Masking in autism and ADHD: discuss

[cara susanna]

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I don't work with children, so I can't comment.

Here's a paper I cite when physicians refer adults to me for differential diagnosis of ADHD.

For reference, when I say movement disorder, I mean something akin to Parkinson's (also treated dopaminergically) or Huntington's.

Do you have a full text of that article? It would be super useful when psychiatrists are giving me guff about declining ADHD testing consults.

 

[AcronymAllergy]

That's interesting, because there was a neuropsychologist who told me that it was extremely rare to find childhood ADHD without any hyperactivity. I'm honestly not sure if that's true because I am by no means an expert.

I'm not a peds person, but I believe this to be generally true. True, never-hyperactive/impulsive ADHD has been conceptualized as a separate disorder by some (Sluggish Cognitive Tempo).

 

[cara susanna]

I'm not a peds person, but I believe this to be generally true. True, never-hyperactive/impulsive ADHD has been conceptualized as a separate disorder by some (Sluggish Cognitive Tempo).

Oh, that's that subscale in the BAARS-IV that I never pay attention to!

 

[R. Matey]

Oh, that's that subscale in the BAARS-IV that I never pay attention to!

It's not really that meaningful clinically because there is a lot of disagreement and essentially no interventions that have been shown to act on SCT aside from one study that looked at study skills with children using SCT as an outcome measure (at least the last time I looked). Conceptually, there is a also a healthy amount of disagreement in whether it's a unitary or multifactored construct, and if the latter, whether those factors are better accounted for by other factors (e.g., effortful/cognitive control, processing speed).

I'm also skeptical of the BAARS total score due to the way the scale was developed, but I admit I haven't look at a any bifactor modeling that may justify it.

 

[bcliff]

I'm not a peds person, but I believe this to be generally true. True, never-hyperactive/impulsive ADHD has been conceptualized as a separate disorder by some (Sluggish Cognitive Tempo).

FWIW, I’ve always preferred the term bradyphrenia over SCT. It seems more specific. It also seems more verifiable (i.e., bradyphrenia implies objective evidence of slowed information processing). I only use this term when there is objective evidence (not just subjective report).

As you can tell, I don’t like ADHD as a diagnostic label, especially as an adult provider. It’s too broad to really mean anything to me. I’m not very wedded to the DSM, in general. I tend to focus on describing specific impairment (e.g., hyperactive/hypomanic, dysexecutive, bradyphrenic, etc.). I don’t like that ADHD forces me to attribute dysfunction to a neurodevelopmental etiology. I guess this perspective is in line with HiTOP, RDoC, and other dimensional approaches to conceptualizing psychopathology.

Here’s another interesting paper—this one showing essentially non-overlapping sets between children and adults diagnosed with “ADHD.”

 

[futureapppsy2]

As with nearly everything, I don't doubt the phenomenon of "masking" is real but it has also been completely mangled by the online reddit-world and has lost all meaning. I think an analogy to other disorders here helps. There are plenty of depressed people who excel at "faking" excessive happiness in social contexts (see: legions of depressed comedians). This seems a form of masking. It sounds exhausting and generally doesn't make the depression better. While there is certainly overlap and shades of grey, I would argue this is distinct from coping. It may reduce functional impairment, but generally not symptoms themselves (perhaps indirectly through retention of social support, etc., etc....hence "shades of grey"). Obviously this looks a bit different in ASD/ADHD where functional impairment is a bit more diagnostically center-stage than it is in depression, but I think the general idea holds. Basically, coping is done to benefit you, but may incidentally benefit others. Masking is done to benefit others, but may incidentally benefit you. It largely is impression management, but I think its reasonable to assume that falls on a continuum. That's just how I've always thought about it.

Now in reddit-land, I think it has become "I self-diagnosed ASD despite having no actual symptoms of ASD. My boss is a jerk who gets mad I keep telling customers to go to hell. How do I get him to understand I shouldn't have to mask and he has to accommodate my ASD?" This is an entirely distinct situation with little-to-no bearing on reality.

Back to the original post, that sounds completely insane but also doesn't surprise me even a little given the state of mental health care. I could certainly see it complicating diagnosis which is always true when there is "a lot going on." Portraying it as "These disorders cancel each other out".........🤣🤣🤣

Yeah, masking is essentially about how you are seen by others, rather than how you are actually functioning or feeling per se, which is different from coping. You can mask well and actually feel worse, because all your energy goes to masking around others.

 

[cara susanna]

FWIW, I’ve always preferred the term bradyphrenia over SCT. It seems more specific. It also seems more verifiable (i.e., bradyphrenia implies objective evidence of slowed information processing). I only use this term when there is objective evidence (not just subjective report).

