Chapter 24: Nervous System

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Welcome back to The Deep Dive.

Today we are walking into what might be, I think for a lot of people, the most intimidating room in the House of Medicine.

Uh, let me guess.

The attic.

The attic, the wiring closet, the mainframe.

We are talking about chapter 24 of Bates Guide, the nervous system.

Ah, yes.

The chapter that launches a thousand panic attacks in medical students everywhere.

It really is.

It's seen as the beast of the physical exam.

It feels incredibly dense.

The anatomy is, well, it's complex.

And frankly, it just feels like a black box.

It does.

You can't see the brain working, right?

You can't palpate the spinal cord directly.

But our mission today is to, um, strip away that intimidation.

We're going to try and prove that this is actually the most logical, almost mathematical system in the entire body.

I could not agree more.

It's not a black box at all.

It's a circuit board.

If you have the wiring diagram, which is the anatomy of the exam, it just solves itself.

It's purely deductive reasoning.

And that's the goal.

We're going to follow the text Bates exactly as it's laid out from that basic wiring diagram all the way through to the bedside maneuvers you do.

But we aren't just memorizing steps.

No, that's pointless.

We are going to get at the why.

Why does the toe go up in a Babinski reflex?

You know, why do we bother testing the corneal reflex?

What does it tell us?

Exactly.

I mean, if you're just memorizing stroke the foot, look at the toe, you're a technician.

We want you to think like a diagnostician.

To get us started on that path, the text actually gives us two guiding questions.

It calls them stars of every single neurological assessment.

Before you even touch the patient, you should be trying to answer them in your head.

Right.

And question one is localization.

Where is the lesion?

That's it.

Is it in the brain cortex?

Is it deep in the brain stem?

Is it in the spinal cord?

Maybe it's a nerve root getting pinched or is it all the way out in the muscle itself?

Because just saying a patient has weakness isn't a diagnosis.

But saying they have weakness caused by a lesion at the C5 nerve root, well, that's a diagnosis.

Precisely.

And that leads right into question two, which is pathophysiology.

What is the nature of the problem?

I mean, what is it?

Is it vascular, like a stroke blocking a blood vessel?

Is it infectious, like meningitis?

Or a neoplastic, like a tumor pressing on something.

Exactly.

So if you can answer, where is it and what is it, there, you've solved the case.

The rest is just details.

Okay.

So to answer where is it, we absolutely need the map.

Let's open up part one of the chapter, anatomy and physiology.

Right off the bat, the text divides the nervous system into two massive territories.

The central nervous system, the CNS and the peripheral nervous system or the PNS.

The CNS is the headquarters, the main office.

Correct.

The CNS is just the brain and the spinal cord.

Basically, if it's encased in bone, so the skull or the vertebrae, it's CNS.

It's the command control center.

And the PNS.

That's the entire delivery network.

The peripheral nervous system is all the wiring that leaves the central command.

So the cranial nerves, the spinal nerves, all the peripheral nerves that project out to the rest of the body, to the skin, to the muscles.

Okay.

So let's zoom in on headquarters first.

The brain.

Bates gives us these great diagrams, figures 24 to one and 24 to two.

And structurally, we see this constant interplay between gray matter and white matter.

This is absolutely fundamental.

You have to get this.

Think of gray matter as the computer chips.

It's where you have these big aggregations of neuronal cell bodies.

This is where the actual processing, the thinking happens.

And it's on the surface.

It rims the entire surface of the brain.

That's the cerebral cortex.

And it also forms these important clusters deep inside the brain.

And so the white matter is the cabling connecting all those chips.

That's the perfect way to think about it.

Those are the neuronal axons and they're coated in myelin.

Myelin is a fatty substance that acts like insulation on a wire and it speeds up the signal transmission.

It's white because of all that fat.

So yes, white matter just connects the gray matter chips to each other and to the rest of the body.

So within the brain, we have the four lobes we all learn about frontal, parietal, temporal, occipital.

But deep inside buried under that cortex are some other structures the text points out as being really critical, like the basal ganglia.

The basal ganglia are these big clusters of gray matter.

So processors deep in the brain.

You can think of them as the gatekeepers of movement.

They don't start a movement, but they facilitate it.

And maybe more importantly, they inhibit unwanted movements.

So what happens when they go wrong?

Well, when the basal ganglia fail, you get diseases of movement.

The classic one is Parkinson's disease, where you lose that facilitation and inhibition.

So you get rigidity, slowness, and tremors, unwanted movements.

Then there's the thalamus.

Grand central states.

I mean, literally almost every sensory signal from your body pain, touch, vision, sound, it all stops at the thalamus before it gets relayed to the conscious brain cortex.

It is the primary sensory relay center.

And right next to it, the hypothalamus.

The thermostat.

Its whole job is to maintain homeostasis.

It's constantly monitoring and monitoring your heart rate, your blood pressure, thirst, hunger.

It's what keeps your internal environment stable while the rest of your brain is dealing with the chaos of the outside world.

Okay.

So moving down from the big cerebrum, we hit the brain stem.

Midbrain, pons, and medulla.

This is what I call the high rent district.

It's a tiny, tiny piece of real estate, but it connects the entire upper brain to the spinal cord.

