There is considerable overlap between anxiety and depressive disorders in symptomatology, treatment modalities and possible causalities. Many symptoms are common to both types of disorder, while relatively few differentiate the disorders from each other. Many antidepressant treatments, both pharmaco- and psycho-therapeutic in nature, are effective in treating the various anxiety disorders. Indeed, the SSRIs in particular are so well established that anxiety disorders are generally believed to have a serotonergic origin. On the other hand, anxiolytic drugs are relatively ineffective in the treatment of depressive disorders, except as augmenting agents for treatment resistance in the case of buspirone or as a means to combat early insomnia and anxiety induced by some antidepressants in the case of the benzodiazepines.

Evidence is emerging that some depressive disorders, particularly psychotic depression and severe melancholia, are characterized by loss of hippocampal volume. There is as yet only preliminary evidence that successful antidepressant treatment restores hippocampal volume to normality, although in experimental animals all antidepressant modalities seem to stimulate neurogenesis in the dentate gyrus. Speculation about the role of a dysfunctional HPA axis resulting in excess levels of neurotoxic glucocorticoids has led to the development of selective antagonists of glucocorticoid receptors as putative antidepressants. Within the anxiety disorders, PTSD also involves loss of hippocampal volume which can be restored by treatment with SSRIs or the antiepileptic phenytoin.
It is likely that some depressive and anxiety disorders have a common biological causality in terms of changes in brain plasticity