Chapter 17: Schizophrenia Spectrum & Other Psychotic Disorders

Welcome back to the deep dive.

I hope you are ready because today we are tackling a massive topic.

We really are.

Yeah.

I'm looking at the stack of notes here and we have research, we have clinical guidelines, and specifically we are cracking open Chapter 17 of Essentials of Psychiatric Mental Health Nursing.

It is a heavy chapter.

I mean, in many ways, this is the chapter that defines psychiatric nursing for a lot of students.

Definitely.

We are talking about schizophrenia spectrum disorders and other psychotic disorders, and I want to set the tone right away.

I think for a lot of people, even nursing students, this topic is, well, it's intimidating.

Oh, absolutely.

It's arguably one of the most complex areas of healthcare and it is definitely one of the most misunderstood.

Misunderstood is an understatement.

It is the most stigmatized condition we treat.

Right.

When you say the word schizophrenia, people have immediate images from movies, you know, violence,

unpredictability, padded rooms, straight jackets and all that.

Exactly.

And our mission today is to dismantle that.

We need to take this dense academic chapter and break it down into a clear digestible guide for you.

We are going to look at the biology, the why, and the evidence -based care.

The how, because if you are a nurse, you need to know how to connect with a human being who is experiencing a reality that is completely different from your own.

That is the whole crux of it.

So let's start at the very beginning.

The core concept here is psychosis.

We hear that word a lot casually, like, oh, that's psychotic.

But clinically, what are we actually talking about?

We have to be precise here.

Psychosis isn't a personality trait.

It is defined as a syndrome of neurocognitive symptoms.

Meaning it's brain -based.

Right.

It involves the brain's ability to process information.

It impairs cognitive capacity.

It leads to deficits in so how you see and hear the world.

And it severely impacts functioning and social relatedness.

Essentially, it is a break from reality.

A divorce from reality.

Yes.

But the source material makes a really critical distinction right out of the gate.

Not all psychosis is schizophrenia.

Right.

And this is crucial for the nursing process.

We have to distinguish between primary and secondary psychosis.

Let's unpack that.

What's the difference?

Primary psychosis is psychiatric in origin.

That is what we are focusing on today.

Schizophrenia spectrum disorders are the prototype of primary psychosis.

The disease is the psychosis.

The wiring of the brain itself is the issue.

Yes.

And secondary.

Secondary psychosis is when that break from reality is caused by something organic or medical.

It's secondary to another problem.

Like substance use.

Exactly.

Think about substance intoxication.

If you are hallucinating because you are

or you have taken LSD, that is secondary.

Or medical issues like delirium from a high fever, a urinary tract infection in an elderly patient, or dementia.

So if I have a patient in the ICU who starts seeing spiders because their electrolytes are messed up, that is secondary psychosis.

Correct.

You treat the electrolytes and the spiders go away.

But with primary psychosis, you are treating a chronic neurodevelopmental condition.

And to make it even more complex, the text points out that they aren't mutually exclusive.

You can have a patient with schizophrenia, which is primary, who also uses substances.

Which would be secondary.

Right.

And that detentiates or worsens the symptoms.

Now, the title of the chapter isn't just schizophrenia.

It's schizophrenia spectrum disorders.

Why the shift to using the word spectrum?

This is a relatively recent shift in how we understand the pathology.

It's not a binary you have it or you don't situation.

It's a gradient.

Because schizophrenia isn't one homogenous disease.

Exactly.

You have schizophrenia, which is the prototype, the most severe in disabling.

But leading up to it on the spectrum, you have other disorders.

Like schizotypal personality disorder.

Yes, which is more about eccentric behavior and social awkwardness, but not full -blown psychosis.

You also have delusional disorder, where the person might function quite well, but has one fixed false belief.

And schizoaffective disorder.

Right.

Which is like a hybrid of schizophrenia and a mood disorder like bipolar.

They all sit on the spectrum.

But for this deep dive, we are focusing on schizophrenia.

Because if you understand that, you understand the mechanism of the entire spectrum.

Makes sense.

Let's set the stage with some numbers.

I think people might be surprised by how common this is.

The prevalence is roughly 1 % worldwide.

That's one in every 100 people.

Yeah.

If you walk into a stadium with 50 ,000 people, 500 of them fall on the spectrum.

And what is fascinating and frankly validation that this is a biological condition, is that this 1 % holds true regardless of race, culture, social status, or environment.

