TY - JOUR
T1 - A review of heterogeneity in attention deficit/hyperactivity disorder (ADHD)
AU - Luo, Yuyang
AU - Weibman, Dana
AU - Halperin, Jeffrey M.
AU - Li, Xiaobo
N1 - Publisher Copyright:
© 2019 Luo, Weibman, Halperin and Li.
PY - 2019/2/1
Y1 - 2019/2/1
N2 - Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that affects approximately 8%–12% of children worldwide. Throughout an individual’s lifetime, ADHD can significantly increase risk for other psychiatric disorders, educational and occupational failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or sufficient to cause ADHD. The multifactorial causation of ADHD is reflected in the heterogeneity of this disorder, as indicated by its diversity of psychiatric comorbidities, varied clinical profiles, patterns of neurocognitive impairment and developmental trajectories, and the wide range of structural and functional brain anomalies. Although evidence-based treatments can reduce ADHD symptoms in a substantial portion of affected individuals, there is yet no curative treatment for ADHD. A number of theoretical models of the emergence and developmental trajectories of ADHD have been proposed, aimed at providing systematic guides for clinical research and practice. We conducted a comprehensive review of the current status of research in understanding the heterogeneity of ADHD in terms of etiology, clinical profiles and trajectories, and neurobiological mechanisms. We suggest that further research focus on investigating the impact of the etiological risk factors and their interactions with developmental neural mechanisms and clinical profiles in ADHD. Such research would have heuristic value for identifying biologically homogeneous subgroups and could facilitate the development of novel and more tailored interventions that target underlying neural anomalies characteristic of more homogeneous subgroups.
AB - Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that affects approximately 8%–12% of children worldwide. Throughout an individual’s lifetime, ADHD can significantly increase risk for other psychiatric disorders, educational and occupational failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or sufficient to cause ADHD. The multifactorial causation of ADHD is reflected in the heterogeneity of this disorder, as indicated by its diversity of psychiatric comorbidities, varied clinical profiles, patterns of neurocognitive impairment and developmental trajectories, and the wide range of structural and functional brain anomalies. Although evidence-based treatments can reduce ADHD symptoms in a substantial portion of affected individuals, there is yet no curative treatment for ADHD. A number of theoretical models of the emergence and developmental trajectories of ADHD have been proposed, aimed at providing systematic guides for clinical research and practice. We conducted a comprehensive review of the current status of research in understanding the heterogeneity of ADHD in terms of etiology, clinical profiles and trajectories, and neurobiological mechanisms. We suggest that further research focus on investigating the impact of the etiological risk factors and their interactions with developmental neural mechanisms and clinical profiles in ADHD. Such research would have heuristic value for identifying biologically homogeneous subgroups and could facilitate the development of novel and more tailored interventions that target underlying neural anomalies characteristic of more homogeneous subgroups.
KW - ADHD
KW - Cognitive impairments
KW - DTI
KW - Functional MRI
KW - Heterogeneity
KW - Neuroscience model
KW - Risk factors
KW - Structural MRI
UR - http://www.scopus.com/inward/record.url?scp=85069538129&partnerID=8YFLogxK
U2 - 10.3389/fnhum.2019.00042
DO - 10.3389/fnhum.2019.00042
M3 - Review article
AN - SCOPUS:85069538129
SN - 1662-5161
VL - 13
JO - Frontiers in Human Neuroscience
JF - Frontiers in Human Neuroscience
M1 - 42
ER -