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Attention deficit hyperactivity disorder (ADHD) is widely theorized to stem from dysfunctional inhibitory processes. However, the definition of inhibition is imprecisely distinguished across theories. To clarify the evidence for this conception, the author relies on a heuristic distinction between inhibition that is under executive control and inhibition that is under motivational control (anxiety or fear). It is argued that ADHD is unlikely to be due to a motivational inhibitory control deficit, although suggestions are made for additional studies that could overturn that conclusion. Evidence for a deficit in an executive motor inhibition process for the ADHD combined type is more compelling but is not equally strong for all forms of executive inhibitory control. Remaining issues include specificity to ADHD, whether inhibitory problems are primary or secondary in causing ADHD, role of comorbid anxiety and conduct disorder, and functional deficits in the inattentive ADHD subtype.

Disinhibition is a common focus in psychopathology research. However, use of inhibition models often is piecemeal, lacking an overarching taxonomy of inhibitory processes. The author organizes key concepts and models pertaining to different kinds of inhibitory control from the cognitive and temperament/personality literatures. Within the rubrics of executive inhibitory processes, motivational inhibitory processes, and automatic attentional inhibition processes, 8 kinds of inhibition are distinguished. Three basic temperament traits may address key executive and motivational inhibitory processes. Future developmental psychopathology research should be based on a systematic conceptual taxonomy of the kinds of inhibitory function relevant to a given disorder. Such an approach can clarify which inhibition distinctions are correct and which inhibition deficits go with which disorders.

Although the field is young, studies pertinent to genetic hypotheses have accumulated for several personality disorders. Genetic links to personality disorders from the domains of normal personality and Axis I disorders are reviewed. Evidence of a link to schizophrenia is clearest for schizotypal and less conclusive for paranoid and schizoid personality disorders. A genetic association between borderline personality disorder and affective disorders has not been clearly supported, but there may be a subtype genetically linked to affective disorders. Evidence of genetic influence is mixed for obsessive-compulsive personality disorder. In general, greater attention to dimensional phenotypic measures and multivariate designs can yield more definitive answers regarding the correct subtyping and probable etiology of personality disorders.

To study malevolent representations, earliest memories were reliably coded on scales of affect tone. Ss were diagnosed with borderline personality disorder: 31 without and 30 with concurrent major depression. Nonborderline comparison subjects had either major depressive disorder (n = 26) or no psychiatric diagnosis (n = 30). Borderline subjects were discriminated from comparison subjects by their more malevolent representations; they more frequently produced memories involving deliberate injury; and they portrayed potential helpers as less helpful. Results suggest the diagnostic significance of malevolent representations, which need to be explained by any theory of borderline personality disorder.