Abstracts

Rationale: Auras reflect abnormal stimulation of brain areas in close proximity to where clinical seizures originate. In standard temporal lobectomy part or all of the amygdala and it's neuronal projections may remain intact. The purpose of our study was to investigate whether fear auras as measurement of abnormal amygdala activity are associated with a higher rate of mood and anxiety disorders before and 1 year after temporal lobectomy. Methods: 22 patients with fear auras (F) were compared to matched groups with other auras (A) and no auras (N). Neurological and neuropsychological evaluations before and 1 year after surgery were reviewed for mood and anxiety disorders (DSM-IV), and psychotropic medication treatment. Data analysis was performed using a logistic regression model to simultaneously examine effects of group and status (preop mood/anxiety disorder, postop auras and seizures, preop treatment) on psychiatric status 1 year postop. Results: Preop, 16/22 (F), 12/22 (A) and 8/14 (N) patients were identified as experiencing depression (F=14 A=9 N=8), anxiety disorder (F=2 A=3 N=0) and (hypo-)mania (F=0, A=1 N=0). 1 year postop, 18/21 (F), 7/22 (A) and 3/14 (N) patients experienced depression (F=9, A=5, N=2), (hypo-)mania (F=4, A=1, N=1) and anxiety disorder (F=5, A=1, N=0). Groups did not differ preop with respect to mood and anxiety disorders but differed postop. Postop aura status did not differ amongst groups and was not associated with psychiatric status. Postop seizure status did not differ amongst the groups. Postop mood and anxiety disorders were more prominent in the group with preop fear auras (p=.0009), particularly if seizure free (p=.03). Psychotropic treatment did not differ preop (F=5/22 A=2/22 N=2/14), but differed postop (F=16/21 A=6/22 N=2/14) (p=.0001). Discussion: Patients with auras arising from the amygdala experienced a higher rate of mood and anxiety disorders after temporal lobectomy and psychotropic treatment, particularly if seizure free. These findings may be explained by models of epileptic kindling, forced normalization and conditioned fear responses.