In the second of his two-part series on dizziness, Toby Commerford writes about the importance of distinguishing dizziness from a strok. You can find part 1, here.
UNTIL recently, I thought that “dizziness” was a bad word, a lay term to be quickly translated into something more medical. In 1972, an influential article kick-started the idea that dizziness should be repackaged into entities of “vertigo”, “presyncope”, “disequilibrium” and “other”.
Using this bedside approach, I vividly recall beseeching patients to tell me which one of these terms best described their predicament, yet “dizzy” was often all they could muster. Even if patients were clear that their symptoms were vertiginous, I remained uncertain how to move ahead towards a rigorous diagnosis (“something in the inner ear” was about the depth of my reasoning).
Others may have felt this uncertainty too, given the observation that vertigo is sometimes seen in case notes as a primary diagnosis – even though it is simply a presenting symptom. Such practice risks missing serious inciting pathologies, especially vertebrobasilar posterior circulation strokes.
A further problem is the frequent treatment of undifferentiated vertigo with a vestibular sedative, commonly prochlorperazine. This drug blocks dopamine, histamine and acetylcholine receptors in the central nervous system (CNS), potentially leading to sedation, parkinsonism and impaired cognition in older people if taken prophylactically or long term. As such, it may chronically heighten falls and fracture risk, the very thing one wishes to avoid. Excessive use can also impair crucial vestibular compensation following acute pathologies. Many causes of dizziness can be treated with less toxic management, such as canal-repositioning manoeuvres for benign paroxysmal positional vertigo, or deprescribing for hypotension or hypoglycaemia.
Happier days ahead
Nowadays, however, the landscape may be slowly changing for the better. Experts in neuro-otology and other disciplines worldwide have sought to rectify the problems associated with approaching dizziness. In this brave new world, three modern observations are key:
- It is now known that complaints of vertigo or presyncope do not necessarily correlate with the pathologies one would expect. People with labyrinthine diseases may complain of light-headedness, while those with hypotension may describe vertigo. This means that we must break away from the mentalities such as “spinning = inner ear” and “faintness = cardiovascular”. The word “dizziness” may be used by patients to describe an array of vestibular symptoms. An overview of the vestibular system is depicted in Figure 1.
- Given the lack of diagnostic accuracy achievable via the traditional approach of dissecting “dizziness” into its qualities (spinning etc), it is now known that the time course of the vestibular symptoms and their association with any preceding triggers or exposures are instead the pivotal metrics. The new approach to history-taking centres on a “timing and triggers” rather than “qualities” mentality. Accurate diagnosis of pathologies or drug toxidromes inciting dizziness is best aided by discovering how long the symptoms have been present and what may have brought them on.
- Forearmed with some knowledge of the basic functional anatomy of vestibular pathways, modern bedside examination techniques can reliably ensure that we no longer miss strokes and wrongly assign them to benign peripheral disease states. This is prognostically important: posterior circulation strokes have high mortality rates, and there is always the issue of secondary stroke prevention.
It’s all in the timing
Regarding time courses, most cases will fall into one of three categories, as follows:
- An acute vestibular syndrome (AVS) is an attack of severe vestibular symptoms starting quickly, persisting for at least 24 hours, and sometimes lasting weeks. It is often a cataclysmic event in life, rather than being a recurrent paroxysmal presentation. An AVS is highly distressing, worsened by head-motion, and is often encountered in emergency departments. Symptoms may resolve slowly over weeks or months via vestibular compensation. With acute unilateral vestibulopathies (eg, labyrinthitis), the CNS may choose to disregard the erroneous head motion signal stemming from pathological asymmetry of vestibular inputs; multisensory cell networks may start placing greater weight on visual motion as the preferred cue hinting at bodily motion (ie, visual dependency results). Gradually, restoration of the symmetry between the diseased and non-diseased sides may ensue via plasticity mechanisms, but this may be impeded if the use of vestibular sedatives extends beyond 72 hours (though early use of prochlorperazine is appropriate to treat vertigo and vomiting in the dreadful first 2–3 days). Over time, patients may recover from the vertigo, the jerk nystagmus, tilts of the perceived vertical, and the pulsion associated with unhelpfully-activated spinal righting reflexes. Contrastingly, however, the vestibulo-ocular reflex (VOR) may never fully recover; patients with a past AVS may be left with chronic difficulty avoiding visual blur when the head moves, such as when walking.
