All Swedish residents have their health records tracked through unique personal identity numbers. That makes it possible to identify psychiatric and medical disorders with great accuracy across an entire population, in this case encompassing more than five and a half million adults aged 18 to 64. A subgroup of more than 1.6 million persons between the ages of 50 and 64 enabled a separate examination of disorders in older adults.

Slightly over one percent of the entire population (about 61,000) were diagnosed with ADHD at some point as an adult. Individuals with ADHD were nine times as likely to suffer from depression as were adults not diagnosed with ADHD. They were also more than nine times as likely to suffer from anxiety or a substance use disorder, and twenty times as likely to be diagnosed with bipolar disorder. These findings are very consistent with reports from clinical samples in the USA and Europe.

Adults with ADHD also had elevated levels of metabolic disorders, being almost twice as likely to have high blood pressure, and more than twice as likely to have type 2 diabetes. Persons with ADHD but without psychiatric comorbidities were also almost twice as likely to have high blood pressure, and more than twice as likely to have type 2 diabetes.
Similar patterns were found in men and women with ADHD, although comorbid depression, bipolar disorder, and anxiety were moderately more prevalent in females than in males, whereas substance use disorder, type 2 diabetes, and hypertension were more prevalent in males than in females.

ADHD was less than a third as prevalent in the over-50 population as in the general adult population. Nevertheless, individuals in this older group with ADHD were twelve times as likely to suffer from depression, anxiety, or substance use disorders, and more than 23 times as likely to be diagnosed with bipolar disorder as their non-ADHD peers. They were also 63% more likely to have high blood pressure, and 72% more likely to have type 2 diabetes.

The authors noted, “Although the mechanisms underlying these associations are not well understood, we know from both epidemiologic and molecular genetic studies that a shared genetic predisposition might account for the co¬existence of two or more psychiatric conditions. In addition, individuals with ADHD may experience increased difficulties as the demands of life increase, which may contribute to the development of depression and anxiety.” As for associations with hypertension and type 2 diabetes, these “might reflect health ¬risk behaviors among adult patients with comorbid ADHD in addition to a shared biological substrate. As others have noted, inattention, disinhibition, and disorganization associated with ADHD could make it difficult for patients to adhere to treatment regimens for metabolic disorders.” They concluded that “Clinicians should remain vigilant for a wide range of psychiatric and metabolic problems in ADHD affected adults of all ages and both sexes.”

REFERENCES
Qi Chen, Catharina A. Hartman, Jan Haavik, Jaanus Harro, Kari Klungsøyr, Tor¬Arne Hegvik, Rob Wanders, Cæcilie Ottosen, Søren Dalsgaard, Stephen V. Faraone, Henrik Larsson, “Common psychiatric and metabolic comorbidity of adult attention-deficit/hyperactivity disorder: A population-based cross-sectional study,” PLoS ONE (2018), 13(9): e0204516. https://doi.org/10.1371/journal.pone.0204516.

Stephen V. Faraone, PhDA working group of the International League Against Epilepsy (ILAE), consisting of twenty experts spanning the globe (U.S., U.K., France, Germany, Japan, India, South Africa, Kenya, Brazil), recently published a “consensus paper” summarizing and evaluating what is currently known about comorbid epilepsy with ADHD, and best practices.

ADHD is two to five times more prevalent among children with epilepsy. The authors suggest that ADHD is underdiagnosed in children with epilepsy because its symptoms are often attributed either to epilepsy itself, or to the effects of antiepileptic drugs (AEDs).

The working group did a systematic search of the English-language research literature. It then reached consensus on practice recommendations, graded on the strength of the evidence.

Three recommendations were graded A, indicating they are well-established by evidence:

  • Children with epilepsy with comorbid intellectual and developmental disabilities are at increased risk of ADHD.
  • There is no increased risk of ADHD in boys with epilepsy compared to girls with epilepsy.
  • The anticonvulsant valproate can exacerbate attentional issues in children with childhood absence epilepsy (absence seizures look like staring spells during which the child is not aware or responsive). Moreover, a single high-quality population-based study indicates that valproate use during pregnancy is associated with inattentiveness and hyperactivity in offspring.

