Database : MEDLINE
Search on : Dyskinesias [Words]
References found : 18305 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 1831 go to page                         

  1 / 18305 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29508924
[Au] Autor:Beck G; Maehara S; Chang PL; Papa SM
[Ad] Address:Yerkes National Primate Research Center, Emory University, Atlanta, Georgia, USA.
[Ti] Title:A selective phosphodiesterase 10A inhibitor reduces l-dopa-induced dyskinesias in parkinsonian monkeys.
[So] Source:Mov Disord;, 2018 Mar 06.
[Is] ISSN:1531-8257
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Phosphodiesterase 10A is a member of the phosphodiesterase family whose brain expression is restricted to the striatum. Phosphodiesterase 10A regulates cyclic adenosine monophosphate and cyclic guanosine monophosphate, which mediate responses to dopamine receptor activation, and the levels of these cyclic nucleotides are decreased in experimental models of l-dopa-induced dyskinesia. The elevation of cyclic adenosine monophosphate/cyclic guanosine monophosphate levels by phosphodiesterase 10A inhibition may thus be targeted to reduce l-dopa-induced dyskinesia. OBJECTIVES: The present study was aimed at determining the potential antidyskinetic effects of phosphodiesterase 10A inhibitors in a primate model of Parkinson's disease (PD). The experiments performed in this model were also intended to provide translational data for the design of future clinical trials. METHODS: Five MPTP-treated macaques with advanced parkinsonism and reproducible l-dopa-induced dyskinesia were used. MR1916, a selective phosphodiesterase 10A inhibitor, at doses 0.0015 to 0.05 mg/kg, subcutaneously, or its vehicle (control test) was coadministered with l-dopa methyl ester acutely (predetermined optimal and suboptimal subcutaneous doses) and oral l-dopa chronically as daily treatment for 5 weeks. Standardized scales were used to assess motor disability and l-dopa-induced dyskinesia by blinded examiners. Pharmacokinetics was also examined. RESULTS: MR1916 consistently reduced l-dopa-induced dyskinesia in acute tests of l-dopa optimal and suboptimal doses. Significant effects were present with every MR1916 dose tested, but the most effective was 0.015 mg/kg. None of the MR1916 doses tested affected the antiparkinsonian action of l-dopa at the optimal dose. The anti-l-dopa-induced dyskinesia effect of MR1916 (0.015 mg/kg, subcutaneously) was sustained with chronic administration, indicating that tolerance did not develop over the 5-week treatment. No adverse effects were observed after MR1916 administration acutely or chronically. CONCLUSIONS: Results show that regulation of striatal cyclic nucleotides by phosphodiesterase 10A inhibition could be a useful therapeutic approach for l-dopa-induced dyskinesia, and therefore data support further studies of selective phosphodiesterase 10A inhibitors for PD therapy. © 2018 International Parkinson and Movement Disorder Society.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1002/mds.27341

