ADHD: A Modest Proposal

February 1, 2012

I’m reluctant to write a post about ADHD.  It just seems like treacherous ground.  Judging by comments I’ve read online and in magazines, and my own personal experience, expressing an opinion about this diagnosis—or just about anything in child psychiatry—will be met with criticism from one side or another.  But after reading L. Alan Sroufe’s article (“Ritalin Gone Wild”) in this weekend’s New York Times, I feel compelled to write.

If you have not read the article, I encourage you to do so.  Personally, I agree with every word (well, except for the comment about “children born into poverty therefore [being] more vulnerable to behavior problems”—I would remind Dr Sroufe that correlation does not equal causation).  In fact, I wish I had written it.  Unfortunately, it seems that only outsiders or retired psychiatrists can write such stuff about this profession. The rest of us might need to look for jobs someday.

Predictably, the article has attracted numerous online detractors.  For starters, check out this response from the NYT “Motherlode” blog, condemning Dr Sroufe for “blaming parents” for ADHD.  In my reading of the original article, Dr Sroufe did nothing of the sort.  Rather, he pointed out that ADHD symptoms may not entirely (or at all) arise from an inborn neurological defect (or “chemical imbalance”), but rather that environmental influences may be more important.  He also remarked that, yes, ADHD drugs do work; children (and adults, for that matter) do perform better on them, but those successes decline over time, possibly because a drug solution “does nothing to change [environmental] conditions … in the first place.”

I couldn’t agree more.  To be honest, I think this statement holds true for much of what we treat in psychiatry, but it’s particularly relevant in children and adolescents.  Children are exposed to an enormous number of influences as they try to navigate their way in the world, not to mention the fact that their brains—and bodies—continue to develop rapidly and are highly vulnerable.  “Environmental influences” are almost limitless.

I have a radical proposal which will probably never, ever, be implemented, but which might help resolve the problems raised by the NYT article.  Read on.

First of all, you’ll note that I referred to “ADHD symptoms” above, not “ADHD.”  This isn’t a typo.  In fact, this is a crucial distinction.  As with anything else in psychiatry, diagnosing ADHD relies on documentation of symptoms.  ADHD-like symptoms are extremely common, particularly in child-age populations.  (To review the official ADHD diagnostic criteria from the DSM-IV, click here.)  To be sure, a diagnosis of ADHD requires that these symptoms be “maladaptive and inconsistent with developmental level.”  Even so, I’ve often joked with my colleagues that I can diagnose just about any child with ADHD just by asking the right questions in the right way.  That’s not entirely a joke.  Try it yourself.  Look at the criteria, and then imagine you have a child in your office whose parent complains that he’s doing poorly in school, or gets in fights, or refuses to do homework, or daydreams a lot, etc.  When the ADHD criteria are on your mind—remember, you have to think like a psychiatrist here!—you’re likely to ask leading questions, and I guarantee you’ll get positive responses.

That’s a lousy way of making a diagnosis, of course, but it’s what happens in psychiatrists’ and pediatricians’ offices every day.  There are more “valid” ways to diagnose ADHD:  rating scales like the Connors or Vanderbilt surveys, extensive neuropsychiatric assessment, or (possibly) expensive imaging tests.  However, in practice, we often let subthreshold scores on those surveys “slide” and prescribe ADHD medications anyway (I’ve seen it plenty); neuropsychiatric assessments are often wishy-washy (“auditory processing score in the 60th percentile,” etc); and, as Dr Sroufe correctly points out, children with poor motivation or “an underdeveloped capacity to regulate their behavior” will most likely have “anomalous” brain scans.  That doesn’t necessarily mean they have a disorder.

So what’s my proposal?  My proposal is to get rid of the diagnosis of ADHD altogether.  Now, before you crucify me or accuse me of being unfit to practice medicine (as one reader—who’s also the author of a book on ADHD—did when I floated this idea on David Allen’s blog last week), allow me to elaborate.

First, if we eliminate the diagnosis of ADHD, we can still do what we’ve been doing.  We can still evaluate children with attention or concentration problems, or hyperactivity, and we can still use stimulant medications (of course, they’d be off-label now) to provide relief—as long as we’ve obtained the same informed consent that we’ve done all along.  We do this all the time in medicine.  If you complain of constant toe and ankle pain, I don’t immediately diagnose you with gout; instead, I might do a focused physical exam of the area and recommend a trial of NSAIDs.  If the pain returns, or doesn’t improve, or you have other features associated with gout, I may want to check uric acid levels, do a synovial fluid analysis, or prescribe allopurinol.

