Mild Traumatic Brain Injury and ADHD

Abstract

Objective: This study investigated the association between mild traumatic brain injury (mTBI) and ADHD, which increases risk of injuries and accidents. Method: We conducted a systematic review and meta-analysis of studies that examined the relationship between mTBI and ADHD. Results: Five studies, comprising 3,023 mTBI patients and 9,716 controls, fit our a priori inclusion and exclusion criteria. A meta-analysis found a significant association between ADHD and mTBI, which was significant when limited to studies that reported on ADHD subsequent to mTBI and when the direction of the association was not specified, but not for studies that reported mTBI subsequent to ADHD. Heterogeneity of effect size and publication biases were not evident. Conclusion: The literature documents a significant association between mTBI and ADHD. Further clarification of the relationship and direction of effect between mTBI and ADHD and treatment implications could have large clinical, scientific, and public health implications.

Keywords

ADHD traumatic brain injury meta-analysis review

Introduction

Mild traumatic brain injury (mTBI) or cerebral concussion is a leading cause of morbidity in the United States. It is also the largest category of brain injury, representing 70% to 90% of TBI complications (Langlois, Rutland-Brown, & Wald, 2006; Ruff, 2011). According to the Centers for Disease Control and Prevention, mTBI is estimated to result in 1.6 to 3.8 million cases each year and is described in a 2003 report to the U.S. Congress as a silent epidemic (National Center for Injury Prevention and Control, 2003; Ruff, 2011). In recent years, public and legislative concern about sport-related concussions and mTBI has greatly increased (Giza et al., 2013; Harmon et al., 2013). Public interest has been further catalyzed by the increased focus on the morbidity of injured athletes, recent highly publicized deaths of professional athletes associated with repetitive brain injury (Guskiewicz et al., 2005; Guskiewicz et al., 2007; Omalu et al., 2006; Omalu et al., 2005; Ruff, 2011). Given its high and increasing prevalence and pervasive deleterious sequelae, efforts to help identify factors that may put individuals at greater risk to develop an mTBI or complicate its course are of clinical, scientific, and public health significance.

The potential association between ADHD and mTBI is of potential interest for several reasons. ADHD is a persistent childhood onset neurobiological, neurodevelopmental disorder associated with impulsivity, risk-taking behavior, accidents, and injuries (Barkley, Guevremont, Anastopoulos, DuPaul, & Shelton, 1993; Barkley, Murphy, & Fischer, 2010; Biederman & Faraone, 2005; Fischer, Barkley, Smallish, & Fletcher, 2007; Lambert, 1995; Ramos Olazagasti et al., 2013). Thus, ADHD might place individuals at greater risk of mTBI. Furthermore, some investigators have hypothesized that mTBI could result in secondary ADHD. Considering that ADHD is a treatable disorder, clarifying the relationship between mTBI and ADHD would promote a better standard of care for patients with mTBI.

To assess the association between ADHD and mTBI, we conducted a systematic review and meta-analysis of the extant literature to assess evidence for ADHD being a risk factor for mTBI and for mTBI being a risk factor for the subsequent development of ADHD.

Method

Search Strategy and Selection Criteria

We performed a literature search through PubMed utilizing the following search algorithm: (Attention deficits OR hyperactivity OR attention deficit hyperactivity disorder OR attention deficit disorder OR hyperkinesis) AND (Traumatic brain injury OR brain injury OR concussion). This search resulted in 1,046 articles. A search of MeSH terms (attention deficit hyperactivity disorder AND [traumatic brain injury OR Brain concussion]) were used to cross-check the search and resulted in no additional studies. References were also reviewed and added if applicable to search criteria.

We included only original studies that specifically evaluated the relationship between ADHD and mTBI. We implemented the following inclusion criteria: (a) articles written in English, (b) original research, (c) specific mention of both ADHD and mTBI as disorders, and (d) studies that included a control group. Articles were excluded if they failed to (a) differentiate syndromatic pictures of ADHD from non-specific “attentional deficits,” (b) differentiate ADHD from learning disorders, (c) differentiate mild TBI from other severities of traumatic brain injury, or (d) evaluate the relationship between ADHD and TBI. We noted and extracted author definitions of ADHD and mTBI including use of the Glasgow Coma Scale (GCS) and Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria. Other exclusions comprised reviews, editorials, letters, and case reports.

Data Extraction

The following variables were extracted: (a) numbers of participants with ADHD in the mTBI and control groups, (b) age group (pediatric, adolescent, adult), (c) mode of mTBI diagnosis, (d) mode of ADHD diagnosis, (e) study design, and (f) type of control population.