So it's not a Western disease or a poverty disease?

No.

Poverty can make the outcome worse, but the incidence is a human condition.

It's wired into the human genome.

And it hits young.

Yeah.

That's the part that always gets me.

It steals potential.

That's the tragedy of it.

The chapter says for men, the onset is typically between 18 and 25 years old.

Think about that age.

You're graduating, starting a career, falling in love.

For women, it's a bit later, usually 25 to 35.

Childhood onset is actually very rare.

Is there a difference in severity between men and women?

Generally, yes.

The data shows that men tend to have an earlier onset and a poorer prognosis.

They often have more structural brain abnormalities and more prominent negative symptoms.

Which we will get to in a bit.

Right.

Women tend to respond a bit better to medication and have a slightly better long -term outcome.

Which brings us to a really heavy part of the epidemiology section comorbidities.

These patients aren't just dealing with the voices or the delusions.

They're dealing with a lot of other health issues.

The statistics here are stark.

If you are a nurse, you cannot just treat the hallucination.

You have to treat the whole person.

Over 50 % of individuals with schizophrenia have a substance use disorder.

And specifically, tobacco.

Tobacco use disorder is massive.

About 50 % of this population smokes.

That is way higher than the general population.

Why is that?

Is it just stress?

There is a biological theory there.

Nicotine stimulates alpha -7 nicotinic receptors in the brain.

It actually temporarily improves some of the cognitive deficits in schizophrenia.

Like sensory gating.

Yes.

Filtering out noise.

So, in a way, they are self -medicating.

But, obviously, it destroys their physical health.

And cannabis.

The source material highlights a strong link there.

And I feel like this is something we need to clarify because there is a lot of debate about it.

The tunt is clear.

There is a strong epidemiological association between cannabis use and the risk of developing a psychotic disorder.

It implies a shared genetic vulnerability.

Exactly.

The risk factors that make a brain susceptible to schizophrenia also make that person more likely to use cannabis.

And crucially, cannabis use can trigger the onset in a vulnerable brain.

It's the second it theory.

Biology loads the gun and the environment, in this case cannabis, pulls the trigger.

But the most alarming comorbidity is suicide.

It is the leading cause of premature death in this population.

About 20 % of people with schizophrenia will attempt suicide.

And 6 to 10 % will complete it.

And here is a counterintuitive fact from the text that I really want to pause on.

The risk factors for suicide include having a higher IQ and high pre -morbid functioning.

It seems backward, doesn't it?

You'd think, oh, they're smart.

They can cope better.

But in schizophrenia,

suicide risk is often driven by insight.

Insight into what they've lost.

Exactly.

Imagine you were a high -functioning 21 -year -old.

You have a scholarship, a partner, a future.

Then the illness hits.

You lose the ability to think clearly.

You drop out.

You lose the relationship.

If you have high insight, you are painfully aware of the gap between the life you had and the life you are living now.

And that awareness drives the despair.

That is heartbreaking.

It is.

And beyond suicide, we have physical health.

Adults with schizophrenia die, on average, 3 .5 times earlier than the general population.

3 .5 times earlier?

That is a staggering loss of life years.

Yes.

And while suicide plays a part, the biggest killer is cardiovascular disease.

We see a massive prevalence of something called metabolic syndrome.

We're going to talk about this more when we get to pharmacology, but let's define metabolic syndrome right now.

It's a cluster of conditions.

Dyslipidemia, so bad cholesterol and high lipids, hypertension or high blood pressure, obesity,

specifically abdominal obesity,

and insulin resistance leading to type 2 diabetes.

And the prevalence is high in this population.

Twice that of the general population.

And unfortunately, the very medications we use to treat the psychosis, antipsychotics often drive this metabolic syndrome.

So nurses are constantly in this no -win situation where they are balancing mental stability against physical longevity.

It requires vigilant monitoring.

You can't just prescribe and walk away.

The chapter also mentions polydipsia as a risk factor.

Yes.

Compulsive water drinking or water intoxication.

It can lead to fatal hyponatremia.

It's another physical health risk nurses have to watch for on the unit.

Okay, let's pivot to the why.

The etiology.

I think for a long time, historically there was this idea that maybe it was bad parenting.

The schizophrenogenic mother.

We need to bury that idea right now.

It caused so much damage in the 20th century.

The text is explicit.

