AD(H)D as a medical model: searching for stability

Abstract

Since time immemorial, medicine has faced the expectation of developing explanatory models and deriving possible courses of action when people experience physical or psychological distress. Since these explanatory models were placed on a scientific basis, the resulting possibilities for action have undergone previously unimaginable expansion. This gave rise to the expectation that knowledge of a causal organic finding would enable targeted and effective help. Where such an attribution initially seems impossible, the regular co-occurrence of various “symptoms” raises the hope of eventually finding an organic factor as the “cause.” They are then grouped together as a “syndrome.” Behavioral abnormalities in severe brain damage led to the assumption that ultimately all such abnormalities must have an organic cause. When this assumption was disappointed and no organic factor was found, the term “dysfunction” was adopted. In the 1990s, the long-held hope of replacing the vague concept of “dysfunction” with the secure foundation of reliable organic findings finally seemed to be fulfilled. New imaging techniques, which for the first time could visualize metabolic processes in the brain, appeared to demonstrate AD(H)D-specific abnormalities of brain metabolism—particularly regarding the role of the neurotransmitter dopamine. Despite methodological shortcomings, these findings were soon treated as established facts and led to the idea that AD(H)D was fundamentally a brain-metabolism disorder. Further developments, however, showed that the significance of all these findings was not as clear as it had initially appeared (Lupke, 2001). Nevertheless, the “brain-metabolism disorder” is still sometimes defended aggressively as an “established fact.” This points to another dimension in the current relevance of the AD(H)D topic: a need for support, certainty, and solid ground—so strong that doubts are ignored and disappointments denied.