The etiology of ADHD
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Attention Deficit/Hyperactivity Disorder (“ADHD”) is a complex multi-factorial disorder that was first described in the late 1800s as a defect in moral control. By the early 1900s, ADHD shifted away from being a behavioral-based to a neurobiological-based disorder. During this period, individuals with ADHD were classified as having minimal brain damage. Early studies focused on the clinical presentation of ADHD. As advances in neuroimaging and molecular marker techniques started to develop, researchers were able to focus more on the neurobiological aspects of ADHD. This shift was instrumental to both the diagnosis and treatment of ADHD. This paper surveys the existing literature on ADHD in an attempt to elucidate its etiology. While several areas of research seem promising, so far, no single major contributor to ADHD has been identified. This paper first looks at the history behind ADHD. The historical background was instrumental in directing the course of ADHD research. Next, the Diagnostic and Statistical Manual of Mental Disorders (“DSM”) is examined with a focus on the changes made to DSM-IV and reflected in DSM-V. While DSM is a valuable diagnostic tool, its purpose in elucidating the etiology behind ADHD is questionable. Despite that, discussion of the DSM is necessary as it is impossible to study a disorder without delineating the normal from the abnormal. What follows this discussion is a brief overview of comorbidities that are often associated, and possibly share, a common etiology with ADHD. The paper then examines the theories promulgated by researchers as to the neurobiological basis of ADHD. This examination is followed by a discussion of recent findings into the pathology behind ADHD, which mainly centers around differences in brain structure and connectivity. Further analysis of these studies reveals that sex plays an instrumental role in the type of brain abnormalities found in ADHD children. In addition, delays in brain development are analyzed, and age is discussed as a factor in the presentation of ADHD. This paper goes on to examine genetics as a contributor to the etiology of ADHD. This examination proves fruitful as several genes of interest seem to indicate a hereditary component of ADHD. Finally, treatment options such as psychosocial therapy and medications that help ADHD patients maintain a quality of life, are discussed. By studying the mechanism of action underlying these medications, additional clues as to the etiology of ADHD may be discovered. There is still a long way to go before a complete picture of ADHD emerges. Already, studies are showing that race and environmental factors play a role in how ADHD presents. These two areas have rarely been studied and doing so will only serve to enhance the current understanding of ADHD. Despite an incomplete picture, the scientific community has come a long way from the 1800s where ADHD was thought to result from a defect in moral control. With early diagnosis and proper treatment, the ADHD individuals of today can live a life as close to that of their neurotypical peers as possible.