Effects of fluoxetine and venlafaxine on serum brain derived neurotrophic factor levels in depressed patients

Background

Several studies demonstrated that depressed patients had low serum BDNF levels which correlated with the severity of their depression, and antidepressant treatment increases levels of serum BDNF in depressed patients. It was speculated that agents acting on both noradrenergic and serotonergic transporters might have a greater influence on BDNF levels. The aim of our study was to determine effects of venlafaxine vs. fluoxetine on serum BDNF levels in depressive patients.

Methods

Forty-three patients diagnosed as major depressive disorder according to DSM-IV are included in the study. Forty-three patients were randomized to take fluoxetine (22 cases) or venlafaxine (21 cases). Serum levels of BDNF were measured by ELISA at baseline and 6 weeks after the start of treatment.

Results

Baseline levels of BDNF were not significantly different between the patient group and the controls. But male patients and the male controls showed statistical differences with respect to baseline BDNF levels. BDNF levels of the patient group did not change with treatment. Yet, the increase of BDNF levels was close to statistically significant in the fluoxetine group, whereas not significant in the venlafaxine group. There were no significant differences in baseline and 6th week BDNF levels between the responders and the non-responders.

Conclusion

Further studies controlling for a wide variety of confounding variables are needed, which may help to reach a clear conclusion about the potential of BDNF as a biomarker for depression or as a predictor of antidepressant efficacy.     

Relationship between CSF biomarkers of Alzheimer's disease and rates of regional cortical thinning in ADNI data

Previously it was reported that Alzheimer's disease (AD) patients have reduced amyloid (Aβ 1-42) and elevated total tau (t-tau) and phosphorylated tau (p-tau 181p) in the cerebro-spinal fluid (CSF), suggesting that these same measures could be used to detect early AD pathology in healthy elderly (CN) and mild cognitive impairment (MCI). In this study, we tested the hypothesis that there would be an association among rates of regional brain atrophy, the CSF biomarkers Aβ 1-42, t-tau, and p-tau 181p and ApoE ε4 status, and that the pattern of this association would be diagnosis specific. Our findings primarily showed that lower CSF Aβ 1-42 and higher tau concentrations were associated with increased rates of regional brain tissue loss and the patterns varied across the clinical groups. Taken together, these findings demonstrate that CSF biomarker concentrations are associated with the characteristic patterns of structural brain changes in CN and MCI that resemble to a large extent the pathology seen in AD. Therefore, the finding of faster progression of brain atrophy in the presence of lower Aβ 1-42 levels and higher p-tau levels supports the hypothesis that CSF Aβ 1-42 and tau are measures of early AD pathology. Moreover, the relationship among CSF biomarkers, ApoE ε4 status, and brain atrophy rates are regionally varying, supporting the view that the genetic predisposition of the brain to amyloid and tau mediated pathology is regional and disease stage specific.     

An unusual type of lateral compression injury of the pelvis tilt fracture with anterior displacement

Tilt fracture is the most unusual variant of pelvic lateral compression injury. The major problem was reported to be protrusion of the pubic ramus into the perineum by posterior–inferior displacement of the fragment. Tilt fragment with anterior and inferior displacement has not been reported in English speaking literature to our knowledge. Anterior tilt fragment can cause significant morbidity in terms of vascular injury, pelvic stability and acetabular fracture.     

Proton magnetic resonance spectroscopic analysis of changes in brain metabolites following electroconvulsive therapy in patients with major depressive disorder

Abstract

Objectives: The aim of this study was to evaluate the metabolic changes in the anterior cingulate cortex (ACC) induced by electroconvulsive therapy (ECT) in patients with MDD via ¹H-MRS.

Methods: The study was conducted on 13 MDD patients receiving ECT treatment and 14 healthy controls matched in terms of age, gender and education. The patients underwent six sessions of ECT. ¹H-MRS imaging and psychometric evaluations obtained before 1st and after the 6th sessions. The control group also went through the same procedures except for ECT. N-Acetyl aspartate (NAA), choline (Cho) and creatine (Cr) metabolite levels and the creatine to metabolite ratios were measured.

