Differentiating Stroke from Benign Vestibular Disease
When disease strikes the vestibular apparatus, there follows symptoms of vertigo, nausea, vomiting. The patient is very unsteady and has nystagmus and they are reluctant to move, are pale and sometimes sweaty. This picture is known as acute vestibular syndrome and it is caused by vestibular neuritis, labyrinthitis, and by posterior circulation stroke, amongst others.
This page discusses the way in which a benign, self-limiting disease such as vestibular neuritis can be differentiated from a life-threatening one that requires immediate intervention such as a stroke affecting the posterior fossa circulation.
The differentiation is entirely clinical. Imaging of the brain in the acute phase of vestibular syndrome will often be normal by MRI and CT scanning lacks sensitivity. Neither can be relied upon to rule out a stroke in the first few hours.
First we will look at the two disease that need to be differentiated and then at the HINTS exam that is able to do this at the bedside.
Posterior circulation stroke
The cerebellum and brainstem are the important structures in relation to this topic. They are supplied by a variety of arteries but most importantly by: the superior cerebellar artery, the anterior inferior cerebellar artery (both from the basilar artery), and the posterior inferior cerebellar artery (from the vertebral artery).
Blood supply of the cerebellum
Blood supply of the labyrinth
AICA - Anterior inferior cerebellar artery
LA - Labyrinthine artery
AVA - Anterior vestibular artery
CCA - Common cochlear artery
PVA - Posterior vestibular artery
Posterior circulation strokes account for about 20-25% of all strokes and, by virtue of the complex neuroanatomy of the brain stem and cerebellum, create a wide range of neurological deficits. They are considered harder to diagnose than anterior circulation strokes and delay in diagnosis may cause preventable death or severe disability.
Symptoms and signs encountered include: dizziness, diplopia, dysarthria, dysphagia, ataxia and visual field deficits, and unilateral limb weakness.
With all of these present it may seem a surprise that strokes can be so easily confused with simple vestibular neuritis or labyrinthitis. However, it is quite possible for an ischaemic event only to affect those portions of the AICA that supply the labyrinth and thus to only present with acute vestibular syndrome. These are just as important to spot, as extension of the stroke to the brain stem or cerebellum are possible. They are also harbingers of sudden more severe strokes in the future.
Vestibular neuritis and labyrinthitis
These two diseases are distinct and covered elsewhere in more depth. Suffice it to say here that VN causes acute vestibular syndrome; vertigo, nausea, vomiting, nystagmus and labyrinthitis causes vestibular syndrome plus sensory deafness and tinnitus. Both of these conditions are viral in origin and self-limiting.
This is true of labyrinthitis except when there is a suppurative labyrinthitis present. This unusual condition follows acute otitis media or cholesteatoma and may lead on to meningitis. Accordingly, it must not be missed.
Distinguishing self-limiting causes of acute vestibular syndrome from stroke
Differentiating inner ear causes of acute vestibular syndrome from stroke is possible at the bedside using a simple battery of three clinical tests collectively known as ‘HINTS’.
The three tests are:
Head impulse test HI
Examination of nystagmus N
Test of skew deviation TS
This is a test of the vestibulo-ocular reflex (VOR). The VOR is the reflex eye movement that occurs when we are looking at something and then turn our heads.
Look at the ‘X’ and then turn your head to the left. Your eyes move to the right so that you can keep seeing the ‘X’ sharply. This reflex allows for clear vision while we are moving around. Turning to the left increases the activity of the left horizontal semicircular canal.
When one of the ears is damaged one of the VORs is damaged with it and this fact can be exploited clinically. We ask the patient to look at something intently and then we quickly turn their head to the right and then the left.
As long as the VOR is working the eyes will stay on the target during quick passive head movements. If the VOR is weakened the eyes will move with the head and will then need to jump back to see the object. The examiner can see this as a quick corrective movement of the eyes.
The beauty of this test is that we can test the left and right ears separately. Turning the head to the left activates the left VOR and vice versa. Thus, if during a passive, quick left head turn the eyes cannot keep looking at the target and must jump back to the target, the left VOR is affected and the left ear diseased.
In a stroke, the VOR is unaffected.
Here are two videos; the first showing an abnormal head impulse test and the second a normal one.
When the head is jerked to the right the eyes move with it and must jump back towards the object the patient is looking at.
In this case the VORs are intact on both sides.
While the head impulse test is very good it is not 100% reliable. So, further tests are used to supplement it.
The jerky movement known as nystagmus is the second of these. Examination for this involuntary movement is critical. Nystagmus of central origin (the brain) behaves differently from that caused by the ear.
Ear generated nystagmus is mono-directional and obeys Alexander’s law. Its direction is unaffected by which way the patient is looking. This means that a left-beating nystagmus remains left-beating whether the patient is looking forwards, left, right, up or down. True, its intensity may vary depending on the direction of gaze but its mono-directional nature persists.
Ear generated nystagmus also obeys Alexander’s law. The law states that nystagmus is more intense when the patient gazes in the direction of the fast phase and is less intense when the patient looks in the direction of the slow phase. Thus, in a left-beating nystagmus the nystagmus is much easier to see when the patient looks left and less easy to see when they look to the right.
This all seems a lot to take in so look at a video.
The patient has nystagmus that is mono-directional in all directions of gaze. In this case it is a left-beating nystagmus. When they look to the left the nystagmus is accentuated. When they look to the right (in the direction of the slow phase) the nystagmus is less obvious. It is, however, still a left-beating nystagmus even though they are looking to the right.
The nystagmus obeys Alexander’s law and is, therefore, of peripheral origin – from the ear.
Nystagmus generated by brain disease e.g. cerebellar or brain stem ischaemia behaves differently. It may be vertical nystagmus, disconjugate or gaze evoked in type, to name a few.
Gaze evoked nystagmus is nystagmus that appears when the eyes are moved from their primary position and it changes direction depending upon which way the patient is looking.
Looking to the left the nystagmus is left-beating
Looking to the right it is right-beating
This does not happen with nystagmus of ear origin (which is mono-directional wherever the patient looks).
In the video, the patient looks left and demonstrates left beating nystagmus. When she looks to the right the nystagmus changes to a right-beating one. Direction changing nystagmus is a feature of brain stem / cerebellar disease.
Test of Skew
Skew deviation is a term used to describe the position of the eye within the orbit or, more properly, the vertical height of the iris when seen from the front. In the image below the patient’s left iris seems to be at a higher level than the right one. This is skew deviation and it is a feature of brainstem / cerebellar disease.
The left eye is said to be hypertropic. When an alternate cover test is applied to the patient the higher eye moves downwards and the lower one rises up. See the next video for a demonstration. The effect is more obvious in his right eye.
The schema above shows the movement of the eyes when each is covered.
Taken together the three tests are a reliable way of differentiating an ear cause of acute vestibular syndrome from a stroke affecting the AICA territory. Research suggests that it is more sensitive than an MRI scan within the first 24 hours of onset.
Ear disease if all of the following are present:
Head impulse positive i.e. abnormal on one side
Nystagmus is uni-directional and obeys Alexander’s law
No skew deviation
Consider stroke if any of the following are present:
Head impulses are normal
Direction changing nystagmus is present