Statistical Analyses

Our meta-analysis used the random effects model of DerSimonian and Laird (1986) that computes a pooled standardized mean difference weighted by sample size. We used the I² index to assess the heterogeneity of effect sizes (Higgins, Thompson, Deeks, & Altman, 2003). Its value lies between 0 and 100 and estimates the percentage of variation among effect sizes that can be attributed to heterogeneity. A significant I² suggests that the effect sizes analyzed are not estimating the same population effect size. We used meta-analytic regression to assess the degree to which effect sizes varied with methodological features (Hedges & Olkin, 1985; Hunter & Schmidt, 1990). The meta-analyses and meta-analytic regressions were weighted by the reciprocal of the variance of the effect size. We used Huber–White robust standard errors in the meta-analytic regression framework to adjust for the fact that the same studies provided multiple data points to some analyses. We used Peter’s method to assess for publication biases. We re-ran the meta-analysis, deleting one observation at a time to determine if the statistical significance of the pooled effect could be accounted for by any one observation.

Role of the Funding Source

This work was supported by the Pediatric Psychopharmacology Council Fund. The corresponding author (J.B.) had full access to all the data in the study and had final responsibility for the decision to submit for publication.

Results

Although our literature search produced 1,053 articles, only 5 articles met our a priori inclusion and exclusion criteria (see Figure 1). One of these articles reported on three independent non-overlapping populations (Segalowitz & Lawson, 1995), which were analyzed separately in our review. Another had two independent populations, with only one of those meeting our inclusion criteria and therefore analyzed with our data (Max et al., 2004). Thus, our literature search resulted in five independent populations with 3,023 mTBI patients and 9,716 controls.

Figure 1.

PRISMA flow diagram.

Table 1 describes key features of the samples analyzed in the meta-analysis. All studies but one used healthy controls. The single exception used an orthopedic-injury control group (Max et al., 2004). Only two studies were prospective. Most samples were of children and adolescents, but the three samples provided by Segalowitz and Lawson (1995) also included adults. The column labeled “Sequence” indicates if the authors studied ADHD occurring prior to mTBI or subsequent to mTBI. Two studies provide information about ADHD prior to mTBI, two provide information about ADHD subsequent to mTBI, and five did not clarify the sequence, that is, they only indicate if participants had both diagnoses at some time in their lives. The studies by Max et al. (2004) and Fann et al. (2004) provided data in two of these sequence categories.

Table 1.

Articles Included in the Meta-Analysis.

First author	Year	TBI n	Control n	Age range or M	Sequence	mTBI diagnostic method	ADHD diagnostic method	ADHD diagnostic system	Type of control	Design
McKinlay	2009	76	839	14-16	Unknown	Medical record	Best estimate	DSM-III	Healthy	Prospective
Max	2004	19	20	5-14	mTBI first	Medical record	Interview	DSM-III	Orthopedic injury	Retrospective
Max	2004	24	24	5-14	ADHD first	Medical record	Interview	DSM-III	Orthopedic injury	Retrospective
Segalowitz^a	1995	397	694	16.8 (M)	Unknown	Self-report	Self-report	Unknown	Healthy	Retrospective
Segalowitz^a	1995	70	126	17.8 (M)	Unknown	Self-report	Self-report	Unknown	Healthy	Retrospective
Segalowitz^a	1995	593	1666	22.8 (M)	Unknown	Self-report	Self-report	Unknown	Healthy	Retrospective
Fann	2004	620	2196	>15	Unknown	Medical record	Medical record	ICD-9-CM	Healthy	Retrospective
Fann	2004	803	2817	>15	ADHD first	Medical record	Medical record	ICD-9-CM	Healthy	Retrospective
Massagli	2004	421	1334	0-14	mTBI first	Medical record	Medical record	ICD-9-CM	Healthy	Prospective

Note. The Max and Fann studies are repeated twice because they used one sample to provide data relevant to different sequences of ADHD and mTBI (see column “Sequence”); TBI = traumatic brain injury; mTBI = mild TBI; DSM-III = Diagnostic and Statistical Manual of Mental Disorders (3rd ed.; American Psychiatric Association, 1980); ICD-9-CM = International Classification of Diseases, Version 9, Clinical Modification.

Segalowitz et al. provided three separate samples.

Figure 2 shows the results of the meta-analysis stratified by the directionality of the effect.

Figure 2.