As you can tell, I don’t like ADHD as a diagnostic label, especially as an adult provider. It’s too broad to really mean anything to me. I’m not very wedded to the DSM, in general. I tend to focus on describing specific impairment (e.g., hyperactive/hypomanic, dysexecutive, bradyphrenic, etc.). I don’t like that ADHD forces me to attribute dysfunction to a neurodevelopmental etiology. I guess this perspective is in line with HiTOP, RDoC, and other dimensional approaches to conceptualizing psychopathology.

Here’s another interesting paper—this one showing essentially non-overlapping sets between children and adults diagnosed with “ADHD.”

Honestly, I wish that ADHD couldn't be diagnosed in adulthood. It's too difficult to rule in or out.

 

[Ceke2002]

It also removes the frustrating "and/or" element of our current ADHD diagnostic label (i.e., attention-deficit [and/or] hyperactivity disorder), which has watered down the diagnosis to something largely unfalsifiable IMO. The emphasis on hyperkinesis also fits with the neurobiological models of the disorder that implicate frontostriatal circuitry (which is admittedly a literature I take with a large grain of salt).

Given its origins as "hyperkinesis" and the subcortical link I mentioned above, I've posed questions to pediatric colleagues about whether they think of (hyperactive-impulsive) ADHD as a movement disorder. All have said that they do not.

I do sometimes wonder if Hyperkinetic Reaction of Childhood and ADHD are in fact two separate disorders, albeit with potential overlap (or one is perhaps a subset or variation of the other). That is so not worded correctly, but am I kind of curious to think what the diagnostic landscape would be like today if they had kept Hyperkinetic Reaction of Childhood and added ADHD in the DSM III alongside it.

I have glanced through some studies comparing diagnostic rates of ADHD as per DSM III for those mid teens and adults who were previously diagnosed under the DSM II criteria for Hyperkinetic Reaction of Childhood. The outcomes ranged from a low of only 4% through to 36% of participants who met the criteria for ADHD past a childhood diagnosis of Hyperkinetic Reaction of Childhood.

I think this is one of the studies I've looked at briefly.

https://psychiatryonline.org/doi/full/10.1176/ajp.155.4.493

 

[PsyDr]

Idk if anyone else has a copy of the DSM-II, but its not like the criteria for Hyperkinetic Disorder of Childhood were ultra specific. I do think the attention deficit components were probably overstated in future iterations of the DSM though.

308.0* Hyperkinetic reaction of childhood (or adolescence)*
This disorder is characterized by overactivity, restlessness, distractibility,
and short attention span, especially in young children; the
behavior usually diminishes in adolescence.
If this behavior is caused by organic brain damage, it should be
diagnosed under the appropriate non-psychotic organic brain syndrome
(q.v.).

 

[Ollie123]

308.0* Hyperkinetic reaction of childhood (or adolescence)*
This disorder is characterized by overactivity, restlessness, distractibility,
and short attention span, especially in young children; the
behavior usually diminishes in adolescence.
If this behavior is caused by organic brain damage, it should be
diagnosed under the appropriate non-psychotic organic brain syndrome
(q.v.).

Yeah, I can kinda see why this was not specific enough 🤣
That describes virtually every single child under the age of 6-7 that I have met in my entire lifetime. Including my own, who quite literally runs laps around the house in between bites of food.

 

[futureapppsy2]

Yeah, I can kinda see why this was not specific enough 🤣
That describes virtually every single child under the age of 6-7 that I have met in my entire lifetime. Including my own, who quite literally runs laps around the house in between bites of food.

I don’t disagree, but isn’t that where developmental appropriateness and impairment come into the diagnostic equation? I’ve seen kids with hyperactive ADHD who definitely moved more than their peers in really noticeable ways.

 

[Shiori]

I wish we could turn this thread into a CEU. I've gotten way more out of this than some of my other official credits.

 

[Ollie123]

I don’t disagree, but isn’t that where developmental appropriateness and impairment come into the diagnostic equation? I’ve seen kids with hyperactive ADHD who definitely moved more than the peers in really noticeable ways.

Oh without a doubt. I'm just making light of it - its pretty clear if we wanted a rigorous "Diagnostic Manual" it behooved us to get at least a bit more specific than that. Imagine if the GAD criteria started and ended with "characterized by extensive worries."

 

[oliversacks4thewin]

It also removes the frustrating "and/or" element of our current ADHD diagnostic label (i.e., attention-deficit [and/or] hyperactivity disorder), which has watered down the diagnosis to something largely unfalsifiable IMO. The emphasis on hyperkinesis also fits with the neurobiological models of the disorder that implicate frontostriatal circuitry (which is admittedly a literature I take with a large grain of salt).

