FULL-LENGTH ORIGINAL RESEARCH
Evaluation of depression risk in LGI1 mutation carriers
Article first published online: 26 JUL 2010
Wiley Periodicals, Inc. © 2010 International League Against Epilepsy
Volume 51, Issue 9, pages 1685–1690, September 2010
How to Cite
Heiman, G. A., Kamberakis, K., Gill, R., Kalachikov, S., Pedley, T. A., Allen Hauser, W. and Ottman, R. (2010), Evaluation of depression risk in LGI1 mutation carriers. Epilepsia, 51: 1685–1690. doi: 10.1111/j.1528-1167.2010.02677.x
- Issue published online: 2 SEP 2010
- Article first published online: 26 JUL 2010
- Accepted May 28, 2010; Early View publication July 26, 2010.
- Partial seizures
Purpose: Depression is the most common comorbid condition in epilepsy. The cause of this comorbidity is unknown, and could involve psychosocial consequences of epilepsy, treatment side effects, seizure manifestations, or common neurobiologic mechanisms. One hypothesis of particular interest is a shared genetic susceptibility to epilepsy and depression. We tested this hypothesis by studying depressive symptoms in families with an identified genetic form of epilepsy: autosomal dominant partial epilepsy with auditory features caused by mutations in the leucine-rich, glioma inactivated 1 gene (LGI1).
Methods: A standardized depression screen was administered to 94 individuals from 11 families with mutations in LGI1, including 38 mutation carriers with epilepsy (AC), 11 clinically unaffected mutation carriers (UC), and 45 noncarriers (NC).
Results: Current depressive symptom scores were significantly higher in AC than in NC, an association that remained after excluding depressive symptoms that appeared likely to be caused by antiepileptic medication use. However, scores did not differ between UC and NC.
Discussion: Although LGI1 mutation carriers who were clinically affected with epilepsy had increased depressive symptoms, mutation carriers without epilepsy did not. These findings suggest that the increase in depressive symptoms in affected individuals from these families is related to epilepsy or its treatment rather than to LGI1 mutations per se.