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Welcome back to the Deep Dive.
Today we're really getting into some core concepts from child and adolescent psychiatry.
We're pulling directly from the textbook to tackle two areas that can be complex, attachment disorders and movement disorders.
That's right.
Our goal is to give you the key insights, the stuff that really matters for understanding these conditions, especially focusing on what the latest research, like what's in the DSM -5, tells us.
We want to make it clear, break down the diagnostic criteria, the theories behind them without, you know, overwhelming you.
Think of it as the essentials for anyone studying this or just curious.
And we're focusing on two main pillars.
First up, those attachment disorders that arise from really severe neglect,
reactive attachment disorder, RAD, and disinhibited social engagement disorder, DSED.
We'll highlight a crucial difference in how they respond to better care.
Okay.
Then we'll pivot to stereotypic movement disorders, SMD.
These are those repetitive movements and the causes are surprisingly varied.
Great.
So let's start with pillar one, attachment.
You can't really grasp the disorders without understanding normal attachment first.
John Mulby really laid the groundwork here.
He absolutely did.
Yeah.
Mulby defined attachment as this fundamental bio -behavioral system.
It's not just about feeling close.
It's about survival.
Uh -huh.
It's this constant balancing act.
You know, the child needs safety.
He needs to stay close to their caregiver, but they also have this drive to explore, to learn about the world, gain mastery.
And feeling secure with that caregiver is what makes the exploration possible.
Exactly.
Seeking proximity leads to that internal feeling of security.
That's the engine driving it.
And this isn't new thinking, is it?
I mean, researchers were noticing related things quite a while ago.
Oh, definitely.
You had people like Renee Spitz back in the 1940s talking about anaclitic depression in infants who lost their primary caregiver.
Serious emotional and physical decline.
It was an early glimpse.
And later research, like Barbara Tizard's work with kids and institutions, started to pinpoint these different patterns of behavior we now categorize more formally.
Right.
But it's super important to distinguish between general attachment patterns and actual disorders.
The famous strange situation procedure helps identify patterns like secure, avoidant, resistant, disorganized.
Okay.
These are really useful clinically.
They tell us about risk or resilience, but they are not diagnoses themselves.
They're only two specific DSM -5 diagnoses we're focusing on here.
And that brings us to the big shift in DSM -5.
This was heavily influenced by some major studies, right?
The English -Romanian Adoption Study, ERA, and the Bucharest Early Intervention Project, BEIP.
Precisely.
Those studies were game changers.
They provided strong evidence to split what used to be subtypes under one umbrella into two distinct disorders.
Which are now under trauma and stress -related disorders.
Correct.
And those two are reactive attachment disorder, RAD.
And disinhibited social engagement disorder, DSED.
Okay, let's nail down the core features.
RID first.
That's the withdrawn one.
Exactly.
RAD is marked by an emotionally withdrawn, inhibited pattern towards caregivers.
You see minimal social and emotional responsiveness to others, limited positive affect.
And they don't seek comfort.
They rarely or minimally seek comfort when distressed.
And they respond minimally to comfort when it's offered.
It's like they've learned not to expect emotional support from adults.
Okay.
And DSED.
That's the flip side.
Completely.
DSED is about being indiscriminately social or disinhibited.
The key feature is behavior involving approaching and interacting with unfamiliar adults.
So none of that typical shyness around strangers.
None.
Stranger weariness usually pops up around seven to nine months.
These kids lack it.
They'll be overly familiar verbally or physically.
Maybe reduced hesitation about going off with someone they don't know.
They don't check back with their caregiver.
All right.
Now, this is maybe the most critical piece, the part that often surprises people.
Both RBRED and DSED require that history of severe neglect or insufficient care.
That's a prerequisite.
Yes.
Things like social neglect, repeated changes of primary caregivers, or growing up in institutions where forming selective attachments is hard.
And the child has to be developmentally at least nine months old with symptoms starting before age five.
But here's the kicker.
What happens when these kids do get into a stable, caring environment?
The BEAP and ERA studies found very different paths for RAD and DSED.
This is crucial.
For IRISE, the symptoms often decrease significantly, sometimes quite rapidly, once the child is in an adequate caregiving setting.
Really.
So if the core issue is the lack of attachment, providing the chance to attach often fixes it.
In many cases, yes.
The inhibited behaviors tied to not having a secure attachment figure tend to resolve as that forms.
But DSED is different.
It often is, yes.
For a notable minority of children with DSED, those indiscriminate social behaviors, that lack of boundaries,
persist even after they've formed a secure attachment with their new caregivers.
Wait.
So they are attached, they feel secure with their new family, but they still run up to strangers.
Exactly.
And that persistence really changes how we think about the underlying problem in DSED.
