Vertigo

Context

Patients frequently present to the emergency department (ED) complaining of dizziness. This term is used by patients to refer to a range of different symptoms and also includes patients with vertigo.

Classification

Detailed history is essential to differentiate vertigo from other non-rotatory dizziness. For example, lightheadedness triggered by postural change, but not head positional change, may have orthostatic hypotension.^1,2

A 2018 systematic review suggested that around 44% of patients presenting with “dizziness” in primary care have peripheral vertigo,³ and another review suggested the lifetime incidence of vertigo may be as high as 10%.⁴

Whilst vertigo often has a benign or self-limiting cause, prospective studies reported dizziness as a presenting symptom in 47% to 75% of patients with posterior circulation strokes.^5,6 Therefore, distinguishing between the benign and serious causes of vertigo is essential. This requires an understanding of the features of these aetiologies, careful clinical assessment and appropriate investigations.

Definition

Vertigo is a false perception of movement. This may be the feeling that the external world is moving around the individual (objective vertigo) or the feeling that the individual themselves is moving (subjective vertigo).

The control of balance and awareness of oneself in space is a highly complex process requiring input from, and integration of, sensory information from the eye, joints and the vestibular apparatus of the inner ear.

This information is integrated and processed by neurological pathways and connections involving cranial and peripheral nerves, the brain stem and higher brain centres.

Disorders in any of the sensory or integrating components can result in symptoms of dizziness or vertigo, but the disorders can be divided into:

• Central causes (vestibular nucleus and above)
• Peripheral causes

Peripheral causes are the more common of the two.

Learning Bite 

Peripheral causes account for about 80% of all vertigo cases.

Central Causes Vertigo

Table 1 – Common central causes of vertigo

Central vertigo arises due to defects of the vestibular nucleus or higher central nervous system connections.

Brainstem vestibular nuclei, the cerebellum and their connections may be affected by a number of pathological processes including:

• Haemorrhage
• Infarction
• Ischaemia
• Demyelination
• Tumour compression

Central causes of vertigo are often associated with other features of brainstem or cranial nerve dysfunction. There may be a new onset headache, and patients with cerebrovascular causes of vertigo may have pre-existing cardiovascular disease or risk factors.

The mechanism by which migraine causes vertigo is not well understood, but it can be associated with migraine headache in susceptible individuals.

Peripheral Causes of Vertigo

Table 2 – Common peripheral causes of vertigo

Peripheral vertigo is vertigo attributable to disorders of the inner ear vestibular apparatus or the peripheral neurological pathways.

Inner ear vestibular apparatus

The inner ear labyrinth is comprised of the vestibule (utricle and sacule) and three semicircular canals. These interconnected structures are filled with endolymph and receptors, which inform the brain of the head’s position and movement.

Disorders affecting the labyrinth are the commonest peripheral causes of vertigo, e.g. benign paroxysmal positional vertigo (BPPV), vestibular neuritis and Meniere’s disease.

Common peripheral causes include:

BPPV

Receptors in the utricle contain calcium oxalate crystals, or otoliths, which can become displaced and enter the semicircular canals. This usually occurs in the posterior canal, as it lies inferiorly, and otoliths are more likely to ‘fall’ into this canal.

Displaced otoliths can continue to stimulate movement receptors after cessation of head movement. This has been implicated as the cause for BPPV.

It is thought that the perception of room movement or rotation results from the brain’s attempt to resolve the conflicting information received from the inner ears, various proprioceptors and the eyes.

Classic cases of BPPV exhibit a positive Dix-Hallpike Test and the displaced otoliths can be repositioned with the Epley manoeuvre.

Learning Bite

Posterior semicircular canal otoliths are the commonest cause of BPPV.

Vestibular neuritis

Vestibular neuritis describes inflammation in the vestibular part of the VIIIth cranial nerve, and is thought to result from viral or post-viral inflammation, although there is no clear history of viral infection in 50% of cases.

Vestibular neuritis is associated with relatively rapid onset of severe persistent vertigo, nausea and vomiting.

