Testing and medication

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mypointlesspov

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Hi everyone,

I'm getting back into testing after four years and was looking for some perspective on medication use. I'm testing someone for ADHD and they're already on guanfacine (prescribed for a different dx). From my experience in grad school, we asked people to not take any stimulant medication if they were being tested for that dx as it would not give us valid results. Guanfacine isn't a stimulant and, to my knowledge, not a med that you can just stop for a day or two. I was planning on asking the person's psychiatrist about this but wanted to get perspective from you folks as well.

Thanks!
 
Hi everyone,

I'm getting back into testing after four years and was looking for some perspective on medication use. I'm testing someone for ADHD and they're already on guanfacine (prescribed for a different dx). From my experience in grad school, we asked people to not take any stimulant medication if they were being tested for that dx as it would not give us valid results. Guanfacine isn't a stimulant and, to my knowledge, not a med that you can just stop for a day or two. I was planning on asking the person's psychiatrist about this but wanted to get perspective from you folks as well.

Thanks!

Considering that the testing results should not inform the diagnosis in any way whatsoever, you should probably just keep them on the medication as prescribed.
 
Considering that the testing results should not inform the diagnosis in any way whatsoever, you should probably just keep them on the medication as prescribed.
Agreed. I can see situations in which stopping medication can be worthwhile (e.g., if you have someone with, say, MS who's on Adderall to help with their fatigue and cognitive complaints). But making an ADHD diagnosis probably isn't one of those situations, unless it's also a psychoeducational evaluation for accommodations, or there's some other reason that getting an "unmedicated" view of cognition (and assessing cognition via objective testing to begin with, rather than just doing a thorough clinical interview with some possible self-/informant-report measures thrown in) would be helpful and warranted (e.g., research).
 
1). Why are they on guanfacine?

a. If it's for hypertension, any testing is useless. If you find ADHD, they cannot take a stimulant without risking cardiac effects.

b. If it's for one of those amorphous diagnoses like POTS or "long covid", your testing won't help due to the confound of another potential cause of attention problems.

2) I would have a real talk with the patient about “What are you hoping to get out of testing?”

a. If they’re looking for adderall, it's not going to happen if they’re hypertensive. Testing isn’t going to help.

b. If they’re having attention problems, the MTA study would indicate that behavioral therapy would be the most efficacious approach. That would be cheaper than testing.

c. If they are looking for academic accommodations: that’s a different story.
 
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Why are they on guanfacine?



If they’re having attention problems, the MTA study would indicate that behavioral therapy would be the most efficacious approach. That would be cheaper than testing.

I'm assuming you mean that in combination with stimulants, yeah?
 
Couple of thoughts:
  • Am I the only one who views it as a major overstepping of professional boundaries/competencies to ask a patient to stop a prescribed medication for testing?
  • Guanfacine for ADHD is usually dog crap - so it probably won't matter.
 




I'm assuming you mean that in combination with stimulants, yeah?
My understanding of MTA is basically this and I how I explain it patients:

  1. They took a bunch of kids with ADHD and put them into three groups. At the start of study, they all have equal symptoms of ADHD.
  2. The first group was behavior therapy, and you see a some reduction in ADHD symptoms.
  3. The second group was ritalin alone, and later studies show that about 80% have a very positive response and normalize when the med is in their system.
  4. The third group "bums me out as a behavioral psychologist, because combined treatment doesn't lead to a statistically greater improvement on main measure of ADHD symptoms than meds alone. This isn't the case for secondary measures, though." This is remarkable because for nearly all other mental/medical conditions - combined treatments usually work way better than either alone.
  5. Why? Because ADHD isn't really a skill deficit, rather its a performance deficit that is likely more "organic" than many other conditions.
  6. Then I draw a picture of two brain cells and show how they never touch...

IMG_5272.jpg
 




I'm assuming you mean that in combination with stimulants, yeah?
Not really.

"Intensive medication management may only make a persistent long-term difference if it is continued with the same intensity as during the MTA's initial 14-month period. In contrast, starting or adding medication at a less than optimal intensity and too late in child's ADHD clinical course (particularly if a child's behavior is deteriorating) may not only be ineffective but also (if not carefully examined in data analysis) even make medication appear to be associated with worse outcomes"


Also see: Table 1 & 2.


Jensen, P. S., et al. (2007). "3-year follow-up of the NIMH MTA study." J Am Acad Child Adolesc Psychiatry 46(8): 989-1002.
 