  2 / 18305 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28454738
[Au] Autor:Miksys S; Wadji FB; Tolledo EC; Remington G; Nobrega JN; Tyndale RF
[Ad] Address:Centre for Addiction and Mental Health, Campbell Family Mental Health Research Institute, Toronto, Canada; Department of Pharmacology and Toxicology, University of Toronto, Canada. Electronic address: s.miksys@utoronto.ca.
[Ti] Title:Rat brain CYP2D enzymatic metabolism alters acute and chronic haloperidol side-effects by different mechanisms.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;78:140-148, 2017 Aug 01.
[Is] ISSN:1878-4216
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Risk for side-effects after acute (e.g. parkinsonism) or chronic (e.g. tardive dyskinesia) treatment with antipsychotics, including haloperidol, varies substantially among people. CYP2D can metabolize many antipsychotics and variable brain CYP2D metabolism can influence local drug and metabolite levels sufficiently to alter behavioral responses. Here we investigated a role for brain CYP2D in acutely and chronically administered haloperidol levels and side-effects in a rat model. Rat brain, but not liver, CYP2D activity was irreversibly inhibited with intracerebral propranolol and/or induced by seven days of subcutaneous nicotine pre-treatment. The role of variable brain CYP2D was investigated in rat models of acute (catalepsy) and chronic (vacuous chewing movements, VCMs) haloperidol side-effects. Selective inhibition and induction of brain, but not liver, CYP2D decreased and increased catalepsy after acute haloperidol, respectively. Catalepsy correlated with brain, but not hepatic, CYP2D enzyme activity. Inhibition of brain CYP2D increased VCMs after chronic haloperidol; VCMs correlated with brain, but not hepatic, CYP2D activity, haloperidol levels and lipid peroxidation. Baseline measures, hepatic CYP2D activity and plasma haloperidol levels were unchanged by brain CYP2D manipulations. Variable rat brain CYP2D alters side-effects from acute and chronic haloperidol in opposite directions; catalepsy appears to be enhanced by a brain CYP2D-derived metabolite while the parent haloperidol likely causes VCMs. These data provide novel mechanistic evidence for brain CYP2D altering side-effects of haloperidol and other antipsychotics metabolized by CYP2D, suggesting that variation in human brain CYP2D may be a risk factor for antipsychotic side-effects.
[Mh] MeSH terms primary: Brain/drug effects
Brain/enzymology
Cytochrome P450 Family 2/metabolism
Haloperidol/adverse effects
[Mh] MeSH terms secundary: Animals
Brain/metabolism
Catalepsy/chemically induced
Haloperidol/blood
Liver/enzymology
Male
Microinjections
Nicotine/administration & dosage
Nicotine/pharmacology
Propranolol/administration & dosage
Propranolol/pharmacology
Rats
Tardive Dyskinesia/chemically induced
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:6M3C89ZY6R (Nicotine); 9Y8NXQ24VQ (Propranolol); EC 1.14.14.1 (Cytochrome P450 Family 2); J6292F8L3D (Haloperidol)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:170430
[St] Status:MEDLINE

  3 / 18305 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29521236
[Au] Autor:Lemos A; Meloc R; Preto AJ; Almeida JG; Moreira IS; Cordeiro MNDS
[Ad] Address:LAQV/REQUIMTE, Department of Chemistry and Biochemistry, Faculty of Sciences, University of Porto, Rua do Campo Alegre s/n, 4169-007 Porto. Portugal.
[Ti] Title:In silico studies targeting G-protein coupled receptors for drug research against Parkinson's disease.
[So] Source:Curr Neuropharmacol;, 2018 Mar 08.
[Is] ISSN:1875-6190
[Cp] Country of publication:United Arab Emirates
[La] Language:eng
[Ab] Abstract:Parkinson's Disease (PD) is a long-term neurodegenative brain disorder that mainly affects the motor system. The causes are still unknown, and even though currently there is no cure, several therapeutic options are available to manage its symptoms. The development of novel anti-parkinsonian agents and an understanding of their proper and optimal use are, indeed, highly demanding. For the last decades, L-3,4-DihydrOxyPhenylAlanine or levodopa (L-DOPA) has been the gold-standard therapy for the symptomatic treatment of motor dysfunctions associated to PD. However, the development of dyskinesias and motor fluctuations (wearing-off and on-off phenomena) associated to long-term L-DOPA replacement therapy have limited its antiparkinsonian efficacy. The investigation for non-dopaminergic therapies has been largelyexplored as an attempt to counteract the motor side effects associated to dopamine replacement therapy. Being one of the largest cell membrane protein families, G-Protein-Coupled Receptors (GPCRs) have become a relevant target for drug discovery focused in a wide range of therapeutic areas, including Central Nervous System (CNS) diseases. The modulation of specific GPCRs potentially implicated in PD, excluding dopamine receptors, may provide promising non-dopaminergic therapeutic alternatives for symptomatic treatment of PD. In this review, we focused on the impact of specific GPCR subclasses, including dopamine receptors, adenosine receptors, muscarinic acetylcholine receptors, metabotropic glutamate receptors, and 5-hydroxytryptamine receptors, on the pathophysiology of PD and the importance of structure- and ligand-based in silico approaches for the development of small molecules to target these receptors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.2174/1570159X16666180308161642

