Chapter 30: Neuromuscular & Muscular Dysfunction in Children

Welcome to Last Minute Lecture.

This free chapter overview is designed to help students review and understand key concepts.

These summaries supplement not replaced the original textbook and may not be redistributed or resold.

For complete coverage, always consult the official text.

Welcome back to The Deep Dive.

Today we are opening up a massive file.

We're talking about

of Wong's Essentials of Pediatric Nursing.

The title of the chapter is The Child with Neuromuscular or Muscular Dysfunction.

It is a bit of a mouthful, isn't it?

Yeah.

But honestly, this is one of those chapters that, I mean, it really defines

pediatric nursing.

It's dense, it's complex, but it is absolutely critical.

It feels high stakes just reading the outline.

We're dealing with the brain, the spinal cord, the nerves, the muscles.

It all just sounds so intimidating.

It can be, for sure.

But if we, you know, if we strip away the medical jargon for a second, what we really talk about here is mobility.

Okay.

And for a child, mobility isn't just about getting from the bedroom to the kitchen.

It is fundamental to who they are.

Right.

It's about development.

It's how they learn.

Exactly.

Mobility is how a child explores their world.

It's how they clay, how they learn cause and effect, how they develop independence.

So if a child has a muscular disorder, that ability to move is compromised.

And that has a ripple effect.

A huge one.

It touches everything.

Their cognitive development, their social skills, their self -esteem.

So our mission for this deep dive is pretty clear.

We want to take all that complex pathophysiology, all the scary neurological terms,

like, I don't know, periventricular leukomalacia,

and translate it.

Translate it into safe, effective nursing practice.

Yeah.

We want to help you visualize the child.

That's the key.

We don't want you just memorizing a list of symptoms for an exam.

We want you to be able to picture the patient in the crib or the wheelchair and, you know, understand what you are seeing and what you need to do next.

And the scope of this chapter is huge.

I mean, we are going to cover conditions a child is born with, like cerebral palsy and spina bifida.

And then we'll get into genetic conditions that show up later, like muscular dystrophy.

And then even acquired things, injuries or infections that can happen to a, you know, perfectly healthy child.

Right.

And the common thread connecting all of these, the nurse's role in observation.

Whether it's acute or chronic, congenital or acquired,

safe care relies on you spotting the subtle signs.

A lag in a motor milestone.

A change in muscle tone when you change a diaper.

That is what we are here to sharpen.

Okay.

So let's map out our roadmap for this deep dive.

We are going to start with the congenital disorders, specifically cerebral palsy and neural tube defects.

Then we will move into the genetic and degenerative disorders, like spinal muscular atrophy and Duchenne muscular dystrophy.

And we will wrap up with the acquired conditions, Guillain -Marie,

tetanus, botulism,

and spinal cord injuries.

And along the way, we're going to stop at the key tables and diagrams mentioned in the text.

Right.

Because I know when you're reading, it's so easy to just skim over a chart, but we want to show you how those charts are actually clinical tools.

Exactly.

So let's jump in with the big one, section one.

Cerebral palsy, or CP.

CP is the most common permanent physical disability of childhood.

That's a heavy statistic to start with.

The definition in the text is interesting.

It says it's a group of permanent disorders of the development of movement and posture, causing activity limitation.

But it also says it's non -progressive.

That one seems strange.

That phrase non -progressive trips people up all the time.

It means the brain injury itself, the initial insult to the developing brain, is done.

It's static.

It doesn't get worse.

It doesn't spread like a cancer.

But the child looks different as they get older.

The condition seems to get worse.

Well, the clinical picture changes as the child grows.

That's the distinction.

Because the child gets bigger.

Exactly.

A toddler with CP has a different set of challenges than a teenager with CP.

The bones grow, the muscles get tighter, the body gets heavier.

So while the brain injury stays the same, the deformities and the functional limitations can definitely progress if we don't intervene.

Okay, that makes sense.

Now I want to address a myth immediately.

I feel like the general public, and maybe even some new nursing students, believe CP is almost always caused by a traumatic birth.

Oh, absolutely.

You know, the cord wrapped around the neck, the baby didn't get oxygen during delivery.

That is a massive misconception, and the text is very specific about correcting this.

While birth asphyxia that lack of oxygen during delivery is a cause, it's actually a relatively small percentage.

Really?

Yeah.