Four more were graded B, meaning they are probably useful/predictive:

  • Poor seizure control is associated with increased risk of ADHD.
  • Data support the ability of the Strengths and Difficulties Questionnaire (SDQ) to predict ADHD diagnosis in children with epilepsy: “Borderline or abnormal SDQ total scores are highly correlated with the presence of a validated psychiatric diagnosis (93.6%), of which ADHD is the most common (31.7%).” The SDQ can therefore be useful as a screening tool.
  • Evidence supports the efficacy of methylphenidate in children with epilepsy and comorbid ADHD.
  • Methylphenidate is tolerated in children with epilepsy.

At the C level of being possibly useful, there is limited evidence that supports that atomoxetine is tolerated in children with ADHD and epilepsy, and that the combined use of drugs for ADHD and epilepsy (polytherapy) is more likely to be associated with behavioral problems than monotherapy. In the latter instance, “Studies are needed to elucidate whether the polytherapy itself has resulted in the behavioral problems, or the combination of polytherapy and the underlying brain problem reflects difficult‐to‐control epilepsy, which, in turn, has resulted in the prescription of polytherapy.”

All other recommendations were graded U (for Unproven), “Data inadequate or conflicting; treatment, test or predictor unproven.” These included three where the evidence is ambiguous or insufficient:

  • Evidence is conflicted for the impact of early seizure onset on the development of ADHD in children with epilepsy.
  • Tolerability for amphetamine in children with epilepsy is not defined.
  • Limited evidence exists for the efficacy of atomoxetine and amphetamines in children with epilepsy and ADHD.

There were also nine U-graded recommendations based solely on expert opinion. Most notable among these:

  • Screening children with epilepsy for ADHD beginning at age 6.
  • Reevaluation of attention function after any change in antiepileptic drug.
  • Screening should not be done within 48 hours following a seizure.
  • ADHD should be distinguished from childhood absence epilepsy based on history and an EEG with hyperventilation.
  • Multidisciplinary involvement in transition and adult ADHD clinics is essential as many patients experience challenges with housing, employment, relationships, and psychosocial well‐being.

REFERENCES
Stéphane Auvin et al., “Systematic review of the screening, diagnosis, and management of ADHD in children with epilepsy. Consensus paper of the Task Force on Comorbidities of the ILAE Pediatric Commission,” Epilepsia (2018), doi: 10.1111/epi.14549. [Epub ahead of print].

 

Stephen V. Faraone, PhDA Norwegian team based at the University of Bergen recently performed a population study using the country’s detailed national health registries. With records from more than two and a half million Norwegians, the team examined what, if any, associations could be found between ADHD and nine autoimmune diseases: ankylosing spondylitis, Crohn’s disease, iridocyclitis, multiple sclerosis, psoriasis, rheumatoid arthritis, systemic lupus erythematosus, type 1 diabetes, and ulcerative colitis.

After adjusting for age and maternal education, the team found no association between ADHD and five of the nine autoimmune disorders: type 1 diabetes, rheumatoid arthritis, iridocyclitis, systemic lupus erythematosus, and multiple sclerosis. In the case of ankylosing spondylitis, it found no association with males with ADHD, but a negative association with females. Females with ADHD were less likely to have ankylosing spondylitis. The adjusted odds ratio (aOR) was 0.56 (95% CI 0.32-0.96).

Positive associations were found for only three autoimmune diseases. The strongest was for psoriasis, with adjusted odds ratios of 1.6 (95% CI 1.5-1.7) for females and 1.3 (95% CI 1.2-1.4) for males. When further adjusted for education, smoking, and body mass index (BMI), however, the adjusted odds ratio for females with ADHD dropped to 1.3 (95% CI 1.0-1.6).

The second strongest association was with Crohn’s disease. But here it was only among women. The odds ratio in this case was 1.4 (95% CI 1.2-1.8). Males with ADHD were actually less likely to have Crohn’s disease, with an odds ratio of 0.71 (95% CI 0.54-0.92).