Agreed. I can see situations in which stopping medication can be worthwhile (e.g., if you have someone with, say, MS who's on Adderall to help with their fatigue and cognitive complaints). But making an ADHD diagnosis probably isn't one of those situations, unless it's also a psychoeducational evaluation for accommodations, or there's some other reason that getting an "unmedicated" view of cognition (and assessing cognition via objective testing to begin with, rather than just doing a thorough clinical interview with some possible self-/informant-report measures thrown in) would be helpful and warranted (e.g., research).


It's a psychoeducational eval for a 16 y/o. Sorry, I was trying to be as vague as possible here.
1). Why are they on guanfacine?

a. If it's for hypertension, any testing is useless. If you find ADHD, they cannot take a stimulant without risking cardiac effects.

b. If it's for one of those amorphous diagnoses like POTS or "long covid", your testing won't help due to the confound of another potential cause of attention problems.

2) I would have a real talk with the patient about “What are you hoping to get out of testing?”

a. If they’re looking for adderall, it's not going to happen if they’re hypertensive. Testing isn’t going to help.

b. If they’re having attention problems, the MTA study would indicate that behavioral therapy would be the most efficacious approach. That would be cheaper than testing.

c. If they are looking for academic accommodations: that’s a different story.
1) emotional regulation issues as a child (multiple daily meltdowns w/ physical aggression). this was prescribed 6 years ago. no history of hypertension or other cardiac concerns per parent report.

2) academic accommodations and diagnostic clarity. parent said a previous psychologist described this 16 y/o as "an alphabet soup kid" and they want to know what's driving the symptoms/behaviors. there are some attention problems but they're unsure if they're related to possible ADHD (family history of this), anxiety, or even autism.
 
I'd talk with the psychiatrist to see if stopping the medication would even be helpful (and reasonable) in this case. And/or find literature on its expected impact on testing so that you can take it into account. For a psychoed, there may be strict requirements on medication use, depending on what they're wanting to use the eval for.

I don't view the idea of stopping meds prior to testing to be overstepping professional boundaries. But I would either talk to the provider prescribing the med beforehand, or would require that the patient do so. Which was easier when I was at VA, where I would just walk down the hall and talk to the psychiatrist, or send them a message on Teams.
 
Not really.

"Intensive medication management may only make a persistent long-term difference if it is continued with the same intensity as during the MTA's initial 14-month period. In contrast, starting or adding medication at a less than optimal intensity and too late in child's ADHD clinical course (particularly if a child's behavior is deteriorating) may not only be ineffective but also (if not carefully examined in data analysis) even make medication appear to be associated with worse outcomes"

I'm not really following how this refutes my point, which is that behavioral therapy alone is not as effective as stimulants alone or in combination with stimulants. Even if you take the MTA out of the equation, other studies have not shown that behavioral therapy has same effect sizes as medication. Here's a review from last year by the MTA folks.
 
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I'm not really following how this refutes my point, which is that behavioral therapy alone is not as effective as stimulants alone or in combination with stimulants. Even if you take the MTA out of the equation, other studies have not shown that behavioral therapy has same effect sizes as stimulants. Here's a review from last year by the MTA folks.
I'm not sure why you'd use an article that says, "In studies comparing behaviour therapy with medication, most evidence suggests that medication and behaviour therapy similarly reduce ADHD symptoms." on page 6, to enhance your position.

The Jensen 3 year follow up shows similar effect sizes at 3 years.

So, what am I missing about your cite?
 
1). Why are they on guanfacine?

a. If it's for hypertension, any testing is useless. If you find ADHD, they cannot take a stimulant without risking cardiac effects.

Incorrect. Stimulant medications in clinically used doses have extremely modest impacts on blood pressure and are only really contraindicated by certain kinds of arrhythmia. Having high blood pressure is not actually a reason not to prescribe someone a stimulant unless we are talking about someone who is teetering on the edge of a hypertensive emergency at all times.
 
I'm not sure why you'd use an article that says, "In studies comparing behaviour therapy with medication, most evidence suggests that medication and behaviour therapy similarly reduce ADHD symptoms." on page 6, to enhance your position.

The Jensen 3 year follow up shows similar effect sizes at 3 years.

So, what am I missing about your cite?

I guess two things: (1) similar effect sizes in one study doesn't make a body of literature (see bottom of p. 420) and (2) effect sizes of behavioral therapy vary due to a whole host of factors and do not seem to intervene on symptoms insomuch as they intervene on peripheral sources of impairment. Effect sizes in behavioral therapy also vary due to a ton of delivery factors (dosage, goals, etc.) so it's more responsible to say that it can help, but effects may not be as reliable as meds. In fact, that is what the authors conclude at the end of the section.

