In an article soon to be published in the Journal of Child Psychology and Psychiatry I, with a colleague at the University of Pittsburgh, discuss the need for a new approach to the development of early therapeutic interventions for child depression, as current interventions are, sadly, barely effective (see this article for a more extensive discussion on the efficacy of child depression treatments). Our basic argument is that most current interventions are not designed to address the underlying processes and pathways that lead to the emergence of depression in childhood. This is partially due to a disconnect between what we know about the development of child depression (basic science) and how clinicians are trained to diagnosed and work with these conditions.  So I was not surprised, although I was excited, when I read a new article in the same journal that discussed the need for the development of new early interventions for the treatment of ADHD. In this article, the authors use many of the same arguments we use to advocate for new child depression treatments. I was excited because this is a reflection of the ongoing changes in our entire field that advocate for 1) a reconceptualization of ‘disorder’ and its onset, and 2) more ‘translational science’ or the translation of basic scientific discoveries into clinical and practical applications.

How do we improve early interventions for ADHD?

The authors of this paper present a basic framework that should guide the development of new treatments:

1. That the development of treatment involves the identification of, and targeting, the underlying causes of the condition (rather than only addressing symptoms – see below for more about this)

2. That ’causes’ are framed within a developmental process. That is, rather than seeing causes as fixed events (e.g., a specific physiological anomaly), causes for developmental disorders are indeed ‘developmental processes’ (e.g., anomalies in the development of specific physiological process for a specific developmental period).

3. That treating these processes early can alter the developmental trajectory of this condition and thus prevent the full emergence of the disorder.

Regarding the last point the authors go on to explain how we need to reconceptualize the definition of disorder, or disorder-onset. Traditionally, most diagnostic criteria of psychiatric disorders require that the condition produce functional impairment. Thus, the symptoms must be severe enough to cause actual dysfunction in the person’s personal, occupational, or educational life. Only if the symptoms produce impairment you “have” the disorder. Although there are many valid theoretical arguments for the need of the ‘impairment’ requirement in the current diagnostic definition of most psychiatric disorders, this criteria has a political rather than empirical foundation. That is, the wide application of the ‘impairment’ criteria to most conditions is not consistent with our understanding of the development of many psychiatric condition. Specifically,  in many cases, the syndrome is likely present before there are significant symptoms and consequently before there is noticeable impairment.

But what does this have to do with treatment? How can a change in our conceptualization of disorders improve the prevention of these conditions?

Imagine for a second that oncologists decided that you have to show symptoms that are so apparent that you can actually describe them (e.g., I feel a mass on my back) and that these symptoms have to cause impairment (e.g., it hurts so much I can’t go to work) BEFORE they can provide a diagnosis of cancer, offer treatment, and be reimbursed by insurance companies. We would all think this would be crazy because we know that the effectiveness of cancer treatment increases if you can treat the condition at the earliest possible stage. I know this is an extreme example, but it highlights the current limitations of psychiatry. Our practice of providing diagnoses and interventions once symptoms are observable and producing functional impairment is greatly limiting the effectiveness of current therapeutic approaches. Furthermore, such conceptualization has resulted in a view of disorders that is static  – you have it when it causes impairment — rather than dynamic — disorders have a developmental trajectory and only the end of the trajectory may cause impairment. Today we mostly diagnose and treat the end of the trajectory, when it’s likely too late for too many.

The reference:

Edmund J.S. Sonuga-Barke, & Jeffrey M. Halperin (2010). Developmental phenotypes and causal pathways in attention deficit/hyperactivity disorder: potential targets for early intervention? Journal of Child Psychology and Psychiatry

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12 Responses to Early intervention for ADHD: More thoughts on our definitions of psychiatric disorders

  1. Onyx_jbl says:

    I’m wondering if your analogy to cancer is valid. Are there some sort of physiological markers for depression/ADHD? Because with cancer, you can actually detect physical changes; I didn’t think that was the case with psychological disorders(or at least not these ones). By casting your net wider, you may end up treating people for things they won’t develop, which may have its own negative effects.

    • The risks you mention are true, especially if the net lacks specificity. There are some markers for most disorders, but none specific enough to be used as an early marker that indicates the presence of the disorder.

      But my argument is that the current conceptualization of disorder as “observable symptoms that cause impairment” is an obstacle to research that would help us identify the type of physiological, cognitive, and affective markers of the early stages (pre-impairment) of a disorder. For example, there has not been a single study on possible prodomal processes in child depression that examines “changes” in physiological or cognitive processes prior to the onset of the first depressive episode. The markers may be there, we just don’t know what they are.

      I agree the cancer example is a bit extreme and that this is a complicated but very interesting issue. Thanks.

  2. JulieL says:

    For ADHD the main marker is the development of the prefrontal cortex. It lags behind in it’s development, up to several years (3-4). My question is, just what exact intervention could spead this process up, and is it even plausible. While rhetoric is important, it seems to me what we can tangibly do with it is moreso. But I agree, research for markers, and their possible interventions are indeed very important and much needed.

  3. RAJ says:

    A recent study related to early detection of signs for autism was published that showed no evidence that autism ‘markers’ can identify children as young as six months to be at risk for the development of autism.

    The study recruited infant siblings with a family history of autism, those who were at risk for the development of autism. The siblings were tested for abnormal eye gaze and abnormal affective interaction behaviors with the mothers. Both were thought to be early markers for autism risk.

