VERTIGO
“Relativity”, M.C Escher, Lithograph 1953
Albert Einstein’s theories of relativity showed that the physical world as it appears to us
is not always what it seems, it depends on your vantage point. Time for example is not a
constant entity, it depends on your speed of travel and at the speed of light it stands still!
Patients’ complaints of “dizziness” rarely imply true vertigo. Like the passage of time in
relation to velocity patients will interpret “dizziness” in relation to their own frame of
reference and understanding of what this means. It is important therefore to establish
precisely what a patient means when they complain of the symptom of dizziness.
VERTIGO
Introduction
Vertigo is a false perception of motion.
Patients will frequently complain of “dizziness”, however, this is a virtually meaningless
lay term, (similar to “hot and cold flushes”). It may mean true vertigo or it may refer to
“presyncopal” symptoms. In the elderly non English speaker especially it may simply
mean, “I feel unwell.”
It is important therefore to establish exactly what the patient means by “dizziness”. In
true vertigo there is a perception that the environment or patient is spinning around.
Vertigo is generally divided into peripheral or central causes.
A major initial decision that needs to be made in ED presentations will be whether or not
cerebral imaging is required.
Traditionally clinical rules-of-thumb have been used to distinguish central from
peripheral lesions. The frequent assumption is then made that a peripheral cause is
“benign” and doesn’t require imaging.
However it is essential to appreciate the following:
●
These clinical rules are not definitively reliable, (many cases of central vertigo are
labeled “peripheral” vertigo on purely clinical grounds - which later prove not to
be the case - with suboptimal outcomes resulting).
●
Not all causes of peripheral vertigo are necessarily benign!
The decision to proceed with imaging should be made not only on the basis of the
clinical findings, but also on the basis of a patient’s individual risk profile for
vascular disease.
CT scan is often used as the imaging modality for vertigo because of its ready
availability. This however is at best a “screening” investigation. If symptoms persist,
or are severe enough or the patient’s risk profile high enough, then CT angiogram
will be a better investigation, and MRI/MRA will be the best investigation of all.
Treatment is directed at the symptoms as well as the underlying cause.
Pathophysiology
The sense of spatial orientation:
The sense of spatial orientation depends on:
●
Visual input.
●
Labyrinthine input.
●
Proprioceptive input.
This information is then centrally processed in the cerebellum, brainstem, basal ganglia
and ultimately the cerebral cortex (temporal and parietal regions)
A patient’s sense of spatial orientation may therefore be affected by a lesion in any of
these regions. However only a vestibular (labyrinthine) lesion will result in true vertigo.
The mechanism of nystagmus:
The mechanism of peripheral nystagmus involves a slow and a quick phase. The slow
phase (vestibulo-ocular reflex) is a relatively slow drift toward the side with the (ablative)
lesion. The quick phase is a cortex controlled quick corrective movement back in the
opposite direction. Therefore nystagmus has a quick phase away from the affected side.
The direction of a nystagmus is named for the direction of the quick component.
In peripheral vertigo the patient may feel that either they are moving or that the
environment is moving. They may feel that the environment is spinning in the direction
of the fast component or that their body is spinning in the direction of the slow
component.
Vestibular nystagmus occurs in the plane of the affected semicircular canal and can be
either horizontal or torsional-vertical. Strictly vertical nystagmus is rarely the result of
vestibular involvement and usually means a brainstem lesion.
Causes of Vertigo:
These are traditionally divided into peripheral and central causes.
Peripheral Vertigo (no CNS signs discernable)
No associated deafness or tinnitus:
●
Benign positional vertigo.
●
Vestibular neuronitis.
Associated deafness or tinnitus:
●
Labyrinthitis, (viral or more seriously but rarely bacterial)
●
Ototoxic drugs (aspirin, aminoglycosides, frusemide quinine)
●
Meniere’s disease.
●
Acoustic neuroma
●
Internal auditory small artery disease.
(See also Appendix 1 below for notes on peripheral causes)
Central Vertigo: (usually - but not always - with associated CNS, brainstem or cerebellar
signs)
●
Vascular:
Posterior fossa, i.e. brain stem or cerebellar lesions
♥
Ischemia, (e.g. cerebellar or lateral medullary syndrome or variations
thereof)
♥
Hemorrhagic lesions
♥
Migraine variants.
Less commonly:
●
Central space occupying lesions
●
Demyelination lesions.