- An episodic vestibular syndrome (EVS) is a shorter spell of vestibular symptoms, generally lasting seconds, minutes or a few hours (up to 24 hours). The spells tend to recur over time, and may be less fulminating than AVS presentations. They commonly present in outpatient settings – patients recall the attacks retrospectively when they are well again (“I keep getting dizzy spells”).
- The term chronic vestibular syndrome (CVS) often alludes to presentations where patients complain of vestibular symptoms each and every time they encounter a certain context. For example, after a past AVS (as above), there may be guaranteed visual blur or oscillopsia on walking in certain individuals. Likewise, a bilateral vestibulopathy (eg, gentamicin ototoxicity) can disconnect the labyrinths’ from the VOR circuitry in the medial brainstem, leading to the same phenomenon. Alternatively, vestibular symptoms may arise in some individuals with past AVS when their original vestibular compensation process was suboptimal. Specifically, such people may remain chronically visually dependent, and prone to visual vertigo; this refers to dizziness induced when looking at busy visual scenes, such as cars zipping past or looking at an optodrum. This stems from the CNS interpreting motion in the outside visual world as “I myself am moving”. Outside of such context-dependent scenarios, a CVS may refer to long-lasting vestibular symptoms present for prolonged periods of time (months or years).
With these three time courses in mind (AVS, EVS and CVS), and given that each of these may be either triggered or spontaneous, it becomes possible to see how dizziness presentations commonly fall into one of six main patterns. Pleasingly, if a patient’s case can be assigned to one of these “Big Six”, the differential of illnesses causing their symptoms is reasonably manageable.
Here is a table where an overview of the six modes of presenting are illustrated, and differential diagnoses for each are briefly listed. I have found this system immensely relieving when seeing patients with dizziness. Entries in bold are common yet sinister or dangerous differentials (not to miss).
|Timing of presentation||Triggered or related to a specific exposure, context or event||Spontaneous (no obvious trigger preceded dizziness)|
· Medication toxicities; anti-epileptics, lithium, alcohol, gentamicin
· Carbon monoxide poisoning
· Head injury (traumatic vestibulopathy)
|· Acute labyrinthitis or vestibular neuronitis
· Acute brainstem stroke (commonly posterior inferior cerebellar artery [PICA] territory)
· Acute cerebral stroke
· Multiple sclerosis (attack)
· Wernicke’s encephalopathy (vitamin B1 deficiency)
· Ramsay Hunt syndrome
· Neuroinflammatory or encephalitis states (eg, neurosarcoidosis or paraneoplastic syndromes)
|EVS||· Benign paroxysmal positional vertigo (dizziness typically lasts seconds rather than minutes or hours)
· Orthostatic hypotension
· Postprandial hypotension
· Reflex presyncope (neurocardiogenic, eg micturition, carotid sinus massage, valsalva)
· Exertional (consider coronary ischaemia, anaemia or aortic stenosis)
· Inner ear fistula
|· Vestibular migraine (most common cause of EVS)
· Vertebrobasilar transitent ischaemic attack
· Lateral temporal lobe epilepsy (vestibular epilepsy)
· Meniere’s disease
· Panic attack
· Addison’s disease
· Episodic ataxia (attack)
|CVS||· Following a past AVS ( related to walking, VOR failing, as above)
· Bilateral vestibulopathy complicating ototoxic medication effect (vestibulo-ocular reflex failing)
· Visual vertigo (following previous AVS, as above )
|· Posterior fossa tumours
· Spinocerebellar degeneration
· Paraneoplastic cerebellar disease
· Downbeating nystagmus (cerebellar/medulla)
What about strokes? How can we reliably detect central lesions and avoid missing them?
