“There can be few physicians so dedicated to their art that they do not experience a slight decline in spirits when they learn that their patient’s complaint is giddiness. This frequently means that after exhaustive enquiry it will still not be entirely clear what it is that the patient feels wrong and even less so why he feels it.”
From W B Matthews. Practical Neurology. Oxford, Blackwell, 1963.
Yes folks. It’s true. Very few of us feel excited by dizziness and, if truth to told, some of us are outright hostile to the symptom.
Why?
Perhaps it is because it is just so darn hard to figure out what dizziness means to the patient. Think about it – you have been trained in medical jargon. Can the same be said of your patients?
Giddy, faint, vertigo, spinning, disequilibrium, drunk, wobbly, shaky, unsteady, weak – see what I mean?
Terms like “dizziness” are so vague as to be almost meaningless, at least when taken at face value. For this reason, you really need to be forensic and relentless in trying to pin down what the real problem is.
This article will try and take you through the maze of dizziness so that you can make a decent fist of trying to figure it out.
When they say “dizzy”, what do they mean?
- Do they mean spinning/rotational movement – if so, this is vertigo, and usually from the “ear”
- Do they mean lightheaded/feeling faint – if so, this might be a blood pressure/cardiac issue
- Do they mean unsteady/like they might fall – if so, this might be “neurological” (whatever that means!)
When did it start and how is it behaving?
Everything is always acute onset, to some extent, but this is particularly true of proper, good-going vertigo. One moment you are fine and the next the world is spinning around. In that sense, vertigo is always acute.
When it comes from the ear (labyrinth) or nerve (vestibular) it should always settle down. That is because the problem is either triggered by movement or, if spontaneous, the brain adapts to this rapidly. Chronic vertigo is not a thing.
- Single-episode spontaneous vertigo is usually either labyrinthitis/vestibular neuritis or some sort of brainstem/cerebellar insult (stroke, demyelination).
- Vertigo triggered by head movement is usually Benign Paroxysmal Positional Vertigo (BPPV) (beware – all vertigo is made worse by head movement, but not all vertigo is repeatedly triggered by it).
- Recurrent attacks of vertigo, with tinnitus and hearing loss is Meniere’s disease.
Lightheaded feelings can occur at rest or on standing (orthostatic).
If this comes on soon after standing, think postural hypotension; if it comes on after being upright for a while, vasovagal (pre)syncope might be the cause.
Lightheaded symptoms at rest may be due to a cardiac rhythm disturbance.
“Unsteadiness” can be due to a dizzying (sorry) array of problems. Some of these are fully-fledged neurological giants and some of these are a bit more nebulous and multi-factorial.
The list below is not exhaustive, merely illustrative.
Neurological
- Unsteady when standing and turning – Parkinson’s? Look for cardinal features
- Unsteady with spontaneous backwards falls – Progressive Supranuclear Palsy? Look for eye signs
- Unsteadiness when standing still, relieved by moving around – Orthostatic tremor?
- Unsteady with eyes open or closed – Cerebellar disease? Look for signs and symptoms consistent with this
- Unsteady with eyes closed – sensory loss in lower limbs? Think peripheral neuropathy or spinal cord disease
- Intermittent and associated with headache? Might be migraine
Multifactorial
- Joint disease
- Muscle weakness
- Physical de-conditioning
- Drugs
- Age
- Visual loss
- Cerebrovascular disease (by this I mean evident on scan but not suggestive of stroke or TIA)
- Cognitive decline
- Anxiety
Let’s go through these in a little more detail.
Dizziness – but really acute vertigo
Bear in mind that I am a neurologist, not an ENT person. As such, a decent ENT specialist will read this and sigh (or perhaps get a little angry!). There are great neurologists doing dizziness too who might feel what is to come is a gross over-simplification. All I can say in my defence is:
- I’m just working with the brain I’ve got and have a load of other stuff on
- Mostly we just need a decent understanding to start from
BPPV
Remember that lovely feeling of a merry round or fairground ride as a kid? Remember how much fun it was to spin round and round and then feel dizzy and fall down? If so, you are part way to understanding BPPV.