Finally, females with ADHD were slightly more likely to have ulcerative colitis, with a barely significant odds ratio of 1.3 (95% CI 1.1-1.5), while no such association was found for males with ADHD, whose odds ratio was a statistically nonsignificant 0.9.

Given the large sample size of over two and a half million, this is no underpowered study. It found no association between ADHD and the generic category of autoimmune disorders. Furthermore, it is a stretch to argue that there are any clear and clinically meaningful links between ADHD and any of the specific disorders that were analyzed in this study. The small and often opposite effect sizes may simply reflect limitations with the data (presumed autoimmune disorders were identified based on drugs prescribed), or to other unidentified confounding factors.

REFERENCES
Tor‐Arne Hegvik, Johanne Telnes Instanes, Jan Haavik, Kari Klungsøyr, Anders Engeland, “Associations between attention‐deficit/hyperactivity disorder and autoimmune diseases are modified by sex: a population‐based cross‐sectional study,” European Child & Adolescent Psychiatry, vol. 27 (2018), 663-675.

Stephen V. Faraone, PhDAn international team of researchers has carefully examined the best current evidence and found strong evidence for an association between asthma and ADHD by combining a meta-analysis of prior data with a new analysis of the Swedish population.

The meta-analysis identified 46 datasets with a total of more than 3.3 million persons. It computed an unadjusted odds ratio (OR) of 1.7, which indicates that ADHD patients have about twice the risk of developing asthma compared with people without ADHD. Limiting the meta-analysis to studies that adjusted for confounding factors, 30 datasets with more than a third of a million participants still led to an adjusted odds ratio of 1.5 (95% CI 1.4 – 1.7). The likelihood of obtaining this result by chance in such a large sample would be less than one in ten thousand.

When the team further checked this result against the results for the Swedish population ofmore than one and a half million persons, the odds ratio was an almost identical 1.6. Adjusting for confounding factors reduced it to 1.5 (95% CI 1.41 – 1.48). That means the findings are very robust: asthma and ADHD are associated, with an odds ratio of 1.5, after adjusting for confounding factors.

What does this small but statistically very reliable association between asthma and ADHD mean? For researchers, it suggests that the two disorders may have common risk factors and that the search for these shared risk factors might lead to improved treatments. These risk factors might also be shared with two other somatic conditions for which ADHD patients are at increased risk: obesity and eczema. It is possible that common inflammatory processes account for this overlap among disorders. Clinicians should be aware that children with asthma have an increased risk for ADHD, although given the small association, systematic screening may not be warranted. But given that ADHD might interfere with asthma medication compliance, the disorder should be considered among noncompliant youth, especially those who show other evidence of inattention, poor memory or disorganization.

REFERENCES
Samuele Cortese, Shihua Sun, Junhua Zhang, Esha Sharma, Zheng Chang, Ralf Kuja-Halkola, Catarina Almqvist, Henrik Larsson, Stephen V Faraone, “Association between attention deficit hyperactivity disorder and asthma: a systematic review and meta-analysis and a Swedish population-based study,” Lancet Psychiatry, Published online July 24, 2018.
https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(18)30224-4/fulltext

This article provides a review of the cardiovascular effects of ADHD medications including potential effects on blood pressure, heart rate and risk of cardiovascular events (myocardial infarction, sudden death and stroke).

The article notes that meta-analyses have generally found that the effects of stimulant medications and atomoxetine were generally similar on systolic blood pressure (1-3 mm Hg) and heart rate (2-5 beats/minute); these were felt to be of limited clinical significance, except for patients with elevated blood pressures or heart rate antecedent to starting these ADHD therapies. However, as these are average changes, changes in individual patients may vary and important to monitor. Additionally, the meta-analysis and observational data available also do not find significantly higher risks for MI or stroke in patients receiving stimulant medications. These findings are complicated by the use of clinical trial data in the meta-analysis which specifically limit is the enrollment of patients with higher risks of pre-existing cardiovascular illnesses and the observational data were of relatively short treatment exposures.

