Chapter 13: Dizziness Assessment & Diagnosis

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Welcome back to The Deep Dive.

We are back at it and today we are tackling a beast.

I really don't use that word lightly.

No, this is a big one.

We are talking about a symptom that walks into primary care clinics every single day,

confuses the heck out of patients, and if we're being honest,

probably spikes the blood pressure of quite a few providers too.

I think that's a fair assessment.

We are talking about dizziness.

It is without a doubt one of the most common complaints clinicians face.

It's universal.

I mean, everyone has felt it at some point, but professionally it can be one of the most frustrating encounters you can have.

Right, and I think that frustration, it comes from the language, doesn't it?

Absolutely.

Because dizzy is this junk drawer term.

If I tell you I'm dizzy, I can mean absolutely anything.

I could mean I feel like I'm going to faint because I skipped lunch.

Right.

I could mean the room is doing cart wheels or I could just mean I feel a little off, you know, like I'm walking on a mattress or something.

Exactly, and that ambiguity is the very first hurdle you have to clear.

We're looking at Chapter 13 from Advanced Health Assessment and Clinical Diagnosis in Primary Care, and the text, it opens with exactly this problem.

It sets the stage perfectly.

It does.

It says patients, and the author specifically highlight children and older adults here, they tend to categorize every single sensation of instability under this one umbrella term.

Lightheadedness, unsteadiness, spinning, falling, it all just gets labeled dizziness.

So if the patient's language is vague, our job is to be the translator.

Yeah.

We have to take that messy, kind of vague complaint and filter it through a really rigorous system.

Precisely, and the text provides that system.

We're going to walk through the history, the physical exam, and the differential diagnosis step by step.

Okay.

But before we even start that detective work, we need to set some boundaries.

Because this chapter, and therefore our conversation today, it isn't about every single wobbly feeling a human being can possibly experience.

Right.

We need to clarify the scope.

The text acknowledges things like lightheadedness,

but the real star of the show here is vertigo.

Correct.

The primary focus of this specific text is vertigo.

And we need to be really pedantic about the definition here.

Vertigo is not just feeling woozy.

It is, in a very real sense, a hallucination.

A hallucination.

That's a strong word.

It's the medical reality of it.

It is a specific hallucination of motion.

The patient has the sensation that either their body is moving, which we call subjective vertigo.

So I feel like I'm spinning.

Yes.

Or that the environment is moving around them, which is objective vertigo.

The room is spinning.

Exactly.

And usually this isn't just a gentle drift.

It's described as a spinning or a rotary motion, a very distinct movement.

So if the room isn't spinning, or if they don't feel like they themselves are spinning, we might be barking up the wrong tree if we're thinking true vertigo.

That might be, yes.

But to understand why the room spins, we have to look at the physiology.

And the text paints this picture of balance that's remarkably complex.

It's not just the ear, right?

It's a whole team effort.

Oh, it's a triad.

Think of your sense of balance like a tripod.

It depends on the seamless interconnection of three specific systems.

First, you have the visual system, what your eyes are telling you about where the horizon is.

Second, the vestibular system, your inner ear, which is detecting gravity and acceleration.

The gyroscope.

Your internal gyroscope, exactly.

And third, the sensory system, specifically proprioception, what your feet and your joints are telling you about where your body is in space.

And stability is basically when all three of those systems agree.

Exactly.

When your eyes see a wall that isn't moving, your feet feel the solid floor beneath you, and your inner ear says, we are standing still, you feel balanced.

So vertigo is a riot.

It's a riot.

It's a disruption or a kick.

And when that tripod kicks out and the brain just gets utterly confused.

And when we are trying to figure out which leg of the tripod is broken,

or I guess more specifically where that signal is getting garbled, we generally divide the problems into two massive buckets.

This seems to be the fundamental framework of the entire chapter.

Yes.

The great divide, if you will.

That's a good way to put it.

Central versus peripheral.

And this is it.

This is the big one.

This is the most critical distinction a clinician has to make.

I mean, everything hangs on this.

Central versus peripheral.

So let's define the territory.

When we say central, we are not talking about the middle of the year.

No, not at all.

Central vertigo refers to the central nervous system.

We are talking about the brainstem or the cerebellum.