We now know that 70 to 80 % of CP cases are caused by unknown prenatal factors or existing prenatal brain abnormalities.

Wow.

70 to 80%.

So the damage is usually happening weeks or months before the mother even goes into labor.

Right.

We're talking about genetic factors, maternal clotting disorders, or maternal infections that affect the fetal brain development.

But there is one single risk factor that the text highlights as the most important.

And that is preterm birth.

Specifically, extremely low birth weight and very low birth weight infants, ELBW and VLBW.

If you are working in an NICU, you are looking at the population most at risk for CP.

Why is the preemie brain so vulnerable?

What's happening there?

It's about the anatomy of the developing brain.

It's just fragile.

They are prone to something called entry cerebral hemorrhage or periventricular leukomalacia.

Okay.

Let's unpack periventricular leukomalacia.

That sounds like exactly the kind of term we're trying to decode.

It does sound fancy, but break it down.

Periventricular means around the ventricles of the brain.

The fluid -filled spaces.

Right.

Leuko means white.

Malaysia means softening or death.

So it's the death of the white matter around the fluid -filled spaces in the brain.

And why is that white matter so important?

That white matter is the highway system for nerve signals.

It's the wiring.

If that highway is damaged by a bleed or a lack of blood flow, the signal from the brain can't get to the muscles properly.

That brings us right to the pathophysiology.

The book discusses this concept of an upper motor neuron lesion.

I think this is crucial for understanding why these kids look the way they do.

It is everything.

Think of the nervous system like a command chain.

The upper motor neuron is the boss in the brain.

Okay.

The lower motor neuron is the worker down in the spinal cord that actually connects to the muscle.

In CP, the brain is damaged.

But the worker, the lower motor neuron, is perfectly healthy.

So the worker is just sitting there waiting for instructions.

It's waiting.

And because it's not getting the calm down or modulation signal from the brain, it goes rogue.

The reflex arc is intact, but it's unregulated.

And the result of that is spasticity.

The muscle stays tense, contracted, and hyper -responsive.

And that leads us directly to the classifications

of spasticity.

The most common type is spastic CP.

Right.

About 70 to 80 percent of cases.

This corresponds exactly to that upper motor neuron damage we just talked about.

You see hypertonicity.

The muscles are just tight.

So if you're assessing them.

If you try to fold the arm straight, you feel that resistance.

They have poor control of posture, balance, and coordinated motion.

Then there's dysgenetic CP.

This one looks different.

Very different.

This involves the basal ganglia.

You see two main patterns.

One is also called Korea.

This involves these slow worm -like writhing movements.

It usually affects the extremities, the trunk, neck, facial muscles, and tongue.

And the other pattern.

Dystonic.

This is slow, twisting movements of the trunk or extremities.

It causes abnormal posturing, and it can be triggered by emotion or even just an attempt to move voluntarily.

That must be so frustrating.

Imagine trying to reach for a cup and your arm twists uncontrollably behind your back.

It's incredibly frustrating for the child.

And the third type is a taxic.

Think balance.

This is cerebellar damage.

These kids have a wide base gait.

They're shaky.

They have a hard time with rapid repetitive movements.

Like what?

If they reach for a toy, their hand might tremor and just overshoot the object completely.

Okay, so we have the types.

But as a nurse, you are often the one doing the initial assessment.

Box 30 .2 lists the clinical manifestations.

What are the red flags we are looking for in an infant?

The universal sign, the one you'll see across the board, is delayed gross motor development.

So they're just not hitting the milestones.

The child simply isn't rolling over, sitting up, or crawling on time.

But you have to look closer at how they move.

It's not just about the timing.

The text mentions abnormal motor performance.

Can you give us a specific example of what that looks like?

Okay.

A great one is to look for early unilateral hand preference.

A healthy baby should use both hands pretty equally.

If you see a four -month -old who only ever reaches with the right hand and keeps the left hand fisted up.

That's a problem.

That is a major red flag for hemiplegia.

That's a really actionable tip.

What about crawling?

Look for an asymmetric crawl,

or what's called the bunny hop.

In spastic deplegia, where the legs are really tight, the baby will crawl by using their arms to pull and then hopping both knees forward together.

Instead of alternating.

Right.

Instead of that normal alternating leg movement.

In muscle tone, you said spasticity.

It can start as flaccid or limp, which can be confusing.

But usually, it progresses to stiffness.

Scissoring is the classic sign.

