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Major depressive disorder (MDD) is a highly heterogeneous mental disorder, and its complex etiology and unclear mechanism are great obstacles to the diagnosis and treatment of the disease. Studies have shown that abnormal functions of the visual cortex have been reported in MDD patients, and the actions of several antidepressants coincide with improvements in the structure and synaptic functions of the visual cortex. In this review, we critically evaluate current evidence showing the involvement of the malfunctioning visual cortex in the pathophysiology and therapeutic process of depression. In addition, we discuss the molecular mechanisms of visual cortex dysfunction that may underlie the pathogenesis of MDD. Although the precise roles of visual cortex abnormalities in MDD remain uncertain, this undervalued brain region may become a novel area for the treatment of depressed patients.
Subject(s)
Humans , Depressive Disorder, Major/pathology , Brain/pathology , Antidepressive Agents/therapeutic use , Visual Cortex/pathologyABSTRACT
Major depressive disorder (MDD) is a highly heterogeneous mental disorder, and its complex etiology and unclear mechanism are great obstacles to the diagnosis and treatment of the disease. Studies have shown that abnormal functions of the visual cortex have been reported in MDD patients, and the actions of several antidepressants coincide with improvements in the structure and synaptic functions of the visual cortex. In this review, we critically evaluate current evidence showing the involvement of the malfunctioning visual cortex in the pathophysiology and therapeutic process of depression. In addition, we discuss the molecular mechanisms of visual cortex dysfunction that may underlie the pathogenesis of MDD. Although the precise roles of visual cortex abnormalities in MDD remain uncertain, this undervalued brain region may become a novel area for the treatment of depressed patients.
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It is unclear whether antidepressants have the same effects on the brain function at different periods of treatment.In this paper, in order to improve the understanding of the neurobiological mechanisms of antidepressants from brain network level, find the target of antidepressants, optimize treatment strategy, four common neuroimaging techniques were reviewed to investigate the changes of brain functional imaging in patients with major depressive disorder at different periods (short-term, acute and long-term) after antidepressant treatment.After short-term antidepressant treatment, the changes of brain functional imaging mainly involved the amygdala, insula, prefrontal cortex, dorsal anterior cingulate cortex and so on, and these short-term changes of brain functional imaging could predict acute efficiency.After acute stage of antidepressant treatment, the changes of brain functional imaging were mostly located in the brain regions of cortical-limbic circuit and default mode network.The effect of long-term antidepressant treatment on brain functional imaging still needs to be further studied.In the future, the experimental design should be optimized and multiple neuroimaging techniques should be combined to conduct longitudinal long-term studies at multiple time points.
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Objective To investigate the relevance of brain-derived neurotrophic factor (BDNF) gene polymorphisms and the effects of citalopram antidepressant.Methods The subjects comprised 280 patients according to the diagnostic and statistical manual of mental disorders in the fourth edition (DSM-Ⅳ) criterion for major depressive disorder (MDD).Severity of depression were assessed by 17 Hamilton depression scale (HAMD) at the baseline and 1,2,4,6 weekend.Citalopram were selected for treatment.Polymerase chain reaction (PCR) and DNA sequencing analysis were used to detect the genotype of SNPs rs7124442 and rs6265 of BDNF.SPSS17.0 software was used for statistical analysis.Results (1) There were 280 patients (242 responders and 38 nonresponders;175 remissioners and 105 nonremissioners) accomplished 6 weeks of treatment.No association was found between the polymorphisms and antidepressant drug response or remission (the reduction rate of HAMD score ≥ 50％ was defined as response,conversely,defined as nonresponse;HAMD score more than 7 was named as remission,in contrast,named as nonremission) (P＞0.05).(2) Repeated measures analysis of variance was adopted to compare the change of HAMD scores among the genotypes at different time points.There was a significant difference in rs6265 polymorphism between the GA +AA genotype (the scores of HAMD at 2,4,6 weeks were(9.98±4.97),(8.02±4.50),(5.83±3.49) respectively) and the GG genotype groups (the scores of HAMD at 2,4,6 weeks were(11.90±6.55),(9.34± 4.71),(7.07±4.28) respectively) (P=0.031).Conclusion The results suggest that BDNF rs6265 polymorphisms in part determine the antidepressant response to citalopram.