Processing centers.

Exactly.

The main computers.

And because it's the brain, the causes here are, well, they're the big scary ones.

Neoplastic issues like tumors, vascular issues like strokes or TIAs, transient ischemic attacks, migraines or multiple sclerosis.

Okay.

So central equals brain and brain equals high alert.

Generally, yes.

You need to be thinking with a higher level of urgency.

And then we have the peripheral bucket.

So peripheral vertigo involves the vestibular apparatus itself, the inner ear and the nerve connecting it back to the brain.

This is where we see the more mechanical issues, things like crystals moving where they shouldn't.

That's canelothiasis or nerve inflammation, infections or issues with the inner ear fluid pressure, like in Meniere's disease.

And just to round it out, the text does mention the third category, which is sort of a catch -all, systemic or other.

Right.

Because you can have a perfectly healthy brain and a perfectly healthy ear, but if the blood pumping to them is compromised or if your blood sugar is low or if there's a toxin in your system, the whole system fails.

Power supply is cut.

Exactly.

So this bucket includes psychogenic causes, cardiovascular issues, metabolic problems, trauma or ototoxicity from medications.

But for your diagnostic reasoning, keeping that central versus peripheral dichotomy in the front of your mind is absolutely essential.

It dictates the urgency of your workup.

Okay, let's get into the room with the patient.

This is the diagnostic reasoning phase, starting with the focused history.

You are sitting there, the patient looks absolutely miserable and they say, I'm dizzy.

As we established, that means nothing yet.

How do we start decoding?

You have to force them to be specific.

You cannot accept dizzy as an answer.

The text lists these key questions to drill down on the actual sensation.

You have to ask, do you feel yourself spinning or do you feel the room spinning?

And if they say, yes, spinning, we're in vertigo territory.

We're on the right track.

Correct.

But what if they say, no, no spinning.

I just feel like I'm about to faint, like the lights are dimming.

Sounds completely different.

That sounds more like a blood flow issue.

Exactly.

That is lightheadedness or presyncope.

That triggers a totally different diagnostic pathway.

You're thinking cardiac, you're thinking metabolic.

It's not an ear problem.

And then there's a third option.

I feel like my balance is off.

I feel like I might fall.

I feel wobbly, but nothing is spinning and I don't feel faint.

And that is disequilibrium.

And the text notes something really interesting about disequilibrium.

It usually has a slow, gradual onset.

Why is that?

What's the mechanism there?

Because it's often degenerative.

If a patient has a loss of equilibrium, but no spinning vertigo, you shouldn't be looking at the inner ear primarily.

You should be looking at that third leg of the tripod proprioception.

The sensory input.

Exactly.

Look for peripheral neuropathy.

If you're diabetic and you can't feel your feet touching the floor properly, your brain is missing critical data.

Of course you feel off balance.

That makes perfect sense.

It's like trying to walk on spilt that you can't feel.

Your brain has no idea where they are.

Precisely.

Or it could be a visual impairment.

Or a motor issue like Parkinson's.

But it's rarely the vestibular system acting up in isolation.

It's a different kind of problem.

Now I want to pivot to a specific population the text mentions.

Pediatrics.

Because asking a five -year -old if they are experiencing rotary nystagmus or subjective vertigo is probably going to get you a blank stare.

Or a request for a snack.

Yeah, no, absolutely not.

You have to translate these concepts into their world.

The text suggests using playground language.

Oh, that's smart.

Ask them if it feels like swinging or being on a merry -go -round.

That's brilliant.

Yeah.

It anchors the sensation to a physical memory they actually understand.

It does.

And there's a nuance here that's really helpful for pediatric assessment.

If a child describes just a vague unsteadiness, it might be something like peripheral neuropathy or a middle ear effusion.

But if they describe a feeling of motion, that merry -go -round feeling, it strongly suggests a vestibular issue.

So the sensation of movement is the key differentiator.

It is, regardless of age.

Let's circle back to lightheadedness for a moment.

The text defines this as near syncope.

Right.

The feeling that you are about to pass out.

And it's important to distinguish this from true syncope.

True syncope is a sudden transient loss of consciousness with a loss of postural tone.

Meaning they hit the floor.

They fall down.

