Acute vertigo: quick reference for HINTS and differential diagnosis

Rapid overview

Acute dizziness is managed most safely by first establishing the time course and precipitating circumstances, and then selecting a targeted examination. The patient's description of the quality of the dizziness — rotatory vertigo, unsteadiness or faintness — discriminates poorly between dangerous and benign causes. Ask primarily how the symptoms began, whether they are continuous or episodic, how long an attack lasts, and whether anything actually triggers it [1,2].

The single most important practical rule is:

• Continuous acute dizziness with spontaneous nystagmus: consider HINTS plus, but only if the examiner is trained.
• Brief attacks triggered by the position of the head relative to gravity: perform Dix-Hallpike and, if needed, the supine roll test.
• Spontaneous attacks without a clear trigger: consider vestibular migraine, Ménière's disease, TIA and arrhythmia, among others.
• Acute severe balance disturbance without nystagmus: HINTS does not apply. Assess gait and truncal stability and investigate for a central cause.

Acute vestibular syndrome is often caused by acute unilateral vestibulopathy, commonly called vestibular neuritis, but posterior circulation stroke is the most important dangerous differential diagnosis. Clear focal neurological findings are absent in roughly half of patients with a central cause. A normal routine neurological examination is therefore not sufficient to exclude stroke [3].

Step 1: classify by time course and triggers

This corresponds to the principles of TiTrATE, in which Timing, Triggers And Targeted Examination guide the diagnostic process [1]. International guidelines recommend that emergency physicians be trained in HINTS, Dix-Hallpike and the Epley manoeuvre, since otherwise these examinations are easily applied to the wrong patient or misinterpreted [4].

Trigger or merely aggravation?

Distinguish between a movement that triggers a new attack and a movement that merely worsens dizziness that is already ongoing.

A patient with BPPV is usually relatively free of symptoms between the brief attacks. Lying down, turning over in bed or looking up triggers a new attack.

A patient with vestibular neuritis or stroke, by contrast, is already continuously dizzy. Head movement then worsens the symptoms but is not their actual trigger. The fact that continuous dizziness becomes worse when the patient moves the head is therefore not evidence of BPPV.

Step 2: decide whether HINTS may be used

HINTS stands for Head Impulse, Nystagmus, Test of Skew. HINTS plus adds a simple assessment of new-onset unilateral hearing loss.

HINTS should be used in an ongoing acute vestibular syndrome, typically with:

• new-onset continuous dizziness or unsteadiness
• spontaneous or gaze-evoked nystagmus
• nausea or vomiting
• marked motion intolerance
• difficulty walking
• symptoms present during the examination itself

HINTS should not be used:

• in brief episodic attacks
• when the patient is free of symptoms
• as a screening test for all non-specific dizziness
• in typical positional vertigo, which should instead be examined with positional testing
• in acute balance disturbance without nystagmus
• by an examiner who has not mastered the technique and its interpretation

GRACE-3 recommends HINTS only for trained clinicians and only in the right patient. If such competence is lacking, an uncertain or difficult-to-interpret finding must not be labelled peripheral [4].

In a Cochrane review of 16 studies and 2,024 patients, clinical HINTS was 94.0 percent sensitive and 86.9 percent specific for a central cause. HINTS plus was 95.3 percent sensitive and 72.9 percent specific. The evidence was judged to be of low quality, in part because of variation in patient selection, training and reference standard [5].

Another meta-analysis found a sensitivity of 95.3 percent and a specificity of 92.6 percent for HINTS. Sensitivity was similar among subspecialists and specifically trained non-subspecialists, but specificity was higher among subspecialists. The results cannot be extrapolated to untrained routine use [6].

Step 3: perform HINTS plus

Head impulse test

Ask the patient to fixate on your nose. Hold the patient's head and tilt it slightly forward so that the horizontal semicircular canals lie closer to the plane of examination. Perform small, rapid and unpredictable head impulses to the right and to the left. The excursion should be small, approximately 5 to 15 degrees.

In peripheral unilateral vestibular hypofunction the eyes move with the head when the head is rapidly turned towards the affected side. The patient must then make a corrective saccade back to the fixation target.

