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- ArticleAdams GC, Wrath AJ, Mondal P, Asmundson GJG.Psychiatry Res. 2018 11;269:86-92.Major depressive disorder (MDD) frequently co-occurs with social anxiety disorder (SAD), and their comorbidity (MDD-SAD) increases clinical severity and functional impairment. Still, the specific psychological vulnerabilities of individuals with MDD-SAD are poorly understood. Individual attachment characteristics develop early in life through interactions with primary caregivers, and tend to persist throughout life. Early trauma can worsen attachment insecurity, increasing the risk for future anxiety and depression. The purpose of this study is to examine differences in individual attachment and history of trauma in depressed individuals with or without comorbid SAD and controls. One hundred sixty-two participants were categorized into three groups based on SCID-I interview: healthy controls (HC), individuals with current MDD without SAD (MDD), and individuals with current MDD comorbid with SAD (MDD-SAD). MDD-SAD group had significantly greater attachment anxiety and attachment avoidance compared to the MDD and HC groups. MDD-SAD group had greater clinician-rated depression severity and dysfunction compared to MDD group. In summary, the study further supports the clinical risks associated with MDD-SAD and suggests that insecure attachment might represent an associated vulnerability and a possible pathway which warrants further research and clinical attention.
- ArticleSengupta SM, Fotopoulos N, Devenyi GA, Fortier MÈ, Ter-Stepanian M, Sagliker S, Karama S, Mallar Chakravarty M, Labbe A, Grizenko N, Joober R.Psychiatry Res. 2018 11;269:652-657.Several epidemiological and genetic studies have provided evidence of an overlap between neurodevelopmental disorders. However, the details of the etiological pathways remain to be elucidated. In this study, we garnered the findings of previous GWAS, conducted with schizophrenia and bipolar disorder. We conducted an exploratory study to examine the association between these SNPs and quantitative clinical/ behavioural/ cognitive/ structural brain parameters, as well as response to treatment with a fixed dose of methylphenidate, in a relatively large sample of children with ADHD. Family-based association tests were conducted with nine tag SNPs with 602 nuclear families. In addition, structural magnetic resonance imaging (sMRI) was conducted in a subset of children with ADHD (n = 76). Of the 9 tag SNPs examined, rs1602565 showed a significant association with ADHD, several dimensional measures and response to treatment. An association was also observed between rs1006737 (CACNA1C) and performance IQ. In addition, significant reductions in cortical thickness measurements were observed with the risk allele in rs1006737. These results provide preliminary evidence for putative shared genetic vulnerability between childhood ADHD and other neurodevelopmental disorders.
- ArticleGonzález-Blanch C, Fernando Hernández-de-Hita, Muñoz-Navarro R, Ruíz-Rodríguez P, Medrano LA, Moriana JA, Cano-Vindel A, Psic AP Research Group.Psychiatry Res. 2018 11;269:596-601.This study explores the associations between different disability domains and the most prevalent symptoms of mental disorders in primary care patients (i.e. depression, anxiety, and somatization). A total of 1241 participants from 28 primary care centres completed self-report measures of depression, anxiety, and somatization. This same sample also completed the Sheehan Disability Scale (SDS) to assess functional impairment in work, social life, and family life domains. Associations between the symptoms and each disability domain were examined using hierarchical regression analyses. Depression emerged as the strongest predictor of all three disability domains. Somatization was associated only with the work domain, and anxiety was associated only with the family life domain. Clinical symptoms explained a greater proportion of the variance than sociodemographic variables. In primary care patients, depression, anxiety and somatizations were associated with distinct domains of disability. Early provision of effective treatments in the primary care setting may be crucial to reduce the societal burden of common mental disorders.
- ArticleStone LB, Amole MC, Cyranowski JM, Swartz HA.Psychiatry Res. 2018 11;269:681-687.Childhood emotional abuse impairs emotion regulation and increases risk for major depressive disorder in adulthood. Mounting evidence suggests that decreased resting-state high-frequency heart rate variability, an index of parasympathetic function, represents a transdiagnostic biomarker of emotion dysregulation. We propose that adults with histories of major depressive disorder and childhood emotional abuse represent a subpopulation at particularly high risk to exhibit deficits in parasympathetic control. The current report compared resting-state high-frequency heart rate variability across three groups: (1) depressed women who endorsed childhood emotional abuse (N = 11); (2) depressed women without childhood emotional abuse (N = 19), and (3) never-depressed women without childhood emotional abuse (N = 22). Participants completed childhood trauma self-reports and assessment of resting-state high-frequency heart rate variability. ANCOVAs comparing the three groups after controlling for health-related, psychiatric, and respiratory factors were significant. Depressed women with childhood emotional abuse exhibited lower high-frequency heart rate variability than both groups without childhood emotional abuse (d's ranging from 0.81-0.92). Surprisingly, psychiatric factors were non-significant predictors, indicating that childhood emotional abuse may have a unique impact on autonomic functioning. Future research on larger samples is needed to disentangle the relative and synergistic burdens of depression and childhood trauma on physiologic indicators of emotion dysregulation.