But the key to syncope is that it always has a spontaneous recovery.

They wake up on their own relatively quickly.

If they just feel like they're going to black out but never actually do, that's lightheadedness.

And what are the usual suspects for that lightheaded feeling?

If it's not the ear crystals, what is it?

Usually it's the pump or the pipes.

Orthostatic hypotension is a huge one, especially in the elderly.

Right.

That's an abnormal regulation of blood pressure when you stand up.

The blood pools in the legs.

The brain gets less oxygen for just a moment.

And whoosh, you feel lightheaded.

But it can also be the blood itself, right?

Like the fuel.

Yes.

Anemia.

Not enough red blood cells to carry the oxygen.

Or hypoglycemia.

Not enough fuel for the brain.

And surprisingly often hyperventilation syndrome.

Which brings us neatly to the systemic causes and specifically anxiety.

I feel like anxiety gets blamed for everything in medicine.

But in this case, the mechanism is very real.

It is very real.

And the text notes that anxiety is actually one of the most common causes of dizziness.

But the description the patient gives is usually different.

It's vague.

Not the spinning.

No, they won't say the room is spinning clockwise.

They might describe fatigue, a fullness in the head, or feeling apart from the environment.

A kind of dissociation or derealization.

And physically, if they're anxious, they might be hyperventilating.

Maybe without even realizing it.

Exactly.

And when you hyperventilate, you blow off too much carbon dioxide.

That changes the pH of your blood, which in turn causes cerebral vasoconstriction.

The blood vessels in your brain literally clamp down.

So you really are getting less blood flow to the brain.

Yes.

It's not all in their head.

Well, it is.

But it's physiological, not just emotional.

That explains why the old paper bag trick works.

You're rebreathing the CO2.

Yeah.

OK, so cardiovascular issues.

What else should we look for besides orthostasis?

Vasa motor instability, reduced cardiac output, dysrhythmias.

I mean, if the heart isn't pumping efficiently, the brain is the first organ to complain.

And don't forget, medications, hypertension meds are designed to lower blood pressure.

Sometimes they do their job a little too well, leading to that dizziness on standing.

The text also emphasizes the relationship to activity or movement.

This feels like a cheat code for diagnosis.

The when seems to reveal the what.

It really is a cheat code.

You need to ask specifically,

what are you doing when the dizziness starts?

If the dizziness happens when turning in bed, particularly rolling over to one side, that is almost always vertigo.

And specifically, benign paroxysmal positional vertigo, or BPPV.

Rolling over moves the gravity sensors in the ear.

Exactly.

It moves the debris in the canals.

But if they say, I'm fine in bed, but I get unsteady when I'm walking.

That's a different story.

That points to disequilibrium.

That implies the system fails when it's under load or demand.

And dizziness specifically on standing up.

Decreased cerebral perfusion.

That's your orthostasis.

The gravity change grains the blood from your head, and the body doesn't compensate fast enough.

OK, so we've got a handle on the sensation.

Now let's get to this really high stakes part of the history.

We need to differentiate central, the brain, from peripheral, the ear.

The text lists some red flags for central vertigo.

What are the signals that should make the hair on the back of our neck stand up?

The first big one is headaches.

If a patient has vertigo A and D, a severe headache, you need to be very, very careful.

Right.

Migraine is a vascular -related central cause.

A huge chunk, about one -third, of migraine patients experience vertigo.

It can be an aura before the pain, or it can happen separately as a vestibular migraine.

And there's a specific, rather nasty type of migraine mentioned in the text, right?

Basilar type?

Yes.

Basilar type migraines involve the basilar artery, which is the main artery that supplies the brainstem.

So along with vertigo, these patients get a whole cascade of brainstem symptoms.

Visual changes, tinnitus, and ataxia, that profound loss of coordination.

That sounds terrifying.

What about other neurologic symptoms?

This is a golden rule, and if you take nothing else from this section, take this.

Central vertigo almost always has neighbors.

Neighbors?

What do you mean?

The brainstem is crowded real estate.

All the cranial nerve nuclei are packed in there tightly, side by side.

If you have a lesion like a stroke or a tumor in the brainstem that's causing vertigo, it's extremely unlikely to only hit the vestibular nucleus.