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OBJECTIVE: This study aimed to evaluate the total antioxidant activity (TAA) in patients with major depressive disorder (MDD) and the effect of antidepressants on TAA using a novel potentiometric method. METHODS: Twenty-eight patients with MDD and thirty-one healthy controls were enrolled in this study. The control group comprised 31 healthy individuals matched for gender, drinking and smoking status. We assessed symptoms of depression using the Hamilton Depression Rating Scale (HAMD) and the Beck Depression Inventory (BDI). We measured TAA using potentiometry. All measurements were made at baseline and four and eight weeks later. RESULTS: There was a significant negative correlation between BDI scores and TAA. TAA was significantly lower in the MDD group than in controls. When the MDD group was subdivided into those who showed clinical response to antidepressant therapy (response group) and those who did not (non-response group), only the non-response group showed lower TAA, while the response group showed no significant difference to controls at baseline. After eight weeks of antidepressant treatment, TAA in both the response and non-response groups was similar, and there was no significant difference among the three groups. CONCLUSION: These results suggest that the response to antidepressant treatment in MDD patients might be predicted by measuring TAA.
Subject(s)
Humans , Antidepressive Agents , Depression , Depressive Disorder, Major , Drinking , Potentiometry , Smoke , SmokingABSTRACT
OBJECTIVES: This research aims to study the effect of omega-3 fatty acid as an adjunct to pharmacologic treatment for major depressive disorder occurring in-out patients aged 18-65 years old in a private tertiary hospital of Metro Manila who will receive pharmacologic maintenance antidepressant therapy. With the knowledge that this is a pilot study for Filipinos, the endpoint will be geared towards determining the feasibility of actually prescribing a dietary supplement in the form of omega-3 to further improve the depressive condition of our patients.METHODOLOGY: Patients with a current diagnosis of major depressive disorder, based on Hamilton Depression Rating Scale score of 14-18 or more, which is considered as moderate depression were observed for 4 weeks. The study design was a 4-week, double-blind addition of omega-3 or placebo to ongoing antidepressant therapy. Patients were required to continue their current antidepressant treatment at the same dose they were receiving when they entered the study. Patients were required to continue their current antidepressant treatment at the same dose they were receiving when they entered the study. Patients who were included in the study had been receiving their antidepressant medication for at least three weeks at the therapeutic dose.RESULTS: Twenty-four patients participated. Eighteen were women, and six were men. Their mean age was 39.7 (range=18-63). The mean reduction of HAM-D scale score in patients taking omega-3 was 12.17 points, compared with 9.58 in patients receiving placebo.CONCLUSION: This comparison in the reduction of scores was insignificant. There was no observable significant trends toward the superiority of omega-3 supplements over placebo in reducing depressive symptoms.
Subject(s)
Humans , Male , Female , Middle Aged , Adult , Young Adult , Adolescent , Fatty Acids , Depressive Disorder , Women , Men , LipidsABSTRACT
Objective To examine the values of Regional Homogeneity (ReHo) in first-episode, treatment-naive patients with major depressive disorder before and after antidepressant treatment in order to explore the neural mechanism of antidepressants. Methods Twenty-five first-episode, treatment-naive patients with major depressive disorder, which met with DSM-IV diagnosis criteria underwent fMRI resting-state scans before and after 8-week antidepressant treat-ment. Paired Samples T-test was used to analysis the differences between two groups. Results The ReHo in the patient group after treatment were significantly decreased in the right medial frontal gyrus, left inferior parietal lobule, left middle temporal gyrus, left insula, right precuneus, left cingulate gyrus and posterior lobe of the cerebellum , while significantly in-creased in the right medial frontal gyrus, left medial frontal gyrus, right inferior parietal lobule, left postcentral gyrus and right middle temporal gyrus compared with before treatment. Conclusions E xtensive abnormal activity within the default mode network in the resting-state may be involved in the neuropathophylogical substrate of depression and the abnormal activity can be partly reversed by antidepressant treatment, suggesting that regional homogeneity can be used to dynamical-ly evaluate the effect of antidepressant treatment.