What's that?

If you lift the infant up by the armpits, their legs stiffen, straighten, and cross over each other like a pair of scissors.

And then there's a pistata nose posturing.

That's when the back muscles are so spastic the child arches backward.

It can be really severe.

And clinically, for the parents, this is devastating.

I can't imagine.

To try to cuddle your baby and they stiffen up and arch away from you.

It must feel like rejection.

It does.

And that's a key nursing intervention right there.

Education.

You have to explain this isn't your baby rejecting you.

This is a reflex.

We have to teach them how to handle the child to break that pattern.

One more thing on assessment reflexes.

Yes.

Primitive reflexes like the moro, the startle reflex, or the tonic neck reflex.

Those should disappear by four to six months.

And if they don't.

If you see a persistent moro reflex in a 10 -month old, that is hard evidence of brain dysfunction.

It's one of the earliest signs we can spot.

Let's move to therapeutic management.

The text emphasizes that there is no cure for CP.

So the therapy is what?

Symptomatic and preventive.

Exactly.

The goal is to promote optimum potential.

We want to maximize function.

We use things like ankle foot orthoses, AFOs, those plastic braces to hold the foot in a functional position and prevent foot drop.

And for the spasticity.

I mean, it must be painful to be that tight all the time.

It is.

And it burns so many calories.

We use medications like backloaf and it's a muscle relaxant.

But oral backloaf has a lot of side effects, can make the child drowsy or confused.

So what's the alternative for severe cases?

For severe cases, we use an intrathecal backloaf pump.

This is a surgical implant, right?

Yes.

A small hockey puck sized pump is placed in the abdomen with a tiny catheter that leads to the spinal cord.

It delivers the drug directly into the spinal fluid.

So you need less of it.

A much, much smaller dose with far fewer systemic side effects.

It's a game changer for severe spasticity.

And what about Botox?

I think most people hear Botox and think of wrinkles.

In PEDS, botulinum toxin A is a functional drug.

We inject it directly into a spastic muscle, say the calf muscle.

It paralyzes that specific muscle just enough to let it relax.

And that does what?

That gives the physical therapist a window of opportunity to stretch the muscle and potentially delay or even prevent surgery.

But sometimes surgery is necessary.

The text mentions something called selective dorsal rhizotomy.

That is major neurosurgery.

They open up the spine and they actually cut the specific dorsal nerve rootlets that are sending the abnormal spastic signals to the muscles.

It disconnects the bad signal.

It disconnects the spastic signal.

It can be life -changing for walking, but it's very invasive.

Before we leave CP, let's touch on the day -to -day nursing care.

Because these kids have needs beyond just mobility.

Oh, absolutely.

Nutrition is a battleground.

Why?

Spastic muscles burn a huge amount of calories.

So you have a child with these very high caloric needs who might also have difficulties sucking or swallowing because of poor motor control.

So failure to thrive is a risk.

A huge risk.

Many of these children require gastrostomy tubes, or G -tubes, to ensure they get enough nutrition safely without aspirating.

And dental health.

That surprised me when I was reading the chapter.

It's a combination of things.

There's the difficulty with oral hygiene because of motor control, but also medication.

Many children with CP also have seizures and take finny toine or Dilantin.

And that has a side effect?

A big one.

Gum hyperplasia overgrowth of the gums.

So nurses need to be super vigilant about oral care.

And finally, just handling.

We talked about the stiff baby.

Yeah, yeah.

Nurses need to teach parents how to carry and position the child.

You never pull against the spasticity.

You use slow, gentle movements.

So what's an example?

If a child is in an extensor spasm, all arched back, sitting them up and flexing the hips can help break the spasm.

It's about working with the body, not fighting against it.

OK, let's shift gears.

Section two, neural tube defects,

specifically spina bifida.

This is a failure of the neural tube to close during the first three to four weeks of gestation.

That is incredibly early.

It is.

I mean, most women don't even know they are pregnant yet.

And that is why the text and every public health agency pushes folic acid supplementation for all women of childbearing age, not just women who are trying to conceive.

Right, because by the time you get a positive pregnancy test, the tube should be closed.

If it hasn't, the defect is already there.

Exactly.

You have to have the folic acid on board before conception.

So we have two main categories.

Spina bifida occulta and spina bifida cystica.

Occulta means hidden.

Right.

The defect is in the vertebrae.

The bone didn't fuse.