Basically, in so doing, you are spinning the fluid in your labyrinth as you move. When you stop, the fluid doesn’t, setting up a mismatch between the information your brain is getting: your feet and eye tell it you are still but your vestibular system is telling it you are still spinning. Down you go.
Whilst this is great fun when done deliberately, and in a very “plastic” and adaptable nervous system, imagine what might happen if the sensation of the fluid moving just triggered when you turned your head. Not so fun.
In BPPV you have a problem with debris somewhere it shouldn’t be, triggering the vestibular system and telling your brain that you are in motion. You can see this more clearly in the diagram below.
The most common semi-circular canal to be involved is the posterior canal – so we will just ignore the others!
When chatting to patients, see if they will volunteer triggers. If not, ask about vertigo initiated by rolling over in bed.
Usually, the sense of spinning is relatively brief and settles after a few minutes. It recurs repeatedly over the course of weeks or months and often then goes away for a while, only to reappear later. Don’t ask me why – it just does.
There is a really fun way to diagnose this, and a unique appearance to the eyes that is the clincher. You can cure this condition in about 5 minutes, if you know what you are doing and it is one of the most satisfying parts of the clinic when you can pull this off.
I have managed to get a patient discharged from hospital, having been in for a week with “postural hypotension”, by diagnosing and treating his BPPV. I felt smug all day.
The Dix-Hallpike manoeuvre
Again, a picture paints a thousand words. There are different ways to do this but you need to be careful to explain it first (and get something for folk to throw up into – other than your shoe). Don’t do this to people with terrible necks, for obvious reasons.
You should see nothing for the first 10 seconds (the latent period), then the patient will experience their vertigo. Don’t let them close their eyes because you need to see them. Next you get a crescendo of twisting (torsional) nystagmus and this then attenuates. If you see this then you are home and dry with your diagnosis of BPPV.
The Epley manoeuvre
The next step is to perform the Epley manoeuvre, which handily follows on from the Dix-Hallpike. You have a pretty good chance of curing the BPPV with this procedure.
Patients can do this at home, in a modified format, to improve the chances of recovery.
Follow the link for more.
Labyrinthitis and Vestibular neuritis
This is a presumed viral infection or either part of the vestibular apparatus. Patients develop intense vertigo with nausea and vomiting. They feel absolutely awful and can be found clinging to the bed with their eyes shut and unable to move.
The general rule of thumb is as follows:
- If there is hearing loss, we call in labyrinthitis (as it involves the cochlea as well)
- If the hearing is fine, we call in vestibular neuritis
The symptoms are the same otherwise and the distinction is not all that vital.
This link will take you to a nice history for Labyrinthitis.
Examination is quite interesting. Patients have nystagmus, which has a fast phase only in one direction (unidirectional). By this we mean that, when looking to the right, the fast phase (jerk) is to the right and, guess what, when they look to the left, the fast phase is to the … right as well.
This unidirectional nystagmus is a hallmark of the peripheral system (ear) so is a useful way of reassuring yourself that the patient has not had a stroke (one of the differentials).
Alexander’s Law states that the nystagmus in the peripheral system is:
- worse when they look in the direction of the fast phase (see the video below)
- the fast phase points to the healthy ear AND
- it attentuates with fixation (so don’t get them to follow your finger).
I could tell you why, but then you would have to die (of boredom, probably)
In the recovery phase, if one side remains abnormal, then patients can have an abnormal head impulse test.It can look a bit brutal but is very helpful after the worst of the symptoms have settled.
This is not pass/fail stuff by the way!
The other thing to say is that patients should only have vertigo (with or without hearing loss). They will not want to walk and so you cannot do the full monty of a neuro exam. That said, their speech should be normal, not slurred, and there should be no visual loss, swallowing problems, facial weakness, limb symptoms etc. They must have a pure vertigo or they have something else.
