Author: Jonathan D Whittaker / Editor: Jonathan D Whittaker / Reviewer: Michael Stewart / Codes: CAP5, CAP12 / Published: 24/01/2018 / Review Date: 24/01/2021
Vertigo is a common problem which affects 5% of adults in any one year (1). Consequently, it is a frequent presenting problem to the ED. It is difficult to separate vertigo from the general diagnosis of dizziness but in a 10 year analysis, 2.5% of all attendances to the EDs in the USA were due to dizziness/ vertigo (2).
Vertigo is also an area of Emergency Medicine that is poorly understood by many Emergency Physicians (EPs). A recent survey of 1150 EPs in the UK, Canada, America and Australasia rated the identification of central vertigo as the second highest priority for the development of a clinical decision rule (3).
Vertigo is defined as an illusion of rotatory movement and always implies an imbalance in the vestibular system although the symptom doesnt indicate where the imbalance originates.
It is vital that the EP differentiates vertigo from dizziness, which is a common lay description covering a multitude of meanings. It is useful to classify dizziness into different clinical categories the most commonly described classification (4) is into four types;
- Vertigo an illusion of motion of either the subject or the environment
- Presyncope a feeling of impending faint or loss of consciousness
- Disequilibrium impaired balance and gait in the absence of abnormal head sensation dizziness of the feet
- Light-headedness a non-specific description of symptoms that cannot be identified as one of the above types
Of these four types, vertigo accounts for approximately 30% of dizzy patients in primary care (5), and of all presentations to an ED with dizziness, 43% were found to be due to a peripheral vestibular disorder (6).
Dizziness is not a diagnosis and the EP must learn to differentiate this symptom into specifically defined types.
Vertigo can be physiological or pathological. Pathological vertigo is usefully divided into two types; central and peripheral. Differentiation of these types is crucial to the investigation and management of a patient with vertigo presenting to the ED.
Basic Science and Pathophysiology
The ability of the body to maintain a position of equilibrium relies on sensory inputs from the vestibular apparatus, visual system and proprioceptive stimuli from the neck and rest of the body. The vestibular apparatus consists of the membranous labyrinth contained within the bony labyrinth lying in the petrous temporal bone, which connects via the vestibulococclear nerve to the vestibular nuclei in the brainstem. These nuclei interconnect with neurones in the cerebellum, spinal cord and cerebral cortex.
The membranous labyrinth consists of the three semicircular canals and two chambers, the saccule and utricle. Flow of fluid (endolymph) in the canals stimulates cilia attached to a sensory organ located in the ampulla of each canal, the crista ampullaris. In the saccule and utricle, movement of calcified calcium carbonate crystals (statoconia or otoliths) stimulates cilia of another sensory organ, the macula. Therefore movement of the head in any plane modifies neural impulses transmitted via the vestibular nerve, connected to each of the sensory organs, to nuclei in the brain stem. Vertigo results from an imbalance of either the received signals or information processing in the brainstem.
Vertigo is caused by an imbalance in either the nerve impulses transmitted by the vestibular system or in the processing of this and other sensory inputs to the brain.
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) in 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.
Nystagmus is a useful clinical sign in determining whether vertigo has a central or peripheral origin.
The first decision for the EP, when assessing a patient, is to differentiate vertigo from dizziness of another type. A patients description of the sensation of vertigo may be subjective (I feel like I am moving (or spinning) ) or objective (it feels like the world is moving (or spinning) ). Vertigo is not light-headedness when moving to a standing position (orthostatic hypotension) or a feeling that one is about to pass out (pre-syncope).
The next step is to try and differentiate between central and peripheral vertigo. In general terms, patients with central vertigo require early radiological investigation and hospital admission whereas most patients with peripheral vertigo can be safely discharged home with appropriate follow-up.
Differentiating between central and peripheral vertigo is the cornerstone of the diagnosis and management of patients with vertigo in the ED.
