The patient who presents with sudden onset severe dizziness - in the absence of prior similar episodes - has the “acute severe dizziness” presentation. Patients with acute severe dizziness appear ill due to the dizziness and accompanying nausea and vomiting. Impaired ability to walk is also common. Though rigorous epidemiological studies are lacking, the most common cause is an acute lesion – presumed viral in origin - of the vestibular nerve on one side, so-called vestibular neuritis.9
The mechanism underlying vestibular neuritis is similar to that of Bell’s palsy. The seventh cranial nerve is affected in Bell’s palsy, whereas the eighth cranial nerve is affected in vestibular neuritis. Patients with vestibular neuritis nearly always report true vertigo, which is characteristically described as visualized spinning of the environment. The symptoms are typically severe for 1-2 days with gradual resolution over weeks to months. It is exceedingly rare to have more than one bout of vestibular neuritis, so an alternative diagnosis should be considered whenever more than one episode is reported.
It is now clear that a small stroke within the posterior fossa can present as acute severe dizziness, closely mimicking vestibular neuritis.3-5
The first step to distinguishing vestibular neuritis from stroke is asking the patient about other neurological symptoms such as focal numbness, focal weakness, or slurred speech. Mild double vision can result from a peripheral vestibular lesion so this symptom is not a reliable discriminator. The next step is the physical examination. Patients with vestibular neuritis have highly characteristic exam features. Only in an extremely rare case can all of the vestibular neuritis exam features be mimicked by a stroke.
Nystagmus in Acute Severe Dizziness Presentations
Nystagmus is a term used to describe alternating slow and fast movements of the eyes. These alternating movements give the appearance that the eyes are beating toward one or more directions. Patients with vestibular neuritis have a peripheral vestibular pattern of nystagmus. In this setting, the peripheral vestibular pattern is a unidirectional, principally horizontal pattern of nystagmus. This description means that the nystagmus beats is in only one direction (i.e., a left-beating nystagmus never converts to right-beating, or a right-beating nystagmus never converts to left-beating). Conversely, bi-directional gaze-evoked nystagmus (i.e., right beating nystagmus present with gaze toward the right, and left-beating nystagmus present with gaze toward the left side) is a central nervous system pattern of nystagmus.10
Other central nervous system patterns are pure torsional nystagmus or spontaneous vertical (typically downbeat) nystagmus. With an acute peripheral vestibular lesion, the only pattern of nystagmus that can result is unidirectional nystagmus. In acute severe dizziness presentations, any other pattern should be considered a central nervous system sign. Patients often prefer to keep their eyes closed early on, but the eyes should be opened and the pattern of nystagmus defined.
Nystagmus in vestibular neuritis is spontaneous (i.e., present in primary gaze) for at least the first several hours of symptoms. Following this initial time period, the nystagmus may only be identified during gaze testing (i.e., having the patient look to each side) or if visual fixation is blocked. Patients can suppress peripheral vestibular nystagmus by visual fixation on a target, so removing the patient’s ability to fixate can bring out the spontaneous nystagmus. The simplest way to block fixation is to place a blank sheet of paper a few inches in front of the patient and then observe for spontaneous nystagmus from the side.
The reason for the characteristic pattern of nystagmus in vestibular neuritis is an imbalance in the peripheral vestibular signals to the brain. Normally, the peripheral vestibular system on each side has a baseline firing rate of action potentials that functions to drive the eyes toward the other side. When the peripheral vestibular system on each side is intact, the input from each side is balance so the eyes remain stationary. When an acute lesion occurs on one side, the input from the opposite side is unopposed. As a result, the eyes will be “pushed” toward the lesioned side. This movement of the eyes is the slow phase of nystagmus. When the eyes reach a critical point off center, the brain responds by generating a corrective eye movement to move the eyes back. This is the fast phase of nystagmus. Since the direction of the fast phase gives the appearance that the eyes are beating in that direction, an acute left peripheral vestibular lesion leads to spontaneous right beating nystagmus. Over time, the asymmetry resolves or the brain compensates for the asymmetry.