That’s what medicine is all about:  we see symptoms that suggest a diagnosis, and we provide an intervention to help alleviate the symptoms while paying attention to the natural course of the illness, refining the diagnosis over time, and continually modifying the therapy to treat the underlying diagnosis and/or eliminate risk factors.  With the ultimate goal, of course, of minimizing dangerous or expensive interventions and achieving some degree of meaningful recovery.

This is precisely what we don’t do in most cases of ADHD.  Or in most of psychiatry.  While exceptions definitely exist, often the diagnosis of ADHD—and the prescription of a drug that, in many cases, works surprisingly well—is the end of the story.  Child gets a diagnosis, child takes medication, child does better with peers or in school, parents are satisfied, everyone’s happy.  But what caused the symptoms in the first place?  Can (or should) that be fixed?  When can (or should) treatment be stopped?  How can we prevent long-term harm from the medication?

If, on the other hand, we don’t make a diagnosis of ADHD, but instead document that the child has “problems in focusing” or “inattention” or “hyperactivity” (i.e., we describe the specific symptoms), then it behooves us to continue looking for the causes of those symptoms.  For some children, it may be a chaotic home environment.  For others, it may be a history of neglect, or ongoing substance abuse.  For others, it may be a parenting style or interaction which is not ideal for that child’s social or biological makeup (I hesitate to write “poor parenting” because then I’ll really get hate mail!).  For still others, there may indeed be a biological abnormality—maybe a smaller dorsolateral prefrontal cortex (hey! the DLPFC!) or delayed brain maturation.

ADHD offers a unique platform upon which to try this open-minded, non-DSM-biased approach.  Dropping the diagnosis of “ADHD” would have a number of advantages.  It would encourage us to search more deeply for root causes; it would allow us to be more eclectic in our treatment; it would prevent patients, parents, doctors, teachers, and others from using it as a label or as an “excuse” for one’s behavior; and it would require us to provide truly individualized care.  Sure, there will be those who simply ask for the psychostimulants “because they work” for their symptoms of inattentiveness or distractibility (and those who deliberately fake ADHD symptoms because they want to abuse the stimulant or because they want to get into Harvard), but hey, that’s already happening now!  My proposal would create a glut of “false negative” ADHD diagnoses, but it would also reduce the above “false positives,” which, in my opinion, are more damaging to our field’s already tenuous nosology.

A strategy like this could—and probably should—be extended to other conditions in psychiatry, too.  I believe that some of what we call “ADHD” is truly a disorder—probably multiple disorders, as noted above; the same is probably true with “major depression,” ”bipolar disorder,” and just about everything else.  But when these labels start being used indiscriminately (and unfortunately DSM-5 doesn’t look to offer any improvement), the diagnoses become fixed labels and lock us into an approach that may, at best, completely miss the point, and at worst, cause significant harm.  Maybe we should rethink this.

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Biomarker Envy IV: The Exmobaby

June 12, 2011

To what lengths would you go to keep your child healthy?  Organic, non-GMO baby food?  Hypoallergenic baby lotions and shampoos?  Bisphenol-free baby bottles?  How about a battery-powered biosensor garment that transmits ECG, skin temperature, and other biometric data about your baby wirelessly to your computer or via SMS message to your smartphone in real time?

Never fear, the Exmobaby is here.  Introduced late last year (and shown in the picture above—by the way, I don’t think that’s Jeff Daniels as a paid spokesman), the Exmobaby is a sleep garment designed for babies aged 0-12 months, which contains “embedded, non-contact sensors, a battery-powered Zigbee transmitter pod, a USB Zigbee receiver dongle that plugs into a Windows PC,” and all the necessary software.  Their slogan is “We Know How Your Baby Feels.”

It sounds like science fiction, but in reality it’s just a souped-up, high-tech version of a baby monitor.  But is it an improvement upon the audio- or video baby monitors currently available?  Exmovere certainly thinks so.  And, luckily for them, there’s no shortage of worried parents who are willing to pay for peace of mind (the device starts at $1000 and goes up to $2500, plus monthly data charges). [Note: please see addendum below.]

But while this might be an example of “a fool and his money being soon parted,” Exmovere makes some claims about the product that are highly questionable.  I first learned about the Exmobaby in a post on the KevinMD website, in which Exmovere’s CEO, David Bychkov, commented that “using Exmobaby to observe and record physiological data symptomatic of emotional changes can be useful… if you are a parent of a child with autism.”

