Approach to Acute Dizziness

Welcome back.

Dr. Rybinnik here.

I know you are dizzy with anticipation for this talk...

Dizziness.

Haha.

Get it?

Get it?

Cause it's an acute dizziness talk.

No?

Allright.

Let's talk about the management of acute dizziness.

I'll disclose that I am obviously intentionally simplifying the subject to help understanding.

We are not trying to complete a neuro-otology fellowship in one YouTube lecture.

Allright, let's go.

The objectives for this talk are to discuss the two different approaches to assessing a patient with acute dizziness.

We are talking about quality of symptoms versus timing and triggers To review the 5 anatomical structures of the coordination system important for localization Discuss useful neurological examination maneuvers in the dizzy patient Review 4 major categories of pathologies causing acute dizziness Discuss the usefulness of various diagnostic tests And conclude with a management algorithm to bring it all together

Our extraordinary story begins very simply.

It begins with a man.

He is a 50 year old ape descendant with hypertension, who is about to have a very bad day.

Raising from bed, he suddenly becomes very dizzy falling right back into bed.

The room is not spinning, but he tries to lay very still as he gets more uncomfortable with movement But the dizziness is continuous, and he can’t find comfort in any position He tried walking to the bathroom, and felt very unsteady, became nauseated and vomited twice There were no hearing changes or recent illness

He was hoping that the symptoms would improve, but after 5 hours he said “enough is enough” and finally went to the hospital.

On examination in the emergency department, he had elevated blood pressure, absent corrective saccades on head impulse test, present direction changing nystagmus, and absent skew.

If what I just said did not make any sense, don’t panic.

I will explain all of these exam maneuvers shortly.

Otherwise there were no arm or leg ataxia, or focal neurological findings, but the patient veered to the right when walking.

What is the likely localization of his lesion?

Now is the perfect time to review some anatomy.

"But look at what has been done with hearts, and kidneys" "Heart and kidneys are tinkertoys!

I'm talking about the central nervous system!"

One of the best parts of neurology is the ability to localize lesions.

Localization is reasonably precise, dependable and disease-independent.

So, whenever you are lost, at least you can always start localizing.

Imagine this patient is looking directly at you.

This drawing is a coronal cut through the inner ear.

But our interest really lies with the labyrinth, and the vestibular portion of the 8th cranial nerve.

Here is that same inner ear, but now in an axial view, with patient looking up.

And to complete all three dimensions, here is the sagittal view with the patient looking to the left.

Say you are walking and accidentally trip… How to do you avoid falling?

Well, the labyrinth constantly senses movement and acceleration data and that information is carried by the vestibular portion of the 8th cranial nerve to the vestibular nuclei in the medulla.

What part of the brain really needs that information to make corrections to your gait?

Yep, the cerebellum.

So, vestibular information travels from the vestibular nuclei (in the medulla) via inferior cerebellar peduncle past the pons to the cerebellum.

The cerebellum makes the calculations, and ultimately needs to pass them onto the frontal cortex to make the necessary course corrections.

The information from the cerebellum passes through the superior cerebellar peduncle, to the red nucleus in the midbrain, and then lateral thalamus, and eventually cortex.

And that’s how you avoid falling on your face after tripping.

Here is another way of thinking about it… a visual mnemonic of sorts Say you are testing gait in an unsteady patient.

Patient attempts to walk straight, but staggers to the right… and then to the left.

And if you plot that patient’s course, it sort of looks like a closed curly bracket.

Here are all the lesions that can cause vertigo/unsteadiness – inner ear and cranial nerve 8, vestibular nuclei, cerebellar peduncles by the pons, the cerebellum, the red nucleus, and the thalamus.

The inner ear and cranial nerve 8 are peripheral structures, and the rest are in the CNS.

Here are some distinguishing factors… The inner ear and cranial nerve 8 lesions may cause hearing loss.

Medullary lesions can cause bulbar signs like dysarthria, dysphagia, hiccups, but also crossed sensory signs – numbness of one side of the face and the opposite side of the body (by damaging the ipsilateral cranial nerve nucleus of 5 and contralateral spinothalamic tract) And let’s not forget Horner’s because of damage to descending sympathetics.

Cerebellar peduncles just like cerebellum can cause isolated truncal or limb ataxia.

But because cerebellar peduncles pass by the pons, you can see hemiparesis, facial weakness, and gaze weakness with those lesions.

Red nucleus is in the midbrain.

What else is in the midbrain?

Well, cerebral peduncles and cranial nerve 3 nucleus.

Which means weakness and complete or partial oculomotor palsy Thalamus is the switchboard of the brain, and essentially filters almost all of the inputs before they get to the cortex.

