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Objective: Anxiety symptoms are common in older adults with or without anxiety disorders. Pharmacological options may be limited for these patients. Alternative treatments, such as physical activity (PA), are often indicated, although few trials have evaluated their efficacy. The aim of this review was to evaluate the efficacy of regular PA on improving anxiety symptoms in older adults without anxiety disorders. Potential neuroendocrine, inflammatory, and oxidative mechanisms, as well as cognitive factors to explain these effects are also discussed. Methods: A systematic literature review was performed to identify randomized controlled trials, crosssectional, cohort, and case-control studies, as well as case series including healthy previously sedentary older adults. We searched the PubMed and Web of Science databases for articles published in English, with no set time limits. Results: Eight studies evaluating the effect of PA on anxiety symptoms in healthy older adults were included in this review. In all studies, regular and supervised PA was directly related to decreased anxiety symptoms in older individuals. Conclusion: Regular PA may be effective for improving anxiety symptoms in older adults. More studies are needed to identify the ideal PA modality, frequency, duration, and intensity for optimizing the positive effects of exercise on anxiety in this population.

This long-term extension of an 8-week randomized, naturalistic study in patients with panic disorder with or without agoraphobia compared the efficacy and safety of clonazepam (n = 47) and paroxetine (n = 37) over a 3-year total treatment duration. Target doses for all patients were 2 mg/d clonazepam and 40 mg/d paroxetine (both taken at bedtime). This study reports data from the long-term period (34 months), following the initial 8-week treatment phase. Thus, total treatment duration was 36 months. Patients with a good primary outcome during acute treatment continued monotherapy with clonazepam or paroxetine, but patients with partial primary treatment success were switched to the combination therapy. At initiation of the long-term study, the mean doses of clonazepam and paroxetine were 1.9 (SD, 0.30) and 38.4 (SD, 3.74) mg/d, respectively. These doses were maintained until month 36 (clonazepam 1.9 [SD, 0.29] mg/d and paroxetine 38.2 [SD, 3.87] mg/d). Long-term treatment with clonazepam led to a small but significantly better Clinical Global Impression (CGI)-Improvement rating than treatment with paroxetine (mean difference: CGI-Severity scale -3.48 vs -3.24, respectively, P = 0.02; CGI-Improvement scale 1.06 vs 1.11, respectively, P = 0.04). Both treatments similarly reduced the number of panic attacks and severity of anxiety. Patients treated with clonazepam had significantly fewer adverse events than those treated with paroxetine (28.9% vs 70.6%, P < 0.001). The efficacy of clonazepam and paroxetine for the treatment of panic disorder was maintained over the long-term course. There was a significant advantage with clonazepam over paroxetine with respect to the frequency and nature of adverse events.

HA and SD dimensions are associated with both the occurrence of depressive and anxiety symptoms. There is also some evidence to suggest that high HA and low SD indicates susceptibility to depression. Longitudinal studies are not sufficient to affirm the same about panic disorder up to the present moment.

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The selective serotonin-reuptake inhibitors are widely used in clinical practice in the treatment of panic disorder (PD). This article undertakes an up-to-date, systematic review of the published double-blind, placebo-controlled, randomized, short-term studies with currently available selective serotonin-reuptake inhibitors in the treatment of PD. Sertraline, paroxetine, citalopram, escitalopram, fluoxetine and fluvoxamine have all been proven to be superior to pill-placebo, although the placebo effect has been shown to be extremely important in patients with PD. The authors also explore the anxiolytic mechanism of action of this antidepressant drug class and the preclinical studies that are being developed to clarify the etiopathogenic mechanisms of PD and, more precisely, the role of the serotoninergic system in this pathogenesis. These steps are considered fundamental for the improvement of pharmacological treatment of PD.

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Long-term pharmacotherapy may prevent symptom relapse in GAD patients. As the relapse rate is very high, the data support the continuation of pharmacotherapy for as long as possible.