It's going to hit the houses next door.

It's going to hit the neighbors, too.

So you'll see double vision diplopia.

You'll see facial numbness.

You'll see hemiparesis, which is weakness on one side of the body.

So if a patient comes in with vertigo A and D, their face is numb, or they're slurring their words.

You are sprinting to the MRI.

You are not looking in their ears for crystals.

That is a brain problem until proven otherwise.

Full stop.

The text also mentions cerebellar signs.

Right, ataxia.

If they literally cannot walk, or if their movements are wild and uncoordinated, that suggests the cerebellum, the coordination center, is involved.

Peripheral vertigo makes you feel unsteady, but usually you can still walk, albeit very carefully.

If you can't stand up at all, you have to think central.

Now let's flip it.

What are the characteristics of peripheral vertigo?

What does the ear problem look like?

Usually you have no additional neurologic signs.

No double vision.

No weakness.

No numbness.

But here is a very counterintuitive fact that the text highlights, and it trips up a lot of students.

Nausea and vomiting.

Yeah, I found this surprising.

I would have thought severe vomiting implies something terrible in the brain.

Projectile vomiting sounds like a brain bleed term.

You would think so, and it can be.

But actually, severe nausea and vomiting point toward a peripheral problem, like vestibular neuronitis or labyrinthitis.

Why is that?

The inner ear is hardwired directly to the vomiting center in the brainstem.

When the inner ear goes haywire, the nausea is profound and overwhelming.

Brainstem lesions can cause vomiting, but it's often much more consistent and severe with inner ear pathology.

So don't let the vomit scare you into thinking stroke immediately.

That is a great pearl.

Vomit equals ear, usually.

Let's talk more about timing.

The when and how long seems to matter a lot in building this profile.

Oh, timing is everything.

Start with the time of day.

If it happens upon arising in the morning or with that first movement of the head, it's usually a vestibular disorder.

We talked about that.

And if it's strictly when turning in bed,

think BPPV.

But then you have to ask about duration.

If the episodes last for seconds, I mean, literally, the room spins for 10 seconds and then stops.

That is classic BPPV.

It's triggered by a head movement.

The crystals settle and it stops.

What if it lasts minutes to hours?

That's the sweet spot for Meniere's disease or recurrent vestibulopathy.

Meniere's attacks are episodes.

They come, they wreck your afternoon, and then they fade.

And what if it lasts for days?

If the room spins for days or even weeks and the patient lies completely still in a dark room because any movement is torture.

Suspect vestibular neuronitis, that is an inflammation of the nerve.

It doesn't just settle like crystals.

The nerve is sick and it takes time to heal.

And on the far end of the spectrum,

sudden and prolonged.

If it is a sudden onset, lasts more than 60 minutes and just does not stop, that's dangerous.

Sudden prolonged vertigo suggests central causes like an infarction, a stroke, or a hemorrhage, especially if they have vascular risk factors like hypertension or diabetes.

What about the speed of onset, gradual versus acute?

A gradual onset is typical of a slow growing problem.

Think of an acoustic neuroma.

It's a benign tumor on the nerve.

It grows millimeter by millimeter so the brain has time to compensate.

The vertigo might be mild or just a feeling of unsteadiness.

But an acute, sudden onset, I was fine and then the world flipped over.

It's characteristic of labyrinthitis, Meniere's, or a stroke.

The system was working and then suddenly it wasn't.

Okay, we can't talk about the ear without talking about hearing.

How do hearing loss and tinnitus, that ringing in the ears, factor into the differential?

They're crucial for narrowing down the peripheral causes.

We have the classic triad for Meniere's disease.

You need all three things, vertigo, hearing loss, and tinnitus.

If you have all three, Meniere's is your prime suspect.

The text also mentions syphilis here, which feels like a blast from the past.

It does, but we can't forget it.

Secondary or tertiary syphilis can mimic Meniere's almost perfectly.

It causes inflammation in the labyrinth.

It's known as the great imitator for a reason.

And acoustic neuroma, how does that present with hearing?

That typically presents with unilateral hearing loss and tinnitus, just one side.

And because it's a tumor pressing on the nerve, the hearing loss is progressive and gets worse over time.

Now here is a distinction I need help with.