●
CNS infection (encephalitis, abscess or meningitis)
Clinical assessment
It is important from the outset to carefully establish what the patient means by their
complaint of vertigo or “dizziness”
The main differential in this regard will usually be from orthostatic hypotension - a
completely different problem to vertigo!, (see separate guidelines on orthostatic
hypotension)
Vertigo is also strongly associated with:
●
Nausea/ retching,
●
Vomiting.
●
Pallor and sweating.
As general rules of thumb clinical assessment can help distinguish a peripheral cause of
vertigo from a central cause according to the following table:
Peripheral
Central
Symptoms are intense often with nausea and
vomiting
Symptoms are less well defined
Very position dependent
Not positionaly related
No associated CNS signs (apart from the 8th
cranial nerve - hearing loss or tinnitus)
May be associated with other CNS signs,
brainstem or cerebellar, (but also may not):
●
Ataxia or other cerebellar signs
●
Visual loss
●
Brainstem symptoms:
●
♥
Diplopia
♥
Dysarthria
♥
Dysphagia
Long tract signs, weakness or hemisensory
Fatigable unidirectional nystagmus
Non fatigable multidirectional nystagmus
Nystagmus is inhibited by ocular fixation
Nystagmus is not inhibited by ocular fixation
Conscious state not affected
Confusion / altered conscious state
The above signs however do not always reliably differentiate central from peripheral
causes, and it is important to also take into consideration a patient’s risk profile for
CVS disease, as vertebrobasilar insufficiency is an important condition that should
not be missed. Note that in elderly patients, non English speaking patients,
cognitively impaired patients, and/or very distressed patients accurate clinical
neurological examination may be very difficult if not impossible.
Important risk factors for central vascular disease will include the usual risk factors for
CVS disease in general such as:
●
Age
●
Hypertension
●
Smoking
●
Diabetes
●
Hypercholesterolemia
●
AF/ A. flutter
●
PVD
●
Known carotid / cardiac disease, (CAGS/coronary stents).
In addition the persistent inability of a patient to walk is an important clue that the
problem may relate to a central lesion.
See also appendix 1 below for clinical features of peripheral conditions causing
vertigo.
Once a diagnosis of peripheral vertigo is made it is important to try to further
distinguish between the two commonest causes, BPPV and vestibular neuronitis as
the treatments for these are different.
A positive Dix-Hallpike test will help confirms the diagnosis of BPPV.
Investigations
These will be guided according to the index of suspicion for any given condition.
The following will need to be considered:
Blood tests:
●
FBE
●
U&Es / glucose
ECG:
●
For the documentation of cardiac disease including arrhythmias such as AF or
atrial flutter.
Imaging
In younger patients with clear features of peripheral vertigo routine imaging is not
generally necessary.
If central vertigo is suspected, then imaging is required. CT scan is not the best
investigation but is readily available and is a useful examination to exclude the important
condition of a posterior fossa hemorrhage.
If no hemorrhage is seen, consideration should be given to a follow up contrast
angiogram study in those at high risk of vertebrobasilar insufficiency.
MRA/MRI is the ideal investigation for vertigo of both peripheral and central causes.
Note that in elderly patients, non English speaking patients, cognitively impaired patients,
and/or very distressed patients accurate neurological examination may be very difficult if
not impossible.
A lower threshold for imaging should be maintained for elderly patients or those
with risk factors for cerebrovascular disease. These patients have a higher risk for a
central cause of vertigo, even when no other symptoms manifest.
If there is any doubt about the diagnosis it is best to admit these patients and arrange for a
CT scan/ MRI to rule out a central lesion, (such as lateral medullary infarction or variants
thereof)
CT Scan Brain:
This is not the ideal modality for the investigation of peripheral or central vertigo, yet is
often undertaken simply because of its ready availability.
Its predominate utility is the ruling out of a posterior fossa hemorrhage and is useful
for this indication, as well as being a very important cause to rule out.
CT Angiogram:
This is a better imaging modality than plain CT scan, in cases of vascular ischemic
disease.
It should be considered as a follow-up to CT with has excluded a hemorrhage, in patients
who are at high risk for vertebrobasilar disease. It delineates the carotid and vertebral
vessels and provides a probable diagnosis where high grade stenosis exists.
MRA/MRI:
This is the best imaging modality for patients being investigated for vertigo.
It should be done for patients who are suspected of having vertebrobasilar insufficiency
in the form of TIAs or completed stroke.
It will provide valuable information of the state of the carotid and vertebral circulations.
It will also provide information about areas of established infarction (and hence give a
definitive diagnosis) which CT cannot provide.
It is the best imaging investigation for middle and inner ear pathology as well as for
acoustic neuromas.