The first clues in deciding whether there is a central or peripheral cause is provided by the history (6);
Occasionally very sudden but usually gradual
Nausea and vomiting
Variable usually minimal systemic upset
Effect of head position
Worsened by position, often single critical position
Little change, associated with more than one position
Associated auditory findings (aural fullness, tinnitus, hearing loss etc)
May be present
Associated neurological symptoms (dysarthria/ diplopia, hemiparesis etc)
Speed of onset, systemic upset, effect of head position and associated auditory and neurological symptoms are the key features of the history which help to differentiate central from peripheral vertigo.
Other factors which are useful when taking a history are:
- Is the episode a new event or is there a history of recurrent episodes? For example, short spells of sudden onset vertigo associated with a change in head position are likely to be caused by benign positional paroxysmal vertigo (BPPV)
- Past history of vascular disease, hypertension or stroke all increase the likelihood of a central cause for vertigo
- Recent trauma or infection of the ear makes a peripheral cause more likely
- Drugs that are associated with vertigo include ACE inhibitors, amiodarone, aminoglycosides, beta blockers, cocaine, phenytoin, salicylates, sildenafil
Examination of the patient must include a general assessment, particularly of the cardiovascular system as vertigo may be associated with conditions such as vascular disease and atrial fibrillation.
A general neurological examination may reveal cranial nerve or peripheral deficits associated with a cerebrovascular event or neoplastic lesion e.g. cerebellopontine tumours may present with both vertigo and fifth and seventh cranial nerve palsy. Limb ataxia, revealed by an abnormal finger-nose or heel shin test, suggests cerebellar disease.
The ears must be examined for evidence of vesicles (Ramsay Hunt syndrome) or presence of a tympanic perforation or cholesteatoma.
Gross hearing should be tested by placing a ticking wristwatch (alternatives are whispering or rubbing the fingers together) close to each ear. If a reduction in hearing is found in one ear then Webers and Rinnes tests must be performed (watch this video for a standard technique http://www.youtube.com/watch?v=FNy7dgOwu30 ) looking for evidence of sensorineural hearing loss. Hearing loss or tinnitus almost always indicates a peripheral cause for vertigo.
Examination of a patient with vertigo must include otoscopy, hearing assessment and examination of the cardiovascular and neurological systems, as abnormal findings may indicate the cause of the vertigo.
The HiNTs examination is a clinical test to differentiate between central and peripheral causes, in patients with vertigo. In some studies it has shown a greater sensitivity than MRI to exclude posterior circulation stroke in these patients.
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.
The patient stands in front of the examiner, with their head held between the examiners hands. The patient is asked to fixate on the tip of the examiners nose, and their head is rotated 20 -40 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 vestibule-ocular reflex is disrupted, and so they lose eye contact and correct with a saccade.
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.
The patient again stand 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.
A video demonstration of the examination can be viewed here
Acute Vestibular Neuritis
The most common presentation of prolonged peripheral vertigo seen in the ED. This problem typically occurs in young and middle aged adults and is postulated to be caused by a viral infection, possibly herpes simplex. It is caused by acute inflammation of the vestibular nerve (10) and is correctly termed vestibular neuritis notlabyrinthitis, a label which is often confusingly used and which correctly refers to a separate condition.
The presentation is typical of peripheral vertigo;
- acute onset within minutes / hours
- exacerbated by movements of the head
- accompanying severe nausea and vomiting
- no other neurological deficit
There is however no disturbance of hearing which is often otherwise found in peripheral vertigo.
Spontaneous nystagmus is found in 2/3 of patients (11) and is peripheral in character i.e.
- suppressed by visual fixation
- fast phase away from the affected ear and most evident when looking to the unaffected side (see vnsmall.avi at http://www.dizziness-and-balance.com/sitedvd.htm)
Acute vestibular neuritis is caused by inflammation of the vestibular nerve and is a separate condition to acute labyrinthitis.
An important differential diagnosis to exclude. Compared to acute vestibular neuritis patients are usually older with pre-existing risk factors e.g. atrial fibrillation, diabetes etc.
Onset of symptoms is hyperacute within a few seconds.
The vertigo is central in character i.e.
- unaffected by head position
- little systemic upset
- generally there are co-existing neurological deficits e.g. ataxia, depressed level of consciousness. Rarely, vertigo may be the only finding.
