Acoustic startle response in panic disorder.

The amygdala and the limbic system are important in inducing a fear reaction; if this "fear network" is involved in panic disorder, panic patients might be more sensitive to fear stimuli than healthy subjects. We compared the startle response with an aversive stimulus in a sample of 29 patients with panic disorder and a sample of 29 healthy controls. The intensity of the startle response, induced by a series of aversive loud (100 dB) sounds, was measured by skin conductance recording in each subject. No statistically significant differences between the two groups were found in either the baseline level of skin conductance or in the response to the stimuli. Nonetheless, panic patients reported significantly higher levels of baseline anxiety measured by the State-Trait Anxiety Inventory. In conclusion, our data do not support the hypothesis that patients with panic disorder are characterised by a hyperreactivity, as measured by the skin conductance response, to fearful sudden stimuli or, at least, to those delivered to the auditory system.

Lack of relationship between CO2 reactivity and serotonin transporter gene regulatory region polymorphism in panic disorder.

Changes in the function of the serotonergic system influence both panic phobic symptoms and carbon dioxide (CO2) reactivity in patients with panic disorder. Schmidt et al. [2000: J Abnorm Psychol 109(2):308-320] recently reported a predictive role of the genetic variants of the 5-HTTLPR on the fearful response to CO2 in healthy controls. We tested the hypothesis that the heterogeneity of CO2 reactivity in patients with panic disorder could be related to the allelic variation of the 5-HTT promoter. Ninety-five patients with panic disorder were challenged with 35% CO2. 5-HTTLPR allelic variation in each subject was determined using a PCR-based method. There were no differences for all the measures of CO2 reactivity among the genotype groups. CO2 reactivity of patients with panic disorder seems not to be influenced by the genetic variants of the 5-HTTLPR; this finding does not support a role for the serotonin transporter in the etiopathogenesis of CO2 reactivity in panic disorder.