Given its origins as "hyperkinesis" and the subcortical link I mentioned above, I've posed questions to pediatric colleagues about whether they think of (hyperactive-impulsive) ADHD as a movement disorder. All have said that they do not.

I have to say, I really struggle with the concept of lumping ADHD (I am assuming strict reference to the predominately hyperactive subtype, based on description) into the category of movement disorders. You alluded to some overlap in dopaminergic dysfunction and basal ganglia involvement between ADHD and movement disorders, but the clinical and pathological features remain distinct. You referenced Parkinson's and Huntington's disease correlates and referenced dopaminergic processes implicit in those, but I feel like the comparison is a bit lacking in neuropathophysiological distinctions that make each condition so unique.

For a simple example, if it was truly all treated "dopaminergically" as you alluded to, why not treat PD and HD with stimulant medications, which is not considered routine or best practice approach? In fact, VMAT2 inhibitors are actually the only recommended treatment for the choreatic movements in HD, which is interesting in that these are also what are sometimes recommended in tic/Tourette's treatment too... which I feel is much more representative of a movement disorder than ADHD. Conversely, why not treat ADHD with Sinemet? It also does not speak to why alpha-2-adrenergic agonists and an SNRI like Strattera that blocks NET, has demonstrated efficacy in treating the hyperactivity (hyperkinetic?) symptoms.

While I am not personally, the biggest proponent of a2a agonists, I have to recognize that they act by stimulating presynaptic alpha-2 receptors, thereby inhibiting the release of norepinephrine. This results in decreased neuronal firing in the locus coeruleus and enhanced prefrontal cortical function, which is associated with better regulation of attention, impulse control, and activity level. I have preference for Strattera, which
treats hyperactivity in ADHD by selectively inhibiting the presynaptic norepinephrine transporter, increasing norepinephrine levels in the PFC, which improves behavioral control and reduces hyperactive/impulsive symptoms. Regardless, it's more PFC vs. basal ganglia.


For more on the specifics about how they differ, Movement disorders such as Parkinson's and Huntington's are defined by involuntary motor abnormalities, tremor, rigidity, bradykinesia, chorea, dystonia, arising from specific neurodegenerative changes in motor control circuits, particularly the basal ganglia and related pathways. Parkinson's disease, for example, is characterized by progressive loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies, leading to hallmark motor symptoms and pathologically confirmed neurodegeneration. Huntington's disease is marked by involuntary choreic movements and cognitive decline, with selective neuronal loss in the caudate and putamen.

While ADHD does involve increased voluntary activity (hyperactivity), these movements are purposeful and not due to abnormal motor system function. Neuroimaging and neurobiological studies show that ADHD is associated with delayed cortical maturation and dysfunction in frontostriatal and mesolimbic circuits, but not with the neurodegenerative changes or involuntary motor phenomena seen in movement disorders .Although there is some overlap in dopaminergic dysfunction and basal ganglia involvement between ADHD and movement disorders, the clinical and pathological features remain distinct. ADHD does not present with the involuntary, progressive motor symptoms or structural brain changes (e.g., substantia nigra degeneration) that define Parkinson's or Huntington's disease. Motor control difficulties in ADHD are subtle, often related to executive dysfunction and response inhibition, and do not meet criteria for movement disorder diagnosis.

Happy to discuss further and can certainly produce cited literature (excluded from here because this is already a long post lol) if you would like.

 

[bcliff]

I have to say, I really struggle with the concept of lumping ADHD (I am assuming strict reference to the predominately hyperactive subtype, based on description) into the category of movement disorders. You alluded to some overlap in dopaminergic dysfunction and basal ganglia involvement between ADHD and movement disorders, but the clinical and pathological features remain distinct. You referenced Parkinson's and Huntington's disease correlates and referenced dopaminergic processes implicit in those, but I feel like the comparison is a bit lacking in neuropathophysiological distinctions that make each condition so unique.

For a simple example, if it was truly all treated "dopaminergically" as you alluded to, why not treat PD and HD with stimulant medications, which is not considered routine or best practice approach? In fact, VMAT2 inhibitors are actually the only recommended treatment for the choreatic movements in HD, which is interesting in that these are also what are sometimes recommended in tic/Tourette's treatment too... which I feel is much more representative of a movement disorder than ADHD. Conversely, why not treat ADHD with Sinemet? It also does not speak to why alpha-2-adrenergic agonists and an SNRI like Strattera that blocks NET, has demonstrated efficacy in treating the hyperactivity (hyperkinetic?) symptoms.

