There is now evidence that repeated administration of interferon-alpha (IFN-alpha) to patients with chronic active hepatitis and cancers induces depressive symptoms. There is also evidence that induction of the cytokine network modulates the serotonergic system and that major depression is related to activation of the cytokine network and disturbances in the serotonergic metabolism. The aims of this study were to examine the effects of IFN-alpha-based immunotherapy on the development of depressive symptoms in relation to its effects on plasma tryptophan and kynurenine and serum serotonin (5-HT). Eighteen patients affected by chronic active hepatitis C were treated with IFN-alpha (3-6 million units subcutaneously three to six times a week for 6 months) and had measurements of the previous parameters before starting immunotherapy and 2, 4, 16, and 24 weeks later. Severity of depression and anxiety were measured with the Montgomery-Asberg Depression Rating Scale (MADRS) and the Hamilton Rating Scale for Anxiety (HAM-A) scale, respectively. Immunochemotherapy with IFN-alpha (1) significantly increased the MADRS and HAM-A scores and serum kynurenine concentrations and (2) significantly reduced plasma tryptophan and serum 5-HT concentrations. IFN-alpha-based immunotherapy significantly increased the kynurenine per tryptophan quotient, which estimates the activity of indoleamine 2,3-dioxygenase, the major tryptophan-catabolizing enzyme, which is induced by IFNs. There are significant relationships between the IFN-alpha-induced changes in the MADRS score and serum kynurenine (positive) and 5-HT (negative) concentrations. Immunotherapy with IFN-alpha significantly increases the severity of depressive symptoms. The latter is related to changes in the serotonergic system, such as depletion of serum 5-HT and induction of the catabolism of tryptophan to kynurenine. It is suggested that the IFN-alpha-induced changes in the serotonergic turnover could play a role in the development of IFN-alpha-induced depressive symptoms.

In a single-center, case-control study, we investigated the frequency and types of psychiatric disturbances in 89 consecutive patients with various primary focal dystonias (34 had cervical dystonia (CD), 28 blepharospasm (BPS), 16 laryngeal dystonia (LD), and 11 arm dystonia), 62 healthy control subjects and as controls for BPS, 26 patients with hemifacial spasm (HFS). Patients and controls underwent a full psychiatric evaluation. Diagnosis was based on the structured clinical interview for DSM-IV, obsessive-compulsive disorder (OCD) was assessed with the Yale-Brown Obsessive-Compulsive scale, anxiety with the Hamilton Rating Scale for Anxiety, the severity of depression with the Beck Depression Inventory. Of the 89 patients with focal dystonias studied, 51 patients (57.3%) had a diagnosis of psychiatric disorders compared with only 15 of 62 healthy subjects (24.1%) and 9 of the patients with HFS (34.6%). Depressive disorders were more frequent in the CD and BPS groups than in healthy controls, whereas the frequency of anxiety disorders, OCDs or adjustment disorders approached that of healthy subjects. No difference was found in the frequency of any specific psychiatric disorder in patients with LD and arm dystonia and healthy controls. In 35 of 51 patients who had psychiatric disorders, these started before and in 16 patients after the onset of dystonia. No differences were found in age, dystonia severity, and duration of botulinum toxin treatment between patients with and without psychiatric disturbances. The most common psychiatric features in patients with CD and BPS are depressive disorders.

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Atrial fibrillation (AF) is the most widely recognized arrhythmia. Systemic arterial hypertension, diabetes, obesity, heart failure, and valvular heart diseases are major risk factors for the onset and progression of AF. Various studies have emphasized the augmented anxiety rate among AF patients due to the poor quality of life; however, little information is known about the possibility of triggering atrial fibrillation by anxiety. The present review sought to underline the possible pathophysiological association between AF and anxiety disorders and suggests that anxiety can be an independent risk factor for AF, acting as a trigger, creating an arrhythmogenic substrate, and modulating the autonomic nervous system. The awareness of the role of anxiety disorders as a risk factor for AF may lead to the development of new clinical strategies for the management of AF.