This article is important for clinicians because it reviews the cardiovascular safety profiles of current ADHD medications and also recommends monitoring of blood pressure and pulse at baseline and during treatment. Furthermore, the authors recommend baseline screening patients for significant cardiovascular histories via family history of cardiovascular disease and sudden death.

REFERENCES
https://www.healio.com/psychiatry/journals/psycann/2018-7-48-7/%7B426ecc52-e3d9-4f38-afc6-34cbf88548c7%7D/review-of-cardiovascular-effects-of-adhd-medications#divReadThis

Stephen V. Faraone, PhDAn international group of twelve experts recently published a consensus report examining the state of the evidence and offering recommendations to guide screening, diagnosis, and treatment of individuals with ADHD-SUD comorbidity.[1]

In a clear sign that we are still in the early stages of understanding this relationship, five of the thirteen recommendations received the lowest recommendation grade (D), eight received the next-lowest (C), and none received the highest (A and B). The lower grades reflected the absence of the highest level of evidence, obtained from meta-analyses or systematic reviews of relevant randomized controlled trials (RCTs).

Nevertheless, with these limitations in mind, the experts agreed on the following points:

Diagnosis

  • The strongest recommendation, the only one based on a 2+ level of evidence (well-conducted case control or cohort studies with a low risk of confounding or bias and a moderate probability that the relationship is causal) is that the “Short Version of the Adult ADHD Self-Report Scale (ASRS-SV) screener is currently the most widely used and investigated screening tool in individuals with ADHD and comorbid SUD, with good sensitivity and specificity across studies.”
  • Two other recommendations were graded C: The diagnostic process should include current and past substance abuse and seek to involve partners and relatives in evaluating symptoms and functional impairments.
  • Four recommendations got the lowest grade, D. The experts suggested starting the diagnostic process as soon as possible and focusing on drug- and alcohol-free periods in the patient’s life during history taking. They also recommended that physicians and clinical psychologists should only make diagnoses if they have extensive training in diagnosing ADHD, as well as experience with adults with ADHD and with addiction care, and that they should consider treating adults with sufficiently severe ADHD symptoms.

Treatment

  • In general, evidence was stronger in this area, and only one of the six recommendations was graded D. The other five recommendations were graded C, with the highest level of evidence being 2 (cohort or case and control studies with undetermined risk of bias), although in three cases it was level 3 (non-analytical studies, such as case reports and case series).
  • The grade D recommendation was to always consider a combination of psychotherapy and pharmacotherapy.

The grade C recommendations included considering adequate medical treatment of both ADHD and SUD; integrating ADHD treatment with SUD treatment as soon as possible;
considering psychotherapy targeting both; use of long-acting methylphenidate, extended-release amphetamines, and atomoxetine because of their low potential for abuse; and careful clinical management to avoid abuse and diversion of prescribed stimulants.

[1] Cleo L. Crunelle at al., “International Consensus Statement on Screening, Diagnosis and Treatment of Substance Use Disorder Patients with Comorbid Attention Deficit/Hyperactivity Disorder,” European Addiction Research, published online March 6, 2018, DOI: 10.1159/000487767.

ADHD Affects the Efficacy of Treatment for Eating Disorders in Adult Women

Stephen V. Faraone, PhDSwedish researchers examined outcomes for adult women who sought treatment at the Stockholm Centre for Eating Disorders over a period of two years and nine months. Out of 1,517 women who came to the clinic 1,143 remained eligible for the study, after excluding women whose symptoms did not fulfill the DSM-IV criteria for eating disorders or had incomplete records.

Of these, seven hundred patients could not be reached or declined to participate, leaving 443 for follow-up. To guard against the possibility that the follow-up group might not be representative of the overall treatment group, researchers compared age, body mass index, and scores on tests for depression, anxiety, compulsivity, inattention, and hyperactivity. The only statistically significant differences were small ones. The median age of the group lost to follow-up was one year younger, they were less likely to be living alone, and on average scored a single point higher on the depression test. Otherwise they were broadly similar.

