In This Issue

Faces with emotional expressions that were incongruent with label wording—such as a fearful face labeled "HAPPY"—revealed an inability to adapt to emotion-related conflict in patients with generalized anxiety disorder. Whereas healthy subjects reacted faster when an incongruent trial followed another incongruent trial than when an incongruent trial followed a congruent trial, this adaptation was lacking in patients with generalized anxiety disorder. Likewise, the healthy subjects, but not the patients, showed an increase in activity in the pregenual anterior cingulate after two consecutive incongruent trials, with a decrease in connectivity between the pregenual cingulate and the amygdala. The tests by Etkin et al. (CME, p. 545) also demonstrated that healthy individuals were unaware of this adaptation. In an editorial on p. 489, Dr. Monique Ernst notes that the deficit characterized in this study "might very well explain the inability of generalized anxiety disorder patients to dampen feelings of anxiety."

A 5-year study of 3,521 randomly selected older adults confirms that clinically significant depression is associated with the development of diabetes mellitus. Campayo et al. (p. 580) report that depression and diabetes were assessed through standardized interviews and that treatment with antidepressants was not related to the increased diabetes risk. Instead, new-onset diabetes was associated with nonsevere depression, as well as persistent or untreated depression, body mass index, and a family history of diabetes. The editorial by Dr. Constantine Lyketsos on p. 496 points out that "somewhat unexpectedly, less severe depression was associated with a higher risk of diabetes, compared to severe depression, perhaps because it was less likely to be treated."

Many psychiatrists believe that mood disorders increase the severity of personality disorders. Morey et al. (CME, p. 528) found evidence that the contrary is true: 6 years after an index episode, patients with personality disorder had similar stability in the symptoms of their personality disorders over time, regardless of the presence or absence of major depressive disorder at baseline. However, patients with comorbid personality disorders and mood disorder had more prolonged depression than those with mood disorder alone, and those patients who failed to resolve their depression also had more persistence of their personality disorder symptoms. In an editorial on p. 487, Dr. Robert Michels comments that "clinicians who know how to diagnose personality pathology should be able to do so whether or not the patient is simultaneously depressed." Gunderson et al. reported previously that comorbid bipolar disorder does not affect the course of borderline personality disorder (Am J Psychiatry 2006; 163:1173–1178).

Wright et al. (CME, p. 502) present a case of neuropsychiatric illness in systemic lupus erythematosus in a patient with erotomania and the Geschwind syndrome. Geschwind syndrome includes hyperreligiosity and hyper- or hyposexuality related to temporal brain lesions and dysfunction, most commonly epilepsy. The presentation of this syndrome in a patient with systemic lupus erythematosus raises the clinical issue of whether the behavioral symptoms are due to lupus or to its pharmacological treatment or to another psychiatric illness. The authors make the point that behavioral symptoms in lupus do not always follow laboratory measures of severity. Brain dysfunction is often related to the autoimmune disease process, including brain vascular damage from autoantibodies, but brain involvement may precede peripheral signs of the illness, such as arthritis, and it may also arise from seizure activity or infarcts caused by the illness. These latter effects may persist even when the lupus itself is treated. These nuances are often not appreciated by other physicians caring for these complex patients.