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Antidepressant Response (antidepressant + response)
Selected AbstractsAntidepressant efficacy and cognitive effects of repetitive transcranial magnetic stimulation in vascular depression: an open trialINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 9 2004I. Fabre Abstract Background Beneficial effects of repetitive transcranial magnetic stimulation (rTMS) were demonstrated by many controlled studies in major depression. Moreover, this promising and non invasive therapeutic tool seems to be better tolerated than electroconvulsive therapy. Vascular depression is a subtype of late-life depression, associated with cerebrovascular disease and means a poorer response to antidepressant treatment. We employed rTMS over the left prefrontal cortex in 11 patients with late-onset resistant vascular depression. The primary purpose of this two-week open study was to examine antidepressant efficacy of rTMS in vascular depression. The secondary aim was to evaluate cognitive effects of rTMS in our sample. Methods Clinical status, as measured with the Hamilton Depression Rating Scale (HDRS), and cognitive effects, as evaluated by neuropsychological tests, were assessed at baseline and after two weeks of rTMS. Brain measurements to obtain an index of prefrontal atrophy were performed at both the motor cortex and prefrontal cortex. Results Five out of 11 resistant patients with late-onset vascular depression were responders. They showed a clinically meaningful improvement in HDRS scores, with a decrease of 11, 4 points (p<0.01). Antidepressant response is correlated to the relative degree of prefrontal atrophy (p = 0.05). After two weeks, verbal fluency and visuospatial memory improved. No cognitive performance deteriorated except for verbal memory, as the delayed recall decreased significantly in the responders' group. Conclusions Our preliminary observations prompt to perform a subsequent controlled study to examine if rTMS may constitute an alternative to electroconvulsive therapy. Copyright © 2004 John Wiley & Sons, Ltd. [source] Brain functional changes during placebo lead-in and changes in specific symptoms during pharmacotherapy for major depressionACTA PSYCHIATRICA SCANDINAVICA, Issue 4 2009A. M. Hunter Objective:, Brain functional changes during placebo lead-in have been associated with antidepressant response in clinical trials for major depressive disorder (MDD); however, the relationship between such non-pharmacodynamic changes in brain function and changes in specific symptoms is unknown. Method:, Fifty-eight adults with MDD completed a 1-week single-blind placebo lead-in preceding 8 weeks of double-blind randomized treatment with fluoxetine or venlafaxine (n = 30) or placebo (n = 28). Brain functional change during lead-in was assessed using quantitative electroencephalographic (qEEG) prefrontal theta-band cordance. Symptoms were assessed using the Symptom Checklist-90-Revised (SCL-90-R). Results:, The multiple regression model examining the qEEG parameter in relation to SCL-90-R subscales was significant [F(9,9) = 4.27, P = 0.021, R2 = 0.81] in females, with a significant association for the interpersonal sensitivity subscale (beta coefficient = 1.94, P = 0.001). Conclusion:, Prefrontal neurophysiologic change during placebo lead-in may indicate subsequent antidepressant-related improvement in symptoms of interpersonal sensitivity. [source] The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticityDEVELOPMENTAL NEUROBIOLOGY, Issue 5 2010Eero Castrén Abstract Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 2010 [source] The antidepressant effects of running and escitalopram are associated with levels of hippocampal NPY and Y1 receptor but not cell proliferation in a rat model of depressionHIPPOCAMPUS, Issue 7 2010Astrid Bjørnebekk Abstract One hypothesis of depression is that it is caused by reduced neuronal plasticity including hippocampal neurogenesis. In this study, we compared the effects of three long-term antidepressant treatments: escitalopram, voluntary running, and their combination on hippocampal cell proliferation, NPY and the NPY-Y1 receptor mRNAs, targets assumed to be important for hippocampal plasticity and mood disorders. An animal model of depression, the Flinders Sensitive Line (FSL) rat, was used and female rats were chosen because the majority of the depressed population is females. We investigated if these treatments were correlated to immobility, swimming, and