Ruth Cunill
Icahn School of Medicine at Mount Sinai
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Featured researches published by Ruth Cunill.
Psychoneuroendocrinology | 2007
Daphne Simeon; Rachel Yehuda; Ruth Cunill; Margaret Knutelska; Frank W. Putnam; Lisa M. Smith
Mature defenses comprise one well-validated indicator of resilience. We investigated the relationships of resilience to trauma, attachment, temperament, cortisol, and cognitive performance in adult healthy volunteers. Participants were administered the Defense Style Questionnaire; the Relationship Questionnaire; the Childhood Trauma Questionnaire, and the Tridimensional Personality Questionnaire. Cortisol determinations included 24-h urinary, mean hourly plasma, response to low-dose dexamethasone suppression, and reactivity to the Trier social stress test (TSST). Mathematical performance during the TSST was quantified. Twenty-five women and 29 men participated. Resilience was significantly negatively correlated with childhood interpersonal trauma and with harm avoidance. Resilience was significantly positively correlated with urinary cortisol, secure attachment, reward dependence, and superior performance. In a linear regression analysis, the strongest predictor of resilience was childhood trauma, followed by math performance under stress and harm avoidance. We conclude that in young adults without manifest psychiatric disorder, resilience was associated with developmental, biological, and cognitive measures which merit further investigation.
Pharmacoepidemiology and Drug Safety | 2013
Ruth Cunill; Xavier Castells; Aurelio Tobías; Dolors Capellà
Atomoxetine is a non‐stimulant drug that could be an alternative to methylphenidate, whose benefit : risk balance for the treatment of adults with attention deficit hyperactivity disorder (ADHD) has recently been shown to be unclear. This study aimed to compare all‐cause discontinuation rate between atomoxetine and placebo in adults with ADHD. Secondarily, efficacy and safety were investigated.
Psychiatry Research-neuroimaging | 2013
Ruth Cunill; Elena Huerta-Ramos; Xavier Castells
The presence of obsessive-compulsive symptoms (OCS) and obsessive-compulsive disorder (OCD) is frequent in patients with schizophrenia and has been associated with greater functional impairment. The impact of these features on cognitive function is unclear. In this article, we performed a systematic review and meta-analysis to assess the effect of OCS/OCD on executive functions in schizophrenia patients. Results indicate that schizophrenia patients with OCS/OCD were more impaired in abstract thinking than schizophrenia patients without OCS/OCD. This finding provides support to the double jeopardy hypothesis and may partially explain the greater functional impairment shown in schizo-obsessive patients compared to those with schizophrenia. Inconsistent results were found for set-shifting, cognitive flexibility, cognitive inhibition and verbal fluency, as indicated by the high statistical heterogeneity found. Potential sources of heterogeneity such as definition of OCS/OCD, age of onset, severity of negative symptoms and premorbid intelligence were planned to be explored but there was an insufficient number of studies to perform these analyses. Our findings highlight the complexity of the relationship between OCS/OCD and schizophrenia and warrant further investigation of the cognitive function of schizo-obsessive patients.
Archive | 2011
Ruth Cunill; Xavier Castells
Obsessive-compulsive features are common in schizophrenia. The term schizo-obsessive has been proposed to delineate this subgroup of schizophrenia patients who also present OCS/OCD. Research into clinical, neuropsychological and functional profiles of schizo-obsessive patients has been extensive during these last years although a specific profile has yet to emerge. In addition, the neurobiological and genetic underpinnings of this association have recently begun to be investigated with preliminary but promising results. This chapter reviews the validity of schizo-obsessive disorder. The clinical and neuropsychological profile is elucidated and possible pathophysiological mechanisms and etiologic factors are discussed. Finally, a suitable therapeutic approach is also suggested.