In other words, this isn’t just a fancy monitoring device, this is a high-tech way of understanding your child’s thoughts and emotions—an “emotional umbilical cord between mother and child”—and, quite possibly, a way to diagnose a psychiatric, neurodevelopmental disorder in your newborn, all in the comfort of your own home.

I surfed over to the Exmobaby web site, whose home page shows a smiling, happy infant wearing these newfangled jammies.  Cute!  And the device (?) looks harmless enough.  But the FAQ page is where it gets interesting (or scary, depending on your position).  One question asks, “how is it possible to detect emotional states using Exmobaby?”  The response sounds like pure 21st century biobehavioral mumbo jumbo:

Detection of emotion involves software that compares heart rate, delta temperature and movement data (arousal) to heart rate variability and skin temperature (valence). These data, if tracked over time, enable a system to “guess” from a series of words that could be used to describe an emotional state: anger, fatigue, depression, joy, etc….In the case of babies, Exmovere is asking its users to try something new: name states. Exmobaby software will monitor trends in vital states. Parents will be asked to name states, such as “giggly” or “grumpy,” and the system can and will alert them when the underlying readings that match those states are detected. The idea is … to create a deeper level of communication between babies and their parents at the beginning of such a critical relationship.

In plain English: they’re asking parents to correlate data from the Exmobaby software (rather than their direct observations of the baby, which is how parents used to interact with their kids) with what they consider to be the baby’s emotional state.  Thus:  “My baby’s happy because the software says he is” rather than using old-fashioned signs—you know, like smiles and giggles.

The Exmovere website also includes an article, clearly written for parents, on “Exmobaby and Autism.”  Now, autism and “autism-spectrum disorders” (ASDs) are hot topics receiving a great deal of attention these days.  ASDs currently have an estimated prevalence of 1 in 110 (and rising rapidly), with an average age of diagnosis of approximately 4 years.  Nonetheless, parents of children with ASDs begin to identify concerns by the age of 12 to 18 months, and finding a “biomarker” to enable earlier diagnosis would allay the fears and insecurities of new parents.

But is Exmovere preying on precisely these fears and insecurities?  Well, let’s first ask: is it even reasonable to think about diagnosing ASDs before the age of 12 months (when the Exmobaby garment would be worn?).  A recent study showed that ASDs could be diagnosed as early as 14 months of age, based on social and communication development (but no biometric measures).  The American Association of Pediatrics recommends ASD screening (an interview with the parents and structured observation of the child) at ages 18 and 24 months, no earlier.  And a recent article in Pediatrics remarked that there are few measures sensitive and specific enough to detect ASD before 2 years of age (and, again, no “biological” measures to speak of).

The Exmobaby handout (which I’ve uploaded here), on the other hand, is a perfect example of a drug/device manufacturer capitalizing on the fears of parents by conflating statistics, commentary, and recommendations in a way that makes their device sound like a vital necessity for healthy infant development.  It’s deceptive marketing, pure and simple.

For example, it states “One of the ‘red flags’ in early diagnosis of ASDs is a lack of response from baby to the use of their name. Parents can potentially use Exmobaby to record times when baby’s name was said so that the reports will correlate any movement or vital sign response.”  Also, “specific tests can be designed in consultation with pediatricians to use Exmobaby to assist with diagnoses of ASDs and related developmental disorders.”  Never mind that there’s nothing in the literature correlating movement or vital-sign responses with diagnosing ASDs in this age group.

Conveniently, Exmovere also included its marketing strategy on its website (available here). It’s clear they’re planning to market Exmobaby as a garment (“a $5 billion per year worldwide market”) and not as a medical device.  That’s probably a good idea.  Or is it?  Bypassing medical professionals and tapping into a wide market of “worried well” might be good for business, but what about the “downstream” impact on our health care system?

So many questions.  But I’ll have to address them some other time, because I need to go make a sandwich.  I just got a text message telling me I’m hungry.

Addendum:  After posting this article, I received an email from Exmovere’s Investor Relations Advisor who pointed out that the $1000-$2500 prices I quoted above are for Evaluation Kits, specifically for distributors, researchers, and hospitals.  Exmobaby is not available for retail purchase at this time.  They anticipate a lower cost when the device/garment is sold directly to end users.