  4 / 18305 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29407218
[Au] Autor:Morissette M; Morin N; Rouillard C; Di Paolo T
[Ad] Address:Neuroscience Research Unit, Centre Hospitalier Universitaire de Québec, CHUL, Quebec City G1V 4G2, Canada.
[Ti] Title:Membrane cholesterol removal and replenishment affect rat and monkey brain monoamine transporters.
[So] Source:Neuropharmacology;133:289-306, 2018 Jan 31.
[Is] ISSN:1873-7064
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The dopamine transporter (DAT) is abundantly expressed in the striatum where it removes extracellular dopamine into the cytosol of presynaptic nerve terminals. It is the target of drugs of abuse and antidepressants. There is a loss of the DAT in Parkinson's disease affecting release of levodopa implicated in levodopa-induced dyskinesias. This study investigated the effect of cholesterol on DAT, serotonin transporter (SERT) and vesicular monoamine transporter 2 (VMAT2) in monkey and rat brains in vitro. DAT protein levels measured by Western blot remained unchanged with in vitro methyl-ß-cyclodextrin (MCD) incubations to remove membrane cholesterol or with incubations to increase membrane cholesterol content. By contrast, striatal DAT specific binding labelled with [ I]RTI-121 or with [ I]RTI-55 decreased with increasing concentrations of MCD and increased with cholesterol loading. Moreover, [ I]RTI-121 specific binding of striatal membranes depleted of cholesterol with MCD was restored to initial DAT content with addition of cholesterol showing its rapid and reversible effect. By contrast, striatal VMAT2 and SERT specific binding showed no or limited changes by cholesterol manipulations. Similar results were obtained for monkey caudate nucleus, putamen and nucleus accumbens. Membrane microviscosity was assessed by fluorescence polarization spectroscopy, using the probe 1,6-diphenyl-1,3,5-hexatriene. DAT changes positively correlated with changes of membrane microviscosity in rat and monkey brain regions investigated and with membrane cholesterol contents. Similar findings were observed with desmosterol but to a lower extent than with cholesterol. These results show an important effect of cholesterol on the DAT associated with microviscosity changes that should be considered in drug therapies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  5 / 18305 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29511826
[Au] Autor:Perez-Lloret S; Rascol O
[Ad] Address:Institute of Cardiology Research, University of Buenos Aires, National Research Council (CONICET-ININCA), Buenos Aires, Argentina.
[Ti] Title:Efficacy and safety of amantadine for the treatment of L-DOPA-induced dyskinesia.
[So] Source:J Neural Transm (Vienna);, 2018 Mar 07.
[Is] ISSN:1435-1463
[Cp] Country of publication:Austria
[La] Language:eng
[Ab] Abstract:L-DOPA induced dyskinesias (LIDs) may affect up to 40% of Parkinson's disease (PD) and impact negatively health-related quality of life. Amantadine has demonstrated significant antidyskinetic effects in animal PD models and in randomized double-blind placebo-controlled trials (RCTs) in patients with PD. These effects are thought to be related to the blockade of NMDA receptors modulating cortico-striatal glutamatergic-dopaminergic interactions involved in the genesis of LIDs. There are three pharmaceutical forms of amantadine currently available in the market: an oral immediate-release (IR) formulation, which is widely available; an extended-release (ER) formulation (ADS-5102) which has been recently developed and approved by the FDA; and an intravenous infusion (IV) solution, which is not commonly used in clinical practice. RCTs with amantadine IR or ER, involving more than 650 patients have shown consistent and long-lasting reductions in LIDs. Interestingly, ADS-5102 not only reduced LIDs, but also reduced significantly at the same time the duration of daily OFF-time, a unique finding compared with other antiparkinsonian medications that usually reduce time spent OFF at the cost of worsening of LIDs. Amantadine IR might also have possible effects on other PD symptoms such as apathy or fatigue. The most common adverse reactions with amantadine are constipation, cardiovascular dysfunction including QT prolongation, orthostatic hypotension and edema, neuropsychiatric symptoms such as hallucinations, confusion and delirium, nausea and livedo reticularis. Corneal degeneration is rare but critical. In summary, amantadine immediate and extended-release are effective and safe for the treatment of LIDs.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1007/s00702-018-1869-1

