Once the child is in school, the attention deficit becomes a more troubling, practical problem. Now these children must sit still, watch and listen to the teacher when she speaks to another child, and not react to distracting stimuli. They cannot stay at their desks, take turns in reciting, be quiet, or control their impulsivity. The teacher finds it difficult to discipline them and the school often insists that the parents seek medical consultation for the child. A few are so hyperactive that they cannot attend regular classes. Their behavior verges on the “organic drivenness” that has been known to occur in children whose brains have been injured by encephalitis. In certain families, the disorder is probably inherited (Biederman et al). In about half the hyperactivity subsides gradually by puberty or soon thereafter, but in the remainder the symptoms persist in modified form into adulthood (Weiss et al).
It has also become clear that there is a large group of children who have difficulty sustaining concentration but do not manifest hyperactivity or behaviors that betray the attention deficit. It is presumed that they share a similar core problem with hyperkinetic children, and it has been observed that they may be helped in studying and school performance by the same stimulant drugs that are used for the treatment of more overt ADHD. A precise relationship between motor hyperactivity and the inability to concentrate and stay focused on a series of tasks has not been established. It would seem that these are but two aspects of the same fundamental disorder of drive and attention, but it is clear that there are individuals who have difficulty concentrating but who are not manifestly hyperactive. This becomes a particular issue in adults with ostensible ADHD who feel they have always had trouble focusing as discussed further on.
For a number of years there was a tendency to consider children with the hyperkinetic syndrome as having a form of minimal brain disease. “Soft neurologic signs” such as right–left confusion, mirror movements, minimal “choreic” instability of the hands, awkwardness, finger agnosia, tremor, and borderline hyperreflexia were said to be more frequent among them. The issue of mild developmental disorders of coordination constitutes its own subject independent of ADHD. The notion of this type of clumsiness has been known for over a century and was called debilite motrice by Dupre. The connection to ADHD, however, is evident in Annell’s description (taken from the review by Kirby and Sugden) “… awkward in movements, poor at games, hopeless in dancing and gymnastics, a bad writer and defective in communication. He is inattentive, cannot sit still, leaves his shoelaces untied, does buttons wrongly, bumps into furniture, breaks glassware, slips off his chair, kicks his legs against the desk, and perhaps reads badly.” Dyslexia is found in approximately 20 percent and a similar clumsiness is known to occur in many developmental disorders and forms of cognitive delay. These signs, however, are seen so often in normal children that their attribution to disease is invalid. Consequently, Schain and others substituted the term minimal brain dysfunction, which is no more accurate and simply restates the problem and, furthermore, may not be true in many cases.
Lacking altogether are clinicoanatomic and clinicopathologic correlative data, but some morphologic and physiologic data are available. In an MRI study of the brains of 10 children with ADHD, Hynd and colleagues found the width of the right frontal lobe to be smaller than normal; also fairly consistently, there was a reduction in the volume of the dorsolateral, cingulate, and striatal regions. Unlike dyslexics, in whom the planum temporale tends to be equal in the two hemispheres, the left planum was larger in the attention-deficit cases, just as it is in normals. Also, functional imaging studies have suggested that changes in the striatum underlie the inability of these children to block impulsive reactions and the improvement that is seen with methylphenidate. One would expect the prefrontal cortex to be implicated in such a disinhibitory syndrome but what data exist have been complex and difficult to interpret.