If the child is securely attached now, the ongoing disinhibition likely isn't just about attachment failure anymore.
So what is it then?
It points towards something more fundamental, possibly a deficit in social boundary development, or maybe inhibitory control systems in the brain.
Is there any biological evidence for that?
There's emerging neurobiology research.
Some studies suggest early deprivation can lead to differences in brain activity, like less mature EEG patterns, or even structural changes like reduced gray and white matter.
And specifically for DSED, some fMRI research has shown that kids with persistent DSED behaviors had reduced ability in the amygdala, the brain's threat detector, to tell the difference between their mother and the stranger.
Wow.
So the brain's warning system for social danger isn't working properly.
That seems to be part of the picture, yes.
If your amygdala doesn't flag stranger as different or potentially risky compared to caregiver,
that natural caution just isn't there.
That's fascinating and really underscores why DSED might persist.
What about treatment then?
Obviously safety first.
Absolutely.
First priority is always ensuring the child's safety and meeting basic needs.
Then the goal is establishing that primary attachment figure, a stable, sensitive, responsive caregiver.
For RED, you said placement often leads to resolution.
Often, yes.
Supportive placement is key.
For DSED, because those boundary issues can persist, there's a clinical suggestion, though not heavily researched yet, that caregivers might need to actively manage the child's interactions.
Like limiting contact with unfamiliar adults for a while?
Sort of, yeah.
The idea is to help consolidate the attachment to the primary caregivers by reducing those opportunities for indiscriminate interaction for a period, maybe a few months.
Dyadic therapies like circle of security or attachment and bio -behavioral catch -up, ABC, are also used to help the caregiver -child relationship.
Makes sense.
Okay, let's use that neurobiology link, the idea of brain systems being affected, to transition to our second pillar.
Stereotypic movement disorders, or SMD, were shifting from attachment systems to motor systems.
It's a good bridge.
SMDs involve repetitive, rhythmic movements that look purposeful, but don't actually achieve anything functional.
Think hand waving, body rocking, head banging, even complex things like nail biting.
And just to be clear, we're talking about these movements as described in DSM5TR, not when they're better explained as a core part of something else, like autism.
Unless they're severe enough to cause self -injury or really interfere with life, then they might warrant a separate SMD diagnosis even alongside autism or another neurodevelopmental condition.
Got it.
Where does our understanding of these come from?
Well, they've been observed for ages, but a key idea came from Reginald Lorry around 1949.
He suggested that many of these rhythmic movements start as normal precursors to more complex motor skills, like an infant might rock before they crawl, but they become stereotyped or pathological if they hang around way too long, past the typical developmental window.
Or if they're particularly intense, you see them often in kids with intellectual disabilities, for example.
So the causes, the etiology, it seems pretty multi -layered.
Very much so.
You've got developmental factors.
Basically, the movement just didn't fade out like it should have.
You see this persistence in conditions like Down syndrome.
Then there are behavioral factors, like reinforcement.
Right.
The behavior might continue because it gets positively reinforced, maybe it feels good, or it gets attention, or negatively reinforced, meaning it helps the person avoid something unpleasant, like it's distracting or self -soothing.
And that ties into psychodynamic ideas too, like self -soothing, thumb sucking, nail biting.
Exactly.
But then you get into the more organic theories focusing on brain chemistry.
One prominent idea involves endogenous opioids, the body's natural pain relievers, and pleasure chemicals.
The stereotypic movement might trigger their release, reinforcing the behavior.
Is that why they've tried opioid blockers like Naltrexone?
That's the rationale, yes, though the results have been pretty inconsistent.
Another major biological pathway involves dopamine.
Dopamine supersensitivity seems to play a role, especially in severe cases or specific syndromes like Lush -Nihan, which involves severe self -injury.
You also see stereotypies, sometimes induced by stimulant medications, which act on dopamine.
It's useful to remember how common these are initially.
You said up to 80 % of typically developing kids show some rhythmic behaviors.
Yeah, things like body rocking or head banging in infancy or toddlerhood are quite common, but they usually disappear by age four.
If they stick around or are severe, that's when it becomes a clinical concern.
And the prevalence goes way up with intellectual disability.
Dramatically.
Maybe 20 % of individuals with severe ID have significant stereotypies, and things like head banging occur in maybe 3 % to 15 % of young children generally.
And some specific examples, bruxism, nail biting.
Right, bruxism teeth grinding happens in over half of infants, usually transiently, but it can cause major dental problems if it persists into adulthood.
And nail biting on acophagia affects maybe 50 % of kids at some point.
Interestingly, there seems to be a strong genetic link there.
Much higher rates in identical twins compared to fraternal twins.
So how does DSM -5 define SMD for diagnosis?