As the vestibular system plugs into the brainstem (via cranial nerve VIII), a brainstem lesion (usually stroke) can cause vertigo as well. Usually, there are other brainstem symptoms and signs.
Often, the nystagmus is what we call “direction-changing”. This means that the fast phase jerks to the left on left gaze and then jerks to the right on right gaze.
Basically, direction-changing nystagmus is never from the ear.
The really great videos below cover BPPV, vesibular neuritis and central nystagmus in one fell swoop.
Meniere’s disease
I draw the line at doing this one. I am definitely not the guy to tell you about this.
These guys have a nice summary, so I can recommend this.
What I would say is this – it is massively over-diagnosed in primary care and far too many patients end up on a drug called betahistine for years and years. Betahsitine is not a treatment for “dizziness”, it is a treatment for Meniere’s disease. In addition, it causes drug-induced Parkinsonism if used in the long-term and so it bugs me to see it dished out like Smarties (other crispy chocolate snacks are available) for the wrong reason.
Dizziness – but really lightheadedness
Okay folks, are you really going to make me do a bit on this?
I hate you all…
Where to start?
Okay, so lightheaded feelings are familiar to us all, usually when we stand up too quickly. Usually, our postural reflexes kick in pretty fast, leading to vasoconstriction and a slight quickening of the pulse (very poetic of me). Soon enough, the BP is back up again and all is well.
Imagine a situation where this correction doesn’t happen. In this situation, folk continue to hypoperfuse their brains and, if they don’t sit down, then they will collapse and either faint (syncope) or almost faint (pre-syncope). This is made more common by a number of factors:
- Age
- Anti-hypertensive medications
- Other nebulous medications
- De-conditioning and prolonged bed rest
- Dehydration
- Various neurological disorders (Parkinson’s, Multiple System Atrophy)
So look for these factors in the story.
Obviously, there are loads of other reasons for the BP to drop – blood loss, heart failure, arrhythmia etc. so you do need to apply a little critical thought to this one.
It is possible to have dizziness due to low blood pressure when you have been upright for a longer period of time. Usually, in young people, this is vasovagal syncope and happens when your control centre for pulse/BP is a little oversensitive. In this situation, dizziness occurs after standing for a while, rather than when first upright.
Investigations are pretty obvious:
- Lying and standing BP – look for a significant drop in mmHg along with symptoms (usually > 20 mmHg)
- ECG
And sometimes
- Heart monitor
- ECHO
- Tilt-table test
These articles are good ones for covering it in more, and better, detail.
Dizziness – but really unsteadiness
This is more my thing, if I’m honest. As neurologists, we see loads of folk with unsteadiness and it can be really tricky to figure out what is going on.
Start by ruling out the other types of dizziness. If you are left with a feeling of imbalance and unsteadiness then it may be “neuro”. If the patient is falling, without blacking out, then this is even more likely to be a neurological in nature.
Let’s go back to our list from earlier.
- Unsteady when standing and turning?
- Unsteady with spontaneous backwards falls?
- Unsteadiness when standing still, relieved by moving around?
- Unsteady with eyes open or closed?
- Unsteady with eyes closed – sensory loss in lower limbs?
- Intermittent and associated with headache?
A good place to start is to think about where balance and movement comes from. Obviously we’re assuming that the vision is okay and the vestibular system is not damaged. Beyond that, you need to know where your legs are (sensory nerves), you need to have a system that coordinates your motor system (cerebellum) and you need to be able to allow the limbs to move (basal ganglia), and rectify your movement if it goes awry (brainstem reflexes).
If any of these go wrong then you have a problem that could be described as “dizziness”.
Let’s start with the sensory system.
You have two types of sensory nerve in your peripheral system – big ones and little ones (who said neurology was complicated?). The big ones send information quickly and the little ones … well, you get the idea.
What sensory information to you want transmitted quickly – proprioception or pain/temperature?
If you want to rectify your balance then you need the proprioception first. In our terms this is joint position sense and vibration. It doesn’t matter if pain is a little slower to get to your brain.