The Head-Thrust Test
A recently described bedside test, the “head-thrust test,” is now an important component of the bedside evaluation in acute severe dizziness presentations.11, 12
The test allows the examiner to assess the vestibulo-ocular reflex (VOR) on each side. The VOR is the component of the vestibular system that triggers eye movements in response to stimulation. In different settings, the VOR has long been tested using the doll’s eye test of the coma exam and caloric stimulation (i.e., the laboratory caloric test or the bedside cold caloric test in a comatose patient). To test the VOR using the head thrust test, the examiner stands in front of the patient and grasps the patient’s head with both hands. The patient is instructed to focus on the examiner’s nose and then the examiner initiates a quick 5-10° movement of the pa tient’s head to one side. When there is a lesion of the VOR on one side – as occurs with vestibular neuritis – a corrective eye movement (i.e., a corrective “saccade”) back to the examiner’s nose is seen after the head is moved toward the affected side.12
In contrast and serving as an internal control, the eyes will stay on target (i.e., the examiner’s nose) after the head thrust test toward the normal side because the VOR is intact on that side. These features can be appreciated even when spontaneous nystagmus is present. The reason for the corrective saccade with a peripheral vestibular lesion is rooted in the physiology of the vestibular system.10
When the head is moved quickly in one direction, the reflex (i.e., the VOR) that moves the eyes toward the opposite direction is generated by the side the head moved toward. Thus a patient with vestibular neuritis of the left side will present with right-beating unidirectional nystagmus and have a positive head thrust test with movements toward the left side.
Vascular Causes of Acute Severe Dizziness
Although vestibular neuritis is the most common cause of the acute dizziness presentation, no laboratory or imaging test exists to confirm a viral etiology. A peripheral vestibular lesion can be caused by a vascular occlusion of the blood supply to the peripheral vestibular components, though presumably this cause is much less common.
Stroke should be a serious consideration in the patient who presents with the acute dizziness presentation. Dizziness is a symptom of stroke in 50% of stroke presentations.13
Most stroke patients that report dizziness as a symptom have other prominent central nervous system features, but a small stroke of the cerebellum or brain stem can present with isolated dizziness (i.e., dizziness without other accompanying central nervous system signs or symptoms). In a population-based study, about 3% of patients with dizziness had a stroke etiology, but less than 1% of patients with isolated dizziness had stroke as the etiology.14
However, a prospective study of 24 patients with acute severe dizziness reported 6 patients (25%) with stroke etiology.3
Patients with stroke presenting as isolated dizziness may report imbalance, true vertigo, a more vague dizziness sensation, or a combination of these. Nausea and vomiting are also common, as they are with vestibular neuritis. Unfortunately, computerized tomography (CT) scans are an extremely insensitive test for acute stroke presentations in general,15
and particularly so for infarction within the posterior fossa.16, 17
A stroke within the posterior fossa may not appear on a CT scan for days or weeks because of artifacts or poor resolution. Because of this, CT should never be considered as a means of excluding stroke. Magnetic resonance imaging (MRI) is a much more sensitive test, but is not a practical test to screen for stroke in emergency department dizziness presentations. Like CT, the sensitivity of the test is the lowest for stroke of the posterior fossa.18
The key features discriminating stroke from vestibular neuritis are the pattern of nystagmus and the results of the head thrust test. Down-beating nystagmus or bidirectional gaze-evoked nystagmus are both immediate indications that the localization must be in the central nervous system. These patterns are not caused by lesions of the peripheral vestibular system. This is the reason that an examination of ocular movements is required before a diagnosis is even considered. Another highly suspicious pattern of nystagmus is a pure torsional pattern. There are now case reports of patients who have unidirectional horizontal nystagmus and a stroke etiology so the pattern of nystagmus should not be the sole criterion.3-5
A patient with unidirectional nystagmus, a positive head thrust in the direction opposite the fast phase of nystagmus, and no other neurological features can be diagnosed with vestibular neuritis with a high level of certainty. It would take a well placed and small stroke to cause the peripheral vestibular pattern of nystagmus and a corresponding positive head thrust test without any other central nervous system features. Though all patients with vestibular neuritis are unsteady walking, the inability to walk is another red flag.5
Finally, a person’s risk for stroke based on stroke risk factors should be considered. Though no validated scale exists to grade stroke risk based on stroke risk factors in this population, a stroke work-up is reasonable in patients with a high risk for stroke. One should not be over reliant on stroke risk factors as discriminators, however, since other stroke mechanisms – such as arterial dissection – occur in the absence of stroke risk factors.
Management of Acute Severe Dizziness
The management of the acute dizziness presentation begins with supportive care. If stroke is suspected then a neuro-imaging study should be considered. Though CT could serve as the initial study, a normal result on CT should provide little confidence that stroke can be excluded. In this situation, an MRI or hospital admission for close observation should be considered. If stroke is confirmed to be the cause and the patient presents within three hours of onset, thrombolytic treatment should be considered. A short course of corticosteroids should be considered for patients with vestibular neuritis. A randomized controlled trial showed that patients with vestibular neuritis treated with corticosteroids within three days of symptom onset had a higher likelihood of recovery of the peripheral vestibular caloric response at 12 months.19
However this study did not test whether the patient’s functional or symptomatic outcome improved, and corticosteroids are not without potential side effects. After the initial severe symptomatic time period, it is important that patients resume activities because this helps the brain to compensate for the asymmetry of vestibular signals. A formal vestibular therapy program has been shown in a randomized trial to improve outcomes in patients with vestibular neuritis.20