OBJECTIVE: Posttraumatic stress disorder (PTSD) and panic disorder (PD) are two anxiety disorders with prominent psychophysiological symptoms. The PTSD criterion of persistent hyperarousal suggests autonomic dysregulation, and the disorder has been associated with elevated heart rate. In contrast, PD has been associated with respiratory abnormalities such as low end-tidal Pco(2). An integrated analysis of automatic and respiratory function in a direct comparison of these anxiety disorders is currently lacking. METHODS: Electrodermal, cardiovascular, and respiratory psychophysiology was examined in 23 PTSD patients, 26 PD patients, and 32 healthy individuals at baseline and during threat of shock. RESULTS: At baseline, the PTSD patients, in contrast to the other two groups, were characterized by attenuated parasympathetic and elevated sympathetic control, as evidenced by low respiratory sinus arrhythmia (a measure of cardiac vagal control) and high electrodermal activity. They also displayed elevated heart rate and cardiovascular sympathetic activation in comparison with healthy controls. PD patients exhibited lower Pco(2) (hypocapnia) and higher cardiovascular sympathetic activation compared with healthy controls. PTSD patients, but not PD patients, sighed more frequently than controls. During the threat of shock phase, the PTSD group demonstrated blunted electrodermal responses. CONCLUSIONS: Persistent hyperarousal symptoms in PTSD seem to be due to high sympathetic activity coupled with low parasympathetic cardiac control. Respiratory abnormalities were also present in PTSD. Several psychophysiological measures exhibited group-comparison effect sizes in the order of 1.0, supporting their potential for enhancing differential diagnosis and possibly suggesting utility as endophenotypes in genetic studies of anxiety disorders.
OBJECTIVE:Posttraumatic stress disorder (PTSD) and panic disorder (PD) are two anxiety disorders with prominent psychophysiological symptoms. The PTSD criterion of persistent hyperarousal suggests autonomic dysregulation, and the disorder has been associated with elevated heart rate. In contrast, PD has been associated with respiratory abnormalities such as low end-tidal Pco(2). An integrated analysis of automatic and respiratory function in a direct comparison of these anxiety disorders is currently lacking. METHODS: Electrodermal, cardiovascular, and respiratory psychophysiology was examined in 23 PTSDpatients, 26 PDpatients, and 32 healthy individuals at baseline and during threat of shock. RESULTS: At baseline, the PTSDpatients, in contrast to the other two groups, were characterized by attenuated parasympathetic and elevated sympathetic control, as evidenced by low respiratory sinus arrhythmia (a measure of cardiac vagal control) and high electrodermal activity. They also displayed elevated heart rate and cardiovascular sympathetic activation in comparison with healthy controls. PDpatients exhibited lower Pco(2) (hypocapnia) and higher cardiovascular sympathetic activation compared with healthy controls. PTSDpatients, but not PDpatients, sighed more frequently than controls. During the threat of shock phase, the PTSD group demonstrated blunted electrodermal responses. CONCLUSIONS: Persistent hyperarousal symptoms in PTSD seem to be due to high sympathetic activity coupled with low parasympathetic cardiac control. Respiratory abnormalities were also present in PTSD. Several psychophysiological measures exhibited group-comparison effect sizes in the order of 1.0, supporting their potential for enhancing differential diagnosis and possibly suggesting utility as endophenotypes in genetic studies of anxiety disorders.
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