Big fibres are myelinated and plug into the back of the spinal cord (dorsal columns) via the dorsal root ganglion. Small fibres are unmyelinated and cross the spinal cord to move up the spinothalamic pathways.
This means that damage to the large fibres (demyelinating or axonal), dorsal root ganglion or dorsal columns leads to a profound sense of imbalance. Patients walk with a broad-based gait, staring at their feet. They will fall if their eyes are closed (Romberg’s sign) and describe sensory symptoms (of course) and have abnormal sensory examination.
Conditions like neuropathy (GBS, CIDP, Diabetes, Alcohol), dorsal root ganglionopathy (Sjogren’s, paraneoplastic) and dorsal column damage (syphilis, B12 deficiency) all cause sensory ataxia.
It should, therefore, be easy to pick these patients up – if you think about it.
Follow the link for obscene levels of detail!
If they are ataxic, but the sensory system is OK …
Then think cerebellum. The gait pattern is more or less the same as in sensory ataxia – broad in base, unsteady, cautious.
Expect some other ataxic bits as well:
- Ataxic eyes – nystagmus, hyper metric movements
- Ataxic speech – dysarthria
- Ataxic swallow – dysphagia
- Ataxic arms – dysmetria, clumsy tapping
- Ataxic legs – heel-shin testing impaired
So really, if your patient has a cerebellar disorder then you should be able to spot this fairly easily.
Here is a useful page on how to examine for ataxia.
There are loads of causes of cerebellar ataxia and none are really “core” knowledge. Dig deeper here for more information.
Unsteady with or without falls
Patients with basal ganglia disorders also complain of “dizziness” and “unsteadiness”. Some are prone to orthostatic hypotension, just to confuse matters, but loads of basal ganglia things mess up your balance – PD, PSP, MSA, DLB – the list goes on.
Always try and look at your patient walk and turn. PD patients usually have a narrow, normal base to their gait. Stride length is reduced and they are stooped and may not swing their arms. When turning, they take small steps and may find it hard to get going again. This is a huge clue to the diagnosis but you will miss it if you don’t look at the gait.
- Parkinson’s disease – asymmetrical bradykinesia, rigidity, tremor, postural instability
- Progressive Supranuclear Palsy – vertical gaze loss, backwards falls, frontal dementia syndrome
- Multiple System Atrophy – Parkinsonism, Ataxia, Autonomic failure (bladder, bowel, blood pressure)
- Dementia with Lewy bodies (DLB) – Parkinsonism, dementia, visual hallucinations, autonomic failure
All of these make you unsteady on your feet.
Unsteady when standing still
There is a rare tremor disorder that only really comes on when you stand still. It is relieved by moving around and so patients hate shopping queues as a result. Patients usually think you think they are mad – but you can smile knowingly and amaze them with your diamond diagnosis of the month – Orthostatic tremor.
This is a great video that covers how it presents and why often people miss it.
The diagnosis is firmed up when you auscultate their legs (Yes, really!) and hear the sound of a distant helicopters. EMG studies show a 13-17Hz tremor on standing.
Spotting this is a good way to look and feel great about your day.
Dizziness with headache
Some migraine patients seem to get brainstem type symptoms when they develop their attacks. This is a diagnosis of exclusion, usually, as the symptoms are abrupt-onset and quite nasty. As such, we usually end up scanning to rule out strokes – at least for the first presentation (often the second or third!). Rotatory vertigo in the context of migraine is a bit of the clue to this.
Chronic “dizziness”
This is the heart sink situation. The approach is to look for all the other stuff (above) and tick it off your list. Sometimes, it is just easier to say what it isn’t than what it is.
Usually, patients in this category have a normal examination and normal tests. They may have many other medical issues and the symptoms are multi-factorial. Treating chronic dizziness is generally unrewarding for both patents and clinicians alike.
But, if you want to read more, and why not given all the time you guys have on your hands, then I can recommend these dizziness experts – not all heroes wear capes!