Epidemiological data consistently indicate that depression and anxiety occur more frequently among individuals with epilepsy compared to the general population and other medical conditions. The relationship between depression and anxiety requires further study to examine the complexities and interconnectedness of the two disorders. Depression and anxiety frequently co-occur both in the general population, and it appears, in epilepsy. Depression, anxiety and epilepsy appear to share related neurobiological mechanisms, and the interplay between the three disorders is not clear. It has been noted time and time again in the epilepsy literature that psychiatric disorders, more specifically depression and anxiety, are frequently under-recognized and under-treated. Yet, there are very few randomized controlled studies for either pharmacological or psychotherapeutic interventions for depression, anxiety or co-occurring depression and anxiety in epilepsy. As researchers and clinicians in epilepsy there is much for us to learn. Psychiatric comorbidity in epilepsy is wrought with complex neurobiological systems that are only just beginning to be understood.
There are a number of implications for future research. First and importantly, we must begin to aggressively study treatment options, both pharmacological and psychotherapeutic, in order to reduce the negative impact of the disorders on the lives of individuals with epilepsy. Second, we must continue to conduct neuroana-tomical studies to obtain more knowledge about the neurobiological link between epilepsy, anxiety, and depression. Third, we must continue to explore the neuro-pathogenic mechanisms of all three disorders, and the potential implications of the dynamic relationship on the expression of these disorders. This knowledge could inform the development of medications to treat depression, anxiety, and epilepsy. Finally, it will be important to identify environmental and psychosocial risk factors for anxiety and depression. It is clear that neurobiological and genetic mechanisms are influenced by environmental factors and their expression is based on exposure to particular stimuli, and thus these factors cannot be ignored. Although clinicians and researchers have been discussing psychiatric comorbidity in epilepsy for several decades, there is much more work to be done.
Was this article helpful?