Besides, sensory thalamic nuclei are right next door to the cerebellar inputs.

So in addition hemiataxia, thalamic lesions can also cause hemianesthesia, disorientation and cognitive deficits, like “being in a fog.”

Now that we understand the vestibular system, how do we examine it?

The eye are window to the soul.

Pupils are the window to the brain.

And gaze is the window to the vestibular system.

Turning a patient’s head to one side causes a compensatory turn of the eyes to the other side.

This is called the vestibulo-ocular reflex, or dolls eyes maneuver.

This relationship between the vestibular and oculomotor system is really the basis for examining a vertiginous patient.

Let review how this is accomplished.

The head is turned to the left, and that motion is detected by the left semicircular canals.

The information then travels along the vestibular portion of the left 8th cranial nerve to the left vestibular nuclei in the medulla.

Left vestibular nucleus then activates the contralateral (right) pontine paramedian reticular formation.

You may know it as the cranial nerve 6 nucleus or the pontine horizontal gaze center.

6th nerve then activates the right lateral rectus, and causes the right eye to move out.

Then, PPRF send a signal through the left MLF to the left cranial nerve 3 nucleus.

And the left 3rd nerve then activates the left medial rectus to get the left eye medially.

And the complicated ballet is complete.

So, bottom line, oculomotor dysfunction is your best bet of detecting vestibular dysfunction.

Let’s see how to apply it at the bedside.

In addition to the general screening neurological examination, another powerful examination tool in your toolbelt is the HINTS exam.

What is the HINTS exam?

Well, I'm glad you asked.

H.I.N.T.S.

stands for: Head impulse, nystagmus, test of skew, and I also added "C" and "D."

"C" stands for coordination and gait, (assessing for appendicular and truncal ataxia) And finally, "D" is for Dix Hallpike maneuver.

Let’s take a closer look.

Here is head impulse test assessing the vestibulo-ocular reflex in a normal patient.

The patient sits in front of the examiner and focuses gaze on the examiner’s nose.

Then, the head is quickly and passively turned (about 10-20 degrees of arch) to one side, and the examiner observers the patient’s ability to keep the eyes locked on target.

You can see what happens mechanistically in this simplistic cartoon.

The left semicircular canals (mostly horizontal) activate the left vestibular nuclei, the right PPRF, and left CN3 nucleus to compensate for the head turn and keep the eyes locked on target.

Now take a look at this patient.

Can you spot the problem here?

When the patient’s head is rotated to the left, the eyes are dragged off of the target, and there is a quick catch-up saccade to get the gaze back on target.

What is going on?

The impaired vestibular portion of the 8th cranial nerve, (for example in cases of vestibular neuritis), causes a delay in a vestibular compensation and eye movement lags behind head movement, creating a need for a corrective saccade.

This would be considered a positive head impulse test to the affected (left) side.

Positive head impulse test is highly localizing to the vestibular nerve – basically a peripheral lesion.

But, remember that the cell bodies for the vestibular part of 8th nerve are in the vestibular nuclei, and whatever deficits nerve lesions cause, can theoretically also be caused by a nucleus lesion.

These are the same neurons after all.

So occasionally you can be fooled by positive head impulse.

We can’t just rely on the head impulse alone to distinguish central and peripheral lesions, and we need more tests to be sure.

Enter nystagmus – the “N” in hints.

Nystagmus is basically repetitive involuntary eye movements with a slow drift component, and a fast correction.

This lovely furry patient is my dog, Pandora.

Pandora from Greek mythology, not the music service.

Although she does sing sometimes.

To properly check for nystagmus, have your patient slowly track your finger to the extremes of gaze and then pull back about 30 degrees of arc and hold.

Watch the patient's eyes.

.

Pandora is doing what many patients would do when tracking your finger, and that is to move the head.

So you have to remind them not to do that.

Here is an example of a normal patient. There are my different types of nystagmus.

Your job is to look out for the malignant types of nystagmus – direction changing nystagmus, where eyes beat to the left when looking to the left, and beat to the right when looking to the right.

And spontaneous vertical nystagmus.

Both of direction-changing and vertical nystagmus are really worrisome, and they suggest a central lesion.

Take a look at this patient.

Is there a nystagmus?

Should we be worried?

I would say “yes” and “yes.”

There is direction-changing nystamus.

Next, test of skew.

Ask the patient to fixate on your nose, and cover one of their eyes briefly with your hand.

Then rapidly uncover the eye and quickly look to see if the eye has shifted position, and moves to re-align.

Repeat with the other eye.

In a normal patient with functioning vestibular system, removing visual fixation by covering one eye should still keep eyes in alignment.

If the eye drifts when covered, that would be suggestive of positive test of skew.,

of skew., and that is highly suggestive of a lesion in central vestibular pathways.