The most sinister differential cause of an AVS is a stroke, though they are often missed. To detect strokes, the most obvious solution would seem to be “get a scan”. However, when early following a stroke, imaging is not always reliable. Co-existing neurological signs (such as hemibody ataxia, dysarthria, diplopia and neglect) may further hint at a central lesion. However, this is not always the case, as up to 20% of strokes present with an isolated AVS, and no other localising clues. About 10% of cerebellar strokes have symptoms mimicking benign vestibular neuronitis.
Bearing these problems in mind, recent studies have highlighted that detection of brainstem strokes is greatly aided by three rapid bedside assessments of the eyes and their movements. Confidently performing these examinations in AVS cases depends, from the outset, on a basic understanding of relevant functional anatomy, summarised below. Ninety per cent of brainstem strokes occur in the PICA territory.
- The VOR circuit is shown in Figure 2 (yellow). Its ability to move the eyes just the right amount for any given head movement is performance-checked by the visual cerebellum, the flocculus. This receives feedback regarding visual blurring; if the VOR is thus not working perfectly, the flocculus tunes the VOR accordingly. The VOR is commonly thought to be testable by the doll’s eye manoeuvre; however, in reality, its intactness can only be examined by a more vigorous horizontal head movement, called the head thrust or head impulse test (HIT): the “doll’s eyes on steroids”.
- Another visual-stabilisation system reliant on head-motion data is maintaining prolonged gaze to the sides of our vision. The extra-ocular muscles are somewhat elastic – when the eyes are deviated left or right to stare at an object for more than a few seconds, there is a pull dragging them back to their central position. To keep the eyes fixed on the target, a network of neurons in the medulla and cerebellum (the neural integrator) kicks in, giving a sustained push of neural firing. This achieves prolonged gaze holding laterally (like holding a spring-door ajar which wants to slam shut). Disease in the medulla and cerebellum (as in PICA infarcts) means that patients cannot fix gaze (hold a stare) in either direction, left or right for more than a brief moment; on attempting to gaze at something on the left, the eyes slowly drift back to the centre by elastic recoil. The brain then fires a quick saccadic movement to take them back to the left, only to fail, and the cycle repeats itself. In a nutshell, this is the genesis of direction-changing gaze-evoked nystagmus: an important bedside sign helping detect PICA strokes.
- In some central lesions, there is an incorrect conclusion by the CNS that the body is rotating sideways, as if performing a cartwheel or rolling in an aeroplane. The normal response to real-life movement like this is to tilt and tort one eye higher than the other, so-called skew deviation. Detecting a skew deviation at the bedside can further help detect brainstem strokes.
To remember these three eye-related bedside tests, the acronym “HINTS” has been used (ie, head impulse; nystagmus, gaze-evoked; skew-deviation). The HINTS examination has shown better sensitivity than magnetic resonance imaging (MRI) in the early detection of strokes presenting with AVS. This is of great potential importance for emergency and primary care doctors dealing with patients who are severely dizzy, in whom missing a stroke would be disastrous – especially so in rural areas lacking MRI access.
The presence of a PICA stroke is suggested by one or more of the following:
- An intact VOR, shown by a normal head thrust/HIT. Neurons passing through the pons from the labyrinth towards the VOR circuitry are spared in PICA strokes. AVS cases with an abnormal HIT are more likely to be peripheral or benign (eg, labyrinthitis).
- Gaze-evoked nystagmus discovered on testing gaze-holding laterally, left and right.
- Skew deviation found on inspection.
Dr Toby Commerford is a consultant geriatrician at Royal Adelaide Hospital, is course coordinator for geriatrics at the University of Adelaide’s Rural School, and practices remote and rural outreaches to Port Augusta and Murray Mallee. He is also the lead singer in a rock band.
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