Nystagmus is also typically central;
- Horizontal, rotatory or vertical see http://uk.youtube.com/watch?v=_KtMS7hx5c4
- Not suppressed by visual fixation
Patients with a cerebellar stroke or TIA usually have co-existing risk factors and present with very sudden onset of central vertigo and nystagmus.
Both acute and chronic ear infections may either directly infect or release toxins into the labyrinth, causing an acute labyrinthitis and peripheral vertigo. The patient will normally complain of fever, ear pain, headache and hearing loss. Otoscopy will reveal evidence of infection.
Paroxysmal Vertigo recurrent or first onset
For patients presenting with paroxysmal vertigo, it is useful to subdivide them into vertigo without and with hearing loss.
Without hearing loss
Transient Ischaemic Attack (TIA)
Although a TIA rarely presents as isolated central vertigo, the temporary features are identical to those of cerebellar stroke.
Benign Positional Paroxysmal Vertigo (BPPV)
Very common and caused by the dislocation of statoconia into the posterior semicircular canal. Vertigo is related to changes in head position e.g. turning over in bed or reaching upwards, and typically affects women between 60 and 70.
The vertigo is peripheral and short lasting with fatiguing nystagmus in one direction. Diagnosis is confirmed by the Hallpike manoeuvre and can be treated with the Epley manoeuvre which, once taught, can be effectively self administered (12). Both manoeuvres can be viewed here http://www.emedicine.com/emerg/topic57.htm
The vertigo associated with BPPV is short lasting and characteristically related to changes in head position.
Migraine typically presents with episodic headaches accompanied by photophobia, nausea and vomiting. Vertigo with either central or peripheral features (13) may occur in up to 25% of patients with acute migrainous vertigo (14).
With Hearing Loss
The commonest cause of acute paroxysmal vertigo with hearing loss and is caused by an increase in the pressure and volume of endolymph. A patient will normally present with an initial aura of aural fullness, followed by increasing tinnitus, fluctuating hearing loss and peripheral vertigo. It is a clinical diagnosis and all investigations serve to rule out other diagnoses.
Acoustic neuroma is more correctly called a vestibular schwannoma a benign tumour of myelin forming cells of the vestibulococclear nerve. Unusually for a central cause of vertigo, gradual progressive hearing loss and tinnitus are common symptoms. Episodic central vertigo may also be a feature.
It is not always possible to make a definite diagnosis in patients with vertigo. The key to managing patients with vertigo in the ED is to separate central from peripheral vertigo. All patients with central vertigo need further investigation either as an in-patient or urgent out-patient basis.
If peripheral vertigo is diagnosed, most patients can be discharged home with arrangements for follow-up either with their GP or in an appropriate ENT clinic, provided they have an appropriate carer to look after them. Some patients may benefit from occupational therapy and/or social services. A few required admission for intravenous rehydration due to inability to tolerate oral fluids even after treatment.
In all cases of prolonged vertigo, both the sensation of vertigo and the commonly associated nausea and vomiting, are distressing to the patient. Vestibular suppressants and antiemetics are the mainstays of treatment.
Vestibular suppressants include low dose benzodiazepines (e.g. diazepam 2mg, lorazepam 0.1mg), anticholinergics (e.g. hyoscine) and antihistamines with anticholinergic (and antiemetic) properties e.g. cinnarizine, cyclizine. Antiemetics such as prochlorperazine and metoclopramide are also commonly used but may be associated with acute dystonic reactions.
It is widely thought that recovery from, and brain adaptation to, short lasting peripheral vestibular dysfunction (e.g. vestibular neuritis) may be hampered by immobilisation and the continuing use of vestibular suppressants (15).
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.
Patients with other than mild, short-lived, self-limiting vertigo because of vestibular dysfunction may, therefore, benefit from vestibular exercises.
In 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 options exist for several causes of vertigo.
Canalith repositioning manoeuvres have been used in an attempt to move canaliths out of the semicircular canal to treat BPPV.
The Epley manoeuvre is used to treat BPPV due to posterior canal canaliths (>90% of cases of BPPV) and has been shown to be safe, and effective, at least in the short term. It can be used in the ED. However, recurrence rates may be as high as 50% over 5 years, although the manoeuvre can be repeated or even taught.