While I am not personally, the biggest proponent of a2a agonists, I have to recognize that they act by stimulating presynaptic alpha-2 receptors, thereby inhibiting the release of norepinephrine. This results in decreased neuronal firing in the locus coeruleus and enhanced prefrontal cortical function, which is associated with better regulation of attention, impulse control, and activity level. I have preference for Strattera, which
treats hyperactivity in ADHD by selectively inhibiting the presynaptic norepinephrine transporter, increasing norepinephrine levels in the PFC, which improves behavioral control and reduces hyperactive/impulsive symptoms. Regardless, it's more PFC vs. basal ganglia.


For more on the specifics about how they differ, Movement disorders such as Parkinson's and Huntington's are defined by involuntary motor abnormalities, tremor, rigidity, bradykinesia, chorea, dystonia, arising from specific neurodegenerative changes in motor control circuits, particularly the basal ganglia and related pathways. Parkinson's disease, for example, is characterized by progressive loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies, leading to hallmark motor symptoms and pathologically confirmed neurodegeneration. Huntington's disease is marked by involuntary choreic movements and cognitive decline, with selective neuronal loss in the caudate and putamen.

While ADHD does involve increased voluntary activity (hyperactivity), these movements are purposeful and not due to abnormal motor system function. Neuroimaging and neurobiological studies show that ADHD is associated with delayed cortical maturation and dysfunction in frontostriatal and mesolimbic circuits, but not with the neurodegenerative changes or involuntary motor phenomena seen in movement disorders .Although there is some overlap in dopaminergic dysfunction and basal ganglia involvement between ADHD and movement disorders, the clinical and pathological features remain distinct. ADHD does not present with the involuntary, progressive motor symptoms or structural brain changes (e.g., substantia nigra degeneration) that define Parkinson's or Huntington's disease. Motor control difficulties in ADHD are subtle, often related to executive dysfunction and response inhibition, and do not meet criteria for movement disorder diagnosis.

Happy to discuss further and can certainly produce cited literature (excluded from here because this is already a long post lol) if you would like.

I ask the question mostly rhetorically.

I don't really buy into the concept of ADHD as a unitary disorder with a neurodevelopmental etiology. The DSM classifies it as such but then proceeds to define the disorder entirely in terms of behavioral signs and symptoms.

Like I mentioned earlier, I generally ascribe to HiTOP, RDoC, and other dimensional conceptualizations of psychopathology more than the DSM. Rather than ADHD as a unitary construct, I focus more on measurable behavioral and cognitive findings, like bradyphrenia, hyperactivity/hypomania, executive dysfunction, disinhibition/impulsivity, etc., the etiology of which is likely multifactorial (rather than exclusively/definitely an irregularity in neurodevelopment).

 

[PsyDr]

providers who are legally confined to behavioral interventions:

“Let’s argue about biology that we can’t change”

 

[quickpsych]

This is the camp I tend to fall into, as well. I'm open to the exploration of the topic, but also recognize, it's technically not a DSM criteria...

There are measurements that attempt to parse apart what makes masking unique, like the CAT-Q, mentioned in the following article: Camouflaging in autism spectrum disorder: Examining the roles of sex, gender identity, and diagnostic timing - PubMed but I recognize their construct validity is still shaky, at best. I do like that studies on these alludes to recognition in social anxiety and ADHD, as it highlights everything you have all said. That these are all behaviors, endured with discomfort, and attempts to cope/compensate around.

I fully appreciate your sentiment @WisNeuro as it seems to excuse all poor behavior by calling it "masking." I feel like the misuse of the construct in the mainstream, makes it harder to define for sure. In my experience, patients with overt ASD still demonstrate masking-like behaviors, where they will attempt to match social reciprocity, so they "don't seem weird." In fact, I have had a number of individuals with ASD who will fiercely maintain eye contact with me, because, I am certain, there were negative consequences for not doing so in the past, even though the new eye contact, is now abnormal. It's not exactly a prosocial behavior but kind of like an attempt to be seen as socially more to the norm, even if it is clearly not. When I think about "masking" these are more of the kinds of behaviors I'm thinking of. It's an attempt to adhere to the "rules" but is based on observed data, rather than inherent fundamental understanding of the concept.

100% spot on. Well said.

 

[oliversacks4thewin]

providers who are legally confined to behavioral interventions:

“Let’s argue about biology that we can’t change”

Haha, I get the sentiment, but

1) I am a prescribing psychologist, so I am legally authorized to provide psychotherapy and prescribe.

2) To ignore the biology, is to see only half the picture. Skinner, himself, believed that biology would one day fill the gaps in the causal chain, but it would not invalidate the behavioral principles discovered through experimentation. Both can operate in harmony, and it is only to our advantage to explore the biological correlates we have continued to learn more and more about (Thank you MRI discoverer!) in the past few centuries.