Let’s take a look at a video example.

Do you see the problem?

Yep, when you cover the patient's right eye, it drifts and uncovered, it re-fixates.

These findings are really subtle, and you won't find them unless you look for them.

Let’s summarize: Positive head impulse, absent central-type nystagmus (meaning direction changing or vertical), and absent skew are highly suggestive of a peripheral vestibular lesion.

The opposite, with a negative head impulse, presence of direction-change or vertical nystagmus, and presence of skew are highly suggestive of a central lesion.

By the way, all three of these results do not need to be positive to suspect a CNS lesion.

I would definitely be worried even if I saw a central-type nystagmus or skew on its own.

Since we are on the subject of a neurological exam, we should review one more test – the Dix Hallpike.

This is the gold standard for the diagnosis of one particular type of peripheral vestibulopathy – benign paroxysmal positional vertigo, and even then with a lesion specifically involving the posterior semicircular canal, which is most common.

The patient begins sitting up.

Their head is oriented 45 degrees toward the ear to be tested.

While keeping the head rotated, you then lie the patient down quickly with their head past the end of the bed and neck extended 20 degrees below the horizontal.

The head is handing off the bed.

In that position, watch the patient's eyes for delayed short-lasting nystagmus triggered by this maneuver.

Later in the talk, we will review an example of abnormal Dix Hallpike.

But meanwhile, let’s get back to our patient.

Let me remind you, he is a 50-year-old hypertensive man with acute spontaneous continuous dizziness.

On examination, he had negative head impulse test, present direction changing nystagmus, and absent skew.

Otherwise, there were no focal neurological findings or limb ataxia, but the patient veered to the right when walking.

Back to my original question, what is the likely localization of the lesion?

Let me give you a moment.

Well, negative head impulse, positive direction-changing nystagmus, and right truncal ataxia are highly suggestive of a central lesion, even though the test of skew is normal.

The fact that other than the truncal ataxia, we have no focal neurological deficits so that make makes medullary, pontine, midbrain and thalamic lesions much less likely.

We are left with the cerebellum, and maybe the cerebellar peduncles.

Speaking of the neuro exam and localization, if you patient can do this, there is nothing wrong with their vestibular system...

system...

[Philippe Petit] "By now, I am becoming aware of the people on the ground below, my audience.

And even though this is something that a wire walker should never do, I look down.

Now it’s a good time to discuss pathologies.

And every good discussion of pathology begins with understanding the chief complaint.

Our patient presented his story to the ER physician who rightfully asked, ”Well, what do you mean by dizziness?”

What do patients mean when they say they are acutely dizzy?

Well it turns out, actually they mean at least 5 things: They could be vertiginous.

Vertigo is a sensation of self-motion when no self-motion is occurring, or the false sensation that the visual surround is moving.

A patient could be lightheaded or pre-syncopal, which is a sensation of impaired spatial orientation without a false or distorted sense of motion.

unsteady (disequilibrium or imbalance essentially means the same thing).

Patients can be experiencing oscillopsia, which is the false sensation that the visual surround is moving And finally, non-specific dizziness.

Symptoms too vague to classify, and a little bit of each of the previous categories So say your patient describes his or her symptoms in the following ways: “I feel wobbly on my feet, like I am on a ship.”

“I feel like the world spinning around me” “I feel dizzy with a constant feeling of nausea and desire to vomit.”

“I feel like I am constantly being pushed when I walk.”

“I feet lightheaded and unsteady with difficulties focusing.”

Which one of these potentially implies a problem with the vestibular system?

Well, all of these!

It’s painfully clear that it's very difficult for patients with acute dizziness to pinpoint their exact chief complaint, and that’s been supported by literature.

On the flip side, doctors are even worse at understanding what their patients mean.

Say you have long list of disorders that can cause dizziness: Cerebrovascular, inner ear, inflammatory, metabolic, infectious, cardiovascular, traumatic, psychiatric or functional, primary headache disorders like vestibular migraine,

temporal lobe seizures, neurodegenerative or congenital, neoplastic...

neoplastic...

Whew! [blows air out] I'm dizzy just reading this list to you.

How do we narrow it down to something manageable – say 3 differentials per patient?

We’ve tried using the “quality of symptoms” approach to diagnosing patients with acute dizziness.

Is it vertigo?

Is it pre-syncope?

Is it disequilibrium?

But I just showed you that it doesn’t really work in the acutely dizzy patient.

Even though we still try to elicit the quality of symptoms, it’s more useful to focus on the timing and triggers Is the dizziness continuous or episodic?

Is there a clear trigger or does it happen spontaneously?