This is a no -fault biological illness.

It is a disease of the brain, just like diabetes is a disease of the pancreas.

Exactly.

It is not caused by a cold mother or bad parenting.

So if it's the brain, what is actually breaking?

It's a combination of chemistry and structure.

The classic theory is the dopamine hypothesis.

I feel like every nursing student learns that dopamine equals schizophrenia.

That's the shorthand.

But we need to nuance that.

It's not just too much dopamine everywhere.

It's about where the dopamine is.

Break down the geography for us.

The theory is that there is hyperactivity, too much dopamine in the limbic regions of the brain.

That's the emotional center.

That excess drives the positive symptoms like hallucinations and delusions.

But simultaneously, there might be hypoactivity to little dopamine in the prefrontal cortex.

Which is the CEO of the brain.

Exactly.

When the CEO is starved of dopamine, you get the cognitive issues, the lack of motivation, the poor judgment.

So it's a traffic jam in one area and a ghost town in another.

That's why treating it so hard.

If you block dopamine everywhere, you fix the voices, but might make the motivation worse.

And it's not just dopamine either, is it?

No.

Serotonin, glutamate, and GABA are all dysregulated.

It's a symphony of neurotransmitters playing out of tune.

And genetics plays a huge role.

Huge.

If you have a sibling with schizophrenia, your risk is 10%.

If you have an identical twin with it, your risk jumps to 50%.

But notice it's not 100%.

Right.

That tells us it's not purely genetic.

Environment matters.

But the source material mentions a specific gene that I found fascinating.

The C4 gene.

Yes.

This is a breakthrough finding.

The C4 gene is responsible for a process called synaptic pruning.

Synaptic pruning?

It sounds like gardening.

That's exactly the metaphor.

Think of a rose bush.

During adolescence, the brain naturally prunes back weak or redundant neural connections to make the brain more efficient.

It's a normal part of growing up.

But the hypothesis is that in schizophrenia, this C4 gene goes into overdrive.

It over prunes.

It's an aggressive gardener.

It cuts back too many connections.

Which explains the onset timing.

Exactly.

That's why we see the onset in late adolescence.

Because that is exactly when this pruning process is happening.

It creates a disconnectivity syndrome.

The brain regions stop talking to each other effectively.

That makes so much sense.

And when we look at the brain scans, the neuroanatomy, we actually see this, don't we?

We do.

We see decreased gray and white matter.

We see enlarged ventricles.

Explain the ventricles for anyone fuzzy on neuroanatomy.

Ventricles are the fluid -filled spaces in the brain.

If they're getting bigger on a scan, it's not because they are growing.

It's because the brain tissue around them is shrinking or atrophying.

Particularly in the frontal lobe, the fluid just fills the empty space.

So we have genetics, we have chemistry, we have structure.

What about the environment?

Can stress cause schizophrenia?

Stress doesn't cause it, but it precipitates it in vulnerable individuals.

It's the diathesis stress model.

You have the genetic loading and the environment is the trigger.

The chapter lists prenatal stressors too?

Yes.

Things like viral infections,

specifically influenza during pregnancy, poor nutrition, exposure to toxins, or lack of oxygen at birth.

Even paternal age plays a role.

Fathers over 45 have a higher risk of having children with schizophrenia.

So it's a perfect storm of biology and environment.

Now let's walk through the clinical picture.

What does this look like in a patient?

It doesn't just happen overnight, right?

Usually not.

It's a slow burn.

There are phases.

It starts with the prodromal phase.

This can happen a month to a year before the first psychotic break.

What are the signs?

They're subtle, mild changes.

Social withdrawal is a big one.

Deterioration and functioning.

Maybe grades drop or they stop showering as much.

The text also mentions magical thinking.

Right.

Odd beliefs, maybe getting really into obscure religious ideas.

Sleep changes.

The text emphasizes that early recognition here is key for prevention.

But it's often missed because it looks like teenage angst or depression.

Then comes the acute phase.

This is the floored phase.

Severe symptoms, hallucinations, delusions.

This is usually what brings them to the hospital or the attention of law enforcement.

Then stabilization, where symptoms decrease.

And finally maintenance, where the goal is remission or managing mild residual symptoms.

Exactly.

Now when we talk about symptoms in the acute phase, the text breaks them down into four dimensions from figure 17 .1.

This is critical for nursing students to understand because the treatment is different for each.