An unstable gait and abnormal vestibular-ocular reflexes are often seen, but neurological examination is otherwise normal.

Hearing is typically unaffected. When ipsilateral sensorineural hearing loss occurs with vestibular neuritis, the term labyrinthitis is used. Acute symptoms usually last for 1-2 days, and attacks rarely recur.

Learning Bite

When ipsilateral hearing loss is associated with the symptoms of vestibular neuritis the term labyrinthitis is used.

Meniere’s disease

The cause of Meniere’s disease, also called endolymphatic hydrops, is unknown.

It is associated with excess endolymphatic fluid and inner ear dysfunction resulting in recurrent attacks of vertigo, vestibular dysfunction, tinnitus, ear fullness and sensorineural hearing loss.

Exacerbations may last for several days and recur over months to years.

Learning Bite

Meniere’s disease is associated with recurrent vertigo, tinnitus and hearing loss.

Careful clinical assessment through history and examination is key to the evaluation of patients with suspected vertigo.

Distinguishing vertigo from other causes of dizziness is an essential step.

True vertigo requires a history of perceived movement of the patient, or their surroundings.

Other conditions where dizziness results from global cerebral hypo-perfusion, such as postural hypotension, must be excluded.

History

When taking a history from a patient with vertigo, the following areas should be considered:

Current symptoms

Details of current symptoms must be identified:

• Type of vertigo (subjective or objective)
• Duration of symptoms
• Onset (sudden or insidious)
• Continuous or paroxysmal, and if paroxysmal then duration of paroxysms
• Aggravating factors, or precipitants of paroxysmal vertigo
• Any associated symptoms such as vomiting, altered hearing, cranial nerve dysfunction or limb weakness.

Risk factors

Risk factors should be identified:

• Previous episodes of vertigo
• Ear problems
• Head trauma
• Use of ototoxic drugs
• Known cardiovascular disease, or risk factors for cardiovascular disease such as increasing age, smoking, hypertension and diabetes.

Identifying potentially life-threatening central causes of vertigo is a crucial aspect of the assessment.

Central Causes

Central causes may be gradual or sudden in onset, but typically present as persistent rather than paroxysmal vertigo.

There may be significant instability, such that the patient struggles to stand and walk.

Other features such as severe head or neck pain or symptoms of brainstem dysfunction such as cranial nerve palsies or cerebellar symptoms are often present.

Central vascular causes are more common in older people and those with vascular risk factors.

Peripheral Causes

Peripheral vertigo may be associated with symptoms of cochlear dysfunction such as tinnitus or hearing loss, depending on the cause. However, the absence of hearing disturbance does not exclude a peripheral cause such as vestibular neuritis. Recurrent, very short attacks of vertigo precipitated by particular head movements, e.g. rolling in bed, are typical of BPPV, in which hearing is not usually affected.

Examination

Central or peripheral features may be further elicited on careful neurological examination.

Nystagmus

Nystagmus is an important clinical sign which may indicate the underlying cause of vertigo. It consists of an initial smooth movement in one direction followed by a rapid movement (saccade) to the opposite direction. Nystagmus is described according to the direction of its fast component. The fast component is also interchangeably used with the term ‘beat’, e.g. when the fast component is downwards = downbeat nystagmus. Nystagmus can be physiological (e.g. looking out of the window of a moving train) or pathological. It is normal to see a few self-limiting beats of nystagmus on extreme lateral gaze. When pathological, it is very useful in deciding whether vertigo has a central or peripheral cause.

Central causes of nystagmus may produce horizontal, vertical or rotational nystagmus. Importantly, the nystagmus does not suppress with visual fixation, is typically bi-directional and may change direction with gaze.

Peripheral causes of nystagmus produce typically unidirectional horizontal or horizontal-rotational nystagmus and is usually suppressed with visual fixation.

In the case of BPPV, it can be precipitated by head movement, e.g. Dix-Hallpike manoeuvre, but fatigues (habituates) with time with the head in the same position.

Learning Bite

Peripheral nystagmus is typically horizontal and unidirectional. Nystagmus that is bi-directional, vertical or torsional is more likely to be central.

