Loss of control of pre-motor activation in anxious agitated and impulsive depressives. A clinical and ERP study.

1. Current research uses a variety of traditional validation methods in order to test the clinical expression of biological models in psychiatry. The application of these methods has resulted in a paradoxical situation which requires the definition of new objectives in biological and pharmacoclinical research: the biological specificity of new psychotropic drugs does not assume any congruence between their pharmacological and their therapeutic effects, but raises the question of the relationship between biological systems and clinical symptomatology. The dimensional description of psychopathological disorders may be more appropriate to biological studies in psychiatry. 2. A study was undertaken on a population of twenty-one in-patients fulfilling the DSM III-R criteria for major depressive episode. They were divided into two groups on the basis of contrasting clinical dimensions: anxious-agitation and impulsiveness versus retardation and affective blunting. 3. Significant clinical differences between the two groups on mood profiles were echoed by contrasts in event-related potentials during a go-nogo task: only anxious agitated and impulsive patients developed an abnormal cortical activity, as measured by contingent negative variation (CNV), in the nogo condition. 4. This paper suggests how a paradigm with control of motor action leads to specify premotor activation abnormalities in the agitated impulsive depression subtype.