Labyrinthitis versus vestibular neuronitis.

They sound so similar.

They both cause severe vertigo and nausea.

They both can follow viral infections.

How do we tell them apart in the history?

It comes down to anatomy and hearing.

Vestibular neuronitis is inflammation of the vestibular nerve only.

The cochlear nerve, the hearing nerve runs right next to it, but it isn't affected.

So you get vertigo without hearing loss.

And labyrinthitis.

Labyrinthitis involves the labyrinth itself, the entire inner ear structure.

That includes the cochlea.

So you get the vertigo plus hearing loss.

Hearing loss is the tiebreaker.

Fantastic.

So no hearing loss equals neuronitis.

Hearing loss equals labyrinthitis.

Got it.

Moving on to section three.

Other historical considerations.

We mentioned meds briefly, but let's list the offenders.

We're always taught to blame the meds first.

Always.

You have to review the list.

You have salt retaining drugs like steroids and phenylbutazone fluid retention can affect the inner ear pressure, which can mimic manures.

Then you have the directly ototoxic drugs that actually poison the ear.

Like what?

Streptomycin, gentamisin are big ones.

And high dose aspirin.

Aspirin.

I didn't know that.

Yes.

In high doses, aspirin is well known to cause tinnitus and vertigo.

And furosemide, which is LASIX, a very common diuretic.

If you push it too fast or the dose is too high, it can hit the ear.

And recent illness.

We touched on this, but it's vital.

If they just had a viral infection like a URI or the flu that often precedes vestibular neuronitis, the virus inflames the nerve.

And kids, look for a middle ear effusion fluid behind the drum from an ear infection.

It's a very common cause of balance disturbance because the middle ear mechanics are dampened.

The text also brings up trauma.

Obviously, a head blow can cause dizziness, concussion, and all that.

But there's this specific thing called a paralymp fistula.

It sounds like a plumbing problem.

It essentially is.

It's a leak between the middle and inner ear.

It can happen from head trauma like whiplash or a direct blow to the head.

But interestingly, the text notes it can also happen from barotrauma.

Pressure changes.

Exactly.

Like snoozing violently, lifting something incredibly heavy, or even from scuba diving.

Wait, sneezing?

You can get vertigo from a sneeze.

If you stifle a massive sneeze, the pressure spike can be immense.

It can literally blow a tiny hole in the round or oval window membrane.

The fluid leaks out, and the patient gets vertigo.

New fear unlocked.

Don't hold in your sneezes.

Okay, let's move from talking to the patient to touching the patient.

The focused physical exam.

Where do we start?

Vitals.

But not just slap the cuff on.

You need to get orthostatic blood pressure.

You need to check for a drop.

How does the text define a positive result?

What are we looking for?

You measure them lying down, Supine.

Then you have them stand.

You measure again within a few minutes.

You are looking for a drop of 30 millimeters of mercury systolic or 20 millimeters of mercury diastolic.

That's a significant drop.

That's not just a blip.

It is significant.

That confirms orthostatic hypotension is at play.

Then just look at the patient, their general appearance.

If they are lying perfectly still, eyes closed, looking miserable, and holding a bucket.

Suspect vestibular neuronitis.

They have learned that any movement equals torture.

And if you suspect, it's anxiety.

You can try to reproduce the symptoms.

You can have them hyperventilate intentionally for a minute or two.

If that brings on their specific feeling of dizziness, you have a strong clue, it's psychogenic.

You've reproduced the mechanism right there in the office.

Now the head and neck exam.

Eyes and ears.

Check vision first.

New glasses, bifocals, or a sudden change in acuity can cause imbalance because the visual input is distorted.

But the ear exam is key.

You're looking for infection.

You're looking for a fusion.

And you're looking for a cholesteatoma.

Describe that for us.

It's a pretty distinct finding.

It is.

You're looking for a shiny white irregular mass behind the eardrum or sometimes a foul smelling discharge.

It's a destructive growth of skin cells in the middle ear space.

It can erode into the inner ear and cause vertigo.

And pneumatic otoscopy.

That's where you puff air into the ear canal.

Usually we use this to see if the eardrum moves, which helps check for fluid.

But here, if puffing that air triggers a sudden violent episode of vertigo and nystagmus, that is a positive sign for a fistula.