All the cables have to run through here.

And that's not all.

Not at all.

It also houses the nuclei for almost all of the cranial nerves.

And the text specifically mentions a system here that's absolutely vital.

The reticular activating system.

That sounds like something out of a science fiction movie.

What is its job?

It's the on switch for your brain.

It's a diffuse network of neurons that regulates arousal and consciousness.

If a patient is comatose.

If a patient is comatose, it usually means there is a problem with one of two things.

Either both of their cerebral hemispheres are damaged or their reticular activating system is out.

You can actually lose a lot of your cortex and still stay awake.

But if you knock out the brain stem, the lights go out immediately.

Let's keep moving down.

We exit the skull and we get to the spinal cord.

Figure 24 to 4 in the book.

This is the main highway.

But here's a fact that I think it catches a lot of students off guard.

The spinal cord is not as long as the spine.

It is not.

Not even close.

The vertebral column, the bones, grows much longer than the cord itself during development.

So in a typical adult, the solid spinal cord actually ends way up at the level of L1 or L2.

So it's in the lower back but still pretty high up.

Right.

So what's in the rest of the spinal canal then?

Below L2.

Can't be empty.

No, it's filled with nerve roots.

Because the solid cord stops, all the nerves for the legs and pelvis have to dangle down from the end of the cord to at the lower levels.

They hang down in the spinal fluid like a horse's tail.

And in Latin, that's cauda equina.

And there is a massive clinical safety tip just buried in this piece of anatomy.

Oh, it's huge.

If you need to do a lumbar puncture, a spinal tap to get cerebrospinal fluid, the one thing you are terrified of is sticking that needle into the solid spinal cord.

That causes permanent devastating damage.

So where do you go?

You go where the cord isn't.

You go below L2.

Usually the spot is L3, L4, or L4, L5.

You insert the needle where the solid cord has already ended and you're just in that sack of fluid with the floating nerve roots.

The roots just get pushed out of the way by the needle.

It's so much safer.

That makes perfect sense.

Now let's talk about the traffic on this highway.

We have signals going out to the body and signals coming back in.

Let's start with the going out signals, the motor pathways.

The absolute star of the show here is the cordaha spinal tract.

It's also sometimes called the pyramidal tract.

This is the primary pathway that allows you to voluntarily move your body.

Okay, so walk me through the commute.

I'm sitting here and I decide I want to wiggle my left big toe.

What happens?

Right.

The thought starts in the motor cortex on the right side of your brain.

The right side because it controls the left body.

Exactly.

That signal, that electrical impulse, travels down through the white matter, down through the internal capsule, through the brain stem, and it reaches the medulla.

And at the medulla, something absolutely critical happens.

It's called the pyramidal deixation.

Deixation just means crossing over, right?

Yes.

It's a fancy word for crossing.

The nerve fibers from the right side of the brain cross over to run down the left side of the spinal cord and the ones from the left brain cross to the right.

This is the anatomical reason why the left brain controls the right body and vice versa.

So the signal crosses in the medulla, goes down the spinal cord on the left side, and then what?

It gets to the right level for your big toe and there it synapses.

It connects with a nerve cell in the spinal cord.

That cell is called the anterior horn cell.

And this brings us to probably the single most important concept in motor physiology.

The difference between the upper motor neuron and the lower motor neuron.

I remember this being so confusing.

UMN versus LMN.

Can you break it down for us?

I'll try.

Think of it like a company.

The upper motor neuron or UMN is the boss in the corporate office.

The office is the brain.

The lower motor neuron or LMN is the worker on the factory floor.

The LMN is the nerve that actually goes from the spinal cord out to the muscle.

Okay, so boss in the brain, worker in the field.

I can picture that.

So the boss, the UMN, sends instructions down to the worker.

It says contract this muscle, do this work.

But the boss also sends constant inhibitory signals.

It says don't work too hard, don't go crazy, stay calm.

The boss keeps a really tight leash on the entire operation.

Okay, so let's play this out.

What happens if the boss, the UMN, is killed?

Say a stroke happens in the brain.

Okay, so the boss is gone.

But the worker, the LMN, and the spinal cord is still alive.

It still has its connection to the muscle.

But now it has no boss.

It has no one telling it to chill out.

No inhibition.

So what does the worker do?

It goes rogue.

It goes absolutely rogue.

It becomes hyperactive.

The muscle tone goes way UP.

We call that spasticity.

The reflexes become hyperactive.

We call that hyperreflexia.

The muscle is tight and twitchy and over -responsive because nobody is telling it to calm down.

So spasticity and super high reflexes means you have a boss problem.

A UMN problem.

Exactly.

Now let's flip it.

What if the worker, the LMN, is killed?

Let's say you have a herniated disc that crushes the nerve root as it leaves the spine.

Well, if the worker's gone, nothing gets done at the factory.

Nothing.

The muscle gets no signal at all.

The factory completely shuts down.

The muscle goes limp and floppy.

That's flaccidity.

Over time, it wastes away from disuse.

That's atrophy.

And as that dying nerve sends out its last few sparks, you might see little twitches under the skin.

We call those fasciculations.