Well let’s take our gigantic list, select the disorders that cause acute dizziness and group them by timing and triggers.

Say the symptoms start spontaneously and continue without remission.

What diseases can cause that?

That’s right, a posterior circulation stroke, but also vestibular neuritis, Neuromyelitis Optica spectrum disorders, and multiple sclerosis.

What if the symptoms are continuous, but there is a clear trigger?

Drugs and poisons are a really good example.

You probably remember learning at some point that aminoglycoside antibiotics cause ototoxicity, right?

How about symptoms that come and go without any obvious trigger?

Well, vestibular migraine and Meniere’s disease fit the bill.

And finally, what if dizziness comes in short bouts and is triggered by a change in position?

You are thinking of benign paroxysmal positional vertigo or orthostasis.

Well you get the idea.

By now you have probably figured out that apart from vestibular neuritis, acute spontaneous continuous dizziness is basically synonymous with a CNS lesion and is the most concerning.

[Exclaims] Hold the phone!

Didn’t our patient have acute spontaneous continuous dizziness?!

Allright you overachievers, I know you have a pretty good idea of what this patient is suffering from.

But I’ll keep you in suspense for a moment longer while we meet some of these disorders up close.

Vast majority of strokes causing isolated dizziness are ischemic not hemorrhagic.

As I mentioned before, stroke causes acute continuous vestibulopathy.

We are typically dealing with patients over 50 years of age with vascular risk factors, such as hypertension.

Hearing is usually preserved since central auditory pathways are bilateral, and it’s nearly impossible to get unilateral hearing loss from CNS damage.

The HINTS exam will show a negative head impulse, central-type nystagmus (meaning vertical or direction-changing), and possible skew deviation.

But what’s even more telling are focal neurological findings and dysmetria or gait ataxia, especially when coordination abnormalities localize to one side.

About those focal neurological signs… You remember that in the posterior circulation, the two vertebral arteries join to form the basilar artery, which bifurcates into the two posterior cerebral arteries.

PICA is a branch of the vertebral artery, and AICA and SCA are branches of the basilar artery.

And if you look at the axial cuts of the MRI where the patient is looking up and vascular territories are conveniently color coded You might also remember that: PCAs supply the thalami, occipital lobes and large parts of the midbrain.

So PCA strokes may cause contralateral sensory loss and visual field cut, but also ipsilateral CN3 palsy and contralateral hemiparesis and ataxia.

Basilar artery supplies the base of the brain, mostly the pons and some anterior medulla to be precise.

Basilar occlusions can cause contralateral sensory (spinothalamic) and motor deficits, but also intranuclear ophthalmoplegia horizontal gaze paresis, ipsilateral 7th nerve palsy, and 5th nerve palsy.

SCAs supply the superior cerebellum, and a stroke in that territory just causes ipsilateral ataxia.

AICA mostly supplies the cerebellar peduncles and anterior cerebellum, and a stroke in that territory will be very similar to an SCA stroke, but with one exception --- unilateral hearing loss!

[Exclaims] Hold the phone!

Again!

Didn’t I just say that CNS lesions don’t cause hearing loss?

Yes I did, and they don’t.

But a small branch of AICA called labyrinthine artery supplies the 8th nerve, which is a peripheral structure.

So hearing loss comes from the stroke of the nerve.

And finally, PICA stroke causes lateral medullary syndrome (also known as Wallenberg syndrome), There you will see crossed sensory loss (I mean ipsilateral face and contralateral body numbness), ipsilateral Horner’s, along with bulbar signs like dysarthria and dysphagia.

If you need more information, please watch the Stroke talk.

Here are four different patients with acute spontaneous vertigo caused by ischemic stroke.

These are diffusion weighted imaging or DWI axial sequences of the MRI with patients looking up to the ceiling, and the patient’s left on your right.

DWI is the gold standard for diagnosing acute ischemic stroke.

These scans show hyperintensities (or areas or restricted diffusion) in the right lateral medulla, left middle cerebellar peduncle, left lateral cerebellum, and the right medial midbrain – all of the components of the vestibular system that we talked about earlier.

And to test your recall from the last slide, what are the vascular territories affected?

PICA, AICA, SCA, and PCA.

Now this one is a little confusion.

As I mentioned before, acute spontaneous continuous dizziness raises concern for a CNS lesion.

So, how is vestibular neuritis on this list?

Well, as far as pathological theories are concerned, vestibular neuritis is though to be an infectious or post-infectious process, kind of like Bell's palsy, which is a neuritis of the 7th cranial nerve.

So by all accounts, vestibular neuritis should really be classified as acute continuous dizziness TRIGGERED by infection.

But unfortunately, patients don't read medical books.

I wish they did.