We have positive, negative,

cognitive, and mood.

Let's start with positive symptoms.

And we need to clarify positive doesn't mean good here.

No.

In medicine, positive means the presence of something.

These are add -on symptoms.

Things that are present that should not be there.

Like hallucinations.

Right.

Sensory perceptions with no external stimulus.

Auditory hearing voices is the most common.

But you can have visual, olfactory, gustatory, or tactile.

And within auditory, there is a specific type that is an absolute psychiatric emergency command hallucination.

This is priority number one for safety.

These are voices telling the patient to do something.

Jump out the window.

Hit that person.

If a patient has command hallucinations, the nurse needs to know immediately.

Yes.

Then we have delusions.

These are false fixed beliefs.

And the word fixed is important.

You cannot argue them away.

No amount of logic works.

None.

If you show them proof they're wrong, they will just think the proof is faked.

And there are specific types listed in table 17 .1 of the text.

Persecutory is common.

The FBI is after me.

Granter.

I am the messiah.

Ideas of reference.

The billboard has a secret message specifically for me.

And then the really sci -fi ones.

Thought broadcasting believing people can hear my thoughts.

Or thought insertion.

Where they think outside forces are putting thoughts into their head.

Or thought withdrawal.

Someone is stealing my thoughts.

It's terrifying if you think about experiencing that.

The boundaries of your own mind are dissolved.

You have no privacy in your own head.

The positive symptoms also include alterations in speech.

I love the examples the text gives here.

It perfectly illustrates the disorganized thinking.

You have associative looseness, which is shifting topics with no logical connection.

Neologisms, which is making up words.

Right.

Echolalia.

Repeating what someone else says.

Or word salad.

Just a jumble of meaningless words.

The text gives that example of word salad.

The Christmas mice spread within three round moons.

The devil will be washed away.

It's poetic, almost.

But clinically, it shows a complete breakdown of semantic structure.

Okay, so those are positive symptoms.

Add it on.

Now, negative symptoms.

These are the deficit symptoms.

Things that are taken away.

These are the A's.

And they are much harder to treat with medication and severely affect the quality of life.

Let's run through them.

Anhedonia.

The inability to feel pleasure.

Avalition.

Lack of motivation.

They can't initiate tasks.

Apathy.

Just not caring.

Elogia.

Poverty of speech.

They just don't say much.

And effective blunting.

The face is flat.

No emotion.

These are the symptoms that really impact whether someone can live independently.

It's hard to hold the job or have a relationship when you have abolition and anhedonia.

Precisely.

And often, family members mistake this for laziness.

They say, why won't he just get out of bed?

He's being difficult.

It's not laziness.

No.

It's the disease stripping away the drive system of the brain.

The nurse has to educate the family that this is a symptom, not a choice.

The third dimension is cognitive symptoms.

Impairment in memory, trouble with executive functioning, and problem solving.

But the big one here is anasognosia.

Impaired insight.

It's the inability to recognize that you are ill.

It's not denial.

Denial is a psychological defense mechanism.

Anasognosia is a neurological deficit.

The part of the brain that allows for self -reflection is literally damaged.

So they truly believe they are fine and everyone else is crazy.

This is the number one cause of medication non -adherence.

And finally, the fourth dimension, mood symptoms.

Depression, anxiety, and as we discussed, suicidality.

Right.

Now there is one specifier we need to mention from the text, catatonia.

This is extreme abnormal motor behavior.

It can be extreme agitation, but usually we think of the retardation, the slowing down.

Waxy flexibility is the classic sign.

Where you lift the patient's arm and it just stays there.

Like a statue or a wax figure for uncomfortable periods of time.

Or automatic obedience, where they move like a robot following commands.

Ecopraxia is another one, mimicking movements.

Okay, so we have the picture of the patient.

Now we are the nurse.

We're walking into the room.

How do we assess applying the nursing process here?

Assessment guideline number one, rule out medical causes first.

Don't assume it's schizophrenia just because they're hallucinating.

Check for that UTI or drug intoxication.

Exactly.

Next is the safety assessment.

We talked about command hallucinations.

You have to ask directly.

You can't beat around the bush.

Never.

You ask, are you hearing voices?

If yes, what are they saying?

Do you recognize the voice?

And crucial, do you plan to follow the command?

You also need to assess the delusions.

Are they fragmented or organized?

Right.