So flaccidity, atrophy, and weakness.

Yeah.

That sounds like a worker problem.

An LMN problem.

You've got it.

And that distinction is the very first thing you should be looking for in a patient who complains of weakness.

It splits the entire differential diagnosis in half right from the get -go.

OK, that's a huge concept.

Now, besides the main corticospinal tract, the text also mentions the basal ganglia and cerebellar systems.

Right.

And they are different.

They don't cause paralysis, but they refine movement.

We already mentioned the basal ganglia.

They help with muscle tone and automatic movements, like swinging your arms when you walk.

The cerebellum is all about coordination, balance, and equilibrium.

It's the smoothing computer.

Let's switch lanes on the highway now.

The coming -in traffic.

The sensory pathways.

Bates highlights two main roads for this.

Correct.

And just like the motor system, they travel differently, which is really useful for us.

Road number one is the spinothalamic tract.

These are generally small nerve fibers with very little myelin.

They carry pain, temperature, and crude touch.

Crude touch, as in just knowing you're being touched, but not what it is.

Exactly.

Not the fine details.

And then there's road number two.

What is?

The posterior columns.

These are the opposite.

They are large, heavily myelinated fibers.

They're the express lanes.

They carry vibration, proprioception, which is your sense of position in space,

and fine, discriminative touch.

Why does it matter so much that they take different roads up the spinal cord?

It matters because of where they cross over to the other side.

This is key.

The pain and temperature fibers, the spinothalamic tract, they cross over immediately as soon as they enter the spinal cord at whatever level.

OK, so they cross right away.

What about the others?

The vibration and position sense fibers, the posterior columns, they stay on the same side all the way up the spinal cord.

They don't cross until they get way, way up high in the medulla of the brainstem.

That seems needlessly complicated of evolution, doesn't it?

It does, but it's a gift for neurologists.

Because if you have a patient who has an injury to one half of their spinal cord, say, the left half, they will lose pain and temperature sensation on the right side of their body below the lesion.

Because those fibers crossed immediately and were coming up the injured left side.

Correct.

But they will lose vibration and position sense on the left side of their body.

Because those fibers hadn't crossed yet.

They were still on the left side where the injury is.

You got it.

That specific pattern is called Brown -Sequard syndrome.

The anatomy predicts the symptoms perfectly.

It's beautiful.

And clinically, think about diabetic neuropathy.

It can affect small fibers, causing burning pain, or large fibers, causing numbness and balance loss.

The pathways matter.

And before we leave the sensory system, we have to talk about dermatomes.

This is another part of the map.

Yes.

A dermatome is simply the band of skin that is innervated by a single spinal nerve root.

It creates a map on the surface of the body.

So the nipple line is T4.

The belly button is T10.

The thumb and index finger are mostly C6.

The knee is L4.

So if a patient comes in and says, I have this weird numbness just on my thumb and my index finger, you aren't thinking brain tumor or massive stroke.

You're thinking something's going on with the C6 nerve root.

Exactly.

It helps you localize the problem to a very specific spot.

OK, one last piece of the wiring diagram.

Spinal reflexes.

The loop.

The reflex arc is beautiful because it's a shortcut.

It doesn't even need the brain to work.

So it's totally involuntary.

Totally.

When you tap the patellar tendon with a reflex hammer, a sensory signal zips from the knee into the spinal cord.

In the cord, it synapses directly onto a motor neuron, which then zips the signal right back out to the quadriceps muscle, and you kick.

It can happen in milliseconds.

And because that whole loop is hardwired to a specific level of the spine,

testing it becomes a GPS locator for us.

That's the perfect term, a GPS locator.

If the ankle reflex is gone, the problem is at the S1 nerve root level.

If the knee reflex is gone, it's somewhere between L2 and L4.

If the biceps reflex is out, it's a C5, C6 issue.

It is incredibly precise.

OK, so we have our map.

We finally understand the basic wiring.

Now the detective walks into the room.

Let's move to part two.

The health history.

The history is everything.

This is where you really start answering those two fundamental questions, localization and pathophysiology.

You are listening for patterns in the patient's story.

The patient, more often than not, gives you the diagnosis before you even pick up the reflex hammer.

So give me an example.

What's a pattern you might hear?

Well, let's take the common complaint of weakness.

A patient just says, I'm weak.

That could mean a million things.

It could just mean they're tired.

So you have to dig deeper.

You have to ask,

is it proximal or is it distal?

Proximal meaning closer to the center of the body, like the shoulders and hips.

Exactly.

So you ask questions like, are you having trouble combing your hair?

Or do you have to use your arms to push yourself up out of a chair?

That's proximal weakness.

And proximal weakness usually suggests a problem with the muscles themselves, what we call a myopathy or a problem at the neuromuscular junction.

And distal weakness would be the hands and feet.

Right.

So you ask, can you open a jar?

Are you having trouble buttoning your shirt?

Can you use scissors?

That kind of weakness out in the extremities usually points more toward a problem with the peripheral nerves, a neuropathy.

What about sensation?

Numbness is another one of those words that's just so vague.

It is.

You have to pin it down.

First, what does it feel like?

Is it a pins and needles feeling?

The technical term is paresthesia?