Please don't cherry pick text to support your argument.
 
I guess two things: (1) similar effect sizes in one study doesn't make a body of literature (see bottom of p. 420) and (2) effect sizes of behavioral therapy vary due to a whole host of factors and do not seem to intervene on symptoms insomuch as they intervene on peripheral sources of impairment. Effect sizes in behavioral therapy also vary due to a ton of delivery factors (dosage, goals, etc.) so it's more responsible to say that it can help, but effects may not be as reliable as meds. In fact, that is what the authors conclude at the end of the section.

Please don't cherry pick text to support your argument.

I cited the 3yr follow up that shows a similar effect size, and that the timing/intensity of stimulant dosage drastically affects the outcomes. Then you cited an article that said that behavior therapy and medication have similar effectiveness.

I'll obviously agree that the variability in administration of behavior therapy is a huge confound, as cited in the Sibley study. Would you agree that that the variability in administration of stimulants is a huge confound, as cited in the Jensen study? I don't think either of us are wrong, or cherry picking.


Incorrect. Stimulant medications in clinically used doses have extremely modest impacts on blood pressure and are only really contraindicated by certain kinds of arrhythmia. Having high blood pressure is not actually a reason not to prescribe someone a stimulant unless we are talking about someone who is teetering on the edge of a hypertensive emergency at all times.
1) The FDA insert for adderall lists moderate to severe hypertension as a contraindication. I am aware of the AHA, AAP, and AACP guidelines.

2) I've never been able to make sense of the literature regarding the effect of stimulants on BP. It looks like there is an increase in BP and HR, that is not necessarily resulting in cardiomyopathy. You're the physician. Any thoughts?

Mick, E., et al. (2013). "Meta-analysis of increased heart rate and blood pressure associated with CNS stimulant treatment of ADHD in adults." European Neuropsychopharmacology 23(6): 534-541.

Olfson, M., et al. (2012). "Stimulants and Cardiovascular Events in Youth With Attention-Deficit/Hyperactivity Disorder." Journal of the American Academy of Child & Adolescent Psychiatry 51(2): 147-156.

Samuels, J. A., et al. (2006). "Effect of stimulants on 24-h ambulatory blood pressure in children with ADHD: a double-blind, randomized, cross-over trial." Pediatric Nephrology 21(1): 92-95.

Zhang, L., et al. (2024). "Attention-Deficit/Hyperactivity Disorder Medications and Long-Term Risk of Cardiovascular Diseases." JAMA Psychiatry 81(2): 178-187.
 
1) The FDA insert for adderall lists moderate to severe hypertension as a contraindication. I am aware of the AHA, AAP, and AACP guidelines.

Sure. I would say that the FDA saying that something is or is not indicated for something is not a very good guide to the actual facts of whether or not something is safe and effective clinically. Certainly a much less reliable linkage between those two things than would be ideal. So I suppose what I am saying is that FDA contraindication =/= "testing is useless because they won't be able to take it"

2) I've never been able to make sense of the literature regarding the effect of stimulants on BP. It looks like there is an increase in BP and HR, that is not necessarily resulting in cardiomyopathy. You're the physician. Any thoughts?

You may have to be more specific as to the point of confusion. In general I would say that a change in 5 bpm in HR and 2mmHg in SBP are vanishingly unlikely to make a meaningful difference to anybody who is not quite medically fragile to begin with.

Mick, E., et al. (2013). "Meta-analysis of increased heart rate and blood pressure associated with CNS stimulant treatment of ADHD in adults." European Neuropsychopharmacology 23(6): 534-541.

Olfson, M., et al. (2012). "Stimulants and Cardiovascular Events in Youth With Attention-Deficit/Hyperactivity Disorder." Journal of the American Academy of Child & Adolescent Psychiatry 51(2): 147-156.

Samuels, J. A., et al. (2006). "Effect of stimulants on 24-h ambulatory blood pressure in children with ADHD: a double-blind, randomized, cross-over trial." Pediatric Nephrology 21(1): 92-95.

Zhang, L., et al. (2024). "Attention-Deficit/Hyperactivity Disorder Medications and Long-Term Risk of Cardiovascular Diseases." JAMA Psychiatry 81(2): 178-187.
 