But the spinal cord and meninges are tucked inside.

You might not see anything externally.

Or you might see something small.

Or you might see a cutaneous marker on the lower back.

A little dimple, a tuft of hair, or a port wine nevus.

Usually these kids are neurologically fine.

But cystica means there is a visible sac on the back.

Yes.

Now if the sac contains only meninges and spinal fluid, it's a meningocilla.

The nerves are safe.

But if the sac contains meninges, fluid, and nerves,

that is malomeningocilla.

And that's the serious one.

That's the one where we see neurologic deficits, paralysis, sensory loss, and bowel and bladder incontinence below the level of the defect.

Let's put ourselves in the delivery room.

A baby is born with malomeningocilla.

There is a fragile, fluid -filled sac on the back.

What is the immediate number one nursing priority?

Protect the sac.

That is the prime directive.

Why?

If that sac ruptures, bacteria from the skin or from stool can get directly into the spinal canal.

And you have meningitis.

It can be fatal.

So how do we position the baby?

Prone.

Always on the belly.

Hips abducted to counteract tightness.

You cannot lay this baby on their back, period.

Even when mom holds the baby, it has to be prone.

And the care of the sac itself?

We apply a sterile, non -adherent dressing moistened with sterile normal saline.

It must stay moist.

If it dries out, it cracks.

Exactly.

If it dries out, it cracks.

You change it every two to four hours and inspect it constantly for leaks or signs of infection.

Now there is a very strong association with another neurological condition here.

Hydrocephalus.

About 80 to 90 percent of children with a myelomeningocele have something called the Chiari II malformation, which blocks the flow of spinal fluid in the brain.

So while you're focused on the back?

You must be measuring the head circumference daily.

If that head starts growing rapidly or the fontanels bulge, they are developing hydrocephalus and they likely need a shunt.

OK, let's flash forward.

The back is surgically closed.

The shunt is in.

Now we are dealing with the long term management.

The text highlights the genitourinary system as a major focus.

It's called a neurogenic bladder.

The nerves that tell the bladder to squeeze and empty just aren't working.

This causes urinary retention.

And that's dangerous.

Very.

If urine sits there, it gets infected and it can back up into the kidneys.

That's called reflux and cause permanent renal scarring.

So clean intermittent catheterization or CIC is the standard of care.

It is.

We teach parents to catheterize the child every few hours to empty the bladder completely.

And the amazing thing is children as young as six or seven can learn to do this themselves.

It gives them so much control.

And some kids might get a surgery called a Mitrofanoff procedure.

What is that?

That's where the surgeon uses the appendix to create a small channel from the bladder to the surface of the skin, usually at the belly button.

So it's like a stoma.

Exactly.

It makes catheterization much easier for a child than a wheelchair.

They don't have to transfer to a toilet.

They can just access the stoma on their belly.

It's brilliant.

There is one more critical safety alert for spina bifida that you cannot forget for exams or for practice.

Latex allergy.

This is huge, non -negotiable.

Children with spina bifida are the highest risk group for latex anaphylaxis.

Why them specifically?

Because they are exposed to latex constantly from birth capitals, gloves during surgeries, shunts.

Their immune system gets sensitized.

So the nursing environment must be completely latex safe.

Absolutely.

No rubber balloons in the hospital, no latex gloves, no rubber balls for PT.

But the really interesting part and the part that often appears on exams is the cross -reaction with certain foods.

This always fascinates me.

The proteins in latex are structurally similar to proteins in certain foods.

So these kids need to avoid bananas, avocados, kiwis, and chestnuts.

So if a child with spina bifida eats a banana and gets itchy lips.

You have to assume they are allergic to latex.

It's a major clue.

That's a crucial takeaway.

Okay, let's move to section three.

Spinal muscular atrophy or SMA.

This is a different beast altogether.

It's not a brain injury like CP and it's not a structural defect like spina bifida.

This is a genetic motor neuron disease.

So what's happening physiologically?

The anterior horn cells in the spinal cord, the motor units, are degenerating.

The signal from the spinal cord to the muscle is being lost.

It leads to progressive weakness and wasting of the skeletal muscles.

The text highlights type 1

It is.

This is the classic floppy infant.

The onset is early, usually within the first six months of life.

When you lay them down, they assume a frog leg position.

Kips weak, legs just falling open.

What else would you see?

They have a weak cry, a very weak cough, and just generalized weakness.