  6 / 18305 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28454042
[Au] Autor:Rajan R; Popa T; Quartarone A; Ghilardi MF; Kishore A
[Ad] Address:Comprehensive Care Center for Movement Disorders, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala, India. Electronic address: drrooparajan@gmail.com.
[Ti] Title:Cortical plasticity and levodopa-induced dyskinesias in Parkinson's disease: Connecting the dots in a multicomponent network.
[So] Source:Clin Neurophysiol;128(6):992-999, 2017 06.
[Is] ISSN:1872-8952
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Levodopa-induced dyskinesias are motor complications following long term dopaminergic therapy in Parkinson's disease (PD). Impaired brain plasticity resulting in the creation of aberrant motor maps intended to encode normal voluntary movement is proposed to result in the development of dyskinesias. Traditionally, the various nodes in the motor network like the striato-cortical and the cerebello-thalamic loops were thought to function independent of each other with little communication among them. Anatomical evidence from primates revealed the existence of reciprocal loops between the basal ganglia and the cerebellum providing an anatomical basis for communication between the motor network loops. Dyskinetic PD patients reveal impaired brain plasticity within the motor cortex which may be modulated by cortico-cortical, cerebello-cortical or striato-cortical connections. In this article, we review the evidence for altered plasticity in the multicomponent motor network in the context of levodopa induced dyskinesias in PD. Current evidence suggests a pivotal role for the cerebellum in the larger motor network with the ability to integrate sensorimotor information and independently influence multiple nodes in this network. Targeting the cerebellum seems to be a justified approach for future interventions aimed at attenuating levodopa-induced dyskinesias.
[Mh] MeSH terms primary: Cerebellum/physiopathology
Connectome
Dyskinesia, Drug-Induced/physiopathology
Levodopa/therapeutic use
Neuronal Plasticity
Parkinson Disease/physiopathology
[Mh] MeSH terms secundary: Corpus Striatum/physiopathology
Dyskinesia, Drug-Induced/etiology
Humans
Levodopa/adverse effects
Motor Cortex/physiopathology
Parkinson Disease/drug therapy
[Pt] Publication type:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Name of substance:46627O600J (Levodopa)
[Em] Entry month:1708
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE

  7 / 18305 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text
Texto completo