Pharmacoepidemiology and Drug Safety | 2014
Ruth Cunill; Xavier Castells; Aurelio Tobías; Dolors Capellà
We have read the letter written by Ramos-Quiroga et al., in which the authors make a methodological critique of our recent paper, based on two issues: the use of all-cause treatment discontinuation as the main outcome of the study, and the measurement of the clinical efficacy of atomoxetine by means of the standardized mean difference (SMD). We aim to address their critiques in the present letter. The authors of the letter argue that all-cause treatment discontinuation, despite being a valid endpoint in the real-world setting, should not be considered a risk : benefit endpoint because it does not represent a primary outcome in randomized placebo controlled clinical trials (RPCCT), is not included in the European Medicines Agency guidelines for the investigation and clinical assessment of the risk : benefit of medicinal products1 and has never been used or accepted by any regulatory agency as a risk : benefit measure. We partially agree with the observations made but not with the conclusion the authors draw from them. First of all, it is precisely because all-cause treatment discontinuation is a valid endpoint in the real-world setting that it may contribute to add useful translational clinical information to RPCCT. Conversely, surrogated endpoints used in most preauthorisation trials are clinically less informative because their external validity is less clear. Secondly, we consider that all-cause treatment discontinuation does represent a risk : benefit endpoint because it combines both efficacy and safety2 in the following way. If symptom improvement outweighs medicationinduced side effects, treatment discontinuation should be lower with the active medication than with placebo. Conversely, if the improvement on symptom severity does not compensate for the side effects, then treatment discontinuation should be higher with the active compound. The latter is what we found in our study: treatment discontinuation was higher with atomoxetine than with placebo. We are aware that despite the interest that all-cause treatment discontinuation could have, little attention has been given to this endpoint by regulatory agencies and consequently in regulatory trials. In fact, our research aimed to propose to these agencies the use of all-cause treatment discontinuation as an additional endpoint with which to appraise the risk : benefit profile of attention deficit hyperactivity disorder (ADHD) medications.3,4 We agree that many factors may contribute to treatment discontinuation in RPCCT, thereby hindering the interpretation of this endpoint. To improve the understanding of our findings on treatment discontinuation, we investigated the causes that may account for it. We focused this analysis on those causes that have a straightforward clinical interpretation: adverse events and lack of efficacy. It was found that, while AE-induced discontinuation was more than twice as high with atomoxetine thanwith placebo, discontinuation due to lack of efficacy was only slightly higher with placebo than with atomoxetine. These results along with those for all-cause treatment discontinuation suggest that atomoxetine efficacy may not compensate for its side effects. In the light of these results, we cannot share the opinion of the Medicines and Healthcare products Regulatory Agency assessor that there are no concerns regarding treatment discontinuation.5 This discrepancy may have a statistical explanation. When taken individually, most clinical trials show no differences in discontinuation rates between atomoxetine and placebo because their sample size is usually too small to detect these differences, because they are powered to investigate the efficacy of atomoxetine on ADHD symptom severity, following regulatory recommendations.1 When this statistical limitation is overcome by pooling the results of all the available data using meta-analytical techniques as we did, all-cause treatment discontinuation is found to be higher with atomoxetine than with placebo. It is likely that if the Medicines and Healthcare products Regulatory Agency assessor had been aware of this finding his/her opinion on this issue would have been less favourable. Ramos-Quiroga et al. also showed concern about the way the efficacy on ADHD symptom severity was analysed in our study. Instead of analysing it as a continuous endpoint, they proposed comparing the proportion of responders as a more relevant measure of efficacy. First of all, we would like to emphasize
Adicciones | 2016
Ruth Cunill; Xavier Castells
Editorial of vol 28-3.
The Journal of Clinical Psychiatry | 2009
Ruth Cunill; Xavier Castells; Daphne Simeon
Medicina Clinica | 2015
Ruth Cunill; Xavier Castells
European Journal of Clinical Pharmacology | 2013
Xavier Castells; Ruth Cunill; Dolors Capellà
Cochrane Database of Systematic Reviews | 2016
Xavier Castells; Ruth Cunill; Clara Pérez-Mañá; Xavier Vidal; Dolors Capellà