Clinical features of peripheral and central vertigo¹:

Patients with acute vertigo

Patients with acute vertigo should undergo a thorough neurological examination including assessment of gait and cerebellar function.

The presence of other neurological signs suggests a central cause, and patients with vertigo due to stroke nearly always have other evidence of brainstem ischaemia, for example diplopia, dysarthria, numbness or weakness. Conversely, true isolated vertigo or dizziness very rarely indicates a stroke, and is found in less than 1% of such patients. However, it can occur in an isolated cerebellar lesion or infarct.

Many patients with vertigo will feel unsteady on standing. However, those with peripheral vertigo can usually stand unaided, whilst those with a central cause require assistance.

Otoscopy should be performed to exclude outer or middle ear pathology such as vesicles in herpes zoster or otitis media. If there is hearing loss, bedside auditory tests, i.e. Rinne and Webber tuning fork tests, should be performed to distinguish between conductive and sensorineural hearing loss. The presence of either support a diagnosis of peripheral vertigo. However, remember that some common peripheral causes of vertigo, such as vestibular neuritis or BPPV, are not typically associated with auditory symptoms or signs.

Learning Bite

Patients with central causes of nystagmus usually have other signs of cerebellar/brainstem dysfunction.

Patients with suspected BPPV

In patients with suspected BPPV, confirmatory bedside tests such as the Dix-Hallpike manoeuvre can be performed to test for posterior canalithiasis (the commonest cause for BPPV).

The sensitivity of this test ranges from 55% to 88%, but a positive test justifies the use of canalith repositioning manoeuvres, such as the Epley manoeuvre, which may be curative.

Dix-Hallpike Manoeuvre

With the patient sitting upright on a flat trolley, neck extended, the patient’s head is turned 45 degrees to the side, usually supported by the physician, before rapidly lying flat with neck extended over a pillow or end of the trolley (caution in the elderly or those with neck problems is required).

This position is held for 30 seconds during which the patient is encouraged to keep their eyes open. The patient is observed for the onset of nystagmus and associated vertigo suggestive of posterior canalithiasis in the down-most ear.

Typically, these symptoms appear after a short latent period, but settle (habituate) with the patient in the same position, and fatigue with repeated testing.

A positive test suggests the presence of a posterior canal canalith and this procedure may be followed by a canalith repositioning manoeuvre such as the Epley manoeuvre.

Image via Shutterstock

HiNTs examination

The HINTS examination is a clinical test to differentiate between central and peripheral causes of vertigo. One study demonstrated potentially greater sensitivity of HINTS than early MRI to exclude posterior circulation stroke in these patients,⁷ but the exam was performed by a neuro-ophthalmologist using specialist equipment, and this may limit its generalisability to the emergency department – indeed, it has been suggested that performance of the examination by other specialists may have a lower sensitivity.⁸ Other papers have suggested that use of HINTS in ED is variable⁹ further training is required before HINTS can be widely adopted.¹⁰ The test may have a higher positive predictive value in patients with vascular risk factors, so calculating ABCD2 score or similar at the same time may be helpful.¹¹

The HINTS exam comprises three elements, head impulse, nystagmus, and test-of-skew. It is only valid in patients who have continuous, ongoing vertigo at the time of assessment.

A video demonstration of the examination can be viewed here.¹² Correct administration of the test is vital in order to draw accurate conclusions.

Head impulse

The patient stands in front of the examiner, with their head held between the examiner’s hands. The patient is asked to fixate on the tip of the examiner’s nose, and their head is rotated 20 to 40 degrees in each direction, before being rapidly brought back to neutral.

The normal response, which is preserved in posterior stroke, is to maintain a continuous direction of gaze. In peripheral causes of vertigo, the vestibulo-ocular reflex is disrupted, so they lose eye contact and correct with a saccade. Thus, an abnormal response is more indicative of a benign cause of vertigo.

Nystagmus

The patient is asked to look straight ahead, to the left, and to the right, while the direction of nystagmus is observed.