Meta-analysis of the association between ADHD and mTBI stratified by direction of association.

The result of the analysis using all the data, regardless of sequence, indicates a significant association between ADHD and mTBI corresponding to a relative risk of 2.0 (z = 6.5, p < .0005). The I² statistic was 0.0% indicating no heterogeneity among studies when estimating this effect. The results remained statistically significant for each of a series of analyses conducted by removing one study at a time. This shows that no single study was driving the statistical significance of the meta-analysis.

The top panel of Figure 2 shows the results for studies that reported the occurrence of ADHD subsequent to mTBI. For these studies, the pooled relative risk of 0.98 suggests no association of prior ADHD with subsequent mTBI (z = 0.04, p = .97). The mean prevalence of ADHD subsequent to mTBI was 10.6% (range = 7.4%-15.8%) compared with a control prevalence of ADHD of 4.2% (range = 3.5%-5%).

The middle panel of Figure 2 shows the results for studies that did not specify the sequence of ADHD and mTBI. For these studies, the pooled relative risk of 2.1 indicates an association between ADHD and mTBI (z = 5.7, p< .0005). The mean prevalence of ADHD in the mTBI group was 11.1% (range = 1.2%-27%) compared with a control prevalence of ADHD of 5.8% (range = 0.7%-16%). The results remained statistically significant for each of a series of analyses conducted by removing one study at a time.

The bottom panel of Figure 2 shows the results for studies that assessed ADHD occurring subsequent to mTBI. For these studies, the pooled relative risk of 2.2 indicates an association between mTBI and subsequent ADHD (z = 3.5, p < .0005). The mean prevalence of ADHD prior to mTBI was 10.6% (range = 0.4%-20.8%) compared with a control prevalence of ADHD of 8.6% (range = 0.5%-16.7%). There was a very high correlation between the prevalence of ADHD in controls and the prevalence of ADHD in the mTBI group (r = .93, p = .0003).

For each stratum defined by the ADHD/mTBI sequence, the I² statistic was 0.0% indicating no heterogeneity among studies within strata. We found no evidence for publication bias when examining all studies pooled together (t₈ = 0.2, p = .9) or only studies that did not indicate the ADHD/mTBI sequence (t₈ = 0.8, p = 0.5). There were not enough studies in the other two sequence strata to perform publication bias analyses within those strata.

Meta-analysis regression found a significant difference between the relative risks of the three classes of study in Figure 2, F(2, 4) = 17.6, p = .01. The pairwise differences were significant when comparing studies of ADHD prior to mTBI with studies of mTBI prior to ADHD (t₄ = 5.8, p = .004) and studies with an unknown ADHD/mTBI sequence (t₄ = 4.8, p = .008). The two latter types of studies did not differ significantly from one another (t₄ = 1.3, p = .3). Subsequent meta-analysis regressions included the significant difference among ADHD/mTBI sequence groups as a covariate. These analyses found no significant effect for method of mTBI assessment (t₄ = 0.5, p = .7), study design (t₄ = 0.6, p = .6), method of diagnosing ADHD (t₄ = 2.1, p = .1), or diagnostic system used for ADHD (t₄ = 2.7, p = .5).

Discussion

Our meta-analysis provides strong evidence for an association between ADHD and mTBI that cannot be explained by publication biases or the effects of one single study. Sub-analyses attempting to clarify the sequence of ADHD and mTBI were frustrated by the fact that most studies did not specify which came first. Thus, any conclusions about the sequencing of ADHD and mTBI must be made with caution.

With that caution in mind, we did find a significant effect of sequence suggesting that the association between ADHD and mTBI was weaker for ADHD as a predictor of subsequent mTBI than it was for mTBI as a predictor of subsequent ADHD or for studies that did not specify a sequence. The studies of ADHD as a predictor of mTBI estimated a relative risk of 0.98, which is so close to the null value of 1.0 that we cannot attribute the lack of significance to statistical power.