[PMID]: 29341071
[Au] Autor:Bergman H; Soares-Weiser K
[Ad] Address:Cochrane Response, Cochrane, St Albans House, 57-59 Haymarket, London, UK, SW1Y 4QX.
[Ti] Title:Anticholinergic medication for antipsychotic-induced tardive dyskinesia.
[So] Source:Cochrane Database Syst Rev;1:CD000204, 2018 01 17.
[Is] ISSN:1469-493X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Antipsychotic (neuroleptic) medication is used extensively to treat people with serious mental illnesses. However, it is associated with a wide range of adverse effects, including movement disorders. Because of this, many people treated with antipsychotic medication also receive anticholinergic drugs in order to reduce some of the associated movement side-effects. However, there is also a suggestion from animal experiments that the chronic administration of anticholinergics could cause tardive dyskinesia. OBJECTIVES: To determine whether the use or the withdrawal of anticholinergic drugs (benzhexol, benztropine, biperiden, orphenadrine, procyclidine, scopolamine, or trihexylphenidyl) are clinically effective for the treatment of people with both antipsychotic-induced tardive dyskinesia and schizophrenia or other chronic mental illnesses. SEARCH METHODS: We retrieved 712 references from searching the Cochrane Schizophrenia Group's Study-Based Register of Trials including the registries of clinical trials (16 July 2015 and 26 April 2017). We also inspected references of all identified studies for further trials and contacted authors of trials for additional information. SELECTION CRITERIA: We included reports identified in the search if they were controlled trials dealing with people with antipsychotic-induced tardive dyskinesia and schizophrenia or other chronic mental illness who had been randomly allocated to (a) anticholinergic medication versus placebo (or no intervention), (b) anticholinergic medication versus any other intervention for the treatment of tardive dyskinesia, or (c) withdrawal of anticholinergic medication versus continuation of anticholinergic medication. DATA COLLECTION AND ANALYSIS: We independently extracted data from included trials and we estimated risk ratios (RR) with 95% confidence intervals (CIs). We assumed that people who left early had no improvement. We assessed risk of bias and created a 'Summary of findings' table using GRADE. MAIN RESULTS: The previous version of this review included no trials. We identified two trials that could be included from the 2015 and 2017 searches. They randomised 30 in- and outpatients with schizophrenia in the USA and Germany. Overall, the risk of bias was unclear, mainly due to poor reporting: allocation concealment was not described; generation of the sequence was not explicit; studies were not clearly blinded; and outcome data were not fully reported.Findings were sparse. One study reported on the primary outcomes and found that significantly more participants allocated to procyclidine (anticholinergic) had not improved to a clinically important extent compared with those allocated to isocarboxazid (MAO-inhibitor) after 40 weeks' treatment (1 RCT, n = 20; RR 4.20, 95% CI 1.40 to 12.58; very low quality evidence); that there was no evidence of a difference in the incidence of any adverse effects (1 RCT, n = 20; RR 0.33, 95% CI 0.02 to 7.32; very low quality evidence); or acceptability of treatment (measured by participants leaving the study early) (1 RCT, n = 20; RR 0.33, 95% CI 0.02 to 7.32; very low quality evidence). The other trial compared anticholinergic withdrawal with anticholinergic continuation and found no evidence of a difference in the incidence of acceptability of treatment (measured by participants leaving the study early) (1 RCT, n = 10; RR 2.14, 95% CI 0.11 to 42.52; very low quality evidence).No trials reported on social confidence, social inclusion, social networks, or personalised quality of life - outcomes designated important to patients. No studies comparing either i. anticholinergics with placebo or no treatment, or ii. studies of anticholinergic withdrawal, were found that reported on the primary outcome 'no clinically important improvement in TD symptoms and adverse events'. AUTHORS' CONCLUSIONS: Based on currently available evidence, no confident statement can be made about the effectiveness of anticholinergics to treat people with antipsychotic-induced tardive dyskinesia. The same applies for the withdrawal of such medications. Whether the withdrawal of anticholinergics may benefit people with antipsychotic-induced TD should be evaluated in a parallel-group, placebo-controlled randomised trial, with adequate sample size and at least 6 weeks of follow-up.
[Mh] MeSH terms primary: Antipsychotic Agents/adverse effects
Cholinergic Antagonists/therapeutic use
Dyskinesia, Drug-Induced/drug therapy
[Mh] MeSH terms secundary: Biperiden/adverse effects
Biperiden/therapeutic use
Cholinergic Antagonists/adverse effects
Dyskinesia, Drug-Induced/etiology
Humans
Isocarboxazid/adverse effects
Isocarboxazid/therapeutic use
Procyclidine/adverse effects
Procyclidine/therapeutic use
Randomized Controlled Trials as Topic
Schizophrenia/drug therapy
Withholding Treatment
[Pt] Publication type:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Name of substance:0 (Antipsychotic Agents); 0 (Cholinergic Antagonists); 0FRP6G56LD (Biperiden); 34237V843T (Isocarboxazid); C6QE1Q1TKR (Procyclidine)
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD000204.pub2

  8 / 18305 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text
Texto completo