climbing behaviors, which are associated with an overall, serotonergic-like and noradrenergic-like antidepressant response, in the Porsolt swim test (PST). Interestingly, while escitalopram, running and their combination increased the number of hippocampal BrdU immunoreactive cells, the antidepressant-like effect was only detected in the running group and the group with access both to running wheel and escitalopram. Hippocampal NPY mRNA and the NPY-Y1 receptor mRNA were elevated by running and the combined treatment. Moreover, correlations were detected between NPY mRNA levels and climbing and cell proliferation and NPY-Y1 receptor mRNA levels and swimming. Our results suggest that increased cell proliferation is not necessarily associated with an antidepressant effect. However, treatments that were associated with an antidepressant-like effect did regulate hippocampal levels of mRNAs encoding NPY and/or the NPY-Y1 receptor and support the notion that NPY can stimulate cell proliferation and induce an antidepressant-like response. © 2009 Wiley-Liss, Inc. [source] Milnacipran plasma levels and antidepressant response in Japanese major depressive patientsHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 4 2003Hisashi Higuchi Abstract The relationship between antidepressant effects and plasma levels of milnacipran was studied in 49 cases of major depression without psychotic features during 6 weeks of milnacipran treatment. The daily dose of milnacipran was 50,mg/day for the first week, and up to 100,mg/day thereafter. Depressive symptoms were evaluated by the Montgomery and Åsberg depression rating scale (MADRS) before treatment and at 1, 2, 4 and 6 weeks after the beginning of this study. Thirty-four patients (69.4%) were responders (defined as a 50% or greater decrease in the baseline MADRS score). Significant differences of MADRS scores were seen from 1 week after the beginning of this study (p,=,0.004, unpaired t -test) between responders and nonresponders. The mean plasma milnacipran level of responders, 82.0,±,29.4,ng/ml, was similar to that of non-responders, 78.6,±,23.1,ng/ml; there was no significant difference between responders and nonresponders. Neither a significant linear nor a curvilinear relationship was obtained between the final MADRS score and the plasma levels of milnacipran. Although there was no significant relationship between the plasma levels of milnacipran and the antidepressant response, milnacipran should be considered an efficacious agent in the treatment of major depressive patients. Copyright © 2003 John Wiley & Sons, Ltd. [source] Anxiety does not predict response to antidepressant treatment in late life depression: results of a meta-analysisINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 5 2009J. Craig Nelson Abstract Objective Previous studies of mixed aged and older adult samples with major depressive disorder (MDD) reported reduced depression response in anxious patients, but a systematic review and analysis has not been performed. Our aim was to determine if anxiety predicts antidepressant response in previously identified placebo-controlled trials of second generation antidepressants for late-life depression. Method From a previous systematic review that identified ten randomized, placebo-controlled trials of community dwelling patients aged 60 or older with major depression, anxious patients were identified by a score ,7 on the anxiety/somatization factor of the Hamilton Depression Rating Scale (HDRS). Response was defined as 50% or greater improvement on the HDRS or the Montgomery Asberg Depression Rating Scale. A meta-analysis was performed using a random effects model to calculate Odds Ratios (OR). Results Data were available from eight trials having ten drug-placebo contrasts that included 2322 anxious and 1387 non-anxious patients. The odds ratio for response to drug compared to placebo in anxious patients was 1.57 (95% CI 1.15, 2.14; z,=,2.86, n,=,10, p,<,0.001), in non-anxious patients was 1.44 (95% CI 1.15, 1.80, z,=,3.21, n,=,10, p,<,0.001), and did not differ between groups. Pooled response rates to drug and placebo respectively were 49.4% vs 37.4% in anxious patients and 44.2 vs 35.5% in non-anxious patients. Conclusions In randomized, placebo-controlled trials, anxiety in late-life depression was not associated with decreased response to second generation antidepressants. Copyright © 2009 John Wiley & Sons, Ltd. [source] Randomized double-blind placebo-controlled donepezil augmentation