An abnormal impulse test does not, however, prove a peripheral cause. Infarction in the AICA territory can affect the labyrinth, the entry zone of the vestibular nerve or the vestibular nuclei, and thereby produce both an abnormal impulse test and acute hearing loss. Head impulse must therefore never be interpreted in isolation.

In the original prospective HINTS study, the combination of a normal impulse test, direction-changing nystagmus or skew was 100 percent sensitive and 96 percent specific in a selected high-risk population. The study was performed by an expert and had a very high proportion of central disease, which limits generalisability [7].

Nystagmus

Examine first in the primary position and then on gaze to the right and left. Ask the patient to look approximately 20 to 30 degrees to the side. Extreme lateral gaze can provoke physiological end-point nystagmus and should be avoided.

Unidirectional horizontal nystagmus is not synonymous with peripheral disease. Many cerebellar and brainstem infarctions produce horizontal nystagmus resembling peripheral vestibulopathy. Vertical or purely torsional spontaneous nystagmus has high specificity for a central cause but low sensitivity. In a systematic review the sensitivity was only 19.1 percent, while the specificity was 97.7 percent [10].

Suppression of nystagmus by visual fixation supports a peripheral cause but does not exclude central disease. Fixation suppression is difficult to assess qualitatively without Frenzel goggles or video-oculography.

Test of skew

Have the patient fixate on your nose. Cover one eye at a time alternately and move the cover rapidly between the eyes. Observe the eye that has just been uncovered.

Skew is relatively insensitive but, when clearly present, points above all to brainstem involvement. Small vertical deviations can also occur in peripheral vestibulopathy. A clearly visible finding on alternate cover testing must nonetheless be managed as central until proven otherwise [7].

HINTS plus: hearing

Ask about new-onset hearing loss, tinnitus or aural fullness. Compare the ears using finger rub or whispered speech. Perform otoscopy and, if findings are abnormal, also the Weber and Rinne tests.

New-onset unilateral sensorineural hearing loss in acute vestibular syndrome should raise suspicion of ischaemia in the AICA territory or labyrinthine infarction. HINTS plus therefore improves sensitivity for AICA infarction compared with HINTS without hearing assessment. In a meta-analysis, sensitivity for AICA stroke increased from 84.0 to 95.7 percent when hearing assessment was added [6].

Acute hearing loss is not specific for stroke. Differential diagnoses include sudden idiopathic sensorineural hearing loss, Ménière's disease and labyrinthitis. Even so, the combination of acute persistent dizziness and new-onset unilateral hearing loss must not be dismissed as peripheral without adequate assessment.

Overall interpretation

A fully peripheral HINTS plus requires that all of the following findings are consistent:

1. Abnormal impulse test towards one side.
2. Unidirectional, predominantly horizontal nystagmus beating away from the side with the abnormal impulse test.
3. No clear skew deviation.
4. No new-onset unilateral hearing loss.
5. No other focal neurological findings.
6. Gait and truncal stability compatible with peripheral vestibulopathy.

A single central or difficult-to-interpret finding is enough for HINTS to be classified as central or equivocal.

The mnemonic INFARCT can be used for the central findings:

• Impulse Normal
• Fast phase Alternating
• Refixation on Cover Test

HINTS is a combined examination. An abnormal impulse test must never be used on its own to discharge the patient.

Step 4: assess gait and truncal stability

Assess gait in every patient in whom this is safe. If the patient is too nauseated to walk, assess whether he or she can sit upright without holding on to the bed rails or supporting themselves with the arms.

In a meta-analysis, grade 2 or 3 was approximately 71 percent sensitive and 83 percent specific for a central cause. Grade 3 had low sensitivity, 44 percent, but very high specificity, 99 percent [11]. The absence of severe truncal ataxia therefore does not exclude stroke, but inability to stand or sit unaided is a serious red flag.

In a patient without nystagmus but with acute severe unsteadiness, HINTS should not be performed. This is rather an acute balance syndrome, in which a central cause, particularly cerebellar stroke, must be investigated.