Because if a patient believes the CIA is poisoning their food, they might stop eating.

That's a massive safety issue too.

And medication adherence check.

Are they actually taking the meds?

Right.

And mapping these symptoms to nursing diagnoses from table 17 .4.

If they have hallucinations, the diagnosis is disturbed sensory perception.

Delusions would be disturbed thought processes.

Paranoia or command hallucinations maps to risk for violence, self or other.

And the negative symptoms map to social isolation or self -care deficit.

So let's get into the art of this chapter.

The implementation and communication guidelines.

This is where nursing students often freeze up.

A patient says, there are snakes in the corner.

What do you do?

The instinct is to use logic and say, there are no snakes.

But that invalidates their reality.

Or you might want to play along and say, oh no, I'll get a shovel.

But that reinforces the psychosis.

Exactly.

So what is the golden rule?

Validate the feeling, but not the reality.

Yes.

You say, I don't see the snakes, but it must be very frightening for you to see them.

You pivot to the emotion.

Exactly.

I don't hear the voices, but you seem very upset by what they're telling you.

You acknowledge their distress without agreeing that the hallucination is real.

And then you use distraction.

Guide them to reality -based activities.

Let's go play cards.

Let's listen to some music.

Competing auditory stimuli like headphones can actually help drown out the voices.

What about delusions?

If someone says, I am God or the FBI is here.

Do not argue.

You cannot reason a delusion away.

It is a fixed belief.

If you argue, they will just get defensive and you lose trust.

Again, focus on the underlying emotion.

If they are paranoid about the FBI, the theme is fear.

Say, it must be terrifying to feel like you are being hunted.

Cautiously, if appropriate, you can interject doubt.

I know you believe that, but I see it differently.

But mostly keep them grounded in the here and now.

Talk to us about paranoia.

That requires some specific body language, doesn't it?

It does.

The text points out that if a patient is paranoid,

direct eye contact can be perceived as challenging or aggressive.

Standing face to face can feel like an interrogation.

Oh, you sit side by side.

Look at a magazine together.

It's less threatening.

And be careful with warmth.

Wait, don't be warm.

Overly warm, touchy -feely behavior can be highly suspicious to a paranoid person.

They think, well, why is she being so nice?

What does she want?

She's trying to trick me.

You want to be, matter of fact, neutral and consistent.

And the food safety tip.

If they think they are being poisoned.

Offer sealed foods.

A banana they have to peel themselves.

A hard -boiled egg in the shell.

A sealed yogurt.

It gives them a sense of control and safety.

That is such a practical tip.

What about associative looseness, when you literally cannot understand what they were saying because it's a word salad?

Do not pretend to understand.

That's dishonest and breaks trust.

It's OK to say, I'm having trouble following you.

Look for recurring themes.

If they keep mentioning the wires and the pain, you can say, I'm not following the details, but it sounds like you are hurting.

It always comes back to the feeling.

Always.

Let's talk about treatment modalities.

Obviously, milieu therapy and inpatient stays are for acute stabilization structure, safety, stimulation control.

But what about afterwards?

Recovery happens in the community.

The test highlights PAYCT, or ACT,

Program of Assertive Community Treatment.

The hospital without walls.

Exactly.

Multi -disciplinary teams go to the patient in the community.

They handle meds, social work, daily living skills.

It's great for non -adherent patients and reduces hospital re -emissions significantly.

And family psychoeducation.

This is critical for reducing relapse.

We know that high expressed emotion in a family, constantly lots of criticism, hostility, over -involvement, triggers relapse.

Family therapy teaches the family to lower the stress level.

There's also the recovery model.

Which is a philosophy shift.

It's not just about symptom reduction.

It focuses on hope, empowerment, and living a meaningful life despite the illness.

And the RAISE project.

Recovery.

After an initial schizophrenia episode, it's an NIMH initiative for early intervention.

If we catch it at the first break and treat it comprehensively, the long -term prognosis improves dramatically.

Okay, stick with us.

We are moving into the science portion pharmacology, the antipsychotics.

This is where nursing students usually start sweating because of all the side effects.

It's dense, but we can organize it.

First, the overview.

Antipsychotics do not cure.

They manage symptoms.

If you stop them, relapse is 70 to 80 % likely.

So we have two main classes.

First generation are FGAs and second generation are SGAs.

Right.

First generation typical antipsychotics.