Or is the sensation actually gone, like totally dead?

That's anesthesia.

And then you ask about the pattern.

Always the pattern.

The absolute classic one is the stocking love distribution.

Which means it starts in the feet and hands and moves inwards.

Exactly.

It's very common in metabolic nerve diseases like diabetic neuropathy.

The disease process depends on the length of the nerve.

The longest nerves in your body go to your feet so they get sick first.

So the toes and feet go numb.

Then as the disease progresses up the leg,

the next longest nerves, the ones to your hands, start to get affected.

It's like you're slowly pulling on a pair of stockings and then a pair of gloves.

That's a great visual.

Let's hit a few specific red flags that the text warns us about.

First up, headache.

Headache is a massive topic on its own.

But for this deep dive for the thing you absolutely cannot miss, you need to know about the thunderclap headache.

And that is?

If a patient looks you in the eye and says,

this was the single worst headache of my entire life and it hit me instantly, like someone hit me in the back of the head with a baseball bat, that is a subarachnoxoid hemorrhage until proven otherwise.

Which is a bleed in the brain.

A ruptured aneurysm bleeding into the space around the brain.

It is a 9 -leven life -threatening emergency.

Other red flags are a headache with a stiff neck and fever, which could be meningitis, or one that gets worse when you cough or bend over, which could suggest a mass lesion.

Okay, another really confusing symptom for patients is dizziness.

Oh, patients use the word dizzy for absolutely everything.

It's your job to separate it into two main buckets.

You ask them, when you say dizzy, do you feel like you are about to pass out like the lights are going to go out?

That's presyncope.

It's usually a heart or a blood pressure issue.

And the other bucket.

Or you ask, is the room spinning around you?

Or do you feel like you're spinning?

That's vertigo.

And vertigo is a true neurologic or inner ear problem.

They are completely different things.

And that leads into the difference between syncope, which is actually fainting versus a seizure.

This is a really common dilemma in the emergency room.

Someone collapses.

A crowd gathers.

By the time you get there, they're waking up.

Was it a simple faint or was it a seizure?

How can you possibly tell the difference?

The key is in the recovery.

In syncope, you faint because of a temporary drop in blood flow to the brain.

Once you hit the floor, gravity helps blood return to your brain and you wake up pretty fast.

You're usually alert and oriented within a minute or so.

And the seizure.

In a generalized seizure, you have a massive, uncontrolled electrical storm in the brain.

Afterwards, the brain is completely exhausted.

It needs to reset.

So the patient is confused.

They're groggy.

Maybe they're combative or sleepy for a long time afterwards.

That period of confusion is called the postictal state.

If there's a long postictal state, it was almost certainly a seizure.

Tongue biting and incontinence also point towards seizure.

OK, so we've gathered all the clues from the history.

Now we finally get to lay hands on the patient.

Part three, physical examination.

Bates organizes the entire neuro exam into five big buckets.

Mental status, cranial nerves, the motor system, the sensory system, and reflexes.

We should probably clarify.

We do not do every single one of these tests on every single person, every single time, do we?

Oh, God, no.

You'd be there for three hours and the patient would hate you.

The text makes a really clear and important distinction between a screening exam and a comprehensive exam.

For a young, healthy person with no neurologic complaints,

you do a quick screen.

It takes maybe five minutes.

But if you find something wrong.

But if you find a deficit,

say during the screen, you notice their left eye isn't moving correctly, then you do a deep dive.

You go back and you do a comprehensive detailed examination of that specific system.

In this case, the cranial nerves involved in eye movement.

The symptoms guide the exam.

OK, let's start with the first bucket then.

Mental status.

This is a huge topic that has its own chapter in Bates chapter nine.

But for the purpose of the general neuro exam, we're really focused on just a couple of things first.

Arousal and orientation.

First thing you do when you walk in the room.

Are they awake?

Are they alert?

And then are they oriented?

So asking them who they are, where they are and the date.

Exactly.

Oriented to person, place and time.

If they're alert and oriented times three, you can usually move on with the rest of the exam.

If not, then you have to pivot to that full formal mental status exam from the other chapter.

But you're also just observing their dress, their grooming, their mood.

And you're listening to their speech.

Is it slurred?

That's dysarthria.

Is it fluent?

But makes no sense.

That's aphasia.

All right.

On to part four.

The cranial nerves.

There are 12 pairs.

This can feel like just a long random laundry list to memorize.

It can.

And that's the wrong way to approach it.

I find it much easier to group them by function.

It makes the exam flow better for you and for the patient too.

You're not jumping all over the place.

OK, let's do it that way.

Let's start with the eyes.

That seems to cover a whole bunch of them right away.

Good idea.

So CN2 is the optic nerve.

That's all about vision.

So first, can they see?

Check their visual acuity with a pocket eye chart.

Then check their visual fields.

Have them cover one eye.

You cover yours.

And see if they can see your fingers wiggling in their peripheral vision.

And there's one more part to the CN TOEIC exam.

Yes.

The fundoscopic exam.

You have to look in the back of the eye with your ophthalmoscope.

You are looking specifically at the optic disc where the nerve enters the eye.

You're looking for papildama.

Which is what?

