3,053 research outputs found
Circadian rhythms in obsessive-compulsive disorder
The etiopathology and neurobiology of obsessive-compulsive disorder (OCD) are not fully understood. As for altered circadian rhythms associated with OCD, hormonal dysregulation and a delayed sleep phase have come into the focus of research. The novel antidepressant agomelatine is able to resynchronize circadian rhythms and the augmentative administration of this compound has been shown to be of benefit in some OCD patients who are refractory to common forms of pharmacotherapy. Adjunctive chronotherapy might also enhance the outcome in treatment-refractory OCD. The present review summarises the findings regarding circadian abnormalities in OCD
Effects of methylphenidate on memory functions of adults with ADHD
Neuropsychological research on adults with attention deficit hyperactivity disorder (ADHD) revealed considerable impairments in memory functions related to executive control. However, only limited evidence exists supporting the effects of pharmacological treatment using methylphenidate (MPH) on memory functions. The aim of the present study was, therefore, to explore the impact of MPH on various memory functions of adults with ADHD. Thirty-one adults with ADHD treated with MPH, 36 adults with ADHD not-treated with MPH, and 36 healthy individuals were assessed on several aspects of memory, including short-term memory, working memory, retrospective memory, prospective memory, and source memory. Multivariate statistical analyses were applied to compare memory functions between groups. Nonmedicated adults with ADHD showed considerable impairments in memory functions related to executive control. Adults with ADHD treated with MPH showed improved memory functions when compared to nonmedicated patients, but were still impaired when compared to healthy controls. The present study emphasized the severity of memory impairments of adults with ADHD. A pharmacological treatment with MPH appeared to improve memory, but does not normalize functioning. Additional treatment intervention (e.g., cognitive-behavioral therapy) is therefore necessary
The Development of an Embedded Figures Test for the Detection of Feigned Attention Deficit Hyperactivity Disorder in Adulthood
ObjectivesIt has been shown that an increasing number of adults deliberately feign attention deficit hyperactivity disorder (ADHD), which demonstrates the need for new tests designed to detect feigned ADHD.MethodsAn Embedded Figures Test ( EFT) was developed for the detection of feigned ADHD in adulthood. EFT performance of 51 adults with ADHD was compared to the performance of 52 matched healthy individuals, as well as to 268 undergraduate students who were randomly allocated in a simulation design to one of four experimental conditions, i.e. a control group, a naive simulation group, a symptom-coached simulation group or a test-coached simulation group. Furthermore, an independent sample of 11 adults with ADHD as well as a sample of 17 clinicians experienced in the work with adults with ADHD were assessed for further validation of the EFT.ResultsThe EFT was relatively easy to perform for both patients with ADHD and healthy comparisons as shown by low error rates and non-significant group differences. However, simulation groups differed from patients with ADHD by significant and large effects. An EFT index for the prediction of feigned ADHD was derived based on logistic regression coefficients. Receiver Operating Characteristics (ROC) demonstrated good classification accuracy of feigned ADHD relative to ADHD (AUC = 94.8%), i.e. high sensitivity (88%) and specificity (90%).ConclusionsThis study supports the utility of the EFT for the detection of feigned adult ADHD.</p
Polyunsaturated fatty acids in the treatment of attention deficit hyperactivity disorder
Background: Attention deficit/hyperactivity disorder (ADHD) is one of the most common behavioral disorders in children. Insufficient dietary intake of long-chain polyunsaturated fatty acids (LC-PUFAs) has been suggested to have an impact on the development of symptoms of ADHD in children. Individuals with ADHD have been demonstrated to have significantly reduced blood concentrations of PUFAs and, in particular, reduced levels of omega-3 (n-3) PUFAs. These findings suggest that PUFA supplementation may reduce the attention and behavior problems associated with ADHD. Objective: To provide an overview of the efficacy of dietary LC-PUFA supplementation in the treatment of ADHD. Methods: Literature published up until December 2013 on the effects of n-3 PUFA supplementation on ADHD symptoms was obtained using a PubMed search and critically reviewed. Results: Dietary PUFA supplementation appears to have beneficial effects on ADHD symptoms although these effects are small. The clinical relevance of these observations remains to be determined. Conclusion: There is only limited support for the efficacy of PUFA supplementation for the core symptoms of ADHD. Given the small effect sizes regarding PUFA supplementation, it may not be a sufficient therapy for a majority of patients with ADHD
Author correction: Elucidating causative gene variants in hereditary Parkinson's disease in the Global Parkinson's Genetics Program (GP2)
Five-Year Change in Visceral Adipose Tissue Quantity in a Minority Cohort: The Insulin Resistance Atherosclerosis Study (IRAS) Family Study
Nomenclature of Genetic Movement Disorders:Recommendations of the International Parkinson and Movement Disorder Society Task Force – An Update
In 2016, the Movement Disorder Society Task Force for the Nomenclature of Genetic Movement Disorders presented a new system for naming genetically determined movement disorders and provided a criterion-based list of confirmed monogenic movement disorders. Since then, a substantial number of novel disease-causing genes have been described, which warrant classification using this system. In addition, with this update, we further refined the system and propose dissolving the imaging-based categories of Primary Familial Brain Calcification and Neurodegeneration with Brain Iron Accumulation and reclassifying these genetic conditions according to their predominant phenotype. We also introduce the novel category of Mixed Movement Disorders (MxMD), which includes conditions linked to multiple equally prominent movement disorder phenotypes. In this article, we present updated lists of newly confirmed monogenic causes of movement disorders. We found a total of 89 different newly identified genes that warrant a prefix based on our criteria; 6 genes for parkinsonism, 21 for dystonia, 38 for dominant and recessive ataxia, 5 for chorea, 7 for myoclonus, 13 for spastic paraplegia, 3 for paroxysmal movement disorders, and 6 for mixed movement disorder phenotypes; 10 genes were linked to combined phenotypes and have been assigned two new prefixes. The updated lists represent a resource for clinicians and researchers alike and they have also been published on the website of the Task Force for the Nomenclature of Genetic Movement Disorders on the homepage of the International Parkinson and Movement Disorder Society (https://www.movementdisorders.org/MDS/About/Committees--Other-Groups/MDS-Task-Forces/Task-Force-on-Nomenclature-in-Movement-Disorders.htm). © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson Movement Disorder Society
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