Examples are haloperidol, which is heldol, and chlorpromazine, which is thorazine.

These are the old guard.

How do they work?

They are dopamine D2 antagonists.

They block dopamine.

Pros and cons.

Pros, they are cheap and they are very good at crushing positive symptoms.

Cons, they have a high risk of EPS extrapyramidal side effects because they block dopamine in the motor centers of the brain.

Okay, hold that thought on EPS.

Let's compare it to second generation.

SGAs, atypical antipsychotics.

Respiradone, olanzapine, quechipine, sepracidone.

These block dopamine and serotonin.

Pros and cons for these.

Pros, they treat positive and negative symptoms and they have fewer motor side effects or EPS.

That's why they're usually the first line.

But the con is big.

The con is metabolic syndrome.

Weight gain, diabetes, high lipids.

A patient might gain 50 pounds.

That's a huge adherence issue and a severe physical health risk.

There is one special drug in the SGA category we have to cover.

Clozapine or Clozeril.

This is the last resort for resistance schizophrenia.

It works when nothing else does.

But it has a potentially fatal major risk of granulocytosis.

Which is a severe drop in white blood cells.

Right.

You basically have no immune system.

You can die from a simple infection.

So patients on Clozapine require strict blood work monitoring.

If they report a sore throat or fever, it's a red alert.

Absolute emergency.

Well, let's break down those other side effects because this is crucial for testing.

EPS extra -pure middle symptoms.

There are four main ones.

Acute dystonia.

Muscle spasms.

Usually the neck, jaw, or tongue.

It's painful and frightening.

It's an emergency.

You treat it with Iambinadryl or cogentin.

Next is ecathesia.

Internal restlessness.

The patient cannot sit still.

They pace.

It's often mistaken for agitation.

Pseudoparkinsonism.

They look like they have Parkinson's.

Shuffling gait, drooling, stiffness.

And tardive dyskinesia or TD.

This is the long -term one.

Involuntary movements of the mouth and tongue like lip smacking.

It can be permanent.

Ingretza or valbenazine is a new treatment for it.

And nurses use the AIM scale to screen for TD.

Yes, the abnormal involuntary movement scale.

Then there is the big, scary, fatal one.

NMS, neuroleptic malignant syndrome.

This is rare but deadly.

Remember the mnemonic fever.

F for fever, usually high.

E for encephalopathy, so confusion.

V for vitals unstable.

E for elevated CPK, meaning muscle breakdown.

And R for rigidity, lead pipe rigid muscles.

If you see fever plus rigidity, you stop the drug immediately.

Hydrate, cool them down.

It requires ICU -level care.

And one more toxicity to watch for anticholinergic toxicity.

Dry mucous membranes, urinary retention, constipation, blurred vision.

Can't see, can't pee, can't spit, can't...

Well, you know the rest.

Exactly.

So that's the pharmacology.

Finally, the chapter covers evaluation and self -care.

We have to evaluate.

Are the goals being met?

Is the patient safe?

Are they adherent?

But we also have to look at the nurse.

Working with psychotic patients is intense.

It can be frightening or anxiety -inducing.

The text acknowledges that nurses often develop defensive behaviors, like avoidance, because of their own anxiety.

And these behaviors can hinder care.

It's necessary to admit it.

Supervision and peer support are necessary to process those feelings.

So what does this all mean?

We've gone from the C4 gene to the streets with PASI -T teams.

It means that schizophrenia is a whole -person illness.

It affects the brain structure, the chemistry, the thoughts, the body, and the family.

And the nurse is the bridge between that fractured reality and safety.

Here's where it gets really interesting for me as a final thought.

The text mentions a fascinating cultural note.

Yes.

Anthropologists have noted that the experience of hallucinations is shaped by culture.

In the U .S., voices are often violent, harsh, command hallucinations.

But in places like India or Ghana, patients often report rich relationships with their voices.

They might be ancestors or playful spirits.

That is wild to consider.

It forces us to ask, how much of the agony of schizophrenia is biological?

And how much is shaped by a society that stigmatizes the experience?

If we treat the voices as relationships rather than torture, would the brain respond differently?

What does that say about the environment's impact on the brain?

That is certainly something to mull over on your own.

Thank you for joining us on this deep dive into Chapter 17.

To all you nursing students out there, go forth, check for command hallucinations and care with empathy.

From the Last Minute Lecture Team, a warm thank you.

Thank you for listening.