These results suggesting that ADHD does not increase the risk of subsequent mTBI stand in contrast to the literature that documents that individuals with ADHD have higher risk of accidents and injuries than the general population (Bonfield, Lam, Lin, & Greene, 2013; Lam, 2002; Pastor & Reuben, 2006; Swensen et al., 2004). Thus, it is reasonable to hypothesize that they would also be at increased risk of mTBI. Furthermore, there are some problems with the two negative studies about ADHD as a risk factor for subsequent mTBI. The report by Max et al. (2004) used a small sample (N = 24, mTBI cases, and N = 24, controls). They also used an orthopedic control group. Given that ADHD youths are at increased risk of injuries, orthopedic controls might be contaminated with a high rate of ADHD. In support of this idea, the prevalence of ADHD in these controls was 16.7%, much higher than the population rate of ADHD, which is about 5% (Faraone, Sergeant, Gillberg, & Biederman, 2003). This suggests that if ADHD is a risk factor for mTBI, that risk is mediated by ADHD’s known risk of increasing accidents (Antshel et al., 2009; Biederman et al., 2006). The second study suggesting that ADHD is not a risk factor for mTBI was large and used healthy controls (Fann et al., 2004), but its method of determining ADHD diagnoses prior to mTBI may have been insensitive because the rate of ADHD in their control group was only 0.7%, a much lower rate than that expected in the general population. Also, unlike the other studies, Fann et al.’s (2004) participants were mostly adults, with 38% being older than 44 years of age. This may have made it difficult to accurately determine the ADHD/mTBI sequence. Clearly, more work is needed to further evaluate this important issue.

The inconclusive results of the link between prior ADHD and subsequent mTBI are mirrored in the small controlled literature about ADHD and severe TBI. These data also come from Max et al. (2004) and Fann et al. (2004). Neither study found a significant association: Max et al.’s study yields a relative risk of 0.8 and Fann et al.’s yields a relative risk of 1.5. Another study by Fann et al. (2002) yielded a non-significant relative risk of 0.9 when comparing ADHD patients with healthy controls, but it did not distinguish between mild and severe TBI. In a study without non-TBI controls, Gerring et al. (1998) reported a premorbid prevalence of ADHD of 20%, with a 95% confidence interval of 12% to 30%. In another uncontrolled study by Levin et al. (2007), the premorbid prevalence of ADHD among consecutive admissions for TBI was 23%, with a 95% confidence interval of 17% to 31%.

There were only two studies assessing ADHD subsequent to mTBI. Both yielded positive relative risks implicating mTBI as a risk factor for ADHD. One of these is the small Max et al. (2004) study using orthopedic controls. For these analyses, the use of orthopedic controls is of note, because whereas ADHD would be expected to cause accidents leading to orthopedic accidents, such accidents would not be expected to lead to ADHD and they did not in this study.

Other data relevant to the risk for ADHD subsequent to TBI come from studies that did not focus on mild TBI. The Max et al. (2004) study using orthopedic controls also had a severe TBI group. Its relative risk of subsequent ADHD is large (5.7), but not significant. Keenan, Hall, and Marshall (2008) did not specify the severity of TBI in their study. In comparisons with healthy controls, their data yielded a relative risk of 1.9 that is significant. They found an equally high rate of subsequent ADHD in their TBI and burn injury groups, with both groups having more subsequent ADHD compared with healthy controls. These additional data are consistent with studies of mild TBI in suggesting that TBI is associated with the subsequent onset of ADHD. They are, however, ambiguous regarding the specificity of the association. Given Keenan et al.’s (2008) burn injury data, it is possible that some mechanism common to injury, but not involving brain trauma, can explain the mTBI/ADHD association.

Although our review suggests an association between mTBI and ADHD, it also identified significant gaps in the literature. Uncertainties remain as to whether individuals with ADHD are more likely to sustain mTBI. Although we have reviewed studies of this question, they are not conclusive. Second, it remains unclear whether individuals with ADHD experience a more serious initial injury or a different type of injury. For example, Gerring et al. (2000) reported that the development of ADHD subsequent to TBI was greatest for those with lesions in thalamus and basal ganglia. Third, it is unclear whether individuals with ADHD have a different injury recovery trajectory. In a recent study, children and adolescents with ADHD who were admitted to the hospital following mTBI had worse functional outcomes than those who did not have ADHD (Bonfield et al., 2013). Fourth, it remains unclear whether mTBI can cause ADHD de novo, or hasten the onset in a genetically vulnerable individual. Finally, more information is needed as to whether mTBI alters the course of ADHD beyond the acute recovery period.

Considering the large clinical and public health relevance of mTBI and given its high and increasing prevalence and significant consequences, further clarification of the relationship between mTBI and ADHD could have large implications. If ADHD were found to increase the risk of TBI, its identification and treatment could mitigate the development of mTBI. If preexisting ADHD were to be found to increase the risk of mTBI-associated complications, such knowledge may play an important role in providing a prognostic marker for severity and duration of the mTBI course.