    At 18 month followup, none of the siblings thought to be at risk for the development of autism showed any signs of autism. In contrast, three of the siblings who showed no signs of abnormal gaze behavior or abnormal affective interaction behaviors with their mothers at six months were diagnosed with autism at followup.

    http://www.ncbi.nlm.nih.gov/pubmed/19702771?

    There are significant problems with trying to identify those who may be at risk for autism. Siblings with early markers for autism would be referred for intense early intervention and it could then be claimed that since none of the at risk infants who underwent intensive therapy were diagnosed with autism at followup early, diagnosis and referral to intense early intervention prevented autism in the group while those who were not referred to early intervention resulted in three cases who at followup were diagnosed with autism.

    The emotional distress and financial hardships of parents who are told that their babies showed early signs of autism and should immediately undergo intense early intervention is incalculable.

    • RAJ I am 100% in agreement that there are some major risks with ‘early markers’ research, especially in regards to the inappropriate and dangerous adoption of untested treatments based on preliminary basic science data (e.g., immune suppressant therapy in autism). However, the study you mentioned worked precisely how science is supposed to work: potential risk factor was identified, tested, and found to be non-specific and non-predictive. This then in turn should inform future researchers.

      On a related note, early risk and vulnerability factor research is not the same as prodromal research (what I advocate), even though sometimes people incorrectly assume they are the same. Risk and vulnerability factors refer to characteristics of the environment or the individual that may make a person more likely to acquire a disorder. However, prodromal factors are characteristics of the disorder an at early stage in the progression of the disorder. Methodologically, the most important difference between these two perspectives is that true prodromal research examines ‘change’ in the phenomenology of the potential marker (prodrome process) that signal the emergence of the condition within a specific time period. In contrast, risk factor research examines whether the presence (not change) of a factor increases the odds for the disorder in the future. Risk factors inform prevention intervention while prodrome factors inform early treatment interventions.

  4. Farouk says:

    thanks for the detailed explanation

  5. RAJ says:

    Here is the current redefinition of autism under review by the APA’s working group on autism along the lines you discussed:

    http://www.psych.org/MainMenu/Research/DSMIV/DSMV/DSMRevisionActivities/DSM-V-Work-Group-Reports/Neurodevelopmental-Disorders-Work-Group-Report.aspx

    This concept includes a category called normal variation ASD for those who are ‘socially isolated’ or ‘awkward’ which are normal for the developmental age and cause no impairment.

    Just how prevalent are normal variation autistic-like traits in the general population?

    “Plomin et al. (2006) have published what can be invoked as tentative cutoffs for ALT’s in the general population. Using questionnaires completed by parents or teachers from a large sample of twins taken from a British twin registry, Plomin’s group has described the 5% highest scorers as possessing ‘extreme autistic-like traits’ and “Around 10% of all children showed only social impairment, only communicative difficulties or only rigid and repetitive interests and behavior, and these problems appeared to be at a level of severity comparable to that found in children with diagnosed ASD in our sample” ( Plomin et al 2006 ), (Plomin et al 2006 P1218 )”.

    If the working group gets this way, the entire concept of autism and will a become meaningless applied label with a rubber-stamp ‘autism spectrum disorder’ applied to all sorts of children. This will extend the high limits of autism prevelance rates to a spectacular 10% of the entire population who will be under the microscope of child psychology and child psychiatry.

    The redefining of autism as a spectrum disorder will take the concept of diagnostic substitution to its logical end point, and will, obscure the boundaries between a debilitating neurological disorder and common normal trait variations that extend very broadly across the entire general population.

    • RAJ the point you raise is well taken and very applicable to the current DSM-V discussions and I’m in agreement with you about it. That is, I don’t advocate for the ‘continuum” of symptoms perspective. Instead, I advocate for the identification of prodromes: features that reliable predict the onset of the full syndrome before impairment is apparent. This is NOT the same as thinking that normal variations in traits, symptoms, etc, are part of the continuum of a disorder. When I think about disorders having a developmental progression, with only the last phase producing impairment, I don’t see the progression as simply reflecting different intensities or frequencies of symptoms (in the case you discuss: going from a few autism traits to many autism traits). Instead, I see the progression as having a specific temporal pattern of symptoms and features that reliably predict the onset of the syndrome. We are not there yet with ANY disorder, so my thinking is mostly wishful thinking. Nestor.

  6. RAJ says:

    Nestor;
    A last thought. In his 1943 seminal paper that introduced the concept of infantile autism as a distinct, previously unrecognized condition, he quoted Rose Zeligs in the preface to his paper:

    ‘To understand and measure emotional qualities is very difficult. Psychologists and educators have been struggling with that problem for years but we are still unable to measure emotional and personality traits with the exactness with which we can measure intelligence’.
    Rose Zeligs in ‘Glimpses into Child Life’

    This is as true today as it was five decades ago, at least in my opinion.

  7. JulieL says:

    Except that our measurement for intelligence is still flawed. ;)

  8. According to my knowledge Attention deficit hyperactivity disorder (ADHD) is a disorder that affects millions of school-aged children,the disorder can persist into adulthood.The main symptoms associated with ADHD are: hyperactivity impulsive behavior inattentiveness,so its time to buckle up doesn’t remain seated go for meditation will feel better.Thanks for your wonderful thoughts.

  9. Psyche says:

    The best intervention for ADHD is not to validate the alternative. We must first eliminate excessive sugars, trace caffeine and other stimulants from children’s lifestyles before even considering ADHD as we would insist that adult drug addicts get “clean” before a clear diagnosis can be implemented. Let’s not mention the how children are labeled as such for the sake of job security. – http://psy.co

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