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Este estudo teve como objetivo estimar a Qualidade de Vida (QV) em pacientes com transtorno depressivo maior antes e após tratamento antidepressivo eficaz. Participaram do estudo 26 indivíduos (18 a 65 anos) com episódio agudo de Transtorno Depressivo Maior, segundo critérios do DSM-IV. A duração do estudo foi de 8 semanas. Os instrumentos utilizados foram: escala de avaliação de depressão de Montgomery-Asberg (MADRS) e de Hamilton (HAMD-17). QV foi avaliada através da escala de qualidade de vida e satisfação (Q-LES-Q). Os resultados indicaram que sintomas depressivos e QV melhoraram significantemente com o tratamento (p<0,001). Sintomas de depressão e QV são significativamente correlacionados. Antes do tratamento, QV foi positivamente relacionada com o MADRS, mas não com o HAMD-17. Em todas as outras avaliações, a QV positivamente correlacionou-se com ambas as escalas, confirmando que a melhora sintomatológica traduz-se em melhora na qualidade de vida em pacientes com depressão maior
This study aimed to estimate the QoL in individuals with severe Mood Depressive Disorder, before and after effective antidepressant treatment. The Sample consisted of 26 participants with MDD. Duration of study was 2 months. Symptoms were measured with the Montgomer-Asberg depression evaluations scale (MADRS) and the Hamilton Depression Scale (HAMD-17). QoL was measured using the Quality of Life and Satisfaction (Q-LES-Q). Treatment yielded significant improvement of depressive symptoms (HAM-D17: p<0.001 and MADRS: p< 0.001) and of quality of life (Q-LES-Q - p<0.001). As measured by the correlation coefficient, qualify of life and symptom scales were significantly correlated. At baseline, quality of life was positively correlated with MADRS (p=0.037), but not with HAMD (p=0.878). For all other time points, quality of life was positively correlated with MDRS and HAMD (p≤ 0.001); increased scores in the Q-LES-Q corresponded to decreased scores in the MADRS and HAMD scales. Symptomatic improvement is significantly correlated with improved QoL in individuals with MDD
Subject(s)
Humans , Adolescent , Adult , Middle Aged , Quality of Life , Signs and Symptoms , Therapeutics , Depressive Disorder, Major , Pharmacology , DepressionABSTRACT
Objective: To investigate the prevalence of Female Orgasmic Dysfunction (FOD) focusing on the orgasm domain among female patients attending PPUKM Psychiatric clinic. To compare the prevalence of orgasmic dysfunction between female patients on Escitalopram and on Fluoxetine therapy. Methods: A validated questionnaire for sexual function was used to assess orgasmic function. A total of 112 women aged between 24 and 57 participated in this study. The orgasmic dysfunction was compared between patients on selective serotonin reuptake inhibitors (SSRIs) fluoxetine and escitalopram. Results: The prevalence of female orgasmic dysfunction was 58.9% (33/56) among patients treated with Fluoxetine and 41.1% (23/56) among patients treated with Escitalopram. However, there was no statistically significant difference between these two treatment groups (p=0.059). The odds to have FOD among patients on higher dose of antidepressants was found to be higher compared to those patients who were on lower dose of antidepressants (Odds ratio 5.32, p= 0.001). Conclusion: There was no significant difference of Female Orgasmic Dysfunction between patients on Fluoxetine and Escitalopram
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OBJECTIVE: This study was conducted to evaluate the impairment of cognitive functions, which include verbal and visual memory, visuospatial function, and executive function, and also to investigate if there is improvement of cognitive impairment after antidepressant treatment in patients with major depressive disorder (MDD). METHODS: Fifteen female patients with non-psychotic MDD in mild to moderate severity and 25 age-matched female normal control subjects participated in this study. Clinical severity of depression was measured by Beck Depression Inventory (BDI), Zung's Self-Rating Depression Scale (Zung), and Hamilton Rating Scale for Depression (HAMD). Cognitive functions were tested using Ray Complex Figure Test (RCFT) to evaluate visuospatial function and visual memory, Stroop test to evaluate conflict monitoring, Wisconsin Card Sorting Test (WCST) to evaluate executive function, and Seoul Verbal Learning Test (SVLT) to evaluate verbal memory. Both clinical depression scales and cognitive function tests were conducted at baseline and after 12 months of antidepressant treatment. RESULTS: At baseline, there were deficits in immediate and delayed recall of SVLT in patients with MDD compared to normal control subjects, while the impairment in visuospatial function, visual memory, and executive function was not clear. After antidepressant treatment, improvement of executive function, i.e. percent of error response and perseverative response of WCST in MDD patients was greater than that in normal control subjects. Improvement of executive function, however, did not show a significant correlation with the change of clinical severity of depression. CONCLUSION: The verbal memory was the most prominent domain of cognitive dysfunction in non-psychotic depression with mild to moderate severity. Of further note, differential improvement in executive function was observed in MDD patients after antidepressant treatment, although the improvement in executive function was not directly associated with the improvement of clinical depression.