It's swelling of that optic disc.

It makes the edges of the disc look blurry and indistinct.

And it's a critical finding because it means there is high pressure inside the skull, which could be from a tumor or bleeding.

It's a huge red flag in someone with a headache.

OK, so that's seeing.

Then we have the nerves that actually move the eyes.

Right.

That's CN that, the oculomotor nerve.

CN ovi, the trochlear.

And CN the eye, the abducens.

You test all three of them at the same time by checking extraocular movements or EOMs.

So this is the part where you hold up your finger and have them follow it.

Exactly.

You hold up your finger, tell the patient to keep their head perfectly still, and you trace a big H pattern in the air.

This makes their eyes move in all six of the cardinal directions of gaze.

And what are we looking for while they do that?

Two main things.

First, you're looking for a palsy.

Does one eye get stuck?

Does it fail to move in one direction?

That tells you which nerve is weak.

Second, you're looking for nystagmus.

Nystagmus is that, that rhythmic jerking of the eye, right?

Right.

A little bit of fine jerking when they look all the way to the side is, OK, that's called endpoint nystagmus.

But if you see sustained rhythmic jerking, especially in the central field of gaze, that suggests a problem in the brain stem or the cerebellum.

Also, while you're looking at the eyes, you should look for ptosis, a drooping of the upper eyelid.

That's usually a sign of a CN third palsy.

What about the pupils?

Ah, the pupils are a team effort.

CN two, the optic nerve, sees the light coming in.

CN the third, the oculomotor nerve, is what actually constricts the pupil.

So you shine a light in one eye and check that it constricts briskly.

That's the direct response.

And you also look at the other eye, which should also constrict a little.

That's the consensual response.

OK, we're done with the eyes.

Let's move down to the face.

That would be CNV in seventh.

Right.

CNV is the trigeminal nerve.

It's mostly a sensory nerve for the face.

It has three branches.

So you test it by lightly touching the forehead, the cheek, and the jaw on both sides.

And you ask the patient, does this feel the same here as it does here?

But it had the motor part, too, right?

It does.

It controls the muscles of mastication chewing.

So you have the patient clench their teeth and you palpate the masseter and temporal muscles to feel them bulge and confirm they're strong.

What about the corneal reflex?

I remember learning that one.

You usually reserve that for comatose patients, or if you suspect a very specific lesion in the brain stem.

But the way it works is you take a tiny wisp of cotton and you lightly touch the edge of the cornea.

A normal response is a bilateral blink.

The sensation of the touch is carried by CNV, and the motor action of the blink is carried out by CNZ7.

Well, speaking of CNZ7, let's talk about the facial nerve.

This is the money nerve.

It controls all the muscles of facial expression.

So the first thing you do is just inspect their face for any asymmetry at rest.

Is one side drooping?

Is the nasolabial fold flattened?

Then you have them do a series of maneuvers.

Raise your eyebrows up high.

Frown.

Close your eyes as tight as you can and don't let me open them.

Show me your teeth.

Puff out your cheeks.

You're looking for weakness or asymmetry with all of these.

And this is where we absolutely need to stop and explain the classic Bell's Palsy versus Stroke distinction.

This comes up all the time on exams and in real life.

It is so critical.

Here is the rule, and it's all based on the anatomy.

The upper part of your face, your forehead, gets nerve signals from both sides of your brain.

It has a backup supply.

The lower part of your face only gets signals from the opposite side of the brain.

Okay, so let's apply that logic.

What does it look like in a patient?

Okay, if a patient has a stroke, which is a central lesion up in the brain,

the forehead is protected.

It still gets signals from the healthy side of the brain.

So the patient can raise their eyebrows and wrinkle their forehead, but the lower part of their face on the opposite side droops.

So forehead spared means it's a central problem, like a stroke.

Right.

Now contrast that with Bell's Palsy.

In Bell's Palsy, the injury is to the facial nerve itself after it has already left the brain.

It's a peripheral lesion.

It cuts off all the signals to that side of the face.

So the entire side of the face is paralyzed.

They can't wrinkle their forehead.

They can't close their eye tightly, and they can't smile on that side.

So weirdly, if the forehead is involved and the whole face is paralyzed, it's actually better news.

It's more likely to be Bell's Palsy and not a stroke in the brain.

Generally speaking, yes.

The Bell's Palsy looks much more dramatic and scary to the patient, but the underlying cause is usually peripheral and often gets better on its own.

Okay, moving on to the ears.

CNA8.

The vestibulococcal nerve.

This has two parts, hearing and balance.

But at the bedside, we mostly just test hearing.

The easiest way is the whispered voice test.

You stand behind them, have them cover one ear, and you whisper a few words.

If they can't hear the whisper, then you'd move on to using a tuning fork with the Weber and Wren tests to figure out if it's a problem with the ear canal conductive hearing loss or a problem with the nerve itself, sensorineural hearing loss.

Down into the throat.

CNIX and X.

The glossopharyngeal and vagus nerves.

We usually test these together.

First, just listen to their voice.

Is it hoarse or nasal?

Then you have them open their mouth and say,

You watch the soft palate.

Normally, it should rise up symmetrically in the midline.