Other findings that suggest a central cause

Neurological findings

Actively look for:

• dysarthria or dysphonia
• dysphagia
• diplopia
• gaze palsy or internuclear ophthalmoplegia
• facial palsy
• Horner's syndrome
• sensory loss in the face or limbs
• crossed sensory deficits
• limb weakness
• dysmetria or limb ataxia
• visual field loss
• impaired consciousness
• new-onset severe headache
• marked gait or truncal ataxia

The absence of these findings does not exclude stroke. In the original HINTS study, fewer than half of the patients with stroke had clear traditional neurological deficits [7].

Vascular warning signs

A central cause becomes more likely with:

• sudden maximal onset
• atrial fibrillation
• previous stroke or TIA
• hypertension, diabetes, smoking or dyslipidaemia
• known vascular disease
• recent dissection or neck vessel trauma
• new-onset neck pain or occipital headache
• coagulation disorder
• active malignancy
• pregnancy or the early postpartum period

Age over 60 years and vascular risk factors increase the probability of stroke, but younger age does not exclude a central cause. Vertebral artery dissection is an important cause of posterior circulation stroke in younger patients and can present as an acute vestibular syndrome, particularly together with new neck pain, occipital headache, trauma or manipulation.

Head movement that worsens dizziness that is already present, by contrast, is common in both peripheral and central vestibular disease and is in itself not a sign of dissection.

Imaging

CT of the brain

A normal CT of the brain does not exclude cerebellar or brainstem infarction. In a meta-analysis the sensitivity for a central cause was only 28.5 percent, while the specificity was 98.9 percent [12].

CT still has a role when the question is:

• intracranial haemorrhage
• a large mass lesion
• trauma
• a contraindication to MRI
• imaging before acute reperfusion therapy

A normal CT must not be used as an argument for discharge when the history or examination suggests stroke.

MRI of the brain with diffusion

MRI with diffusion-weighted sequences is the first-line method when a central cause is suspected, but early MRI is not a perfect rule-out test. In the meta-analysis of acute dizziness the sensitivity was approximately 80 percent [12]. In HINTS studies, early diffusion-weighted MRI was falsely negative in approximately 12 to 15 percent of stroke patients, particularly with small lesions in the lateral medulla, pons or cerebellar peduncles [6,7].

With a central or equivocal HINTS, serious neurological findings or strong clinical suspicion, the patient should therefore be managed as a possible stroke even if the first MRI examination is normal. Neurological observation and a repeat MRI may be needed.

CT angiography or MR angiography

Vascular imaging is indicated when there is suspicion of:

• vertebral or carotid artery dissection
• basilar artery occlusion
• vertebrobasilar stenosis
• posterior circulation TIA
• other large vessel occlusion

Vascular imaging does not replace parenchymal imaging and does not exclude small infarctions.

Acute stroke treatment

Patients with suspected ischaemic stroke should be assessed immediately according to the local stroke alert protocol. Dizziness and ataxia can be disabling stroke symptoms even at a low NIHSS. A low NIHSS does not exclude serious posterior circulation stroke. Assessment for thrombolysis and thrombectomy should follow current local stroke protocols.

Positional vertigo, BPPV

BPPV is usually caused by otoconia that have detached from the utricle and entered a semicircular canal. The posterior canal is most commonly affected. The diagnosis is made by provoking a canal-specific nystagmus pattern, not merely by the patient becoming dizzy [16,17].

Posterior canal

Perform Dix-Hallpike:

1. Seat the patient on the examination couch.
2. Turn the head 45 degrees towards the side being tested.
3. Rapidly lay the patient back with the neck extended approximately 20 degrees.
4. Observe the eyes for at least 30 to 60 seconds.
5. Ask whether the typical vertigo is provoked.
6. Return the patient to sitting and observe for any reversed nystagmus.
7. Test the other side.

A typical positive test shows:

• upbeating torsional nystagmus
• torsion with the upper pole of the eye towards the lower ear
• a latency of one or a few seconds
• a crescendo followed by decreasing intensity
• duration usually under one minute
• a simultaneous brief attack of vertigo

Fatigability may occur but need not be actively tested by many repetitions. Repeated provocations can reduce the nystagmus and make assessment more difficult.