You are transmitting pressure directly into the inner ear through that leak we talked about.

And hearing tests.

The text mentions the old school Wren and Weber.

Basic but essential tuning fork tests.

You are looking for sensorineural loss.

Remember, with sensorineural loss or nerve damage, the sound in the Weber test lateralizes to the unaffected or good ear.

If the patient has vertigo and the sound goes to the left ear, the right ear might be the culprit.

Okay.

We have arrived at the heavy hitter.

The part of the exam that scares students.

And let's be honest, some doctors too.

Nystagmus.

It can be intimidating, but it is the single most useful tool for differentiating central from peripheral vertigo.

If you master nystagmus, you master the dizzy patient.

So let's define it.

Nystagmus is that involuntary rhythmic eye movement.

Yes.

And think of it as a tug of war.

It has two distinct phases.

A slow drift and a quick corrective jerk.

What's actually happening in the brain and the ear?

The slow drift is the pathology.

The vestibular system is imbalanced, so it effectively pulls the eyes to one side.

The eyes drift off target.

The brain, specifically the cortex, sees this and says, hey, look back at the target.

That snap back is the quick jerk.

So the drift is the ear's fault and the jerk is the brain fixing it.

Exactly.

And here is the convention that's important.

The direction of nystagmus is named by the quick component.

Okay.

Named by the quick jerk.

The text has a critical table.

Table 13 .1.

Let's break it down.

Peripheral versus central nystagmus.

What does peripheral look like?

The ear -related kind.

Peripheral nystagmus, coming from the ear, is usually, for lack of a better word, well -behaved.

It has a fixed direction.

It always beats the same way.

Typically horizontal or rotary.

So if it's beating to the left, it stays beating to the left no matter where they look.

Correct.

Furthermore, if you give the patient a target, ask them to stare at your finger,

peripheral nystagmus gets suppressed.

Visual fixation helps the brain override the faulty ear signal.

That makes sense.

The visual system, that other leg of the tripod, steps in to help stabilize things.

Exactly.

Also, peripheral nystagmus has a latent period.

It takes a few seconds to start after you move them.

And it fatigues.

It gets better if you repeat the maneuver.

The system adapts.

Okay.

Now compare that to central nystagmus.

This is the brainstem acting up.

Central nystagmus behaves badly.

It's erratic.

It can change directions.

It might beat left when they look left and then beat right when they look right.

So it's not fixed.

Not fixed at all.

It also starts immediately.

There's no latency.

It does not fatigue.

It just keeps going as long as you hold the position.

And critically,

visual fixation does not suppress it.

Staring at a dot won't stop the brainstem from misfiring.

And is there a specific direction that is a dead giveaway for central?

Vertical.

Just up and down?

Yes.

If the eyes are beating purely up or purely down, what we call upgaze or down days in nystagmus, that is always central.

Always.

There are no exceptions.

For the purpose of this text and for primary care safety, yes.

You will essentially never see pure vertical nystagmus from an inner ear problem.

The anatomy of the inner ear canals is arranged to create horizontal or rotary movements.

Vertical implies a problem with the central integrators in the brainstem or cerebellum.

That is a massive red flag.

Vertical equals central.

Got it.

Moving to section six.

Maneuvers and reflexes.

We have to talk about the gold standard for BPPV.

The Dix -Hall -Pike maneuver.

This is a maneuver every primary care provider should absolutely master.

It is the definitive diagnostic test for BPPV.

Walk us through it step by step.

You have the patient sit up on the exam table.

You turn their head 45 degrees to one side.

Let's say we're testing the right side first.

Okay.

Then you warn them.

This might make you very dizzy.

And you quickly lower them backward into a lying position.

So their head hangs about 20 to 30 degrees lower than the table edge.

You're extending their neck.

So they are looking up into the right with their head hanging off the table.

And what are we waiting for?

What are we watching?

You are watching their eyes like a hawk.

You are waiting for that latency period.

Usually three to ten seconds.

Then if it's BPPV, you will see a burst of intense vertigo and a very specific rotary nystagmus.

And the patient will probably grab your arm and tell you they hate you?

They often do.

It is very unpleasant.

But that response confirms the diagnosis.