The one-year follow-up on the study group found a substantial difference in rate of recovery from eating disorders between those wEating disorders and ADHDith and without comorbid ADHD. Almost three out of four patients (72%) who scored lower (between 0-17) on the World Health Organization adult ADHD self-report scale had recovered from their eating disorder. Among those scoring 18 and higher, on the other hand, it was less than half (47%). This difference was extraordinarily unlikely (one chance in one thousand) to be due to chance (p=.001).

Another way of expressing this is through odds ratios. Those scoring 18 and up on the ADHD self-report scale were about two and a half times less likely to recover from their eating disorders following treatment. More specifically, they were about three times less likely to recover from loss of control and binging, and almost three and a half times less likely to recover from purging.

To improve outcomes, the researchers suggest “identifying concomitant ADHD symptoms and customizing treatment interventions based on this.” They specifically propose controlled clinical trials to explore the effect of combining stimulant medications with standard treatment for eating disorders.

REFERENCES
Nils Erik Svedlund, Claes Norring, Ylva Ginsberg, Yvonne von Hausswolff‐Juhlin, “Are treatment results for eating disorders affected by ADHD symptoms? A one‐year follow‐up of adult females,” European Eating Disorders Review (2018).

Stephen V. Faraone, PhDAn international group of twelve experts recently published a consensus report examining the state of the evidence and offering recommendations to guide screening, diagnosis, and treatment of individuals with ADHD-SUD comorbidity.1

In a clear sign that we are still in the early stages of understanding this relationship, five of the thirteen recommendations received the lowest recommendation grade (D), eight received the next-lowest (C), and none received the highest (A and B).

The lower grades reflected the absence of the highest level of evidence, obtained from meta-analyses or systematic reviews of relevant randomized controlled trials (RCTs).

Nevertheless, with these limitations in mind, the experts agreed on the following points:

ADHD Diagnosis

  • The strongest recommendation, the only one based on a 2+ level of evidence (well-conducted case control or cohort studies with a low risk of confounding or bias and a moderate probability that the relationship is causal) is that the “Short Version of the Adult ADHD Self-Report Scale (ASRS-SV) screener is currently the most widely used and investigated screening tool in individuals with ADHD and comorbid SUD, with good sensitivity and specificity across studies.”
  • Two other recommendations were graded C: The diagnostic process should include current and past substance abuse and seek to involve partners and relatives in evaluating symptoms and functional impairments.
  • Four recommendations got the lowest grade, D. The experts suggested starting the diagnostic process as soon as possible and focusing on drug- and alcohol-free periods in the patient’s life during history taking. They also recommended that physicians and clinical psychologists should only make diagnoses if they have extensive training in diagnosing ADHD, as well as experience with adults with ADHD and with addiction care, and that they should consider treating adults with sufficiently severe ADHD symptoms.

ADHD Treatment

  • In general, evidence was stronger in this area, and only one of the six recommendations was graded D. The other five recommendations were graded C, with the highest level of evidence being 2 (cohort or case and control studies with undetermined risk of bias), although in three cases it was level 3 (non-analytical studies, such as case reports and case series).
  • The grade D recommendation was to always consider a combination of psychotherapy and pharmacotherapy.
  • The grade C recommendations included considering adequate medical treatment of both ADHD and SUD; integrating ADHD treatment with SUD treatment as soon as possible; considering psychotherapy targeting both; use of long-acting methylphenidate, extended-release amphetamines, and atomoxetine because of their low potential for abuse; and careful clinical management to avoid abuse and diversion of prescribed stimulants.

Note: Andrew Reding is a co-author on this post.

REFERENCES
1Cleo L. Crunelle at al., “International Consensus Statement on Screening, Diagnosis and Treatment of Substance Use Disorder Patients with Comorbid Attention Deficit/Hyperactivity Disorder,” European Addiction Research, published online March 6, 2018, DOI: 10.1159/000487767.