If the patient cannot extend the neck, a side-lying test can be used. Take care in the presence of a current neck injury, marked cervical spine instability, severe cervical spinal stenosis or known dissection.

The Epley manoeuvre

In typical posterior canal BPPV the patient should be treated with a canalith repositioning manoeuvre, usually the Epley manoeuvre [16]:

1. Start in the positive Dix-Hallpike position with the affected ear down.
2. Maintain the position until the nystagmus and vertigo have subsided.
3. Turn the head 90 degrees towards the unaffected side.
4. Roll the patient further in the same direction until the nose points down towards the couch.
5. Help the patient back to sitting.

The manoeuvre can be repeated if clear typical nystagmus persists, but frequent immediate repetitions of Dix-Hallpike can sometimes contribute to canal conversion.

In a Cochrane review, the Epley manoeuvre increased the proportion of patients with complete resolution of symptoms from 21 to 56 percent compared with a sham manoeuvre or control. Conversion from a positive to a negative Dix-Hallpike test also improved clearly. Serious complications were not reported, but nausea was common [18].

Routine restrictions after the manoeuvre, such as sleeping upright or avoiding lying on a particular side, are not recommended [16].

Horizontal canal

Suspect horizontal canal BPPV if the history is typical but Dix-Hallpike shows horizontal or no nystagmus.

Perform the supine roll test:

1. Place the patient supine with the head slightly flexed.
2. Turn the head rapidly to one side.
3. Observe for horizontal nystagmus.
4. Return to the midline.
5. Repeat to the other side.

Treatment can be given with the Gufoni manoeuvre or barbecue roll. When the side is uncertain, the pattern atypical or treatment fails, the patient should be assessed by a physiotherapist, neurologist or ENT specialist with expertise in dizziness.

Central positional nystagmus

The following argue against ordinary posterior canal BPPV:

• purely downbeating nystagmus
• purely vertical or purely torsional nystagmus
• nystagmus that does not correspond to any semicircular canal
• immediate and persistent nystagmus without the typical intensity profile
• marked neurological findings or truncal ataxia
• new severe headache
• repeated unsuccessful repositioning manoeuvres
• a nystagmus pattern that changes between examinations
• severe vertigo out of proportion to the positional finding

Downbeating positional nystagmus is not always central, since rare anterior canal BPPV occurs. That diagnosis, however, requires an anatomically plausible nystagmus pattern and a response to appropriate repositioning. When in doubt, a central cause should be investigated [17].

Typical BPPV without atypical findings does not require CT, MRI or routine vestibular laboratory testing [16].

Vestibular neuritis

The more neutral term is acute unilateral vestibulopathy. The diagnosis requires an acute peripheral vestibular deficit without concurrent central neurological or acute audiological involvement [13].

Typical findings are:

• acute or subacute onset
• continuous dizziness persisting for at least 24 hours
• nausea, vomiting and motion intolerance
• unidirectional horizontal-torsional spontaneous nystagmus
• an abnormal impulse test towards the affected side
• the fast phase of the nystagmus beating away from the affected side
• no new-onset hearing loss
• no clear skew
• no gaze-direction-changing nystagmus
• no other focal neurological findings

Symptoms that resolve completely within 24 hours are less typical of vestibular neuritis. In that case consider TIA, vestibular migraine, Ménière's disease or another episodic vestibular disorder, among others.

Vestibular neuritis is a diagnosis of exclusion. New-onset hearing loss, tinnitus, ear pain or neurological symptoms should lead to reconsideration.

Treatment

Prioritise:

• fluids and correction of electrolyte disturbance when needed
• short-term antiemetic treatment in marked nausea
• early mobilisation
• gaze stabilisation exercises
• balance exercises and vestibular rehabilitation

Vestibular suppressant drugs can be used during the most symptomatic phase but should normally be limited to a maximum of two to three days. Longer treatment can inhibit central vestibular compensation [3].

Early vestibular rehabilitation improves patient-reported dizziness and functional ability. In a meta-analysis of five randomised trials, the Dizziness Handicap Inventory improved at both one and twelve months when early rehabilitation was added to corticosteroids [14]. Another meta-analysis found that vestibular rehabilitation gave better early subjective improvement than corticosteroids, whereas corticosteroids gave better early recovery on caloric testing. No reliable long-term difference could be demonstrated [15].

