Search

BackgroundInfluential theories predict that antidepressant medication and psychological therapies evoke distinct neural changes.AimsTo test the convergence and divergence of antidepressant- and psychotherapy-evoked neural changes, and their overlap with the brain's affect network.MethodWe employed a quantitative synthesis of three meta-analyses (n = 4206). First, we assessed the common and distinct neural changes evoked by antidepressant medication and psychotherapy, by contrasting two comparable meta-analyses reporting the neural effects of these treatments. Both meta-analyses included patients with affective disorders, including major depressive disorder, generalised anxiety disorder and panic disorder. The majority were assessed using negative-valence tasks during neuroimaging. Next, we assessed whether the neural changes evoked by antidepressants and psychotherapy overlapped with the brain's affect network, using data from a third meta-analysis of affect-based neural activation.ResultsNeural changes from psychotherapy and antidepressant medication did not significantly converge on any region. Antidepressants evoked neural changes in the amygdala, whereas psychotherapy evoked anatomically distinct changes in the medial prefrontal cortex. Both psychotherapy- and antidepressant-related changes separately converged on regions of the affect network.ConclusionsThis supports the notion of treatment-specific brain effects of antidepressants and psychotherapy. Both treatments induce changes in the affect network, but our results suggest that their effects on affect processing occur via distinct proximal neurocognitive mechanisms of action.

This article describes a method for the modification of paper with single-wall carbon nanohorns (SWCNHs) to form stable suprastructures. The SWCNHs form stable dahlia-like aggregates in solution that are then self-assembled into superior structures if the solvent is evaporated. Dipping paper sections into a dispersion of SWCNHs leads to the formation of a thin film that can be used for microextraction purposes. The coated paper can be easily handled with a simple pipette tip, paving the way for disposable extraction units. As a proof of concept, the extraction of antidepressants from urine and their determination by direct infusion mass spectrometry is studied. Limits of detection (LODs) were 10 ng/L for desipramine, amitriptyline, and mianserin, while the precision, expressed as a relative standard deviation, was 7.2%, 7.3%, and 9.8%, respectively

Background: Most empirically derived antidepressants increase monoamine levels. The nuclei of cells synthesising these monoamines are located in the brainstem, and projection tracts such as the medial forebrain bundle reach virtually all other brain areas. Two studies of unipolar depressive illness using transcranial ultrasound have reported reduced echogenicity of the brainstem midline in unipolar depressed patients. This may be consistent with disruption of white matter tracts, including the medial forebrain bundle, and it has been suggested that the effect of such disruption could be reversed by antidepressants. Objective: To replicate these findings in a group of unipolar depressed patients and controls. Methods: Fifteen unipolar depressed patients and 15 controls were studied using transcranial ultrasound imaging and diffusion tensor magnetic resonance imaging (DT-MRI). Results: No difference in echogenicity of the brainstem midline of unipolar depressed patients was found. A possible trend (Cohen’s d = 0.39) in the direction of previous studies was found. Although the echogenicity of the brainstem midline of the control group was found to be similar to previous reports, there was no reduction in the patient group. Additionally, no structural abnormality of the brainstem was identified using DT-MRI. Conclusions: While these data do not replicate the findings of previous studies reporting a significant reduction in the echogenicity of the brainstem midline in unipolar depressed patients, the ultrasound investigation indicated that there may be a trend in this direction. Given the importance of identifying the causes of depressive illness, it is important that other groups attempt similar studies.

Background: Prescribed drugs in patients with Alzheimer’s disease may affect the symptomatic progression of their disease, both positively and negatively. Aim: To examine the effects of drugs on the progression of disease in a representative group of patients with Alzheimer’s disease. Methods: Patients with the diagnosis of probable Alzheimer’s disease were recruited from the community. The prescribed drugs taken by 224 patients (mean age 82.3 years) were recorded at initial assessment and then correlated in logistic regression analysis with progression of the disease, defined as an increase of one point or more in the Global Deterioration Scale over the next 12-month period. Results: Patients who were taking antipsychotic drugs and sedatives had a significantly higher risk of deterioration than those who were taking none (odds ratios (ORs) 2.74 (95% confidence interval (CI) 1.17 to 6.41) and 2.77 (95% CI 1.14 to 6.73), respectively). Higher risk of deterioration was observed in those who were taking both antipsychotic and sedative drugs together (OR 3.86 (95% CI 1.28 to 11.7). Patients taking drugs licensed for dementia, drugs affecting the renin–angiotensin system and statins had a significantly lower risk of deterioration than those who were not taking any of these drugs (ORs 0.49 (95% CI 0.25 to 0.97), 0.31 (95% CI 0.11 to 0.85) and 0.12 (95% CI 0.03 to 0.52), respectively). Conclusion: Our findings have implications for both clinicians and trialists. Most importantly, clinicians should carefully weigh any potential benefits of antipsychotics and benzodiazepines, especially in combination, against the risk of increased decline. Researchers need to be aware of the potential of not only licensed drugs for dementia but also drugs affecting the renin–angiotensin system and statins in reducing progression in clinical trials.

Background: In a previous prospective study of 300 consecutive new attenders at neurology outpatient clinics, depressive disorders were diagnosed in 119 patients (40%) and major depressive disorder in 77 (26%). Objective: To describe the eight month outcome of depression in this cohort. Methods: Patients were reinterviewed eight months after their baseline assessment. Mental state was examined using the primary care evaluation of mental disorders (PRIME-MD) interview and the hospital anxiety and depression (HAD) self rating scale. Health status was measured using the medical outcome study 36 item short form scale (SF-36). Results: Of the original cohort of 300, 226 (75%) participated in the follow up. Among them, 88 had a depressive disorder at baseline and 69 (78%) of those were still depressed at follow up; 54 had major depression at baseline and 46 (85%) of those still had a major depressive disorder at follow up. Among the 138 patients who had no depression at baseline, 20 new major depressive disorders had developed by the time of follow up. Resolution of major depressive disorders was associated with an improvement in health status. Conclusions: Most depressive disorders detected in neurology outpatients persist at an eight month follow up, and a substantial number of new cases arise. Resolution of depressive disorders, particularly major depressive disorder, is associated with an improvement in health status.