And if it doesn't?

If one side is paralyzed, the strong, healthy side will pull the uvula over towards it.

So the uvula points away from the side of the lesion.

You can also test the gag reflex, but it's unpleasant and not always necessary.

Finally, let's finish up the cranial nerves with the neck and tongue.

CNXI and XII.

CNTI is the spinal accessory nerve.

This one's easy.

It controls two muscles.

You have them shrug their shoulders up against your hands to test the trapezius muscle.

Then you have them turn their head to each side against your hand to test the sternocleidomastoid muscle.

And last one, CNXII.

The hypoglossal nerve.

This one controls the tongue.

First, you have them stick their tongue straight out.

You inspect it for any atrophy or for those twitchy fasciculations, which are signs of a lower motor neuron problem.

Then you look to see if it deviates to one side.

And which way does it go?

If there's a lesion on one side, the muscles on that side of the tongue are weak.

So when they try to stick it out, the strong muscles on the healthy side overpower the weak side and push the tongue over toward the weak side.

So the tongue licks the wound.

It points directly toward the side of the lesion.

Excellent.

That's a lot, but we got through the head.

Now let's move to the rest of the body.

Part five, the motor system.

Okay, so for the motor exam, before you even start testing strength, you have to just look.

Inspection is the first step.

Look at the patient's body position.

Look for involuntary movements like tremors or tics.

Look closely at the muscles for any signs of wasting or atrophy.

Are there fasciculations?

Look at the hands.

Specifically, atrophy in the muscles between the thumb and index finger is a really subtle but important sign of nerve damage.

And after looking, we test tone.

And tone is different from strength, right?

Yes, completely different.

Tone is the residual tension that's present in a voluntarily relaxed muscle.

To test it, you have the patient relax completely and you move their arm and leg for them.

It should feel loose, but with a tiny bit of smooth, continuous resistance.

So what does abnormal tone feel like?

Well, if it's spastic from that UMN boss problem, it feels tight and resistant.

And then as you push, it might suddenly give way.

We call that clasp knife rigidity, like opening a pocket knife.

If it's rigid, like in Parkinson's, it's stiff and resistant throughout the entire range of motion, sometimes with a ratchet -like jerky feel we call cogwheeling.

And the opposite.

If it's flaccid from that LMN worker problem, it's just floppy.

Like a wet noodle, there's no resistance at all.

Okay, so after tone, we finally get to test strength.

We use that zero to five scale.

And it's important to know what the numbers mean.

Five out of five is normal power, full resistance.

Three is the critical cutoff point.

Three out of five means they can move the limb against gravity, like they can lift their arm up off the bed.

But as soon as you apply any resistance, they collapse.

And below three.

Anything below three is significant weakness.

Two out of five means they can move the limb, but not against gravity.

So they could slide their arm around on the bed, but they can't lift it up.

One is just a flicker of muscle contraction without any actual movement.

And zero is complete paralysis.

So what are the key muscle groups we need to test?

You want to test groups that represent different nerve roots and peripheral nerves.

So in the arms, shoulder abduction for C5, C6, elbow flexion and extension, wrist extension, their grip and finger abduction to test the ulnar nerve.

In the legs, hip flexion, knee flexion and extension, and then ankle dorsiflexion for L4, L5, and plantar flexion for S1.

There's one special motor test that the text really highlights.

The pronator drift.

Yes.

This is an incredibly sensitive test for a very mild weakness from a corticospinal tract lesion, like a subtle stroke.

How do you do it?

You have the patient stand or sit with both arms held straight out in front of them, palms facing up to the ceiling as if they're holding a pizza box.

And then you tell them to close their eyes.

Why do they have to close their eyes?

Because we use our vision to compensate for weakness.

When you take away that visual correction, any subtle weakness will be unmasked.

If there is a slight weakness in the corticospinal tract on one side, that arm will slowly start to drift downward.

And importantly, the palm will turn over or pronate.

That's a positive pronator drift.

It's often the very first sign of a stroke affecting the opposite hemisphere of the brain.

Okay, next up is coordination.

This is really where we're testing the cerebellum.

Exactly.

The cerebellum is the computer that coordinates and smooths out all our voluntary movements.

We test it in a few ways.

First is with rapid alternating movements or rams.

You have them slap their thigh, alternating between the palm and the back of their hand as fast as they can.

And if they can't do that well.

If they are slow, clumsy, or irregular, we call that distidochokinesis.

I just love that word.

It's a great scrabble word.

Next are point -to -point movements.

The classic one is the finger -to -nose test.

You have them touch your finger, then touch their own nose back and forth.

You're looking to see if they consistently overshoot the target, that's dysmatria, or if a tremor develops as they get closer to the target.

That's an intention tremor.

Both are signs of cerebellar disease.

And then of course you have to watch them walk.

The gate.

Watching a patient walk is probably the highest yield single minute of the entire neurologic exam.

You watch their casual walk, then you have them walk heel -to -toe, like on a tightrope, which is called tandem walking.

You have them walk on their toes and on their heels.

And you're looking for specific abnormalities.

Yes.

You're looking for ataxia, which is that wide -based, staggering, almost drunk -like walk.

