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Depression and Anxiety in People with Epilepsy

박성파|권오영
대한신경과학회 (Korean Neurological Association)|2014.07|Journal of Clinical Neurology|제10권 제3호|pp. 175-188|DOI http://dx.doi.org/10.3988/jcn.2014.10.3.175

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참고문헌

키워드

depressionanxietyepilepsy

초록

Many recent epidemiological studies have found the prevalence of depression and anxiety to behigher in people with epilepsy (PWE) than in people without epilepsy. Furthermore, people withdepression or anxiety have been more likely to suffer from epilepsy than those without depression or anxiety. Almost one-third of PWE suffer from depression and anxiety, which is similar tothe prevalence of drug-refractory epilepsy. Various brain areas, including the frontal, temporal,and limbic regions, are associated with the biological pathogenesis of depression in PWE. It hasbeen suggested that structural abnormalities, monoamine pathways, cerebral glucose metabolism, the hypothalamic-pituitary-adrenal axis, and interleukin-1b are associated with the pathogenesis of depression in PWE. The amygdala and the hippocampus are important anatomicalstructures related to anxiety, and γ-aminobutyric acid and serotonin are associated with its pathogenesis. Depression and anxiety may lead to suicidal ideation or attempts and feelings of stigmatization. These experiences are also likely to increase the adverse effects associated with antiepileptic drugs and have been related to poor responses to pharmacological and surgical treatments. Ultimately, the quality of life is likely to be worse in PWE with depression and anxiety than inPWE without these disorders, which makes the early detection and appropriate management ofdepression and anxiety in PWE indispensable. Simple screening instruments may be helpful forin this regard, particularly in busy epilepsy clinics. Although both medical and psychobehavioraltherapies may ameliorate these conditions, randomized controlled trials are needed to confirmthat.

Abstract

Many recent epidemiological studies have found the prevalence of depression and anxiety to behigher in people with epilepsy (PWE) than in people without epilepsy. Furthermore, people withdepression or anxiety have been more likely to suffer from epilepsy than those without depression or anxiety. Almost one-third of PWE suffer from depression and anxiety, which is similar tothe prevalence of drug-refractory epilepsy. Various brain areas, including the frontal, temporal,and limbic regions, are associated with the biological pathogenesis of depression in PWE. It hasbeen suggested that structural abnormalities, monoamine pathways, cerebral glucose metabolism, the hypothalamic-pituitary-adrenal axis, and interleukin-1b are associated with the pathogenesis of depression in PWE. The amygdala and the hippocampus are important anatomicalstructures related to anxiety, and γ-aminobutyric acid and serotonin are associated with its pathogenesis. Depression and anxiety may lead to suicidal ideation or attempts and feelings of stigmatization. These experiences are also likely to increase the adverse effects associated with antiepileptic drugs and have been related to poor responses to pharmacological and surgical treatments. Ultimately, the quality of life is likely to be worse in PWE with depression and anxiety than inPWE without these disorders, which makes the early detection and appropriate management ofdepression and anxiety in PWE indispensable. Simple screening instruments may be helpful forin this regard, particularly in busy epilepsy clinics. Although both medical and psychobehavioraltherapies may ameliorate these conditions, randomized controlled trials are needed to confirmthat.

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