Corticosteroids can be considered early after symptom onset in selected patients, but should not be described as established routine treatment with a certain clinical benefit. An evidence synthesis found low-quality support for improved caloric recovery but a very uncertain effect on patient-reported dizziness and disability [14]. Take into account diabetes, hyperglycaemia, infection, gastrointestinal risk and other contraindications to steroids.

Antiviral treatment is not routinely recommended in uncomplicated vestibular neuritis.

Episodic spontaneous dizziness

When the patient has recurrent attacks but is free or nearly free of symptoms between them, HINTS is normally not useful. The diagnosis rests largely on the duration of the attacks, the associated symptoms and the risk profile [22].

Vestibular migraine

The main diagnostic features are:

• at least five episodes
• moderate or severe vestibular symptoms
• duration of 5 minutes to 72 hours
• current or previous migraine
• migrainous features during at least half of the episodes, for example migraine headache, photophobia and phonophobia, or visual aura
• no better alternative diagnosis [20]

Headache does not have to be present with every attack of dizziness. Vestibular migraine can also produce positionally triggered symptoms, but the nystagmus pattern is then often more persistent and less clearly canal-specific than in BPPV.

A first attack in an older patient or in a patient with vascular risk must not automatically be labelled vestibular migraine.

Ménière's disease

Definite Ménière's disease is characterised by:

• at least two spontaneous episodes of vertigo lasting 20 minutes to 12 hours
• documented low- or mid-frequency sensorineural hearing loss
• fluctuating hearing, tinnitus or a sensation of fullness in the affected ear
• no better alternative diagnosis [21]

Vertigo without documented hearing loss is not sufficient for a definite diagnosis. Audiometry is central.

Posterior circulation TIA

TIA can present as isolated episodic dizziness without residual findings on examination. Suspicion increases with:

• sudden maximal onset
• a new type of attack
• older age or vascular risk
• concurrent diplopia, dysarthria, dysphagia, ataxia or sensory disturbance
• new headache or neck pain
• attacks in the context of known vertebrobasilar vascular disease

Between attacks the neurological examination may be normal, which makes the history particularly important [23,24]. HINTS should not be used once the attack has ended. When TIA is reasonably suspected, urgent stroke workup and usually vascular imaging are needed.

Arrhythmia and presyncope

Presyncope is often described as dizziness. Ask about:

• greying out of vision
• syncope or near-syncope
• palpitations
• chest pain
• dyspnoea
• symptoms on exertion
• gastrointestinal or other bleeding

Check pulse, blood pressure, oxygen saturation and ECG. Consider glucose, full blood count, electrolytes and further cardiac workup according to the clinical picture.

Orthostatic dizziness

Orthostatic dizziness:

• is triggered by standing up or standing
• improves when the patient sits or lies down
• may be accompanied by blurred vision, weakness, cognitive clouding or palpitations
• should be documented with orthostatic blood pressure and pulse [19]

Turning over in bed suggests BPPV rather than orthostatism. Becoming dizzy on sitting up, by contrast, can be due to either and requires a careful history of provocation.

Other differential diagnoses

Drugs and toxins

Common drug-related causes are:

• antihypertensives and diuretics
• benzodiazepines, opioids and other sedatives
• antiepileptic drugs
• antipsychotics
• antidepressants
• aminoglycosides and other ototoxic drugs
• alcohol or other drugs of abuse
• polypharmacy

Drugs often cause diffuse unsteadiness, sedation or orthostatism rather than a typical focal vestibular syndrome. Antiepileptic drug toxicity can produce central nystagmus and ataxia.

Wernicke's encephalopathy

Consider thiamine deficiency in dizziness or ataxia together with malnutrition, alcohol dependence, prolonged vomiting, bariatric surgery or another risk of nutritional deficiency. The classic triad is often incomplete. When clinically suspected, thiamine should be given promptly according to local protocol and not delayed while awaiting laboratory tests.

