Catecholamines such as norepinephrine, epinephrine, and dopamine are closely related to the autonomic nervous system, suggesting that panic disorder may involve elevated catecholamine levels. This study investigated basal and posttreatment catecholamine levels in patients with panic disorder. A total of 29 patients with panic disorder and 23 healthy controls participated in the study. Panic disorder patients received paroxetine treatment for 12 weeks after clinical tests and examination had been conducted. We investigated the difference in basal levels of catecholamine and measured the changes in catecholamine levels before and after drug treatment in panic disorder patients. The basal plasma epinephrine (48.87±6.18 pg/ml) and dopamine (34.87±3.57 pg/ml) levels of panic disorder patients were significantly higher than those (34.79±4.72 pg/ml and 20.40±3.53 pg/ml) of the control group. However, basal plasma norepinephrine levels did not show statistically significant differences between patients and controls. After drug therapy, plasma catecholamine levels were nonsignificantly decreased and norepinephrine levels showed a tendency toward a decrease that did not reach significance. In conclusion, this study suggests the possibility of a baseline increase of plasma catecholamine levels and activation of sympathetic nervous systems in patients with panic disorder which may normalize after treatment with paroxetine.
Panic disorder is a kind of anxiety disorder that is characterized by unexpected and repeated panic attacks which are abrupt surges of intense fear or intense discomfort that reach a peak within minutes, and that are followed by anticipatory anxiety and phobic avoidant behavior as characterized in the DSM-5 (American Psychiatric Association, 2013). Although abnormalities in various neurotransmitter systems have been found in panic disorder, catecholamines such as norepinephrine, epinephrine, and dopamine are regarded as the key neurotransmitters involved in the pathophysiology of panic disorder.
Previous studies that directly measured plasma levels of catecholamine and urinary levels of the norepinephrine metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG) in patients with panic disorder found inconsistent results. Some studies reported an increase in plasma epinephrine (Nesse et al., 1984 and Villacres et al., 1987) and urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) levels (Garvey et al., 1987) in patients with panic disorder, whereas other studies showed no change in baseline plasma norepinephrine (Stein et al., 1992) and MHPG levels (Uhde et al., 1988). Regarding the role of dopamine in panic disorder, previous studies that examined the plasma dopamine level (Roy-Byrne et al., 1986 and Schneider et al., 1987) and cerebrospinal fluid levels of the dopamine metabolite homovanillic acid (HVA) (Eriksson et al., 1991 and Johnson et al., 1994) did not find significant results. However, studies using dopamine agonists including apomorphine (Pitchot et al., 1992) and cocaine (Anthony et al., 1989) suggested abnormalities in the dopamine neurotransmitter system as a possible etiology of panic disorder. As far as we know, no previous studies have investigated plasma catecholamine levels before and after treatment of panic disorder.
The present study assessed whether the basal levels of catecholamines, such as epinephrine, norepinephrine, and dopamine, were higher in panic disorder patients, compared with levels in normal control subjects, and whether the abnormal catecholamine levels in panic disorder patients were significantly decreased after 12 weeks of paroxetine treatment.