Management
There are 4 important considerations when planning the management and disposition of
the patient who presents to the Emergency Department with “vertigo”.
●
Control of the patient’s symptoms
●
Deciding on the need for imaging, and what type of imaging
●
Treatment of the underlying cause of the vertigo, (where possible).
●
The disposition of the patient
Symptomatic treatment
Treatment of symptoms include:
1.
IV fluids:
●
2.
3.
If there has been prolonged nausea and vomiting and/or an ongoing
inability to tolerate oral fluids.
Antiemetics:
●
Prochlorperazine
●
Ondansetron/ granisetron
Diazepam:
This can be an additional option for those with severe symptoms
●
Diazepam 5 to 10 mg orally, 3 times daily. 2
●
4.
Small titrated IV doses may be considered for very severe symptoms, in
those who cannot tolerate anything orally.
Promethazine
●
This is also an alternative option to help alleviate severe symptoms
See latest Therapeutic Guidelines for full prescribing details.
Note that the long-term daily symptomatic treatment of chronic dizziness or vertigo with
the above drugs is not recommended due to the risk of tardive dyskinesia, drug-induced
parkinsonism and dependence. 2
Treatment of the underlying cause
Where possible specific treatment is directed to the underlying cause.
Antiplatelet agents are given in cases of ischemic vertebrobasilar insufficiency
Cases of benign peripheral vertigo can often be helped with mechanical maneuvers.
Cases of vestibular neuronitis should receive corticosteroids.
Disposition
This will obviously depend on the cause of the vertigo as well as the severity of the
symptoms.
All cases of central or suspected central vertigo should admitted for ongoing
assessment
Younger patients with benign causes of peripheral vertigo may be able to be treated as
outpatients.
If symptoms are severe in peripheral causes of vertigo and/ or there are significant
comorbidities admission to hospital will be necessary.
If there is associated acute hearing loss, this may not be simple “peripheral vertigo” and
these cases should be discussed with ENT, before discharge, (see also Acute Hearing
Loss guidelines).
Appendix 1
Features of peripheral conditions leading to vertigo
Benign positional vertigo:
1.
Repeated attacks of vertigo, which are strongly precipitated by changes in
posture, (cf neuronitis which is more severe and constant, though still somewhat
aggravated by movement).
2.
No hearing loss or tinnitus.
3.
Common and usually in the elderly.
4.
Attacks are short lived, lasting seconds to minutes only. They usually subside
over several weeks, (cf neuronitis which lasts days to weeks)
5.
Hallpike’s test helps to confirm the diagnosis.
See also separate guidelines.
Vestibular neuronitis:
1.
Acute onset of peripheral vertigo with severe associated symptoms.
2.
Vertigo comes on spontaneously and persists at rest. There may be some
aggravation with movement but this is not as strong as that seen in BPPV.
2.
Tinnitus may occur though there is no hearing loss.
3.
Lasts days to weeks.
4.
Presumed viral origin.
Labyrinthitis:
This is a less common and more severe condition than vestibular neuronitis.
1.
Acute onset of peripheral vertigo with severe associated symptoms.
2.
There is hearing loss.
3.
Possible viral origin, rarely a bacterial infection.
4.
May be secondary to a traumatic perilymph fistula.
Meniere’s disease:
1.
Uncommon, usually in the elderly over 50 years of age.
2.
Recurrent attacks of severe vertigo, lasting 30 minutes up to 12 hours. There may
be periods of weeks to years between attacks.
3.
There is a progressive background of tinnitus and deafness.
4.
The intensity of attacks generally diminishes and finally ceases as the deafness
progresses.
Acoustic neuroma:
1.
This is a rare neurofibroma of the 8th cranial nerve.
2.
Commonest age group is 35-45 years of age.
3.
There is a progressive deafness, sometimes with a mild tinnitus and vertigo.
4.
The lesion may progress to cause pressure on adjacent structures within the
cerebello-pontine angle to produce:
●
7th cranial nerve lesion.
●
5th cranial nerve lesion:
♥
Weakness of mastication
♥
Loss of corneal reflex.
♥
Facial sensory loss.
●
6th cranial nerve lesion.
●
Ipselateral cerebellar signs.
References
1.
Strupp M et al. Methylprednisolone, Valacyclovir, or the Combination for
Vestibular Neuritis. N Engl J Med July 2004; 351:354-61.
2.
Neurology Therapeutic Guidelines, 4th ed, 2011.
Dr J Hayes
Reviewed 6 September 2012