- ArticleLüdtke T, Pult LK, Schröder J, Moritz S, Bücker L.Psychiatry Res. 2018 11;269:753-762.Depressive symptoms are common, yet only a subgroup of individuals receive adequate treatment. To reduce the treatment gap, several online self-help programs have been developed, yielding small to moderate effects. We developed a smartphone self-help application addressing depressive symptoms. We sought to evaluate its feasibility and efficacy in participants reporting a subjective need for help (a diagnosis of depression was not mandatory). We conducted a randomized controlled trial (N = 90). The primary outcome was a reduction of depressive symptoms measured with the Patient Health Questionnaire-9 (PHQ-9). Secondary outcomes included improved self-esteem (Rosenberg Self-Esteem Scale) and quality of life (WHOQOL-BREF). The intervention group obtained access to the application for four weeks, the wait-list group received access after the post assessment. No group differences emerged in either outcome in intention-to-treat analyses. Per protocol analyses with frequent users (i.e., several times a week or more) yielded a small effect size (η2p = 0.049) at trend level on the reduction of depressive symptoms in favor of the treatment group. However, 39% of the participants did not use the application frequently. Mobile self-help applications represent a promising addition to existing treatments, but it is important to increase patients' motivation to use them.
- ArticleChen MH, Li CT, Lin WC, Hong CJ, Tu PC, Bai YM, Cheng CM, Su TP.Psychiatry Res. 2018 11;269:207-211.Increasing evidence supports the rapid antidepressant effect of a low-dose ketamine infusion in treatment-resistant depression (TRD). Proinflammatory cytokines play a crucial role in the pathophysiology of TRD. However, it is unknown whether the rapid antidepressant effect of ketamine is related to the rapid suppression of proinflammatory cytokines. Seventy-one patients with TRD were randomized into three groups according to the treatment received: 0.5 mg/kg ketamine, 0.2 mg/kg ketamine, and normal saline infusion. Proinflammatory markers, including C-reactive protein (CRP), interleukin (IL)-6, and tumor necrosis factor (TNF)-α were examined at baseline and at 40 min, 240 min, Day 3, and Day 7 postinfusion. Montgomery-Åsberg Depression Rating Scale (MADRS) was assessed for depressive symptoms across time. Log-transformed IL-6 and TNF-α levels differed significantly over time. The decrease in TNF-α between baseline and 40 min postinfusion was positively correlated with a decrease in MADRS scores across time in the 0.5 mg/kg ketamine group. This is the first clinical study to support a positive correlation between changes in cytokine levels after ketamine infusion and improvements in depressive symptoms with TRD. The rapid suppression of proinflammatory cytokines may contribute to the rapid antidepressant effect of the ketamine infusion.
- ArticleWang X, Zhao J, Hu Y, Jiao Z, Lu Y, Ding M, Kou Y, Li B, Meng F, Zhao H, Li H, Li W, Yang Y, Lv L.Psychiatry Res. 2018 11;269:271-277.Schizophrenia presents with a broad range of negative, positive, and cognitive symptoms, and comprehensive treatment is still a challenge. Sodium nitroprusside (SNP) has been reported to rapidly reduce psychotic symptoms and improve cognitive functions in patients with schizophrenia, providing a new possible direction for treatment. In this study, we tested whether SNP can improve psychotic symptoms and cognitive function in schizophrenia patients with longer disease history. This was a randomized, double-blind, placebo-controlled trial conducted between May 2016 and April 2017. Forty-two schizophrenia patients aged 18-45 years were recruited from Henan Province Mental Hospital. Baseline psychiatric symptoms were measured using the Positive and Negative Syndrome Scale (PANSS), and baseline cognitive functions were measured using the Wechsler Adult Intelligence Scale. Patients received two SNP or placebo infusions (0.5 μg/kg per min for 4 h) at a one-week interval. We reassessed psychiatric symptoms and cognitive functions using the same tests shortly after the first and second infusions and 4 weeks after the second infusion. We did not find any significant effect of SNP over placebo on psychotic symptoms or cognitive functions, although SNP was relatively well tolerated with a good safety profile.
- ArticleBonanno S, Giossi R, Zanin R, Porcelli V, Iannacone C, Baranello G, Ingenito G, Iyadurai S, Stevic Z, Peric S, Maggi L.J Neurol. 2022 11;269(11):5858-5867.BACKGROUND: Spinal muscular atrophy (SMA) is an autosomal recessive disease where a deficient amount of SMN protein leads to progressive lower motor neuron degeneration. SMN-enhancing therapies are now available. Yet, fatigue and signs of impaired neuromuscular junction (NMJ) transmission could contribute to SMA phenotype. Amifampridine prolongs presynaptic NMJ terminal depolarization, enhancing neuromuscular transmission.
METHODS: SMA-001 was a phase 2, 1:1 randomized, double-blind, placebo-controlled crossover study. Ambulatory (walking unaided at least 30 m) SMA Type 3 patients, untreated with SMN-enhancing medications, entered a run-in phase where amifampridine was titrated up to an optimized stable dose. Patients achieving at least three points improvement in Hammersmith Functional Motor Score Expanded (HFMSE) were randomized to amifampridine or placebo, alternatively, in the 28-day double-blind crossover phase. Safety was evaluated by adverse events (AE) collection. Primary efficacy measure was the HFMSE change from randomization. Secondary outcomes included timed tests and quality of life assessment. Descriptive analyses and a mixed effects linear model were used for statistics.
RESULTS: From 14 January 2019, 13 patients, mean age 34.5 years (range 18-53), with 5/13 (38.5%) females, were included. No serious AE were reported. Transient paresthesia (33.3%) was the only amifampridine-related AE. Six patients for each treatment sequence were randomized. Amifampridine treatment led to a statistically significant improvement in HFMSE (mean difference 0.792; 95% CI from 0.22 to 1.37; p = 0.0083), compared to placebo, but not in secondary outcomes.
DISCUSSION: SMA-001 study provided Class II evidence that amifampridine was safe and effective in treating ambulatory SMA type 3 patients.
CLINICAL TRIAL REGISTRATION: NCT03781479; EUDRACT 2017-004,600-22.