The functional neuroanatomy of psychiatric treatments

The attraction of this kind of model-building is its rigor. There is an unhealthy indiscipline to psychiatry as long as it remains purely phenomenologic. Clouds are described, then other clouds; then they are related, one to another; then new clouds form, and they too are described. It is a process that could go on forever, but it is too nebulous to win support for very much longer. In contrast, psychiatry that is based on etiopathogenesis, on brain maps, has rigor. It is either true or untrue, like the three models presented above. If it is true, like the frontal lobe hypothesis of dopamine agonists, it will lead somewhere. If it is only a small part of the truth, like the kindling theory of temporal lobe drugs, it will be supplanted, before long, by a more cogent hypothesis. What is more attractive about this kind of thinking, however, is the practical side of it. The KBS hypothesis of autism is not simply an idle exercise. It is a guide to a specific approach to behavioral treatment and a warning to eschew the mindless search for a pharmacologic "bullet." Theories, like every other living thing, have to do something useful before they are ultimately set aside. At least this one lends some common sense to day-to-day events.