It would make my job a lot easier.

[To himself] Hmm... be careful what you wish for.

Only less than half of patients with vestibular neuritis, and that is actually being generous, report a history of recent infectious trigger, like skull-based, or ear infection, or general viral illness.

Hearing is usually preserved, unless the auditory component of the 8th nerve or the cochlea itself is involved.

(Basically a labyrinthitis).

So, neuronitis involves the nerve.

Labyrinthitis involves the labyrinth and the cochlea.

And you can distinguish between the two of them by the presence of hearing loss.

On the exam, this is the prototypical disease that causes a positive head impulse.

You'll see unilateral horizontal nystagmus with or without a torsional component, but not vertical and not direction-changing.

Certainly, there shouldn't be any skew or focal neurologic deficits, because again, that would suggest CNS pathology.

Patients with vestibular neuritis are unsteady when walking.

But then so are patients with stroke and immune-mediated brainstem lesions.

But one key difference, is that vestibular neuritis patients are still able to generally walk without falling.

Finally, just like with Bell's palsy, watch out for signs of acute varicella zoster infection, like cutaneous vesicles around the ear (so-called Ramsay Hunt syndrome).

Next up – immune-mediated disorders, specifically neuromyelitis optica spectrum disorders, and multiple sclerosis Again, both of these can cause acute spontaneous continuous vestibulopathy Multiple sclerosis diagnosis requires dissemination in time/space

and neuromyelitis optica spectrum disorders can also cause optic neuritis and myelitis, which are part of their diagnostic criteria The HINTS exam has features of central vestibulopathy, likely direction-changing or vertical nystagmus and skew deviation, but the head impulse test can actually be positive.

Remember that a positive head impulse usually means damage to the 8th nerve, but occasionally damage to the cell bodies (vestibular nuclei) can produce the same result Just as with stroke, it’s the focal brainstem findings that really differentiate these disorders.

When thinking of NMO and MS damaging the brainstem, the lesions will either be bilateral periventricular (especially in the dorsal medulla right next to the 4th ventricle in the case of NMO), or small unilateral and discrete (in the case of MS).

[Puzzled tone] Hmm... Interesting.

Or at least hope it is.

Why this discrepancy?

Well, NMOSD are usually caused by antibodies against aquaporin 4 channels, and these channels are concentrated throughout the ventricular system, around the 3rd ventricle, cerebral aqueduct, 4th ventricle.

And this is where you find those lesions.

So imagine a young patient with sudden unexplained vertigo, intractable hiccups, nausea and vomiting.

– all symptoms localized to the posterior medulla, so-called the area postrema syndrome.

And here is that patient’s MRI.

You are looking at the T2 based FLAIR sequence, axial cuts through the medulla.

The patient is looking upward with the patient’s left on your right.

What’s the abnormality?

Did you just say there is bilateral hyperintensity in the dorsal medulla in the area postrema right next to the 4th ventricle?

Well, you would be right.

If you didn't say that, just look at the orange arrow, and repeat after me: "bilateral hyperintensity in the dorsal medulla in the area postrema right next to the 4th ventricle."

Yep, you got it!

This is a classic NMOSD lesion.

Here is another perfect example in a different patient.

Same cut, same sequence, just enlarged.

Now, how is this lesion different?

We are again looking at the axial FLAIR imaging, this time through the level of the pons.

The lesion is pontine, unilateral, discrete, and ovoid shaped.

Yep, that’s characteristic of MS. We have a separate talk discussing these immune-mediated disorders, but just remember to think about NMOSD and MS in patients with acute dizziness, especially when they have mild brainstem symptoms, like intranuclear ophthalmoplegia, unexplained hiccups, nausea vomiting.

Now that we've seen several examples of spontaneous continuous dizziness, let's switch gears to continuous triggered dizziness.

A common cause of continuous triggered dizziness is various drugs and poisons.

I can almost bet that if you look at the package insert for almost any drug, you'll find dizziness on the list of side-effects.

The worst offenders are: Antiepilleptics, such as levetiracetam, phenytoin Antidepressants, including SSRIs, and tricyclics Cardiovascular drugs, such as sympathetic blockers, beta blockers, diuretics, vasodilators Antiparkinsonian drugs, including levodopa Phosphodiesterase inhibitors like sildenafil

Poisons and illicit drugs like alcohol, ketamine, and PCP.

Even nicotine can cause nystagmus.

Antibiotics, including aminoglycosides Antipsychotics Narcotics And any sedative/hypnotic drugs.

Incidentally benzodiazepines are sometimes used to treat vertigo, but can cause the very symptoms they are treating.

The whole point is if you have a dizzy patient, just be aware of their medication list.