The movement has to be repetitive, seemingly driven, and non -functional.
Crucially, it must interfere with social, academic, or other activities, or result in self -injurious behavior, SIB, that needs treatment.
And there are severity levels?
Yes, mild, moderate, or severe.
The severity is judged by the degree of interference or the risk of harm.
They provide a case example of Ruth, a middle -aged woman whose head scratching, a stereotypic movement, was so severe she actually wore through her scalp and skull, exposing the brain's outer lining, the dura mater.
That's clearly severe.
Wow, that's intense.
Okay, so how do you tell SMD apart from similar things, like dipetics or OCD compulsions?
It can be tricky.
Ticks are usually less rhythmic, more sudden, brief, and often feel involuntary, though people can often suppress them for a bit.
Think blinking or throat clearing.
And compulsions.
Compulsions, which we see in OCD, are usually more complex and ritualistic.
And critically, they're driven by an urge to reduce anxiety or prevent a feared outcome.
There's a specific mental goal.
Stereotypes are generally simpler, more rhythmic, and while they might be self -ceiving, they lack that specific, if I do this, then this bad thing won't happen, quality of a compulsion.
Got it.
The SM5 also asks you to specify if the SMD is associated with a known medical or genetic condition or a neurodevelopmental disorder, right?
Yes, or if it involves self -injurious behavior.
And if the SIB is present or the stereotype is bad enough to be a main focus of treatment alongside something like autism, you give both diagnoses.
Okay, let's talk treatment.
Safety first, especially with SIB.
What comes next?
Behavior therapy is really the cornerstone.
You start with trying to understand the function of the behavior, what triggers it, what reinforces it, then you use techniques based on positive reinforcement.
Like DRO and DRI.
Exactly.
DRO is differential reinforcement of other behavior, rewarding the child for any period they are not doing the stereotypic movement.
DRI is differential reinforcement of incompatible behavior, rewarding them for doing something that physically prevents the stereotypy.
Like, if a child flaps their hands, you might reward them for holding a toy or keeping hands in pockets.
What about habit reversal training?
That shows good success, too.
It involves awareness training, helping the person recognize when they're about to do the behavior, and then teaching them a competing response, a less noticeable or harmful behavior to do instead.
And medication.
You mentioned the dopamine link and sometimes using antipsychotics for SIB in autism.
Right.
Resperidone and erypiprazole are FDA approved for irritability, aggression, and SIB associated with autism.
They can sometimes help reduce severe stereotypes, too.
But you have to be really careful.
Because of side effects.
Yes.
Particularly the risk of inducing other movement problems,
like tardive dyskinesia, involuntary movements that can sometimes be permanent.
That's a major concern.
Is that where those newer VMAT2 inhibitors come in?
Valbenazine, dutrabenazine?
Exactly.
Those are actually approved specifically to treat tardive dyskinesia.
So their availability gives clinicians more options for managing that risk if antipsychotics are deemed necessary for severe behaviors.
Other medications, like SSRIs or nultrexone, have been tried for SMD, but results are really mixed.
Okay.
So wrapping this up for you listening, let's recap the big takeaways.
First, for the attachment disorders.
Remember that critical split between RA and DSE.
Right.
Art often improves significantly with good care, suggesting it's truly about the absence of
DSED, however, frequently persists even after attachment forms, pointing to deeper issues of social boundaries or maybe inhibitory control.
And remember, both RA and DSED are rare and require that documented history of severe neglect.
They shouldn't be diagnosed lightly.
Absolutely.
Proper assessment is key.
Then for stereotypic movement disorders, the main point is the complexity.
Yeah, it's not just one thing.
Causes underlying neurochemistry involving opioids or dopamine.
Which means treatment has to be multifaceted.
Behavioral approaches are primary, focusing on reinforcement strategies and safety.
But sometimes careful medication use is needed, especially for severe SIB, always weighing those risks and benefits.
So if we circle back to those Romanian adoption studies, the ERA study followed those kids for a long time, right?
Like 20 years.
They did.
And the findings are sobering, also hopeful.
Even two decades later, only about one fifth of the children who had spent significant time in those severely deprived institutions were functioning within the typical range across various measures of psychopathology.
Early deprivation can cast a very long shadow.
But at the same time, the studies clearly showed the incredible positive impact of moving into a supportive, loving family environment.
It made a huge difference.
It did.
So the final thought maybe is this.
You have this lasting risk from early trauma, yet you also see this powerful potential for recovery and resilience through dedicated care.
What does that gap, that tension between enduring vulnerability and the possibility of healing,
teach us about how absolutely critical those early developmental years are?
Something important to reflect on.
Thank you for joining us for this deep dive into these foundational aspects of attachment and movement disorders.