in antidepressant-treated elderly patients with depression and cognitive impairment: a pilot studyINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 7 2008Gregory H. Pelton Abstract Objective To assess combined antidepressant and cognitive enhancer treatment in elderly patients presenting with depression plus cognitive impairment. Methods Twenty-three elderly (>50 years old) depressed, cognitively impaired (DEP-CI) patients participated in a pilot study. We evaluated whether, after 8 weeks of open antidepressant treatment, donepezil HCl (Aricept) would afford added cognitive benefit compared to placebo in a randomized 12-week trial. A subsample continued in an 8-month extension phase of open treatment with donepezil. Neuropsychological testing (NPT) was performed and antidepressant response monitored at baseline and the 8, 20, and 52-week time points. Results At 8-weeks, the antidepressant response rate was 61% (14/23). Improvement in SRT immediate recall (SRT-IR; e.g. episodic verbal memory) was observed in responders compared to non-responders. During the 12-week, placebo-controlled, donepezil add-on trial, patients on donepezil showed further improvement in SRT-IR versus patients on placebo. In the open extension phase, patients who continued open donepezil treatment (n,=,6) maintained improvement in memory and tended to show an advantage over patients who never received donepezil and were evaluated at the 52-week time point (n,=,6). There were no observed significant donepezil effects on non-memory cognitive domains. Conclusion These preliminary findings suggest that addition of a cholinesterase inhibitor (AChEI) following antidepressant medication treatment in elderly Dep-CI patients may improve cognition, and support the need for a confirmatory, larger randomized placebo-controlled trial. Copyright © 2007 John Wiley & Sons, Ltd. [source] Hippocampal volume and antidepressant response in geriatric depressionINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 6 2002Ming-Hong Hsieh Abstract Background Biological markers of treatment response may include structural brain changes seen on neuroimaging. While most imaging studies have focused on cerebrovascular disease, evidence is growing that the hippocampus may play a role in depression, particularly geriatric depression. Method We studied 60 depressed elderly patients enrolled in a longitudinal study who were treated with antidepressant medications using a treatment guideline-based approach. Baseline and 12-week Montgomery-Asberg Depression Rating Scale (MADRS) scores were obtained via interview with a geriatric psychiatrist. All subjects had a baseline magnetic resonance imaging (MRI) brain scan. MRI scans were processed using standard protocols to determine total cerebral volume and right and left hippocampal volumes. Hippocampal volumes were standardized for total cerebral volume. MADRS scores less than 10 were used to define remission. Results When the group with the lowest quartile of standardized hippocampal volumes was compared to those above the first quartile, those with small right and total hippocampal volumes were less likely to achieve remission. In a subsequent logistic regression model controlling for age small standardized right hippocampal volumes remained significantly associated with remission. Conclusion Further studies with larger sample are needed to determine if left-right hippocampal volume differences do exist in depression, and basic neuroscience studies will need to elucidate the role of the hippocampus in geriatric depression. Copyright © 2002 John Wiley & Sons, Ltd. [source] No predictors of antidepressant patient response to milnacipran were obtained using the three-factor structures of the Montgomery and Åsberg Depression Rating Scale in Japanese patients with major depressive disordersPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 2 2008Hisashi Higuchi md Aims:, Milnacipran, a new specific serotonin and norepinephrine re-uptake inhibitor, is as effective as tricyclic antidepressants. Symptomatological predictors of antidepressant response to milnacipran have not been studied until now. Methods:, This study included 101 Japanese patients who fulfilled the DSM-IV criteria for the diagnosis of major depressive disorders and whose score on the Montgomery and Åsberg Depression Rating Scale (MADRS) was ,21. Eighty-three patients were finally included. Patients with a pretreatment MADRS score ,31 points were defined as severe (n = 28), and the rest