dV-I
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
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
For more details, watch the video: t.ly/zu6J
Unidirectional nystagmus indicates a peripheral lesion
Alexander’s law: Nystagmus intensity ↑ when the patient looks toward the fast phase and ↓ when looking toward the slow phase
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
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
For more details, watch the video: t.ly/YGQ
Note: horizontal movement is not skew
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 
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
For more details, watch the video: t.ly/9Sdz
Figure 2: Head Impulse Test
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.
One study in a stroke center showed that the HINTS plus test had a higher sensitivity in detecting stroke than the ABCD² score.
- To confirm the diagnosis of Benign Paroxysmal Positional Vertigo (BPPV).
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:
- 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.
The Five Dangerous D's: Dysphagia, Dysarthria, Diplopia, Dysmetria, and Dysphonia strongly suggest a central cause of vertigo.
- 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).
MRI yields a better diagnostic value than computed tomography (CT) scan in evaluating the posterior fossa lesion and acute ischemic changes.
MRA shows specificity and sensitivity of over 95 percent in detecting stenosis or occlusion of the posterior circulation.
- Laboratory tests: considered based on history and clinical presentation
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.
- 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
- 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
- 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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Medical doctor from Hue University of Medicine and Pharmacy