That's a classic cerebellar sign.

Or you might see the stepage date, where they have to lift their knee really high because they're foot is drooping, a foot drop.

Or the hemiplegic gait after a stroke, where one leg is stiff and spastic and they have to swing it out in a circle to walk.

Now this is a perfect time to clear up a massive misconception that so many students have.

Let's talk about the Romberg test.

Yes.

Please ask any medical student what the Romberg test is for, and I swear 90 % of them will say it tests the cerebellum and they are completely wrong.

But what does it actually test?

It tests position sense, proprioception.

It is a test of the posterior columns, not the cerebellum.

Okay.

Explain the logic behind that.

Why isn't it a cerebellum test?

Okay.

So your ability to maintain balance relies on a three -legged stool of sensory inputs to your brain.

Leg one is vision.

Leg two is your vestibular sense from your inner ear.

And leg three is proprioception, your ability to feel where your feet and joints are in space.

To stand up straight, you need at least two out of those three legs to be working.

Okay.

Two out of three.

Makes sense.

In the Romberg test, you ask the patient to stand with their feet together and then close their eyes.

By having them close their eyes, you have just removed the vision leg of the stool.

Now they're balancing with only their inner ear and their proprioception.

So if their proprioception is also gone?

If their proprioception is also gone, which can happen in things like severe diabetic neuropathy or B12 deficiency,

they now only have one leg of the stool left, and they can't balance on one leg.

They start to sway and fall over.

So positive Romberg tests falling over when you close your eyes is a sign of a sensory problem, not a coordination problem.

Exactly.

A patient with a cerebellar problem is wobbly and unstable, even with their eyes open.

Their coordinating computer is broken, so it doesn't matter how good the input is.

That is a really crucial distinction.

Okay.

Part six, the sensory system.

Bates gives a warning here about the fatigue factor.

Yes.

Sensory testing is subjective and can be really boring for the patient.

If you poke and prod a patient for 20 minutes straight, they're going to stop paying attention and your results will be useless.

You have to be efficient.

So what's the strategy for being efficient?

A few things.

Always compare symmetric areas.

Test the right arm, then immediately test the same spot on the left arm, and go distal to proximal.

Start at the fingers and toes.

If the sensation is perfectly normal there, it's very likely to be normal further up the limb because the longest nerves are the most vulnerable.

And we have to check the different modalities that travel in those different pathways we talked about?

Right.

So you check pain and temperature, which travel in the spinothalamic tract.

For pain, you can use a broken cotton swab to get a sharp end and a dull end.

For temperature, you can use test tubes with hot and cold water, but that's usually only done if pain sensation is abnormal.

And what about the other pathway?

For the posterior columns, you test vibration.

You use a 128 hertz tuning fork and you place it on the big toe joint or the finger joint.

Vibration sense is often the very first sensation to be lost in a peripheral neuropathy, so this is a really important screening test.

And also proprioception or position sense.

Yes.

You grab the patient's big toe and it's important that you hold it by the sides, not the top and bottom.

If you push on the top, they can feel the pressure and just guess the direction.

So you hold it by the sides and you move it upward down a tiny amount and ask them, which way did I move it?

Then the book gets into the fancy cortical tests, the discriminative sensations like stereognosis.

Right.

So for these tests to work, the patient has to have normal primary sensation first.

For stereognosis, you put a familiar object like a key or a coin in their hand while their eyes are closed and you ask them to identify it just by feel.

If they can feel that there's an object there, but they have no idea what it is, that's called a stereognosis.

And it points to a lesion in the parietal lobe of the brain.

The brain can't process the sensory data.

And graphesthesia.

That's a good alternative.

The patient can't move their hand to feel an object.

You use a blunt object like the back of a pen to draw a number on their palm.

They should be able to identify it.

And lastly, extinction.

This is a really interesting one.

You touch the patient on both arms at the exact same time.

Now, a patient with a parietal lobe lesion might feel a touch on their left arm if you do it alone, and they'll feel a touch on their right arm if you do it alone.

But if you touch both sides together, they will extinguish or completely ignore the sensation on the side opposite to the brain lesion.

Their brain just can't handle the dual input and prioritizes the healthy side.

Okay.

Onto our last major section of the exam, part seven, reflexes.

We use that zero to four plus scale for grading.

Yes.

And it's important to remember that two plus is considered normal.

Zero is absent.

One plus is diminished.

Three plus is brisker than average.

And four plus is very hyperactive, and it's usually associated with clonus.

Can you describe what clonus looks like?

Clonus is a series of rhythmic involuntary muscle contractions.

The easiest place to test for it is the ankle.

You support the patient's leg, and you sharply push their foot up into dorsiflexion.

If clonus is present, their foot will start beating rhythmically against your hand, like a tremolo.

It's a very dramatic sign of severe UMN disease, a total loss of that boss's inhibition.

And the main deep tendon reflexes we check are the biceps, C5, C6, the triceps, C6, C7, the brachioradialis, C5, C6, the patellar or knee jerk, L2, L4, and the Achilles or ankle jerk, S1.

But the most famous or maybe infamous reflex of all is the plantar response, also known as the Babinski sign.

This is really evolutionary biology in action at the bedside.