[PMID]: 29341067
[Au] Autor:Soares-Weiser K; Maayan N; Bergman H
[Ad] Address:Cochrane Editorial Unit, Cochrane, St Albans House, 57 - 59 Haymarket, London, UK, SW1Y 4QX.
[Ti] Title:Vitamin E for antipsychotic-induced tardive dyskinesia.
[So] Source:Cochrane Database Syst Rev;1:CD000209, 2018 01 17.
[Is] ISSN:1469-493X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Antipsychotic (neuroleptic) medication is used extensively to treat people with chronic mental illnesses. Its use, however, is associated with adverse effects, including movement disorders such as tardive dyskinesia (TD) - a problem often seen as repetitive involuntary movements around the mouth and face. Vitamin E has been proposed as a treatment to prevent or decrease TD. OBJECTIVES: The primary objective was to determine the clinical effects of vitamin E in people with schizophrenia or other chronic mental illness who had developed antipsychotic-induced TD.The secondary objectives were:1. to examine whether the effect of vitamin E was maintained as duration of follow-up increased;2. to test the hypothesis that the use of vitamin E is most effective for those with early onset TD (less than five years) SEARCH METHODS: We searched the Cochrane Schizophrenia Group Trials Register (July 2015 and April 2017), inspected references of all identified studies for further trials and contacted authors of trials for additional information. SELECTION CRITERIA: We included reports if they were controlled trials dealing with people with antipsychotic-induced TD and schizophrenia who remained on their antipsychotic medication and had been randomly allocated to either vitamin E or to a placebo, no intervention, or any other intervention. DATA COLLECTION AND ANALYSIS: We independently extracted data from these trials and we estimated risk ratios (RR) or mean differences (MD), with 95% confidence intervals (CI). We assumed that people who left early had no improvement. We assessed risk of bias and created a 'Summary of findings' table using GRADE. MAIN RESULTS: The review now includes 13 poorly reported randomised trials (total 478 people), all participants were adults with chronic psychiatric disorders, mostly schizophrenia, and antipsychotic-induced TD. There was no clear difference between vitamin E and placebo for the outcome of TD: not improved to a clinically important extent (6 RCTs, N = 264, RR 0.95, 95% CI 0.89 to 1.01, low-quality evidence). However, people allocated to placebo may show more deterioration of their symptoms compared with those given vitamin E (5 RCTs, N = 85, RR 0.23, 95% CI 0.07 to 0.76, low-quality evidence). There was no evidence of a difference in the incidence of any adverse effects (9 RCTs, N = 205, RR 1.21, 95% CI 0.35 to 4.15, very low-quality evidence), extrapyramidal adverse effects (1 RCT, N = 104, MD 1.10, 95% CI -1.02 to 3.22, very low-quality evidence), or acceptability of treatment (measured by participants leaving the study early) (medium term, 8 RCTs, N = 232, RR 1.07, 95% CI 0.64 to 1.80, very low-quality evidence). No trials reported on social confidence, social inclusion, social networks, or personalised quality of life, outcomes designated important to patients. There is no trial-based information regarding the effect of vitamin E for those with early onset of TD. AUTHORS' CONCLUSIONS: Small trials of limited quality suggest that vitamin E may protect against deterioration of TD. There is no evidence that vitamin E improves symptoms of this problematic and disfiguring condition once established. New and better trials are indicated in this under-researched area, and, of the many adjunctive treatments that have been given for TD, vitamin E would be a good choice for further evaluation.
[Mh] MeSH terms primary: Antipsychotic Agents/adverse effects
Dyskinesia, Drug-Induced/drug therapy
Vitamin E/therapeutic use
Vitamins/therapeutic use
[Mh] MeSH terms secundary: Adult
Disease Progression
Dyskinesia, Drug-Induced/etiology
Humans
Patient Acceptance of Health Care/statistics & numerical data
Psychotic Disorders/drug therapy
Randomized Controlled Trials as Topic
Schizophrenia/drug therapy
Vitamin E/adverse effects
Vitamins/adverse effects
[Pt] Publication type:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Name of substance:0 (Antipsychotic Agents); 0 (Vitamins); 1406-18-4 (Vitamin E)
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD000209.pub3

  9 / 18305 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
SciELO Brazil full text