Multiple sclerosis and other inflammatory disease

Demyelinating lesions in the brainstem or cerebellum can produce an acute vestibular syndrome, particularly in younger patients. Central ocular motor findings, other neurological deficits or previous episodes strengthen the suspicion.

Infection and ear disease

Perform otoscopy in every patient with acute dizziness. Look for:

• otitis
• cholesteatoma
• herpes zoster in the ear canal or on the auricle
• tympanic membrane perforation
• blood or signs of temporal bone trauma

Dizziness together with acute hearing loss or abnormal ear findings often requires assessment by an ENT specialist.

Red flags and common pitfalls

Red flags

• Central or equivocal HINTS.
• New-onset unilateral hearing loss in acute vestibular syndrome.
• Inability to stand or sit without support.
• Diplopia, dysarthria, dysphagia or other focal neurological findings.
• New severe headache or neck pain.
• Sudden maximal onset.
• Ongoing or recently resolved symptoms compatible with posterior circulation ischaemia.
• Anticoagulant treatment or known bleeding risk.
• Fever, meningism or impaired consciousness.
• Chest pain, dyspnoea, syncope or marked palpitations.
• Atypical or treatment-resistant positional nystagmus.

Pitfalls

1. Asking only what the dizziness feels like. Symptom quality is less diagnostic than time course, triggers and associated findings [1,2].

2. Calling all motion sensitivity positional vertigo. Both vestibular neuritis and stroke are worsened by head movement.

3. Performing HINTS in episodic dizziness or without nystagmus. A normal impulse test in a symptom-free patient is normal and does not constitute a central HINTS finding.

4. Using the impulse test on its own. AICA infarction can produce an abnormal impulse test and thereby mimic peripheral vestibulopathy.

5. Interpreting unidirectional horizontal nystagmus as proof of a peripheral cause. Many stroke patients have such a pattern [10].

6. Letting a normal CT exclude stroke. Sensitivity for a central cause in acute dizziness is low [12].

7. Letting an early normal MRI end the workup despite a central clinical picture. Small posterior circulation infarctions can be diffusion-negative early on [6,7,12].

8. Forgetting gait and truncal stability. Marked inability to stand or sit is a strong sign of a central cause [11].

9. Making a diagnosis of vestibular neuritis despite acute hearing loss. Hearing loss is not part of the criteria for acute unilateral vestibulopathy [13].

10. Giving vestibular suppressant drugs for too long. Prolonged treatment can counteract central compensation.

11. Treating BPPV with drugs instead of repositioning. Routine vestibular suppressant drugs are not recommended in BPPV [16].

12. Missing orthostatism, bleeding or arrhythmia. Presyncope may be described as dizziness and requires a different workup from vestibular vertigo.

13. Dismissing stroke because of young age. Dissection and other posterior circulation stroke also occur in younger patients.

14. Calling the patient's condition peripheral when HINTS is incomplete or difficult to interpret. An unclear test is not a negative test.

Practical emergency algorithm

1. Stabilise first. Check vital signs, glucose and the need for acute ABCDE management.

2. Determine the syndrome. Continuous, episodic triggered or episodic spontaneous.

3. Perform a neurological examination and assess gait. Include cranial nerves, coordination, sensation and power.

4. Examine the eyes and ears. Nystagmus in the primary position and on lateral gaze, otoscopy and a simple comparison of hearing.

5. In acute vestibular syndrome with nystagmus: perform HINTS plus if you are trained. A central or equivocal HINTS leads to stroke workup.

6. In acute severe unsteadiness without nystagmus: do not perform HINTS. Assess gait and truncal stability and have a low threshold for MRI.

7. In a typical positionally triggered syndrome: perform Dix-Hallpike and, if needed, the supine roll test. Treat confirmed posterior canal BPPV with the Epley manoeuvre.

8. In spontaneous attacks: consider vestibular migraine, Ménière's disease, TIA, arrhythmia and presyncope.

9. Use imaging selectively but promptly when a central cause is suspected. A normal CT does not exclude infarction. An early normal MRI may need to be repeated.

10. Document the findings. State which ear the impulse test was abnormal towards, the direction of the nystagmus in each gaze position, the presence of skew, the hearing findings and the patient's ability to sit, stand and walk.

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