   
Joseph_Biederman_AIA_rX8AEqAmy_Yule_w_credentials_nHHCtD
While it has been well documented that attention deficit hyperactivity disorder (ADHD) and substance use disorders (SUD) commonly co-occur, little is known about the reasons for this association.  Since both disorders are highly heritable one hypothesis is the high co-occurrence may be due to common genes.  One way to assess for a genetic relationship between ADHD and SUD is through a familial risk analysis.  Familial risk analysis compares the prevalence of an illness in relatives of individuals with a given disorder based on the presence or absence of the same illness in relatives.  Since both ADHD and SUD are known familial illnesses, we can expect relatives of individuals with ADHD and SUD to have a higher prevalence of the same disorders.   

The way in which these two disorders aggregate in families can provide insight as to the nature of the association between the disorders.  If ADHD and SUD are independent disorders we would expect that different relatives of affected individuals with each condition would be affected with the same disorder.  For example, an individual with ADHD would have many relatives with ADHD and an individual with SUD would have many relatives with SUD.  Another possibility is that the genes that produce one disorder (ADHD or SUD) would express both risks in relatives.  For example, an individual with ADHD would have many relatives with ADHD or SUD afflicting different relatives.  A third possibility is that an individual with co-occurring ADHD and SUD would have many relatives who also have co-occurring ADHD and SUD.  This latter scenario is known as co-segregation and it usually suggests that the combined condition is driven by closely linked genes that are inherited together.  

Through the Massachusetts General Hospital longitudinal family studies of boys and girls with and without ADHD and their first-degree relatives we were able to test these hypotheses and examine the nature of the relationship between ADHD and SUD.  These children were first assessed in childhood and followed prospectively onto young adult years (“grown-up child”) through the peak period of risk for the development of addictions.  Our sample consisted of 404 subjects with a mean age of 22 years and their 1,336 relatives.  All individuals who participated in the study were systematically assessed with structured diagnostic interviews. Our findings showed that SUD in a grown-up child significantly increased the risk for SUD in relatives irrespective of having ADHD, and that ADHD in the grown-up child significantly increased the risk for SUD in relatives irrespective of whether or not the grown-up child had a SUD.   Our results also showed that grown-up children with both ADHD and SUD co-occurring together had an excess of relatives in which both conditions were present in the same relative (co-segregation).  Furthermore, we found the risk for SUD was not specific to alcohol or drug dependence indicating that what it is inherited is a general increased risk to develop a SUD. Finally, we documented that these risks were equally operant in boys and girls indicating that these risks are due to ADHD and not the sex of the affected individual.

Taken together, these patterns of familial aggregation point to three overlapping risks for the development of SUD in ADHD that include common familial etiological factors due to genes associated with ADHD, genes associated with SUD, and genes associated with their combined presence.  This triple risk may explain why the risk for SUD is so high in individuals with ADHD.

While these findings support the hypothesis that genetic influences are involved in mediating the risk for SUD in ADHD, we were also interested in examining familial environmental influences such as parental modeling of substance use through exposure to a parent with an active SUD. Our findings revealed that exposure to maternal SUD, but not paternal SUD, during adolescent years was associated with a modest increased risk for SUD in offspring (Yule 2013).  Taken together, these findings suggest that genetic influences are an important determinant of risk for SUD in children with ADHD.  Although modest, exposure to active maternal SUD also has a detrimental effect in moderating the risk for SUD in their adolescent offspring.

Our findings have clinical and public health implications.   Clinically, when a youth presents for treatment of ADHD clinicians should screen for SUD in the child and the family.  When a youth presents for the management of SUD, clinicians should also screen the youth and their family members for ADHD.  Since ADHD typically onsets years before the onset of substance use, ADHD children could benefit for early intervention strategies aimed at mitigating the risk for subsequent SUD.  For example, treatment for ADHD has also been shown to be an important intervention to decrease risk for SUD among youth with ADHD (Biederman 1999).          

In summary, the bidirectional association between ADHD and SUD seems to be due to strong genetic links between the two disorders.  All children within families with ADHD should be closely monitored for SUD.

 

REFERENCE

Yule, A. M., Martleon, M., Faraone, S., Carrellas, N., Wilens, T. E., & Biederman, J. (2017). Examining the association between attention deficit hyperactivity disorder and substance use disorders: A familial risk analysis. Journal of Psychiatric Research(85), 49-55.

