Abstract

Research has shown that reductions in hippocampal volume can result from various forms of stress and are a feature of Major depressive disorder (MDD), with some studies suggesting similar impairments in PTSD. However, there has been little research on the connection between stress and the hippocampus as it relates to other affective and anxiety disorders. The current study examined hippocampal morphology and functioning and their relationship to depressive symptomatology in older adults with Generalized anxiety disorder (GAD). We hypothesized that GAD patients may show lower hippocampal volume and functioning; and having GAD might add to or magnify the impact of depression on the hippocampus. Participants were 15 older adults diagnosed with GAD without co-occurring MDD, and 15 age- and sex-matched non-anxious controls. Participants completed a diagnostic interview; measures of anxiety and depression; neuropsychological tests; and a structural MRI scan. The Verbal Paired Associates (VPA) test (Wechsler, 1997) was used to assess verbal contextual memory, a common index of hippocampal functioning. Higher levels of depressive symptomatology, as measured by the Beck Depression Inventory (Beck & Steer, 1987), were associated with smaller hippocampal volumes, which were in turn associated with lower scores on VPA recall and on the Stroop color test (StroopC; Trenerry, Crosson, DeBoe, & Leber, 1989). The association between depression and the hippocampus was significantly stronger in the GAD sample. In addition, reductions in hippocampal volume and VPA delayed recall and StroopC scores were found in those GAD patients with the highest levels of depression (n = 5), after controlling for several covariates. Findings suggest that alterations in hippocampal morphology and functioning may be evident in a subset of GAD patients, specifically those with higher levels of depression. They also support the idea that, in the context of GAD, even moderate levels of depression that fail to meet diagnostic criteria for MDD may have deleterious effects on the brain and mind. Implications for the conceptualization and treatment of GAD are discussed.

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