as non-severe (n = 55). The three-factor model of MADRS was used for analysis; the first factor was defined by three items, the second factor was defined by four items and the third factor was defined by three items representing dysphoria, retardation, and vegetative symptoms, respectively. Milnacipran was administered twice daily for 6 weeks. The initial dose was 50 mg/day; after a week it was increased to 100 mg/day. Results:, No significant difference was observed in the mean score of first factor, second factor and third factor at pretreatment time between responders and non-responders in both severe and non-severe patients. Conclusions:, No predictor of antidepressant response to milnacipran was obtained using the three-factor structures of the MADRS in Japanese patients with major depressive disorders. [source] Molecular genetics of bipolar disorder and depressionPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 1 2007TADAFUMI KATO md Abstract, In this review, all papers relevant to the molecular genetics of bipolar disorder published from 2004 to the present (mid 2006) are reviewed, and major results on depression are summarized. Several candidate genes for schizophrenia may also be associated with bipolar disorder: G72, DISC1, NRG1, RGS4, NCAM1, DAO, GRM3, GRM4, GRIN2B, MLC1, SYNGR1, and SLC12A6. Of these, association with G72 may be most robust. However, G72 haplotypes and polymorphisms associated with bipolar disorder are not consistent with each other. The positional candidate approach showed an association between bipolar disorder and TRPM2 (21q22.3), GPR50 (Xq28), Citron (12q24), CHMP1.5 (18p11.2), GCHI (14q22-24), MLC1 (22q13), GABRA5 (15q11-q13), BCR (22q11), CUX2, FLJ32356 (12q23-q24), and NAPG (18p11). Studies that focused on mood disorder comorbid with somatic symptoms, suggested roles for the mitochondrial DNA (mtDNA) 3644 mutation and the POLG mutation. From gene expression analysis, PDLIM5, somatostatin, and the mtDNA 3243 mutation were found to be related to bipolar disorder. Whereas most previous positive findings were not supported by subsequent studies, DRD1 and IMPA2 have been implicated in follow-up studies. Several candidate genes in the circadian rhythm pathway, BmaL1, TIMELESS, and PERIOD3, are reported to be associated with bipolar disorder. Linkage studies show many new linkage loci. In depression, the previously reported positive finding of a gene,environmental interaction between HTTLPR (insertion/deletion polymorphism in the promoter of a serotonin transporter) and stress was not replicated. Although the role of the TPH2 mutation in depression had drawn attention previously, this has not been replicated either. Pharmacogenetic studies show a relationship between antidepressant response and HTR2A or FKBP5. New technologies for comprehensive genomic analysis have already been applied. HTTLPR and BDNF promoter polymorphisms are now found to be more complex than previously thought, and previous papers on these polymorphisms should be treated with caution. Finally, this report addresses some possible causes for the lack of replication in this field. [source] Lux vs. wavelength in light treatment of Seasonal Affective DisorderACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2009J. L. Anderson Objective:, Published dosing guidelines for treatment of Seasonal Affective Disorder (SAD) refer to photopic lux, which is not appropriate for short-wavelength light. Short wavelengths are most potent for many non-visual responses to light. If SAD therapy were similarly mediated, standards utilizing lux risk overestimating necessary dose. We investigated antidepressant responses to light using two light-emitting diode (LED) sources, each emitting substantial short-wavelength light, but <2500 lux. Method:, A randomized, double-blind trial investigated 3-week 45 min/day out-patient treatment with blue-appearing (goLITE®) or blue-enriched white-appearing light in 18 moderately-depressed adults (12F, 49.1 ± 9.5 years). Equivalent numbers of photons within the short-wavelength range were emitted, but the white source emitted twice as many photons overall and seven-fold more lux. Results:, Depression ratings (SIGH-ADS; http://www.cet.org) decrease averaged 82% (SD = 17%) from baseline (P < 0.0001) in both white- and blue-light groups. Both sources were well tolerated. Conclusion:, Short-wavelength LED light sources may be effective in SAD treatment at fewer lux than traditional fluorescent sources. [source] | |||||||||||||