I don't expect guanfacine would be used for hypertension:
- Alpha-2 agonists are not used for hypertension with significant frequency, their only mention in AHA guidelines is for amphetamine, cocaine, etc. intoxication, and even then it is second line to benzodiazepines
- Guanfacine is relatively centrally selective, and its vasoactivity caps out relatively early. Clonidine, which is more vasoactive, would be the choice if an alpha-2 is being used for BP

It's a psychoeducational eval for a 16 y/o. Sorry, I was trying to be as vague as possible here.

1) emotional regulation issues as a child (multiple daily meltdowns w/ physical aggression). this was prescribed 6 years ago. no history of hypertension or other cardiac concerns per parent report.

2) academic accommodations and diagnostic clarity. parent said a previous psychologist described this 16 y/o as "an alphabet soup kid" and they want to know what's driving the symptoms/behaviors. there are some attention problems but they're unsure if they're related to possible ADHD (family history of this), anxiety, or even autism.

One thing to consider would be that if the guanfacine is helping with emotional regulation, if you stop it and they become emotionally dysregulated during the eval, you would have a lot of difficulty clarifying that alphabet soup.
 
I'll obviously agree that the variability in administration of behavior therapy is a huge confound, as cited in the Sibley study. Would you agree that that the variability in administration of stimulants is a huge confound, as cited in the Jensen study? I don't think either of us are wrong, or cherry picking.

Yes, and I actually thought about that later: whatever critiques about dosage and follow-up that can be leveled at stimulants in the MTA study can also be leveled at behavioral therapy studies outside the MTA. Arguably, there is a greater amount of variability in behavioral therapy considering that therapist effects, type of interventions, and therapeutic goals are additional sources not seen when you're administering medication (though there could be physiological confounds that I am not aware of).

I cited the 3yr follow up that shows a similar effect size, and that the timing/intensity of stimulant dosage drastically affects the outcomes. Then you cited an article that said that behavior therapy and medication have similar effectiveness.

Not quite sure I agree here. Notice they cite the Jenson study as evidence that the MTA showed that behavioral therapy did not have meaningful effects in childhood. I think this is partly because many people in behavioral condition began using medication after the MTA study ended, which more or less fuddled the comparisons in Jenson due to selection effects. It was also apparent that whatever gains the MTA algorithm had at the time of the study were subsequently lost in follow-up, making them comparable to community care/behavioral treatment. There is also the tendency for ADHD symptoms to reduce or change in development, which may explain some of the effect as well.
 
Since we don't really use performance testing to diagnose ADHD, it's all about history of meeting behavioral criteria so I don't think being on meds is a big deal
 
Incorrect. Stimulant medications in clinically used doses have extremely modest impacts on blood pressure and are only really contraindicated by certain kinds of arrhythmia. Having high blood pressure is not actually a reason not to prescribe someone a stimulant unless we are talking about someone who is teetering on the edge of a hypertensive emergency at all times.
Anecdotally, a colleague of mine has (treated) high blood pressure and a history of cardiac problems (currently corrected in a prior surgery) and still received cardiac clearance for stimulants.
 
Since we don't really use performance testing to diagnose ADHD, it's all about history of meeting behavioral criteria so I don't think being on meds is a big deal
I've had supervisors see a high average cognitive profile and average WMI/PSI/sustained/selective attention and think it's indicative of ADHD, while ignoring other potential confounds and/or normal intra-individual variability. Then proceed to diagnose ADHD without a thorough clinical or family interview and only rely on self-report measures and testing. People rely on testing way too much for ADHD and I'd like to know where exactly that originates from. Wasn't it Barkley that initially emphasized the use of testing then later changed course in that 2019 article? Maybe I'm remembering it wrong.
 
Not quite sure I agree here. Notice they cite the Jenson study as evidence that the MTA showed that behavioral therapy did not have meaningful effects in childhood. I think this is partly because many people in behavioral condition began using medication after the MTA study ended, which more or less fuddled the comparisons in Jenson due to selection effects. It was also apparent that whatever gains the MTA algorithm had at the time of the study were subsequently lost in follow-up, making them comparable to community care/behavioral treatment. There is also the tendency for ADHD symptoms to reduce or change in development, which may explain some of the effect as well.
This point bears emphasizing. This is one reason the follow ups for the MTA were underwhelming - many in the non stim groups were using them on follow up. A rising tide lifts all boats.
 
Since we don't really use performance testing to diagnose ADHD, it's all about history of meeting behavioral criteria so I don't think being on meds is a big deal
I could see it masking symptoms in a patient who was otherwise present as ADHD during a clinical interview if they weren’t medicated, though. Otoh, you would want to make sure any co-morbidities like depression, anxiety, PTSD were being treated. I still don’t think testing is necessary or useful for an ADHD diagnosis, absent other neurological concerns, though.
 