[PMID]: 29340519
[Au] Autor:Barboza LA; Ghisi NC
[Ad] Address:Laboratório de Biologia Molecular, Universidade Tecnológica Federal do Paraná, Dois Vizinhos, PR, Brasil.
[Ti] Title:Evaluating the current state of the art of Huntington disease research: a scientometric analysis.
[So] Source:Braz J Med Biol Res;51(3):e6299, 2018 Jan 11.
[Is] ISSN:1414-431X
[Cp] Country of publication:Brazil
[La] Language:eng
[Ab] Abstract:Huntington disease (HD) is an incurable neurodegenerative disorder caused by a dominant mutation on the 4th chromosome. We aim to present a scientometric analysis of the extant scientific undertakings devoted to better understanding HD. Therefore, a quantitative study was performed to examine the current state-of-the-art approaches that foster researchers' understandings of the current knowledge, research trends, and research gaps regarding this disorder. We performed literature searches of articles that were published up to September 2016 in the "ISI Web of Science™" (http://apps.webofknowledge.com/). The keyword used was "Huntington disease". Of the initial 14,036 articles that were obtained, 7732 were eligible for inclusion in the study according to their relevance. Data were classified according to language, country of publication, year, and area of concentration. The country leader regarding the number of studies published on HD is the United States, accounting for nearly 30% of all publications, followed by England and Germany, who have published 10 and 7% of all publications, respectively. Regarding the language in which the articles were written, 98% of publications were in English. The first publication to be found on HD was published in 1974. A surge of publications on HD can be seen from 1996 onward. In relation to the various knowledge areas that emerged, most publications were in the fields of neuroscience and neurology, likely because HD is a neurodegenerative disorder. Publications written in areas such as psychiatry, genetics, and molecular biology also predominated.
[Mh] MeSH terms primary: Biomedical Research/statistics & numerical data
Huntington Disease/genetics
[Mh] MeSH terms secundary: Brazil
Chorea/genetics
Humans
Huntington Disease/diagnosis
Huntington Disease/therapy
Internationality
Language
Mediator Complex/genetics
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (MED12 protein, human); 0 (Mediator Complex)
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE

  10 / 18305 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 29338466
[Au] Autor:Sarva H; Henchcliffe C
[Ad] Address:a Parkinson's Disease and Movement Disorders Institute , Weill Cornell Medicine/New York Presbyterian Hospital , New York , NY , USA.
[Ti] Title:Valbenazine as the first and only approved treatment for adults with tardive dyskinesia.
[So] Source:Expert Rev Clin Pharmacol;11(3):209-217, 2018 Mar.
[Is] ISSN:1751-2441
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Valbenazine is a selective VMAT2 inhibitor that the FDA approved in April 2017 for the specific treatment of tardive dyskinesia (TD), a movement disorder commonly caused by dopamine blocking agents. Valbenazine acts to decrease dopamine release, reducing excessive movement found in TD. Areas covered: This drug profile reviews the development of valbenazine and the clinical trials that led to its approval as the first treatment specific to TD. The literature search was performed with the PubMed online database. Expert commentary: Two clinical trials assessing the efficacy of valbenazine have shown the reduction of antipsychotic-induced involuntary movement. No life threatening adverse effects were found. Data from a 42-week extension study demonstrated sustained response.
[Mh] MeSH terms primary: Dopamine/metabolism
Tardive Dyskinesia/drug therapy
Tetrabenazine/analogs & derivatives
Valine/analogs & derivatives
[Mh] MeSH terms secundary: Adult
Animals
Antipsychotic Agents/administration & dosage
Antipsychotic Agents/adverse effects
Antipsychotic Agents/pharmacology
Drug Approval
Humans
Tardive Dyskinesia/chemically induced
Tetrabenazine/adverse effects
Tetrabenazine/pharmacology
Tetrabenazine/therapeutic use
Valine/adverse effects
Valine/pharmacology
Valine/therapeutic use
Vesicular Monoamine Transport Proteins/antagonists & inhibitors
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Antipsychotic Agents); 0 (SLC18A2 protein, human); 0 (Vesicular Monoamine Transport Proteins); 54K37P50KH (valbenazine); HG18B9YRS7 (Valine); VTD58H1Z2X (Dopamine); Z9O08YRN8O (Tetrabenazine)
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE
[do] DOI:10.1080/17512433.2018.1429264


page 1 of 1831 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information