Nystagmus due to a peripheral cause is always horizontal, and will always have the fast phase in the same direction, and is often accentuated when the patient looks in the direction of the fast phase. Any vertical or rotational element, or if the direction changes with direction of gaze, is suggestive of a central cause of vertigo.

Test-of-skew

The patient stands in front of the examiner and is asked to fixate on the tip of their nose. The eyes are alternately covered. In a central cause of vertigo, the vertical alignment of the eyes may be different, and a vertical corrective movement will be seen as the eye is covered and uncovered. In peripheral causes, this finding is absent.

Bedside tests should be used to assess for, and exclude, other potential causes of dizziness. These tests include:

• Blood sugar
• ECG
• Postural blood pressures

Any other specific investigations for vertigo will be guided by the clinical picture, and ED investigations may not be required.

Magnetic resonance imaging (MRI) and MR angiography (MRA) are most sensitive for:

• Brainstem infarcts
• Demyelination
• Inner ear pathology
• Acoustic neuromas

However, MRI may not be available in ED, and patients with suspected central causes such as intracranial (e.g. cerebellar) haemorrhage may initially undergo an urgent CT scan of the brain. Early neuroimaging may not be fully sensitive to detect significant central causes of vertigo,⁷ and where there is high suspicion of a central cause consider admission or urgent follow up for specialist assessment and possible delayed neuroimaging.

Specialist assessment and/or neuroimaging should also be considered in those patients with a clinical picture that is not fully consistent with a peripheral cause. This is especially relevant in patients with associated headache, risk factors for stroke or symptoms lasting more than 48 hours.

Learning Bite

Investigations are guided by clinical assessment. Consider neuroimaging in patients for whom a peripheral cause cannot be confidently positively diagnosed. Be aware that early neuroimaging may yield false negatives.

Patients with potentially life-threatening causes of dizziness due to cerebral hypoperfusion (e.g. cardiac arrhythmia, sepsis or hypovolaemia), must be distinguished from those with true vertigo as soon as possible and resuscitated.

Correct diagnosis of the underlying cause of vertigo may allow specific treatments to be given.

Although some diagnoses such as Meniere’s disease have no specific acute treatments in general, the focus should be on excluding treatable and serious causes, and providing symptomatic treatment and rehabilitation where required.

Symptomatic Treatment

Patients may require symptomatic treatment for associated nausea, vomiting and dehydration with antiemetics and intravenous fluids. Admission may be required for patients with particularly severe or persistent symptoms. Some patients with vertigo, especially the elderly or those without social support, may require help from occupational therapy and social services.

Several classes of drugs can be used to treat the symptom of vertigo:

• Centrally-acting antihistamines (e.g. betahistine, cinnarazine)
• Phenothiazines (e.g. prochlorperazine)
• Anticholinergics (e.g. scopolamine)

Betahistine is commonly prescribed for Ménière’s disease, but the mechanism by which it works is incompletely understood. It is believed to be a potent H3 antagonist, acting centrally to increase blood flow to the vestibular apparatus.

Betahistine may be more efficacious for the treatment of Ménière’s disease than cinnarizine¹³ but overall high-quality evidence for the efficacy of betahistine is lacking.¹⁴ Antihistamines are likely to be more effective in the treatment of vertigo than benzodiazepines,¹⁵ and the latter carry significant and well known side effects.

It is suggested that prochlorperazine is effective for management of acute peripheral vertigo,¹⁶ but comparisons with other treatments are lacking.

Anticholinergics may be theoretically efficacious for vertigo, but evidence is lacking, and side effects of dizziness and confusion (particularly in the older patient) are well documented.

For all symptomatic treatments for vertigo, there is a suggestion that long term use may lead to vestibular disequilibrium.

Vestibular Rehabilitation

There is some evidence that the brain can, over time, compensate for vestibular dysfunction from a variety of causes.

Physical therapies utilising ‘vestibular exercises’ have been shown to significantly improve symptoms, and function, for peripheral causes of vertigo, when compared to controls, or no intervention.

If the vertigo is not mild, short-lived or self-limiting, a patient with vestibular dysfunction may therefore benefit from vestibular exercises.