 

Yule, A. (2013). The Impact of Exposure to Parental Substance Use Disorders on Substance Use Disorder Risk in Growing-Up Boys and Girls. Poster presented at the American Academy of Child and Adolescent Psychiatry, Orlando, FL.


Biederman, J., Wilens, T., Mick, E., Spencer, T., & Faraone, S. (1999). Pharmacotherapy of attention-deficit/hyperactivity disorder reduces risk for substance use disorder. Pediatrics, 104(2), e20.

http://medicalwritingtraining.com/Over the past few decades, a consensus has emerged among psychopathologists that some patients exhibit a well-defined syndrome referred to as sluggish cognitive tempo or SCT. There are no diagnostic criteria for SCT because it has not yet been accepted as a separate disorder by the American Psychiatric Association. People with SCT are slow-moving, indolent and mentally muddled. They often appear to be lost in thoughts, daydreaming, drowsy or listless. In reviewing these symptoms and the literature, Barkley suggested that SCT be referred to as Concentration Deficit Disorder (CDD). This term is less pejorative but is not yet commonly used. Becker and colleagues recently evaluated the internal and external validity of SCT via a meta-analysis of 73 studies. Internal validity addresses the consistency of SCT symptoms as measure of an underlying construct. Based on factor analytic studies using more than 19,000 participants, the authors concluded that the items purported to measure SCT are sufficiently correlated with one another to justify the idea that they measure the same underlying construct. Further support for internal validity was found in studies reporting high test-retest and interrater reliability. As regards ADHD, the authors found that SCT correlated significantly with both inattentive (r = 0.72) and hyperactive-impulsive (r = 0.46) symptoms in adults. The greater correlation with inattentive symptoms makes sense given the nature of SCT symptoms. So these data confirm two key points about SCT: 1) it is definitely associated with ADHD symptoms and 2) it is a meaningful construct in its own right. Very little is known about the implications of SCT for the treatment of ADHD. In a naturalistic study of 88 children and adolescents with ADHD, Ludwig and colleagues examined the effect of SCT on the response of ADHD symptoms to methylphenidate. They found no significant differences in treatment response between subjects with and without SCT. McBurnett and colleagues tested the effects of atomoxetine on SCT in children with ADHD and dyslexia (ADHD+D) or dyslexia only. Atomoxetine treatment led to significant reductions in both ADHD symptoms and SCT outcomes. Because controlling for changes in ADHD symptoms did not predict changes in SCT outcomes, the authors concluded that change in SCT in response to atomoxetine is mostly independent of change in ADHD. Although these data are preliminary and in need of replication, they do provide some guidance for clinicians dealing with ADHD patients who also have SCT.
 

REFERENCE
Becker, S. P., Leopold, D. R., Burns, G. L., Jarrett, M. A., Langberg, J. M., Marshall, S. A., McBurnett, K., Waschbusch, D. A. & Willcutt, E. G. (2016). The Internal, External, and Diagnostic Validity of Sluggish Cognitive Tempo: A Meta-Analysis and Critical Review. J Am Acad Child Adolesc Psychiatry 55, 163-78.

Ludwig, H. T., Matte, B., Katz, B. & Rohde, L. A. (2009). Do sluggish cognitive tempo symptoms predict response to methylphenidate in patients with attention-deficit/hyperactivity disorder-inattentive type? J Child Adolesc Psychopharmacol 19, 461-5.

McBurnett, K., Clemow, D., Williams, D., Villodas, M., Wietecha, L. & Barkley, R. (2016). Atomoxetine-Related Change in Sluggish Cognitive Tempo Is Partially Independent of Change in Attention-Deficit/Hyperactivity Disorder Inattentive Symptoms. J Child Adolesc Psychopharmacol.

Barkley, R. A. (2014). Sluggish cognitive tempo (concentration deficit disorder?): current status, future directions, and a plea to change the name. J Abnorm Child Psychol 42, 117-25.