Anterior canal BPPV is rare, and can be a complication of canalith repositioning manoeuvres because the canaliths migrate from the posterior canal into the anterior canal. Such cases may respond to other specialist manoeuvres.
The Epley (canalith repositioning) manoeuvre
Click Next and Previous to navigate forwards and backwards through the animation.
There is evidence that corticosteroids (methylprednisolone) given acutely may improve longer-term vestibular function in patients with presumed viral vestibular neuritis.
Betahistine, or diuretics, are often prescribed for dizziness symptoms in Meziere’s disease, and these are generally well tolerated; though evidence of the efficacy of these treatments is lacking.
Specialist treatments such as intratympanic gentamicin may be of benefit in selected cases.
MedicoLegal and other considerations:
- Dizziness is not a diagnosis. It must be differentiated into one of four more specific types to aid assessment and management. (level of evidence 5)
- Separation of vertigo into central and peripheral types is the key to investigating and managing patients presenting to the ED with vertigo. (level of evidence 4)
- Nystagmus is a useful clinical sign and identification of the effect of visual fixation, fatigability, the direction and duration of nystagmus are all features which help to differentiate a central from a peripheral cause of vertigo. (level of evidence 5)
- Laboratory investigations are very unlikely to be of use in the diagnosis of vertigo. (level of evidence 4)
- Vestibular neuritis is caused by an acute inflammation of the vestibular nerve and is a separate entity to acute labyrinthitis, which is caused by spread of infection from the middle ear. (level of evidence 5)
- Patients presenting with a cerebellar stroke or TIA usually have co-existing risk factors and describe a very sudden onset of central vertigo and nystagmus. (level of evidence 5)
- Patients prescribed a vestibular suppressant for vertigo should be encouraged to mobilise and to use their medication for the shortest time possible. (level of evidence 5)
- Neuhauser HK, von Brevern M, Radtke A et al. Epidemiology of vestibular vertigo: a neurotologic survey of the general population. Neurology 2005;65:898-904
- Kerber KA, Meurer WJ, West BT et al. Dizziness presentations in US emergency departments, 1995-2004. Acad Emerg Med 2008;15:744-750
- Eagles D, Stiell IG, Clement CM et al. International survey of emergency physicians priorities for clinical decision rules. Acad Emerg Med 2008;15:177-182
- Drachman DA. A 69-year-old man with chronic dizziness. JAMA 1998;280:2111-2118
- Hanley K, ODowd T, Considine N. A systematic review of vertigo in primary care. Br J Gen Pract2001;51:666-671
- Herr RD, Zun L, Mathews JJ et al. A directed approach to the dizzy patient. Annals Emerg Med1989;18:664-672
- Halmagyi GM, Curthoys IS. A clinical sign of paresis. Arch Neurol 1988;45:737-9
- Hoffman RM, Einstadter D, Kroenke K. Evaluating dizziness. Am J Med 1999;107:468-78
- Akinci E, Aygencel G, Keles A et al. Role of C-reactive protein, D-dimer and fibrinogen levels in the differential diagnosis of central and peripheral vertigo. Adv Ther 2007;24:1068-77
- Karlberg M, Annertz M, Magnusson M. Acute vestibular neuritis visualised by 3-T magnetic resonance imaging with high dose gadolinium. Arch Otolaryngol Head Neck Surg 2004;130:229-232
- Cooper C. Vestibular neuronitis: a review of a common cause of vertigo in general practice. Br J Gen Pract1993;43:164-7
- Tanimoto H, Doi K, Katata K et al. Self-treatment for benign paroxysmal positional vertigo of the posterior semicircular canal. Neurology 2005;65:1299-1300
- Von Brevern M, Zeisse D, Neuhauser H et al. Acute migrainous vertigo: clinical and oculographic findings. Brain2005;128:365-74
- Kayan A, Hood JD. Neuro-otological manifestation of migraine. Brain 1984;107:1123-42
- Baloh R. Vestibular neuritis. NEJM 2003;348:1027-32
- Strupp M, Zingler, VC, Arbusow V et al. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. NEJM 2004;351:354-61
- Kattah, J. 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. 40(11):35043510.