And also remember that some of these drugs, like furosemide, sildenafil and aminoglycosides can actually be ototoxic.

So now that we understand continuous dizziness, let’s talk about episodic dizziness.

And will we start with episodic dizziness triggered by positional change.

[Announcer voice] Ladies and gentlemen, may we have your attention please for this important public announcement.

All vertigo gets worse with position.

[Normal voice] Say it with me: "All vertigo gets worse with position, but only BPPV completely resolves while being still."

This is the difference between an exacerbating factor and a trigger.

Well, that’s not entirely accurate.

Vertigo in BPPV dramatically improves while not moving, but patients still complain of “not feeling right.”

Patients with BPPV will tell you that their symptoms are continuous.

They are always dizzy.

You need to specifically ask them if the vertigo nearly resolves when they stop moving.

And without motion, the symptoms actually subside quickly - we are talking in 30 seconds or less.

The symptoms with BPPV are so brief that when patients ask me if they need medication to treat their vertigo, I usually joke and say that the vertigo will be gone by the time they unwrap their pill.

HINTS exam should not be done in these patients.

Movement may trigger nystagmus, and you’ll get false positives.

This is where we need the Dix Hallpike test, and a positive test is pathognomonic for BPPV affecting the posterior semicircular canal.

Well, all that is well and good, but what does a positive Dix Hallpike look like?

Here is what happens when you take patient with BPPV, lower them down with their head turned to the affected side, and the head positioned 20 degrees below the horizontal.

After a short delay, you'll see an upward beating nystagmus with the rotational component towards the downward ear – the ear closes to the ground.

This nystagmus persists for less than a minute and then diminishes.

Dix Hallpike test is not considered positive unless you see this delayed rapidly diminishing nystagmus.

[Patient] "I'm dizzy. I'm very dizzy!"

Symptoms of vertigo and nausea don’t count.

Now, you were paying attention.

At this point you are probably wondering, “didn’t you tell us that vertical nystagmus means central lesion?”

Typically yes but I was referring to spontaneous vertical nystagmus.

Vertical nystagmus during a Dix Hallpike test is the exception because it is triggered.

Remember our general motto for this talk: [Ominous voice] Beware of the sudden spontaneous and continuous things.

Those are the symptoms and signs that are most concerning, after all.

What is happening here?

Calcium carbonate crystals are displaced usually into the posterior semicircular canal.

Because… you know… gravity.

And then we position the patient in such a way as to activate the posterior semicircular canal.

So the vestibular portion of the 8th nerve is then activated excessively.

Orthostasis is similar to BPPV in a sense that it is also triggered by sudden postural change and occurs in more often in the elderly.

But in BPPV the positional change is the rotation of the head, where in orthostasis it's actually going from lying to sitting to standing.

Orthostasis doesn’t happen when lying down or rolling over.

Using antihypertensives actually increases the risk of orthostasis, but that’s not that specific.

Many people take antihypertensives.

But the presence of autonomic dysfunction is extremely helpful.

Think of patients with diabetic neuropathy, and neurodegenerative conditions like Parkinson’s disease, multisystem atrophy and dementia with Lewy bodies.

In those diseases, autonomic system degenerates making them more susceptible to orthostasis.

The diagnostic sign here is measuring blood pressure fall from lying to standing.

Orthostatic testing is considered positive if the blood pressure falls by more than 20 mmH systolic or 10 diastolic.

So, here is what happens when we have a patient with orthostasis switch positions.

Blood pressure and heart rate remains stable when lying down.

On standing up, blood pressure suddenly drops, and there is a compensatory increase in heart rate.

The patient complains of dizziness here.

Within about 20 seconds, compensatory mechanisms kick in, blood pressure rises and the symptoms go away.

The final two examples are vestibular migraine and Meniere’s disease We’ll talk about them briefly here, especially since vestibular migraine is the most common cause of recurrent spontaneous vertigo and patients don’t always volunteer that headache history.

Otherwise, I’ll leave the causes for recurrent and chronic vertigo for another talk.

Migraine actually has many triggers, but it's also a good example of a disease that causes episodic, spontaneous vertigo.

It's actually the most common cause of recurrent spontaneous vertigo.

Before you attribute vertigo to migraine you need to: Confirm a history of migraine diagnosis.

Confirm 5 or more episodes of dizziness lasting minutes to days, with at least half of them associated with migranous features like photophobia, visual aura.

You must exclude other causes.

Migraine is a diagnosis of exclusion, which usually means having had negative brain imaging.

And before we call it vertiginous migraine our patient should not have any worrisome signs like central-type nystagmus or clear focal neurological deficits The moral of the story, if you have a patient with episodic spontaneous vertigo get a headache history And with the first ever episode of vestibular migraine, especially lasting hours,

you will need to approach this patient as if they had acute spontaneous continuous dizziness.