If the nystagmus is fixed in direction, has that delay, and lessens when you repeat it, that confirms peripheral BPPV.

And if it starts instantly upon lying back or if it's vertical or it just keeps going without stopping?

That's central.

That's a positive test for a brain issue, not BPPV.

It's next maneuver.

The vestibular ocular reflex or the head thrust test.

What is this for?

This tests the function of the horizontal semicircular canal.

It basically asks the question, is the gyroscope working correctly?

How do you do it?

You ask the patient to stare at your nose.

You hold their head with both hands.

You might move it slowly side to side just to relax them and then snap.

You quickly thrust their head to one side.

It's a small movement, but it has to be fast and unpredictable.

What's a normal response?

Normal is that their eyes stay locked on your nose, like a camera on a gimbal.

The VOR reflex counters the head movement instantly and perfectly.

And abnormal.

What does that look like?

If they have a vestibular pathology on that side, say the nerve is dead from neuronitis, the eyes will move with the head.

They'll lose the target.

Then, a split second later, the brain realizes it and jerks the eyes back to your nose to refixate.

That jerk is the ketchup saccade.

Correct.

If you see that ketchup saccade, it confirms a peripheral vestibular problem on that side.

It's highly specific.

Finally, the neurologic exam basics.

We need to check the cerebellum.

Right.

Gait is the big one.

Specifically, tandem walking, heel to toe.

A vestibular patient might wobble, but a cerebellar patient often cannot do this at all.

You also check rapid alternating movements or rams and past pointing.

The text mentions a really cool way to differentiate vestibular from cerebellar ataxia using a blindfold, or just having them close their eyes.

Yes.

This goes right back to the tripod analogy.

If the ataxia is from vestibular loss from the inner ear, that patient is relying heavily on their eyes to stay upright.

They're using vision to compensate.

Exactly.

So if you blindfold them, taking away the visual leg of the tripod, they get much worse.

They might start to fall.

And if it's cerebellar?

If the ataxia is from cerebellar disease from the brain itself, the coordination is broken regardless of the input.

They are uncoordinated whether their eyes are open or closed.

The blindfold doesn't change much because the processor itself is faulty.

That brings us to section seven, labs and diagnostics.

When do we start ordering the expensive tests?

Well, audiometry is essential if there is any hearing loss.

You need to document the extent and the type of hearing loss.

Electronostagmography, or ENG, is more of a specialist test.

It electronically records eye movements and uses caloric stimulation warm and cool water in the ear to test the vestibular function on each side.

It's very useful for confirming something like manures.

What about the magnet, MRI versus CT?

MRI with contrast is the gold standard for looking at the brain stem in the auditory canal.

It's what you need to find an acoustic neuroma or see MS plaques.

If they have that vertical nystagmus, a severe headache, or a sudden onset with vascular risk factors, you need an MRI.

When would you ever settle for a CT?

A CT is much faster, but the resolution for soft tissue in the brain stem is poor because of bone artifact.

However, it is excellent for seeing blood.

So it's good for a sudden onset in patients with risk factors like renal failure or hypertension if you're looking for an acute hemorrhage.

But for tumors or asthmia, MRI is king.

And other basic labs.

Clucose to rule out hypoglycemia.

A CBC to rule out anemia.

And syphilis serology if you have any reason at all to suspect neurosyphilis.

There's an evidence -based box in the text about the Romberg test.

We all learned the Romberg in school.

Stand with your feet together, close your eyes.

We did.

It's a classic part of the neuro exam.

But the text cites a study noting that the Romberg is really a test of general balance.

It tests the integrity of the dorsal columns of the spinal cord, which is proprioception.

It relies on vision, vestibular input, and proprioception.

So it's not specific.

Right.

A positive Romberg doesn't tell you it's the ear.

It just tells you the patient's balance is impaired when vision is removed.

The text argues it shouldn't be used as the primary screen for vestibular impairment because it's just too broad.

It has low specificity for vestibular disease.

Okay, we have gathered all our clues.

History, nystagmus, maneuvers.

Now, section eight.

The differential diagnosis breakdown.

Let's do the grand tour of the most common causes.

Let's start with peripheral, the inner ear.

First up, BPPV, benign paroxysmal positional vertigo.

