Neurobehavioral Clinical Research Section, Social and Behavioral Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland.
Neurobehavioral Clinical Research Section, Social and Behavioral Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland.
Biol Psychiatry. 2021 Jan 15;89(2):152-161. doi: 10.1016/j.biopsych.2020.06.004. Epub 2020 Jun 14.
Symptoms of attention-deficit/hyperactivity disorder (ADHD) run a variable course through adolescence. While most affected individuals show some improvement, particularly of hyperactivity-impulsivity, symptoms of inattention are more persistent, and some individuals may meet diagnostic criteria for the first time during adolescence. Genetic factors affect adolescent symptom trajectories; those showing persistence likely carry a greater burden of common risk alleles. Rare structural genomic variants, such as copy number variants and point mutations, might also play a role. Although psychostimulant medication is associated with better functional outcomes, an impact on underlying adolescent symptom trajectories has been hard to demonstrate. At a neural level, several studies report that adolescents whose childhood ADHD symptoms have remitted are indistinguishable from neurotypical individuals. This finding could reflect the "carrying forward" of relatively typical childhood neural features among those destined for adolescent remission or the correction of early childhood anomalies with a convergence toward typical dimensions. Other studies have noted unique, possibly compensatory patterns of neural activity among adolescents whose ADHD has improved. Finally, different neural processes might occur in different brain regions. Thus, some functional imaging studies find that subcortical anomalies reflect the onset of ADHD and remain throughout life regardless of symptom change, whereas the variable clinical course of adolescent ADHD is determined by plasticity of the cerebral cortex. Integrating an understanding of the neural processes with genomic risk could elucidate the mechanisms underlying the complex course of adolescent ADHD.
注意缺陷多动障碍（ADHD）的症状在青春期呈多变过程。虽然大多数受影响的个体表现出一些改善，特别是多动冲动，注意力不集中的症状更持久，一些个体可能在青春期首次符合诊断标准。遗传因素影响青少年症状轨迹；那些表现出持续性的个体可能携带更多常见风险等位基因的负担。罕见的结构性基因组变异，如拷贝数变异和点突变，也可能起作用。尽管兴奋剂药物与更好的功能结果相关，但对潜在的青少年症状轨迹的影响很难证明。在神经水平上，几项研究报告说，那些童年期 ADHD 症状已经缓解的青少年与神经典型个体无法区分。这一发现可能反映了那些注定要在青少年期缓解的个体中，相对典型的儿童期神经特征的“延续”，或者是通过向典型维度收敛来纠正儿童早期异常。其他研究注意到，那些 ADHD 改善的青少年中存在独特的、可能是代偿性的神经活动模式。最后，不同的神经过程可能发生在不同的大脑区域。因此，一些功能影像学研究发现，皮质下异常反映了 ADHD 的发作，并持续存在于整个生命中，无论症状是否改变，而青少年 ADHD 的可变临床过程则由大脑皮层的可塑性决定。将对神经过程的理解与基因组风险相结合，可以阐明青少年 ADHD 复杂病程的机制。