Meaning, treat them like an acute stroke until proven otherwise.

As I mentioned, Meniere’s disease is another cause of spontaneous episodic vertigo.

The pathology is increased endolymphatic pressure affecting the structures pictured.

Think of a person in their 3rd to 5th decade of life with recurrent episodes of hearing changes, like tinnitus or ear fullness, followed by intense vertigo.

These episodes last anywhere from half an hour to about a day, and then resolve.

Diagnosis is basically clinical here.

It requires at least two spontaneous episodes of vertigo lasting at least 20 minutes with hearing changes (like tinnitus and/or sensation of ear fullness), and confirmation of progressive sensorineural hearing loss with audiometry.

Ok, back to the case.

We have a 50-year-old man with vascular risk factors who developed sudden onset continuous spontaneous dizziness HINTS examination was concerning for CNS pathology, and we localized the lesion to the cerebellum, or the cerebellar peduncles.

Let’s consult our table of diseases Let’s isolate the continuous column.

Since our patient is suffering from spontaneous continuous dizziness with features of CNS lesion, our differential would include vertebrobasilar ischemic stroke, minor cerebellar hemorrhage or a small discrete MS lesion.

Now both hemorrhage and MS lesion are statistically less likely here.

Now, what the next best step in the management here?

Well, we have to confirm what we already suspect.

Enter diagnostic testing.

In a patient with acute dizziness: Head CT actually has a sensitivity of less than 30% - one third, and even that’s being generous.

Sure, you may pick up a small hemorrhage, but that is fairly rare.

Chances are, you will not pick up acute ischemia, or inflammatory lesions.

Obvious neurological deficits are more helpful, with a sensitivity of about two thirds.

Early MRI within the first 48 hours from symptom onset is even better, but even the MRI may miss up to 20% of lesions - one in five.

When you can do a good HINTS exam, a non-benign HINTS exam (we are talking about direction-changing nystagmus or vertical nystagmus, positive skew, negative head impulse) That's even more reliable.

So, unless your your patient has obvious neurological deficits, the HINTS exam is your best bet for detecting worrisome pathology.

And if head impulse is negative, there is positive directing-changing or vertical nystagmus positive skew, you pretty much need to do an MRI to confirm a CNS lesion.

And if it’s not immediately obvious, when working with incomplete history or unreliable HINTS exam, always assume the worst and get the MRI.

So, our patient clearly needed brain imaging.

And here it is.

Read this MRI.

I’ll give you a second...

I hope you said something like: These are axial DWI and T2 cuts through the medulla (with patient facing upward), and a sagittal T2 slice just left of midline with patient facing your left.

And hopefully, you saw the hyperintensity in the left posterior inferior cerebellum.

And hopefully, you recognized that this lesion is within the vascular territory of the posterior inferior cerebellar artery.

And hopefully, seeing the bright signal on DWI, you came to the conclusion that our patient suffered an acute left PICA stroke.

Let’s conclude with a brief discussion of treatments.

Treatments in the acute setting fall into two groups – disease-specific and symptomatic.

Orthostasis from volume depletion?

Give fluids.

Acute ischemic stroke?

Thrombolysis, blood pressure optimization, antithrombotics.

Vestibular neuritis?

The evidence for corticosteroids is shaky at best, but these can be considered in severe cases.

Just have a risk/benefit discussion with your patient.

Benign positional vertigo?

Epley maneuver.

Now, on the other hand, symptomatic treatments basically just suppress the vestibular system.

We are talking about antiemetics like ondansetron, and metoclopramide, antihistamines like meclizine, (which by the way the drug of choice in pregnant women) and benzodiazepines, which are sedating and are usually the last resort.

Let’s review the Epley maneuver for the treatment of BPPV when posterior semicircular canal is involved.

This maneuver begins very much like a Dix Hallpike test.

Turn the patient's head 45 degrees to the affected side (the side where nystagmus was seen during Dix Hallpike), and then lower the patient down making sure the head rests about 20 degrees below the horizontal.

Now hold that position for about 30 seconds.

Then turn the head 90 degrees to the opposite side, again making sure the head stays below the horizontal.

Hold that for 30 seconds.

Then without getting up, have them turn onto their side and rotate another 90 degrees so the head faces the floor.

Hold for another 30 seconds.

Then have the patient slowly sit up.

Epley maneuver is over 90% effective in patients with posterior canal BPPV.

I always love to say that it's one of the very few treatments in medicine when you can cure a person just by putting your hands on them.

Almost miraculous!

Step one, cure BPPV.

Step two, turn water into wine.

And that’s it.