Biomarker Envy I: Cortical Thickness

May 13, 2011

In the latest attempt to look for biological correlates or predictors of mental illness, a paper in this month’s Archives of General Psychiatry shows that children with major depressive disorder (MDD) have thinner cortical layers than “healthy” children, or children with obsessive-compulsive disorder (OCD).  Specifically, researchers performed brain MRI scans on 78 children with or without a diagnosis, and investigated seven specific areas of the cerebral cortex.  Results showed four areas which were thinner in children with MDD than in healthy children, two which were thicker, and one that did not vary.

These results add another small nugget of data to our (admittedly scant) understanding of mental illness—particularly in children, before the effects of years of continuous medication treatment.  They also represent the bias towards imaging studies in psychiatry, whose findings—even if statistically significant—are not always that reliable or meaningful.  (But I digress…)

An accompanying press release, however, was unrealistically enthusiastic.  It suggested that this study “offers an exciting new way to identify more objective markers of psychiatric illness in children.”  Indeed, the title of the paper itself (“Distinguishing between MDD and OCD in children by measuring regional cortical thickness”) might suggest a way to use this information in clinical practice right away.  But it’s best not to jump to these conclusions just yet.

For one, there was tremendous variability in the data, as shown in the figure at left (click for larger view).  While on average the children with MDD had a thinner right superior parietal gyrus (one of the cortical regions studied) than healthy children or children with OCD, no individual measurement was predictive of anything.

Second, the statement that we can “distinguish between depression and OCD” based on a brain scan reflects precisely the type of biological determinism and certainty (and hype?) that psychiatry has been striving for, but may never achieve (just look at the figure again).  Lay readers—and, unfortunately, many clinicians—might read the headline and believe that “if we just order an MRI for Junior, we’ll be able to get the true diagnosis.”  The positive predictive value of any test must be high enough to warrant its use in a larger population, and so far, the predictive value of most tests in psychiatry is poor.

Third, there is no a priori reason why there should be a difference between the brains (or anything else, for that matter) of patients with depression and patients with OCD, when you consider the overlap between these—and other—psychiatric conditions.  There are many shades of grey between “depression” and “OCD”:  some depressed children will certainly have OCD-like traits, and vice versa.  Treating the individual (and not necessarily the individual’s brain scan) is the best way to care for a person.

To be fair, the authors of the study, Erin Fallucca and David Rosenberg from Wayne State University in Detroit, do not state anywhere in their paper that this approach represents a “novel new diagnostic method” or make any other such sweeping claims about their findings.  In fact, they write that the differences they observed “merit further investigation” and highlight the need to look “beyond the frontal-limbic circuit.”  In other words, our current hypotheses about depression are not entirely supported by their findings (true), so we need to investigate further (also true).  And this, admittedly, is how science should proceed.

However, the history of psychiatry is dotted with tantalizing neurobiological theories or findings which find their way into clinical practice before they’ve been fully proven, or even shown any great clinical relevance.  Pertinent examples are the use of SPECT scans to diagnose ADHD, championed by Daniel Amen; quantitiative EEG to predict response to psychotropics; genotyping for metabolic enzymes; and the use of SSRIs to treat depression.  (Wait, did I say that???)

The quest to identify “biomarkers” of psychiatric illness may similarly lead us to believe we know more about a disease than we do.  A biomarker is a biological feature (an endocrine or inflammatory measure, a genotype, a biochemical response to a particular intervention) that distinguishes a person with a condition from one without.  They’re used throughout medicine for diagnosis, risk stratification and monitoring treatment response.   A true biomarker for mental illness would represent a significant leap ahead in personalized treatment.  Or would it?  What if a person’s clinical presentation differs from what the marker predicts?  “I’m sorry Mrs. Jones, but even though Katie compulsively washes her hands and counts to twelve hundreds of times a day, her right superior parietal gyrus is too thin for a diagnosis of OCD.”

Other fields of medicine don’t experience this dilemma.  If you have an elevated hsCRP and high LDL, even though you “feel fine,” you are still at elevated risk for cardiovascular disease and really ought to take preventive measures (exercise, diet, etc).  (However, see this recent editorial in the BMJ about “who should define disease.”)  But if your brain scan shows cortical thinning and you have no symptoms of depression, do you need to be treated?  Are you even at risk?

Some day (hopefully) these questions will be answered, as we gain a greater understanding of the biology of mental illness.  But until then, let’s keep research and clinical practice separate until we know what we’re doing.  Psychiatry doesn’t have to be like other fields of medicine.  Patients suffer and come to us for help; let’s open our eyes and ears before sending them off to the scanner or the lab.  In doing so, we might learn something important.


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