Though cognitive dysfunction from traumatic brain injuries is frequently managed with stimulant medications, the American Medical Society for Sports Medicine’s position on concussion finds no established role for stimulant medications in the treatment of cognitive deficits after a concussion (Harmon et al., 2013). ADHD, in contrast, is a treatable disorder that responds well to stimulant medications. Thus, if patients with traumatic brain injury meet diagnostic criteria for ADHD, interventions for ADHD could be considered.

This work must be considered in the context of several limitations. Like all meta-analyses, our results are limited by the methods used in the studies providing the data. Although some studies may have also assessed ADHD in TBI patients, they could not be identified if they did not meet our inclusion and exclusion criteria or use appropriate key words allowing us to identify them. The total number of studies was small, especially when considering analyses by subgroups. As a counterbalance to this problem, these studies included a large number of participants (3,023 mTBI patients and 9,716 controls). This provides some reassurance about the findings pooled across all studies, but we must be especially cautious in interpreting the findings from the two strata that each comprised only two studies. Perhaps the most important limitation of the available literature on mTBI and ADHD is the absence of prospective, pre-injury assessment data about ADHD symptoms. Without this information, we cannot determine the temporal relationship between mTBI and ADHD. Prospective longitudinal studies are clearly needed.

Conclusion

Our meta-analysis provides strong evidence for an association between ADHD and mTBI but the directionality of this association remains unclear. There is stronger evidence for the hypothesis that mTBI leads to subsequent ADHD than there is for the idea that ADHD leads to subsequent mTBI. However, due to limitations of the literature, conclusions about directionality must be made with caution.

Footnotes

Declaration of Conflicting Interests

The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Dr. Joseph Biederman is currently receiving research support from the following sources: the Department of Defense, Ironshore, Vaya Pharma/Enzymotec, and National Institutes of Health (NIH). In 2013, Dr. Joseph Biederman received an honorarium from the Massachusetts General Hospital (MGH) Psychiatry Academy for a tuition-funded continuing medical education (CME) course. He received research support from American Professional Society of ADHD and Related Disorders (APSARD), ElMindA, McNeil, and Shire. He has a U.S. patent application pending (61/233,686) through MGH corporate licensing, on a method to prevent stimulant abuse. Dr. Biederman received departmental royalties from a copyrighted rating scale used for ADHD diagnoses, paid by Shire and Sunovion; these royalties are paid to the Department of Psychiatry at MGH. In 2012, Dr. Joseph Biederman received an honorarium from the MGH Psychiatry Academy and The Children’s Hospital of Southwest Florida/Lee Memorial Health System for tuition-funded CME courses. In 2011, Dr. Joseph Biederman gave a single unpaid talk for Juste Pharmaceutical Spain, received honoraria from the MGH Psychiatry Academy for a tuition-funded CME course, and received honoraria for presenting at international scientific conference on ADHD. He also received an honorarium from Cambridge University Press for a chapter publication. Dr. Biederman received departmental royalties from a copyrighted rating scale used for ADHD diagnoses, paid by Eli Lilly, Shire, and AstraZeneca; these royalties were paid to the Department of Psychiatry at MGH. In 2010, Dr. Joseph Biederman received a speaker’s fee from a single talk given at Fundación Dr. Manuel Camelo A.C. in Monterrey Mexico. Dr. Biederman provided single consultations for Shionogi Pharma Inc. and Cipher Pharmaceuticals Inc.; the honoraria for these consultations were paid to the Department of Psychiatry at the MGH. Dr. Biederman received honoraria from the MGH Psychiatry Academy for a tuition-funded CME course.

Dr. Zafonte receives funding from the Department of Defense, the NIH, and the National Institute on Disability and Rehabilitation Research (NIDRR). He receives publication royalties from Elsevier, Oakstone, and Demos.

Dr. Thomas Spencer has received research support from, has been a speaker for or on a speaker bureau or has been an advisor of on an advisory board of the following sources: Alcobra, Shire Laboratories, Inc., Eli Lilly, Glaxo-Smith Kline, Ironshore, Janssen Pharmaceutical, McNeil Pharmaceutical, Novartis Pharmaceuticals, Cephalon, Pfizer, the National Institute of Mental Health and the Department of Defense. Dr. Spencer receives research support form Royalties and Licensing fees on copyrighted ADHD scales through MGH Corporate Sponsored Research and Licensing. Dr. Spencer has a U.S. Patent Application pending (61/233,686), through MGH corporate licensing, on a method to prevent stimulant abuse.