Let’s summarize our approach.

Hopefully a nice and tidy algorithm will lift your spirits and put it all together.

Say you are seeing a patient with acute dizziness.

Dizziness is fairly non-specific and can be caused by a wide variety of medical issues including: myocardial infarction, pulmonary embolism, arrhythmia, hypoglycemia, sepsis.

So as neurologists we really rely on our emergency medicine colleagues to focus on the ABCs and stabilize the patient where appropriate.

They are awesome at dealing with crashing patients.

If ABCs are stable, we need to get history.

And not just any history.

Remember we are trying to figure out if the dizziness is episodic or continuous, triggered or spontaneous.

Presence of hearing loss and focal neurological deficits is helpful.

History of headaches.

(Remember migraine vertigo?)

But also vertebral artery dissection and posterior fossa hemorrhage can present with a headache, but those are generally rare.

Anxiety.

Panic attacks are a common cause of acute episodic spontaneous dizziness.

And history of vascular risk factors, because after all the most feared neurological cause of acute dizziness is a stroke.

Next, let’s do a quick screening neurological exam.

What are we looking for?

Well, brainstem signs and ataxia of the hands and feet, and trunk.

Let me pause here for a second, cause this is important.

It is possible to have a CNS lesion in the posterior fossa which presents only with truncal ataxia.

The rest of your screening neurological exam will be normal.

So as much as it pains you and the patient, dizzy patients really need a gait exam, or at least a decent attempt at one.

Now based on your exam, are there focal neurological signs concerning for a CNS lesion?

Yes?

Is the patient within 24 hours from last known at baseline?

Again yes?

Consider calling a stroke code.

No signs pointing to a CNS lesion, or the patient is beyond the 24-hour window?

Now it’s time to do some thinking.

Say that based on your history, the patient has continuous spontaneous dizziness - the most concerning kind of acute dizziness.

I'll keep repeating this until you hear this in your nightmares: [Ominous] Beware of spontaneous continuous things.

You are probably dealing with: Vascular pathologies, like vertebrobasilar stroke, or rarely posterior fossa hemorrhage Immune mediated pathologies like NMO spectrum disorders, MS, and cerebellitis.

Toxic metabolic pathologies, like electrolyte disturbances and thiamine deficiency.

And infectious pathologies, like vestibular neuritis with or without labyrinthitis Continuous triggered dizziness is usually a medication side-effect.

For the most part here, you will need to differentiate a CNS lesion from vestibular neuritis.

And it’s nice if you have a focal neurological deficit to help you, but when you are not that lucky in one third of cases.

[Fanfare] This is where the HINTS exam comes in.

Remember, positive head impulse, absent central nystagmus, and absent skew suggest a peripheral lesion (vestibular neuritis).

But unless the HINTS exam is benign, we should strongly consider admission to the hospital and MRI of the brain to work up for acute CNS lesion.

Consider adding contrast to your MRI, and performing an LP when CNS infectious/inflammatory causes are suspected.

Just make sure you do that MRI with contrast before the LP, because the LP will affect the pattern of enhancement on MRI.

Occasionally, when our initial MRI misses the lesion we actually can do MRI with thin cuts throughout the brainstem and internal acoustic meatus to better visualize vestibular system structures.

No concerning CNS findings?

Well don’t celebrate just yet.

We still have some work to do.

We are usually dealing with episodic dizziness here.

Triggered presentations like: Inner ear disorders (BPPV and Meniere’s disease) Cardiovascular issues, like orthostasis And disorders causing spontaneous episodic dizziness, like panic attacks and vestibular migraine.

The diagnostic challenge here is BPPV versus orthostasis.

This is where two things are very helpful: Getting a careful history of a positional trigger (remember that orthostatis doesn’t happen when lying down or rolling over) And checking orthostatics and Dix Hallpike testing.

On the Dix Hallpike test, just look for delayed rapidly resolving nystagmus.

It should be upward beating with the rotational component towards the ear closest to the ground.

That phrase just rolls off the tongue, doesn’t it?

"Delayed upward beating nystagmus with the rotational component towards the ground."

Say that three times fast!

These patients usually do not need any brain imaging, and treatment really depends on the underlying cause: Abortive therapy for migraines, fluids for orthostasis, Epley maneuver for BPPV.

Well, you get the idea.

Ok, consider yourselves oriented.

And go forth and diagnose patients with acute dizziness.

Until next time, thanks for listening.

[BLOOPER BEEP] Using antihypertensives increases the risk of orthostasis, but it's not that specific.

Many people take orthostasis...

[Blows air out] Oh man, making sense is hard!

[BEEP] Check out a set of vestibular nuclei on that guy.

[BEEP] Allright where were we...