Urbach-Wiethe disease is an extremely rare autosomal recessive entity characterized by the deposition of hyaline material in the skin and other tissues of the body.5 Bilateral selective calcifications of the amygdala are present in 50% of patients. The fact that the amygdala plays a critical role in the recognition of fear in facial expressions has already been shown by Adolphs et al6 in a patient with bilateral amygdala damage. Herein, we present a patient with bilateral selective lesions of the amygdala due to UWD who developed panic attacks in the course of his disease. At the age of 4 years, the patient was diagnosed as having UWD because of the pathognomonic skin manifestations. Up to the age of 38 years, there were no additional manifestations of the patient's UWD. In particular, the patient had a normal emotional development and exhibited a normal range of mood and affect, without abnormalities in his experience of fear or panic. At the age of 38 years, he developed spontaneous panic attacks, which were characterized by the acute onset of unprovoked and intense anxiety accompanied by rapid breathing, palpitations, and the feeling of imminent death. The attacks occurred in intervals of several days at different times of the day and without any external trigger. In particular, there was no evidence that hyperventilation or increased carbon dioxide or lactate levels triggered panic episodes.7 The diagnosis of panic attacks was confirmed by a psychiatrist according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria. None of the attacks, which lasted from 5 to 20 minutes, was accompanied by loss of consciousness, motor phenomena, amnesia, or any other epileptic symptoms. There was no history of any psychiatric disease or epilepsy, but at the time of the panic attacks the patient developed depressive mood with lack of interest, apathy, sleep disturbances, and social withdrawal. Magnetic resonance imaging revealed bilateral selective calcifications of the amygdala (Figure) without any additional abnormalities in the brain. As the patient did not have any neurological symptoms prior to the onset of his panic attacks, no previous neuroimaging studies were available for a statement as to when the lesions occurred. The patient underwent extended video electroencephalography monitoring over a period of 5 days, including bilateral sphenoidal electrode recordings, which excluded an epileptic etiology of the symptoms. The patient's neuropsychological profile was found to be within the normal range for cognitive parameters, including IQ, memory, attention, and executive functions (Table). In a detailed interview, however, the patient reported that he had noticed a significant decline in his ability to recollect autobiographical episodes over the last years. For example, several weeks after his vacations, the patient was able to recall all cities he visited during his travels but could not remember specific episodes he experienced there. These specific memory deficits were also confirmed in a standardized autobiographic memory interview (Table). After antidepressive treatment with venlafaxine hydrochloride (75 mg/d), both the panic attacks and the depressive symptoms gradually ceased. The memory impairment, however, persisted.