You take a semi -sharp object, like a key or the end of your reflex hammer, and you stroke the lateral aspect of the sole of the foot from the heel up and curving across the ball of the foot.

What should happen in a healthy adult?

In an adult with a mature nervous system, the toes should curl down into flexion.

That's the normal physiological response.

We call that a down -going toe or a negative Babinski.

And if it's positive,

the Babinski sign?

If it's positive, the big toe goes UP into dorsiflexion, and the other toes often fan out.

Why on earth does that happen?

It's fascinating.

That up -going toe response is actually the default primitive setting.

Babies do it.

It's a normal reflex in infants.

But as our brain matures,

the corticospinal tract, our UMN system, sends down a constant signal to suppress that primitive reflex.

If you damage the corticospinal tract anywhere along its path, from the brain to the spinal cord, that suppression is lost.

The primitive reflex returns.

The toe goes up.

So an up -going toe in an adult is a hard sign that the connection from the brain is broken somewhere.

Exactly.

It is a definitive sign of CNS pathology.

Okay.

We are coming into the final stretch here.

Part 8 in the chapter covers special situations, specifically the comatose patient.

This is a huge shift.

The game completely changes.

Now you're dealing with a patient who can't cooperate.

You can't ask them to squeeze my fingers or tell me what you feel.

You have to rely entirely on your powers of observation and on testing brain stem reflexes.

And what's the first priority?

Always, always, always the ABCs.

Airway, breathing, circulation.

You don't worry about their knee reflex if they aren't breathing.

Also, a key don't.

Don't flex the neck until you are absolutely certain there isn't a cervical sprain fracture.

And how do we describe their level of arousal?

We use a gradient of terms.

Alert is awake and interactive.

Lethargic is drowsy, but they'll answer questions when you speak to them.

Obtended means you have to shake them to get a response.

Stuporous means they only respond to a painful stimulus.

And coma means they are completely unresponsive to everything.

Since they can't move on command, we have to check their brain stem reflexes to see if the basic machinery is still working.

Right.

So we check their pupils.

Are they tiny?

Are they fixed and dilated?

That gives us clues.

And we check the doll's eyes maneuver or the oculocephalic reflex.

What is that maneuver?

In a patient where you've cleared the cervical spine, you hold their eyelids open and you turn their head from side to side.

Normally, their eyes should move in the opposite direction of the head turn to stay looking forward, just like a doll's eyes.

If the eyes stay frozen in the head and move with the head as you turn it, that means the brain stem reflex connecting the eyes and neck is gone.

That's a very bad sign.

And posture.

We can't ask them to move, but we can see how they respond to pain.

Exactly.

You apply a painful stimulus, like a sternal rub.

If they respond by flexing their arms in tightly toward their chest with their hands and fists, that's called decorticate posturing.

It implies the lesion is high up in the brain above the brainstem.

If they respond by extending their arms out straight by their sides with their wrists flexed and palms down, that's decerebrate posturing.

That's generally worse.

It implies the lesion is lower down in the brainstem itself.

Okay.

The final part of the chapter, part nine, is about documentation and health promotion.

This is so important.

Your documentation needs to be clear, concise, and precise.

Please, don't just write neuro exam normal.

That means absolutely nothing to the next person reading your note.

So what should a normal note look like?

It should be a summary of your findings.

Mental status alert and oriented by three,

CNII -12 intact, motor strength 55 and symmetric throughout, reflexes two plus and symmetric, gait steady with no ataxia.

That paints a picture.

And if the exam is abnormal?

Then you describe the pattern you found.

Right -sided facial droops bearing the forehead, 45 strength in the right arm with positive pronator drift, right -sided hyperreflexia three plus says,

right Babinski sign is up going.

Anyone reading that note knows exactly where the lesion is.

Left side of the brain, a UMN pattern.

Exactly.

Your note should tell the story and point to the localization.

And finally, the so what for the patient, the health promotion piece.

It all comes back to prevention.

We are looking for these subtle deficits to try and prevent the big catastrophic event.

It's about aggressively controlling blood pressure and cholesterol to prevent stroke.

It's about regularly checking the sensation in the feet of patients with diabetes to prevent ulcers and amputation.

And it's about teaching everyone in the community the fast acronym for recognizing a stroke.

Face drooping, arm weakness, speech difficulty,

time to call 911.

Time is brain.

The faster they get to the hospital, the more brain function we can potentially save.

Wow.

We have covered a massive amount of ground today.

We've gone from the basic chips and cables of the anatomy through the detective work of taking a good history all the way to the specific hands -on maneuvers of the physical exam.

It's a lot, I know.

But always, always remember the mission.

You aren't just learning a series of magic tricks.

You are learning how to trace the wires in the circuit board.

Localization and pathophysiology.

If you keep those two questions at the front of your mind, the beast of the neuro exam becomes, well, maybe not a pussycat, but at least a manageable puzzle.

A very complex but logical pussycat.

Fair enough.

A very logical one.

Thank you so much for guiding us through the nervous system today.

This has been another deep dive from the last minute lecture team.

It was my pleasure.

Keep those reflex hammers handy, everyone.

We'll see you on the next one.

Take care.