Alterations of the hypothalamic-pituitary-adrenal (HPA) axis and of its peripheral indices have been reported in both normal and pathological anxiety with controversial findings. The aim of the present study was to investigate the possible correlations between serum cortisol and dehydroepiandrosterone-sulfate (DHEA-S) levels and DHEA-S/cortisol ratio, and panic-agoraphobic spectrum dimensions in a sample of healthy subjects.

Forty-two healthy subjects of both sexes, with no current or lifetime psychiatric disorders, were assessed by means of the Structured Clinical Interview for DSM-IV (SCID-I/P) and the so-called Panic Agoraphobic Spectrum-Self Report lifetime version (PAS-SR).

Significant, negative correlations were found between cortisol levels and the total score of the separation sensitivity, panic-like symptoms, and medication/substance sensitivity PAS-SR domains. The PAS-SR total and the panic-like symptoms domain scores were positively related to the DHEAS/cortisol ratio. When the sample was divided in women and men, these correlations were present in women only.

These findings, while indicating the presence of significant relationships between panic-agoraphobic traits and some indices of HPA axis functioning in healthy women, would suggest this as one of the factors explaining the greater vulnerability of women to cross the line between normal and pathological anxiety.

Further studies are needed to explore gender differences in the relationships between HPA axis alterations and the panic-agoraphobic spectrum dimensions.

Attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) are frequently co-occurring disorders in children and adolescents. However, their clinical status among adults is still under discussion. This study analyzes how the current clinical presentation of adult ADHD might be influenced by a lifetime history of CD and ODD.

We compared three groups of patients: ADHD without history of CD/ODD (n = 178), ADHD + history of ODD (n = 184), and ADHD + history of CD (n = 96).

A history of CD (and to a lower extent ODD) is associated with a more severe and externalizing profile.

Past CD and ODD entail a significant negative mental health impact on persistent ADHD, reinforcing the importance of actively assessing the developmental history of adult ADHD patients.

The goal of this study was to determine the relationship between age and risk for depression among the old and the oldest old.

MEDLINE, EMBASE, and the Cochrane Library database were used to identify potential studies. The studies were divided into cross-sectional and longitudinal subsets. For each study, the numbers of the total participants, cases (for cross-sectional study), or incident cases (for longitudinal study) of depression in each age group were extracted and entered into Review Manager 4.2 software. Qualitative meta-analyses of cross-sectional studies and of longitudinal studies were performed. For prevalence and incidence rates of depression, odds risk (OR) and relative risk (RR) were calculated, respectively.

The qualitative meta-analyses showed that, compared with younger participants (above vs. below 65 years, above vs. below 70 years, above vs. below 75 years, and above vs. below 80 years), older age groups had a significantly higher risk for depression. (All of the ORs and RRs were significant.) Compared with participants aged 55–89, those aged above 90 years had no higher risk for depression. (Neither the OR nor the RR was significant.)

Despite the methodological limitations of this meta-analysis, older age appears to be an important risk factor for depression in the general elderly population (aged below 80 years), but not in the oldest population (aged above 85 years).

In old age, depressive syndromes often affect people with chronic medical illnesses, cognitive impairment, and disability, which can worsen the outcomes of other medical disorders and promote disability. Repetitive magnetic transcranial stimulation (rTMS) is a simple and effective treatment in patients with treatment-resistant depression. Therefore the use of rTMS could be of particular potential benefit in treatment-resistant elderly patients, who often cannot tolerate the higher doses of drugs needed or show phenomena of intolerance and interaction. However, several studies assessing the efficacy of rTMS found smaller response rates in elderly patients when compared to younger samples. Nevertheless, the correlation between age and response is still a controversial issue, and there is no strong evidence to date. The aim of our study was to retest the effectiveness and safety of low-frequency rTMS in a 3 weeks active treatment in a group of resistant-depressed patients, and to investigate the role of age in the response to stimulation treatment.

Enrolled in this study were 102 treatment-resistant depressed patients. The patients were treated with low-frequency rTMS over the right dorso-lateral prefrontal cortex (DLPFC) for 3 weeks with a simple protocol (420 pulses per session for 15 sessions). At baseline, at the end of the second week, and at the end of the third week of treatment, the Hamilton Depression Rating Scale (HAM-D) and the Hamilton Anxiety Rating Scale (HAM-A) were administered.

Low-frequency rTMS on the prefrontal dorsolateral right area resulted in a statistically significant reduction of mean HAM-D scores in the entire group of patients at the end of treatment. The responder's rate in the whole group at the end of the third week was 56.86%. A significant inverse relationship between HAM-D reduction and age was found in the “older” (>60 years old) group, not in the “younger” (<60 years old) group.

Results from this study show that low-frequency rTMS over the right DLPFC, with a relatively low number of pulses (420 pulses per session) and a relatively short period of treatment, is effective in the treatment of resistant patients (in a sample also including elderly patients) in a 3-weeks treatment protocol with a low reduction with the progress of age. Furthermore, we found a greater response in younger patients and an inverse correlation between age and treatment response. Adaptations of the protocol according to age are reviewed.

We investigated an association between the polymorphism of brain-derived neurotrophic factor (BDNF) gene Val66Met and the response to mirtazapine in Japanese patients with major depressive disorder (MDD). We also examined mirtazapine's effects on the serum BDNF and plasma levels of catecholamine metabolites in these patients.

Eighty-four patients who met the DSM-IV-TR criteria for MDD were treated with only mirtazapine for 4 weeks. The BDNF Val66Met polymorphism was detected by direct sequencing in the region, and serum BDNF levels and plasma levels of catecholamine metabolites were measured by ELISA and HPLC-ECD, respectively.

Mirtazapine treatment for 4 weeks significantly increased serum BDNF levels in the responders, whereas nonresponders showed significant decreases. No association was found between either of the two genotypes (Val/Val vs. Met-carriers) and the response to mirtazapine at T4 or the serum BDNF levels at T0. Mirtazapine did not alter the plasma levels of homovanillic acid (HVA) or 3-methoxy-4-hydroxyphenylglycol (MHPG).

The dynamics of serum BDNF levels, but not plasma levels of HVA and MHPG, reflect the response to mirtazapine treatment; the BDNF Val66Met polymorphism in patients with depression is, however, associated with neither a particular response to mirtazapine treatment nor baseline serum BDNF levels.

Serum BDNF levels, but not plasma levels of HVA or MHPG, and BDNF Val66Met polymorphism are related to the mirtazapine response in MDD.