Commentary on Hyperkinetic Impulse Disorder

Dr. Goldstein continues the laudable practice of reprinting articles of historical significance in the history of ADHD with this selective reprinting of material from the original article by Maurice Laufer, Eric Denhoff, and Gerald Solomons on hyperkinetic impulsive disorder (HID) in children. They were distinguished professionals in their day, highly productive in their clinical research careers and well regarded by their clinical colleagues, so the importance of this article in influencing clinical practice and research at the time cannot be overemphasized. All had worked at the Bradley Home in Rhode Island, which was the site of the first studies of stimulants on hyperactive children by William Bradley in 1937. This article on HID is among the first articles to distinguish a group of children who were seriously hyperactive and impulsive yet who did not have evidence by history of significant brain injury. It also signaled a return to focusing on child behavioral disorders in 1957 after a hiatus in which two World Wars preoccupied the general population and medical professionals alike. In this article, all of the major symptom dimensions that would go on to characterize both minimal brain dysfunction and eventually ADHD were noted, including short attention span, variability of behavior and work performance, impulsiveness, and emotional dysregulation. The latter feature has recently been argued to be just as central to the disorder as the former difficulties with attention, activity, and inhibition (Barkley, 2010; Martel, 2009; Skirrow, McLoughlin, Kuntsi, & Asherson, 2009)—a position that existed throughout much of the history of ADHD dating back to 1798. It was removed from the holy trinity of ADHD symptoms in the Diagnostic and Statistical Manual of Mental Disorders (Second Revision; DSM-II) never to return to its central place in subsequent DSM revisions. Although recognizing that any of these symptoms could have a “purely emotional origin” such as psychodynamic or psychoanalytic conflict, the authors argued that when seen in combination, the symptom complex did not appear to be of psychological origin. Where an etiology could be established, it was most often related to pregnancy or birth complications and their presumed impact on brain development. Specifically, the authors marshaled evidence to argue that the origin of the disorder was within the brain generally and specifically the midbrain structures included under the term diencephalon, and particularly the thalamus. Modern neuroimaging studies now implicate other brain regions in conjunction with ADHD, such as the right prefrontal cortex, anterior cingulate cortex, basal ganglia, and cerebellum (Bush, Valera, & Seidman, 2005; Valera, Faraone, Murray, & Seidman, 2007). Of course, structural or functional neuroimaging devices and procedures were unavailable at the time, making it difficult to objectively determine the presence of functional abnormalities within brain structures in the 1950s when this article was published. So to prove their thesis, the authors administered a drug (Metrazol) to children having HID. This drug is known to affect the threshold for inducing a spike-and-wave pattern on the electroencephalogram (EEG) and a myoclonic jerk of the arms particularly when a strobe light is being flashed, known as the photo-Metrazol method. The threshold was the dose at which these changes in EEG and muscle movement occurred. The authors reported that the HID children developed such signs at a lower dose than the non-HID children, which they argue indicates dysfunction in the thalamus and diencephalon more generally. Although this procedure today would be unlikely to pass review by a human research review committee or institutional review board, it was an acceptable procedure to use at the time under expert medical supervision. The authors subsequently studied the effect of amphetamine on this threshold in children with HID and found it to raise this threshold to within the normal range, on average, whereas removal from medication resulted in a lowering of the threshold. This aspect of the study makes this article among the first to attempt to identify the mechanism of action of the amphetamines in the management of HID (ADHD). To their credit, the authors discuss a number of potential reasons for the presence of the lower photo-Metrazol threshold in the HID cases. They acknowledged the remote possibility that it could even arise from emotional or psychological origins yet also noted the lack of any evidence for this explanation. More convincing was the possibility of adverse pre-, peri-, or postnatal events on the brain and its subsequent development given the high frequency of such adverse events in the histories of many of these children. The authors go on to postulate that HID may arise from a significantly lower 413045 JAD15810.1177/1087054711413 045BarkleyJournal of Attention Disorders © 2011 SAGE Publications