But the tragedy of SMA is the cognitive aspect.

Yes, their sensation and their intellect are completely normal.

These babies are alert.

They watch you.

They have these bright, expressive eyes and they engage socially, but their body is failing them.

And the prognosis.

Historically, it was fatal by age two due to respiratory failure.

But the text mentions new horizons.

We have a game changer.

The drug Neusnersen, brand name Spinraza, is an intrathecal injection again into the spine that modifies the genetic expression.

It basically stops the degeneration.

And what are the results?

We are seeing children with SMA type 1 living, sitting, and some are even standing.

It is essentially the first effective treatment for a previously fatal disease.

It's incredible.

For the nurse at the bedside, what is the priority assessment for a child with SMA?

Respiratory status.

Always.

Always.

These kids have a weak cough.

They can't clear secretions.

A simple cold can be deadly.

So what are the interventions?

Nurses need to use cough assist machines, devices that mechanically simulate a cough and monitor pulse oximetry, especially during sleep, when their breathing can slow down and become shallow.

Okay, section 4 brings us to acquired neuromuscular disorders.

These are conditions that can strike a previously healthy child.

Let's start with the yamber ray syndrome, or GBS.

GBS is an immune -mediated acute demyelination.

Let's break that down.

Basically, the immune system mistakenly attacks the myelin sheath that covers the nerves.

It usually happens about 10 days after a viral infection or a GI bug.

And the hallmark sign is very distinct.

Ascending paralysis.

It starts in the toes and feet and moves up the legs to the trunk and then the arms and even the face.

I always remember it as ground to brain.

That's the perfect way to think of it.

The symptoms move up.

And the big danger zone is when it hits the diaphragm.

Respiratory failure.

Right.

So if you have a child with GBS,

your number one nursing priority is monitoring their respiratory effort.

How do you do that?

Listen to their speech.

If they're getting breathless while talking or they can't finish a full sentence without taking a breath, they are losing their tidal volume.

They might need to be intubated.

And the treatment is IVIG and plasmapheresis.

And what about recovery?

It's usually good.

The paralysis reverses in the opposite order.

It's descending.

So the arms and face come back first, then the trunk and the legs are last.

It can take weeks or months, but most kids recover fully.

Next acquired condition.

Tetanus.

Also known as lockjaw.

This is caused by clostridium tendones spores found in soil and dust that get into a wound.

And this is the complete opposite of the floppy weakness we've been talking about.

This is rigidity.

The text mentions the sardonic smile.

Rhesus sardonicus.

The facial muscles spasm into this fixed grimace.

They have opus atnos, that severe arching of the back,

and incredibly painful muscle spasms.

What triggers the spasms?

Stimulation, anti -stimulation.

Light, noise, touch.

So the nursing care involves creating a very controlled, quiet environment.

Low lighting.

Quiet room.

Grouping your care activities so you aren't disturbing them constantly.

And of course, we prevent this with the Tdap vaccine.

So we have botulism.

Also from a clostridium bacteria, but this is botulinum.

In infants, this is often linked to ingesting honey, which can contain the spores or from environmental soil dust.

Hence the famous rule.

No honey for children under 12 months.

Strictly.

And botulism causes a descending paralysis the opposite of GBS.

But the very first sign in an infant is often constipation.

That's subtle.

Very subtle.

Then you see the generalized weakness, a weak cry, loss of head control, and that flocky appearance.

And we treat it with big view botulism, immune globulin.

Yes, it neutralizes the toxin.

But the recovery is slow because the nerve endings have to physically regenerate.

Section five covers spinal cord injury, or SCI.

In kids, motor vehicle crashes are the leading cause.

But I want to focus on a specific life -threatening complication mentioned in the chapter.

Autonomic dysreflexia.

This is a medical emergency that every nurse must know.

It occurs in patients with spinal cord injuries at level T6 or higher.

What is the mechanism?

What's happening?

Essentially, there is a noxious stimulus below the level of injury.

Usually a full bladder from a kinked catheter or constipation.

The body tries to send a pain signal up to the brain, but it hits the spinal block.

And then what?

The autonomic nervous system panics and triggers a massive unchecked sympathetic discharge.

And the symptoms are dramatic.

Skyrocketing blood pressure.

220 over 110.

A pounding headache.

Breedy cardia.

A slow heart rate.

And flushing and sweating of the face and chest above the level of injury.