For a simple exercise, patients with acute peripheral vertigo can be advised to focus on an object, while moving their head side to side then up and down. Movements should be slow and slight to start with, to prevent nausea, but can gradually be increased and repeated for several minutes, 2 – 3 times per day.

Specific Management

Specific management options exist for several causes of vertigo.

Benign paroxysmal positional vertigo (BPPV)

Other Management

Vestibular neuritis

There is evidence that methylprednisolone given acutely may improve longer-term vestibular function in patients with presumed viral vestibular neuritis,¹⁷ though the editor is not aware of this treatment being widely used.

• Mistaking ‘dizziness’ due to hypotension or other pre-syncopal causes for true vertigo.
• Mistaking a life-threatening central cause of vertigo, for example cerebellar haemorrhage, as a benign peripheral cause such as benign paroxysmal positional vertigo, which may result in a patient being discharged inappropriately.
• Misdiagnosing rare cases of isolated central vertigo as vestibular neuritis, e.g. central cerebellar infarction. This can avoided by paying close attention to the patient’s history and risk factors, the characterisation of the patient’s nystagmus and a full assessment of cerebellar function.

1. Rivlin W, et al. Practical approach to vertigo: a synthesis of the emerging evidence. Intern Med J. 2022 Mar;52(3):356-364.
2. National Institute for Health and Care Excellence (NICE). Vertigo. Clinical Knowledge Summaries (CKS) NICE, 2022.
3. Hanley K, O’Dowd T, Considine N. A systematic review of vertigo in primary care. Br J Gen Pract. 2001 Aug;51(469):666-71.
4. Murdin L, Schilder AG. Epidemiology of balance symptoms and disorders in the community: a systematic review. Otol Neurotol. 2015 Mar;36(3):387-92.
5. Searls DE, Pazdera L, et al. Symptoms and signs of posterior circulation ischemia in the new England medical center posterior circulation registry. Arch Neurol. 2012;69:346–51.
6. Akhtar N, Kamran SI, et al.Ischaemic posterior circulation stroke in State of Qatar. Eur J Neurol. 2009;16:1004–9.
7. Kattah JC, Talkad AV, et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009 Nov;40(11):3504-10.
8. Kerber KA, et al. Stroke risk stratification in acute dizziness presentations: A prospective imaging-based study. Neurology. 2015 Nov 24;85(21):1869-78.
9. Rau CJ, Terling L, Elkhodair S, Kaski D. Acute vertigo in the emergency department: use of bedside oculomotor examination. Eur J Emerg Med. 2020 Oct;27(5):381-383.
10. Warner CL, et al. Clinician’s perspectives in using head impulse-nystagmus-test of skew (HINTS) for acute vestibular syndrome: UK experience. Stroke Vasc Neurol. 2022 Apr;7(2):172-175.
11. MDCalc. HINTS for Stroke in Acute Vestibular Syndrome. Pearls/Pitfalls. MDCalc.
12. EM Crit – HINTS exam for Diagnosing Posterior Stroke. [internet] EM Crit, 2015.
13. Djelilovic-Vranic J, et al. Betahistine or Cinnarizine for treatment of Meniere’s disease. Med Arch. 2012;66(6):396-8.
14. Murdin L, Hussain K, Schilder AG. Betahistine for symptoms of vertigo. Cochrane Database Syst Rev. 2016 Jun 21;2016(6):CD010696.
15. Hunter BR, Wang AZ, et al. Efficacy of Benzodiazepines or Antihistamines for Patients With Acute Vertigo: A Systematic Review and Meta-analysis. JAMA Neurol. 2022 Sep 1;79(9):846-855.
16. Kameswaran M, et al. Effectiveness and Safety of Prochlorperazine in Indian Patients with Acute Vertigo: Results from a Large, Prospective, Post-marketing Observational Study. Indian J Otolaryngol Head Neck Surg. 2023 Dec;75(4):3152-3160.
17. Strupp M, Zingler VC, et al. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med. 2004 Jul 22;351(4):354-61.