I've had supervisors see a high average cognitive profile and average WMI/PSI/sustained/selective attention and think it's indicative of ADHD, while ignoring other potential confounds and/or normal intra-individual variability. Then proceed to diagnose ADHD without a thorough clinical or family interview and only rely on self-report measures and testing. People rely on testing way too much for ADHD and I'd like to know where exactly that originates from. Wasn't it Barkley that initially emphasized the use of testing then later changed course in that 2019 article? Maybe I'm remembering it wrong.

There were a proliferation of performance studies in the 1990s/2000s that showed pretty consistent, but small performance differences on certain cognitive tasks, informed by Barkley's model. Metas that examined the effects concluded they were so small (and moderated by external factors) that they were not clinically meaningful. Here's a decent starting place.
 
I could see it masking symptoms in a patient who was otherwise present as ADHD during a clinical interview if they weren’t medicated, though. Otoh, you would want to make sure any co-morbidities like depression, anxiety, PTSD were being treated. I still don’t think testing is necessary or useful for an ADHD diagnosis, absent other neurological concerns, though.

I've done ADHD clinical interviews with patients who were medicated and I think it's pretty easy to get an idea of what they're like without the meds. The only thing it might impact is the current symptom observer forms, but you could take those responses with a grain of salt.
 
Not quite sure I agree here. Notice they cite the Jenson study as evidence that the MTA showed that behavioral therapy did not have meaningful effects in childhood. I think this is partly because many people in behavioral condition began using medication after the MTA study ended, which more or less fuddled the comparisons in Jenson due to selection effects. It was also apparent that whatever gains the MTA algorithm had at the time of the study were subsequently lost in follow-up, making them comparable to community care/behavioral treatment. There is also the tendency for ADHD symptoms to reduce or change in development, which may explain some of the effect as well.

1) When I'm looking at the Jensen study, Table 1&2 seem to refute the Sibley interpretation. Am I reading this wrong?

1723053204990.png



2) The Molina 8 year follow up MTA study, does seem to support my position.

"Two variables were statistically significant in the planned contrasts at 6-years only, and these effects were small. First, adolescents who received Comb had fewer school services at 6 years than adolescents who received Beh, p=.0204. Second, DISC diagnoses of anxiety or depression differed by group at 6-years. Children who received Beh had a lower rate of these diagnoses (4.3%) than children in the Comb (17.7%), MedMgt (19.1%), or CC (16.4%) groups. The difference was reflected in four statistically significant contrasts: Comb+MedMgt>Beh+CC, p=.0050; Beh<CC, p=.0064; Comb>Beh, p=.0027; Comb+Beh<MedMgt+CC, p=.0132."

3) I really enjoy the collegial exchange. Thank you.
 
1) When I'm looking at the Jensen study, Table 1&2 seem to refute the Sibley interpretation. Am I reading this wrong?

View attachment 390484


2) The Molina 8 year follow up MTA study, does seem to support my position.

"Two variables were statistically significant in the planned contrasts at 6-years only, and these effects were small. First, adolescents who received Comb had fewer school services at 6 years than adolescents who received Beh, p=.0204. Second, DISC diagnoses of anxiety or depression differed by group at 6-years. Children who received Beh had a lower rate of these diagnoses (4.3%) than children in the Comb (17.7%), MedMgt (19.1%), or CC (16.4%) groups. The difference was reflected in four statistically significant contrasts: Comb+MedMgt>Beh+CC, p=.0050; Beh<CC, p=.0064; Comb>Beh, p=.0027; Comb+Beh<MedMgt+CC, p=.0132."

3) I really enjoy the collegial exchange. Thank you.

3. Likewise
2. That's the '08 paper, right? I'll need to look at again, but IIRC SES was a significant predictor of positive outcomes
1. You're not wrong, but the reasons that the differences are minimal is because it was impossible to disentangle effects of MTA study vs. treatment was started after the study concluded. Thus, it's a bit post hoc to infer that differences are minimal due to intervention during the MTA. At least that's my take.
 
My first thought is that an “alphabet soup” kid does not have ADHD but has deficits in functioning for a variety of other reasons. Psychological testing can be helpful to begin to tease out what those factors are. Too often we are looking for a fix or answer for something that does not have one and the patient ends up suffering more and more as they get diagnoses and medications thrown at a complex problem and it just makes it more problematic.
 
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