So you walk into the room, your patient is flushed, complaining of a severe headache, and the BP monitor is screaming, what do you do?

First step.

Step one.

Sit them up immediately.

Elevate the head of the bed to 90 degrees.

Gravity helps lower the blood pressure.

Do not lay them flat.

Okay, step two.

Find and remove the cause is almost always the bladder.

Check the catheter for kinks.

Is the bag full?

If they don't have a catheter, you need to put one in immediately to drain the bladder.

And if the bladder empty?

Then you check the bowel for impaction.

You have to stop the stimulus to stop the sympathetic storm.

If you don't act fast, they can have a seizure or a stroke.

That is a critical sequence.

Sit up.

Check bladder, check bowel.

Okay, finally section six.

Muscular dystrophies.

We are focusing on Duchenne, muscular dystrophy or DMD.

It is the most severe and the most common form of MD.

And it is X -linked recessive.

So it almost exclusively affects boys.

And what's missing in these kids?

What's the core problem?

A protein called dystrophin.

You can think of it like the glue or the shock absorber that holds muscle cells together.

Without it, the muscle fibers just degenerate and are replaced by fat and connective tissue.

This leads to a very confusing clinical sign called pseudohypertrophy.

False enlargement.

These boys, usually diagnosed around age three to five, often have huge bulky calf muscles.

They look strong.

But if you touch the calf, it feels woody and hard.

Because it's not muscle.

It's mostly fat deposits.

The actual muscle inside is incredibly weak.

And there is a classic diagnostic maneuver, the Gower sign.

Yes, figure 30 .8 in the text.

You have to see this.

Because the leg and hip muscles are so weak, these boys cannot just stand up from the floor like you or I would.

So what do they do?

They have to get on all fours, then get into a kneeling position, and then they walk their hands up their shins, then their knees, and then their thighs to push their torso upright.

Like climbing up their own body.

Exactly.

It's iconic for Duchenne.

They also have a characteristic waddling gait and lordosis that sway back posture to try and maintain their balance.

Is there a cure for this?

No cure yet.

We use corticosteroids like prednisone to preserve muscle function for as long as possible.

It can prolong their ability to walk for maybe six months, up to two years.

Two years doesn't sound like a lot.

In the life of a child, two extra years of walking is massive for their independence and their development.

But inevitably, the weakness progresses.

Most boys lose ambulation by around age 12.

And then the focus of care shifts.

It shifts entirely to respiratory and cardiac care.

As the diaphragm and intercostal muscles weaken, they lose the ability to cough effectively.

So a simple cold is a huge threat.

A huge threat.

Respiratory infection is a leading cause of death.

We use BiPAP caesareans at night and cough assist devices aggressively.

And then later in the disease, cardiomyopathy becomes a major concern.

The nursing care here feels very different from the acute care of, say, a fracture.

It's so deeply psychosocial.

It is.

You are supporting a family through a progressive, fatal disease.

You're watching a child lose milestones they once had.

The goal becomes normalization, keeping the child in school, active and independent for as long as humanly possible.

But you're also having to navigate end -of -life discussions.

And palliative care.

It's about managing symptoms, maintaining dignity, and supporting the entire family through an unimaginable journey.

We have covered a huge amount of ground today.

I mean, from the static nature of CP to the repairable defect of spina bifida to the progressive decline of Duchenne.

If we synthesize this, the common thread is clear.

Whether the condition is fixable or fatal, the nurse's role is advocacy and maximization of function.

We look past the wheelchair.

We look past the brace.

We see the child.

We work to prevent the secondary complications, the contractures, the pressure sores, the infections, so that the child can live their life, play, and learn to be a kid.

And here's a final thought to leave you with.

We talked about SMA and that new drug Nusnersen.

We are standing on the edge of a new era in pediatric neurology.

We really are.

For decades, nursing care in this field was supportive.

It was about managing the decline.

But with the rapid advancement of genetic therapies, we are moving toward treating the root cause.

So the nurse's role will change.

How will the role of the nurse evolve when we are administering genetic cures intraphically rather than just managing symptoms?

The future of this specialty is changing incredibly fast.

It's an exciting and hopeful time to be entering the field.

Thank you for diving deep with us today.

Go check out those growth charts and the Gower sign image in your text.

It really helps lock it all in.

Thanks for listening.

This has been the Last Minute Lecture Team.

See you next time.