ABSTRACT
Stress-system dysregulation is thought to increase the risk for anxiety disorders. Here we describe both hypothalamic pituitary adrenal (HPA) axis and autonomic nervous system (ANS) activity in basal non-challenging conditions and after 0.5mg dexamethasone in generalized social anxiety disorder (gSAD) patients. To ensure stress-free sampling we collected saliva and determined cortisol and alpha-amylase (sAA), the latter a relative new marker of autonomic activity. Forty-three untreated gSAD patients without comorbidity were compared with 43 age and gender matched controls in non-stressed conditions on sAA and cortisol after awakening, during the day (including late evening), and after a low dose (0.5mg) of dexamethasone. Cortisol and sAA were analyzed with mixed models. Additional analyses were done with paired t-tests. Apart from the assessments in the morning, gSAD patients had significantly higher diurnal and post-dexamethasone 1600h sAA levels. No differences between gSAD and controls in any cortisol measurements were found. In conclusion, in gSAD in basal, non-stimulated conditions and after dexamethasone, we found hyperactivity of the ANS, as measured with sAA, but not of the HPA-axis. This suggests a relative increased activity of the ANS as compared to the HPA-axis, in line with the observed hyperarousal in gSAD.
Subject(s)
Agoraphobia/metabolism , Anxiety Disorders/metabolism , Hydrocortisone/blood , alpha-Amylases/metabolism , Adult , Agoraphobia/blood , Agoraphobia/psychology , Anti-Inflammatory Agents/pharmacology , Anxiety Disorders/blood , Anxiety Disorders/psychology , Autonomic Nervous System/physiopathology , Circadian Rhythm/physiology , Dexamethasone/pharmacology , Female , Humans , Hypothalamo-Hypophyseal System/physiopathology , Male , Middle Aged , Pituitary-Adrenal System/physiopathology , Saliva/metabolismABSTRACT
Findings from epidemiological, pharmacotherapeutical, genetic and neurobiological studies suggest a possible overlap in the neurobiology of generalized social anxiety disorder (gSAD) and panic disorder (PD). Previously we have found a rapid intravenous m-CPP challenge of 0.1 mg/kg to be highly sensitive and selective in the provocation of panic attacks in patients with PD. We therefore directly compared the behavioural, neuroendocrine and physiological effects of this rapid m-CPP challenge in a small sample of patients with gSAD, patients with PD and matched healthy controls. Panic attacks were significantly more provoked in patients with PD (85%), but not in patients with gSAD (14%) as compared to healthy controls (0%). Effects on the other behavioural parameters, but not on the neuroendocrine and physiological parameters, were significantly greater in patients with PD compared to patients with gSAD and controls. Our preliminary data do not support a shared neurobiology of gSAD and PD.
Subject(s)
Anxiety Disorders/drug therapy , Growth Hormone/metabolism , Hydrocortisone/metabolism , Pain Measurement/drug effects , Panic Disorder/drug therapy , Piperazines/administration & dosage , Serotonin Receptor Agonists/administration & dosage , Adult , Anxiety Disorders/metabolism , Anxiety Disorders/physiopathology , Female , Humans , Injections, Intravenous/methods , Male , Middle Aged , Panic Disorder/metabolism , Panic Disorder/physiopathology , Single-Blind Method , Statistics, Nonparametric , Time FactorsABSTRACT
Fourteen patients with social anxiety disorder (generalized type), according to DSM-IV criteria, were treated with mirtazapine 30 mg for 12 weeks. Twelve patients completed the study. Two patients (14.3%) dropped out due to side-effects. Generally, mirtazapine was well tolerated. Five out of 12 patients (41.7%) were classified as responders, based on a Clinical Global Improvement score of 1 or 2 and a reduction of the Liebowitz Social Anxiety Scale (LSAS) of 40%. The mean total score on the LSAS, as well as the anxiety and avoidance subscores, decreased significantly. This open pilot study suggests that further investigations are warranted to prove the efficacy of mirtazapine in generalized social anxiety disorder.
