The neurological concept involving the frontal lobe in the mechanism of attention deficit hyperactivity disorder is reemphasized by neurologists and geneticists at the Johns Hopkins University School of Medicine, Baltimore, MD. A frontal-motor cortex disconnection syndrome, or “lazy” frontal lobe, in ADHD is hypothesized on the basis of cerebral blood flow and EEG studies, and MRI findings. The concept develops from the function of the frontal lobe as an inhibitor of excessive motor activity, and children with ADHD having disinhibited motor activity. The calming effect of methylphenidate stems from its stimulatory effect on the frontal lobe causing motor inhibition. [1]

COMMENT. The importance of the frontal lobe in relation to hyperactive behavior was demonstrated more than 50 years ago in animal studies by Langworthy and Richter (1939), and later by Livingston, Fulton and colleagues (1948), and Mettler (1967). Two types of hyperactivity were distinguished: overreactivity, an external stimulation or distractibility caused by frontal lobe injury, and essential overactivity, a disinhibitive hyperkinesia due to striatal lesions and release from fronto-cortical-reticular inhibition of ascending systems. (See Progress in Pediatric Neurology III, Ed. Millichap JG, PNB Publ, pp 195-265, for further articles and comments on the neurobiologic organic theory of ADHD). Since the report of 3 children with a temporal lobe arachnoid cyst TLAC/ADHD syndrome [2], three further cases have been uncovered. Different sites and degrees of damage in the cortical striatal circuit might account for the heterogeneous nature of ADHD.