This is the most common cause you'll see.

Give us a profile.

Positional triggers like rolling over in bed.

Very short duration, just seconds.

Hearing is normal.

It's caused by those calcium crystals, the otoliths, migrating into the semicircular canals where they don't belong.

And the diagnosis is made with the Dix -Hall -Pike maneuver.

Next,

Meniere's disease.

The triad, vertigo, hearing loss, and tinnitus.

It comes in recurring attacks that last minutes to hours.

Patients will often describe a feeling of fullness or pressure in the affected ear.

Then the twins,

vestibular neuronitis versus labyrinthitis.

Okay, vestibular neuronitis.

Severe vertigo, nausea, vomiting.

It often follows a viral infection and the key is NO hearing loss.

And labyrinthitis.

Exactly the same presentation.

Severe vertigo and nausea by T.

It includes hearing loss because the cochlea, the hearing part of the inner ear, is also inflamed.

Acoustic neuroma.

That's a benign tumor on cranial neur 8.

The profile is unilateral hearing loss, tinnitus, and a very gradual onset of disequilibrium.

The nystagmus might be subtle because the brain has had time to compensate as the tumor grows so slowly.

And cholesteatoma.

For that one, you need to look for a history of chronic infection, a foul -smelling discharge, and that classic white mass behind the eardrum on exam.

They'll usually have a conductive hearing loss.

Okay, now switch gears to central causes.

The brain.

Brainstem stroke or TIA.

Think acute onset, usually an older adult with vascular risk factors.

And you have to look for those labors, diplopia, weakness, sensory deficits.

And remember the vertical nystagmus.

Multiple sclerosis.

This is a surprisingly common cause of vertigo.

The text says it occurs in roughly 50 % of MS patients at some point.

Onset is usually younger in the third or fourth decade of life, and the MRI will show the characteristic demyelinating plaques.

And migraine.

The history is absolutely key.

A history of headaches, aura, photophobia.

It's often a diagnosis of exclusion after you've ruled out the more dangerous structural stuff.

Finally, that systemic or other category.

Psychogenic.

The symptoms are vague, the patient often seems anxious, and there's no true nystagmus.

The symptoms can often be reproduced by having them hyperventilate.

And last but not least, neurocephalus.

The great imitator.

It can mimic almost anything, but look for the Argyle -Roberson pupil.

Remind me what that is again.

The pupil reacts to accommodation.

It constricts when the patient looks at something up close, but it does not constrict when you shine a bright light in it.

It's a very specific, classic sign.

That is quite the list.

But if you follow the system history first, then nystagmus, then maneuvers, you can sort through it pretty logically.

Absolutely.

The goal isn't to memorize every single disease, but to categorize the patient.

Central versus peripheral, urgent versus benign.

We've covered a lot of ground.

Let's head to the outro and try to summarize this for the listener.

Dizziness is a puzzle, but it's a solvable one.

Start with the sensation.

Is it vertigo?

Is it actually spinning?

If yes, then your job is to classify it.

Is it central continuous vertical nystagmus other neuroscience?

Or is it peripheral intermittent rotary nystagmus?

Maybe some hearing loss.

And don't forget the maneuvers.

They're your hands -on tools.

Never.

The Dix -Hall Pike for a diagnosis of BPPV and the head thrust for a vestibular hypofunction are your best friends in the exam room.

They can give you the answer right then and there.

I want to leave the listeners with a final provocative thought.

Something the text alludes to, but is worth really mulling over.

I think it's the profound impact of age and context on the interpretation of the exact same symptom.

Think about the sensation of spinning.

If a child feels it on a merry -go -round, it's play.

They seek it out.

If an older adult feels the exact same sensation turning over in bed, it's pathology.

It's BPPV.

And if that same older adult feels it suddenly while sitting still, it could be a stroke.

The sensation is identical, spinning.

But the context, the age of the patient, and the history surrounding it completely changes the biological reality.

The history is truly the most powerful tool we have.

It is.

We treat the patient, not the spinning.

Context is king.

Well, that wraps up our deep dive into dizziness in Chapter 13.

Thank you so much for listening.

Hopefully the room has stopped spinning for you by now.

Thank you from the Last Minute Lecture Team.