In the past year, Dr. Faraone received consulting income and/or research support from Akili Interactive Labs, VAYA Pharma, and SynapDx and research support from the NIH. His institution is seeking a patent for the use of sodium-hydrogen exchange inhibitors in the treatment of ADHD. In previous years, he received consulting fees or was on advisory boards or participated in continuing medical education programs sponsored by Shire, Alcobra, Otsuka, McNeil, Janssen, Novartis, Pfizer, and Eli Lilly. Dr. Faraone receives royalties from books published by Guilford Press (Straight Talk About Your Child’s Mental Health) and Oxford University Press (Schizophrenia: The Facts).

Dr. Adeyemo, Ms. Kagan, Dr. Uchida, Ms. Kenworthy, and Dr. Andrea Spencer have no financial disclosures to report.

Funding

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the Pediatric Psychopharmacology Council Fund.

Author Biographies

Bamidele O. Adeyemo, MD, was a neurorehabilitation fellow and clinical neuromodulation research fellow in the Department of Physical Medicine and Rehabilitation at Spaulding Rehabilitation Hospital and Harvard Medical School in Charlestown, Massachusetts. He is currently working as an assistant professor at the Emory School of Medicine Department of Rehabilitation in Atlanta, Georgia. His research interests are in traumatic brain injury, assorted complications of neurological injury, global advocacy for rehabilitation, neuroplasticity, neuromodulation, and non-invasive brain stimulation for brain recovery.

Joseph Biederman, MD, is the chief of the Clinical and Research Programs in Pediatric Psychopharmacology and Adult ADHD, and director of the Alan and Lorraine Bressler Clinical and Research Program for Autism Spectrum Disorders, at Massachusetts General Hospital, Boston. He is a professor of psychiatry at Harvard Medical School, Boston, Massachusetts. He is board certified in general and child psychiatry. His clinical and research interests include ADHD in children and adults, and pediatric mood and anxiety disorders.

Ross Zafonte, DO, is the chairperson of the Department of Physical Medicine and Rehabilitation at Spaulding Rehabilitation Hospital, Harvard Medical School in Charlestown, Massachusetts, and the chief of Physical Medicine & Rehabilitation at Massachusetts General Hospital, Boston. He is known for his work in traumatic brain injury.

Elana Kagan, BA, worked as a clinical research coordinator in the Pediatric Psychopharmacology Program at the Massachusetts General Hospital, Boston. She is currently pursuing a graduate degree in clinical psychology at Temple University, Philadelphia, Pennsylvania. Her interests include improving treatments for psychological disorders.

Thomas J. Spencer, MD, is the assistant chief of the Clinical and Research Programs in Pediatric Psychopharmacology and Adult ADHD at Massachusetts General Hospital, Boston. He is also an associate professor at Harvard Medical School, Boston, Massachusetts. His interests have focused on the effectiveness and safety of standard and novel pharmacologic treatments of ADHD throughout the life cycle.

Mai Uchida, MD, is a staff child and adolescent psychiatrist in the Clinical and Research Programs in Pediatric Psychopharmacology and Adult ADHD, and the Alan and Lorraine Bressler Clinical and Research Program for Autism Spectrum Disorders at Massachusetts General Hospital, Boston. She is also an instructor in psychiatry at Harvard Medical School, Boston, Massachusetts. Her career focus has been on the characteristics, longitudinal course, and treatment of childhood psychiatric conditions.

Tara Kenworthy, BA, is a clinical research coordinator in the Pediatric Psychopharmacology Program at the Massachusetts General Hospital, Boston. Her interests include early identification and treatment for psychiatric disorders in children.

Andrea E. Spencer, MD, is an assistant in psychiatry at Massachusetts General Hospital, Boston, and instructor at Harvard Medical School, Boston, Massachusetts. She currently treats patients at the MGH Chelsea Healthcare Center, where she serves as a consultant psychiatrist to the Pediatrics Unit, and at MGH in the Pediatric Psychopharmacology and Adult ADHD Program and the Alan and Lorraine Bressler Program for Autism Spectrum Disorders. Her research has focused on ADHD and its comorbidities.

Stephen V. Faraone, PhD, is the director of the Medical Genetics Research Center and distinguished professor of psychiatry and neuroscience and physiology at SUNY Upstate Medical University, Syracuse. He is also senior scientific advisor to the Pediatric Psychopharmacology and Adult ADHD program at Massachusetts General Hospital and a lecturer at Harvard Medical School, Boston, Massachusetts. His research contributions include psychiatric genetics, psychopharmacology, diagnostic issues, and methodology.

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