Results: There was no significant difference in the ACC metabolite levels of the patients and those of the controls at the baseline. ECT associated with a statistically significant decrease in the NAA/Cr ratio in ACC. All of the patients had responded to ECT treatment as measured with the clinical scales.

Conclusions: The results has suggested that indirect proof of an increase in energy metabolism without any evidence of impaired neuronal viability in the ACC induced by ECT. The relative increase in Cr levels following ECT in MDD seems to be associated with improvement in clinical severity.

• Key points

• ECT is one the most effective method in the treatment of acute MDD.

• The mechanism of ECT’s antidepressant activity remains unclear but it is thought to be related to the regulation of prefrontal cortical or cingulate areas.

• In this study the patients underwent six sessions of ECT and after ¹H-MRS imaging.

• The study revealed that baseline levels of metabolites in patients with MDD were not significantly different than those of control group.

     

Visualization of the diaphragm muscle with ultrasound improves diagnostic accuracy of phrenic nerve conduction studies

Introduction: Evaluation of phrenic neuropathy (PN) with phrenic nerve conduction studies (PNCS) is associated with false negatives. Visualization of diaphragmatic muscle twitch with diaphragm ultrasound (DUS) when performing PNCS may help to solve this problem. Methods: We performed bilateral, simultaneous DUS–PNCS in 10 healthy adults and 12 patients with PN. The amplitude of the diaphragm compound muscle action potential (CMAP) (on PNCS) and twitch (on DUS) was calculated. Results: Control subjects had <38% side‐to‐side asymmetry in twitch amplitude (on DUS) and 53% asymmetry in phrenic CMAP (on PCNS). In the 12 patients with PN, 12 phrenic neuropathies were detected. Three of these patients had either significant side‐to‐side asymmetry or absolute reduction in diaphragm movement that was not detected with PNCS. There were no cases in which the PNCS showed an abnormality but the DUS did not. Conclusions: The addition of DUS to PNCS enhances diagnostic accuracy in PN. Muscle Nerve 49 : 669–675, 2014     

CSF protein biomarkers predicting longitudinal reduction of CSF β-amyloid42 in cognitively healthy elders

β-amyloid (Aβ) plaque accumulation is a hallmark of Alzheimer''s disease (AD). It is believed to start many years prior to symptoms and is reflected by reduced cerebrospinal fluid (CSF) levels of the peptide Aβ1–42 (Aβ42). Here we tested the hypothesis that baseline levels of CSF proteins involved in microglia activity, synaptic function and Aβ metabolism predict the development of Aβ plaques, assessed by longitudinal CSF Aβ42 decrease in cognitively healthy people. Forty-six healthy people with three to four serial CSF samples were included (mean follow-up 3 years, range 2–4 years). There was an overall reduction in Aβ42 from a mean concentration of 211–195 pg ml⁻¹ after 4 years. Linear mixed-effects models using longitudinal Aβ42 as the response variable, and baseline proteins as explanatory variables (n=69 proteins potentially relevant for Aβ metabolism, microglia or synaptic/neuronal function), identified 10 proteins with significant effects on longitudinal Aβ42. The most significant proteins were angiotensin-converting enzyme (ACE, P=0.009), Chromogranin A (CgA, P=0.009) and Axl receptor tyrosine kinase (AXL, P=0.009). Receiver-operating characteristic analysis identified 11 proteins with significant effects on longitudinal Aβ42 (largely overlapping with the proteins identified by linear mixed-effects models). Several proteins (including ACE, CgA and AXL) were associated with Aβ42 reduction only in subjects with normal baseline Aβ42, and not in subjects with reduced baseline Aβ42. We conclude that baseline CSF proteins related to Aβ metabolism, microglia activity or synapses predict longitudinal Aβ42 reduction in cognitively healthy elders. The finding that some proteins only predict Aβ42 reduction in subjects with normal baseline Aβ42 suggest that they predict future development of the brain Aβ pathology at the earliest stages of AD, prior to widespread development of Aβ plaques.