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[PMID]:28454042
[Au] Autor:Rajan R; Popa T; Quartarone A; Ghilardi MF; Kishore A
[Ad] Endereço:Comprehensive Care Center for Movement Disorders, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala, India. Electronic address: drrooparajan@gmail.com.
[Ti] Título: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] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo: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] Termos MeSH primário: Cerebelo/fisiopatologia
Conectoma
Discinesia Induzida por Medicamentos/fisiopatologia
Levodopa/uso terapêutico
Plasticidade Neuronal
Doença de Parkinson/fisiopatologia
[Mh] Termos MeSH secundário: Corpo Estriado/fisiopatologia
Discinesia Induzida por Medicamentos/etiologia
Seres Humanos
Levodopa/efeitos adversos
Córtex Motor/fisiopatologia
Doença de Parkinson/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
46627O600J (Levodopa)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:29341071
[Au] Autor:Bergman H; Soares-Weiser K
[Ad] Endereço:Cochrane Response, Cochrane, St Albans House, 57-59 Haymarket, London, UK, SW1Y 4QX.
[Ti] Título:Anticholinergic medication for antipsychotic-induced tardive dyskinesia.
[So] Source:Cochrane Database Syst Rev;1:CD000204, 2018 01 17.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo: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] Termos MeSH primário: Antipsicóticos/efeitos adversos
Antagonistas Colinérgicos/uso terapêutico
Discinesia Induzida por Medicamentos/tratamento farmacológico
[Mh] Termos MeSH secundário: Biperideno/efeitos adversos
Biperideno/uso terapêutico
Antagonistas Colinérgicos/efeitos adversos
Discinesia Induzida por Medicamentos/etiologia
Seres Humanos
Isocarboxazida/efeitos adversos
Isocarboxazida/uso terapêutico
Prociclidina/efeitos adversos
Prociclidina/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Esquizofrenia/tratamento farmacológico
Suspensão de Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Cholinergic Antagonists); 0FRP6G56LD (Biperiden); 34237V843T (Isocarboxazid); C6QE1Q1TKR (Procyclidine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD000204.pub2


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[PMID]:29341067
[Au] Autor:Soares-Weiser K; Maayan N; Bergman H
[Ad] Endereço:Cochrane Editorial Unit, Cochrane, St Albans House, 57 - 59 Haymarket, London, UK, SW1Y 4QX.
[Ti] Título:Vitamin E for antipsychotic-induced tardive dyskinesia.
[So] Source:Cochrane Database Syst Rev;1:CD000209, 2018 01 17.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo: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] Termos MeSH primário: Antipsicóticos/efeitos adversos
Discinesia Induzida por Medicamentos/tratamento farmacológico
Vitamina E/uso terapêutico
Vitaminas/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Progressão da Doença
Discinesia Induzida por Medicamentos/etiologia
Seres Humanos
Aceitação pelo Paciente de Cuidados de Saúde/estatística & dados numéricos
Transtornos Psicóticos/tratamento farmacológico
Ensaios Clínicos Controlados Aleatórios como Assunto
Esquizofrenia/tratamento farmacológico
Vitamina E/efeitos adversos
Vitaminas/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Vitamins); 1406-18-4 (Vitamin E)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD000209.pub3


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[PMID]:29352477
[Au] Autor:Bergman H; Bhoopathi PS; Soares-Weiser K
[Ad] Endereço:Cochrane Response, Cochrane, St Albans House, 57-59 Haymarket, London, UK, SW1Y 4QX.
[Ti] Título:Benzodiazepines for antipsychotic-induced tardive dyskinesia.
[So] Source:Cochrane Database Syst Rev;1:CD000205, 2018 01 20.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Tardive dyskinesia (TD) is a disfiguring movement disorder, often of the orofacial region, frequently caused by using antipsychotic drugs. A wide range of strategies have been used to help manage TD, and for those who are unable to have their antipsychotic medication stopped or substantially changed, the benzodiazepine group of drugs have been suggested as a useful adjunctive treatment. However, benzodiazepines are very addictive. OBJECTIVES: To determine the effects of benzodiazepines for antipsychotic-induced tardive dyskinesia in people with schizophrenia, schizoaffective disorder, or other chronic mental illnesses. SEARCH METHODS: On 17 July 2015 and 26 April 2017, we searched the Cochrane Schizophrenia Group's Study-Based Register of Trials (including trial registers), inspected references of all identified studies for further trials and contacted authors of each included trial for additional information. SELECTION CRITERIA: We included all randomised controlled trials (RCTs) focusing on people with schizophrenia (or other chronic mental illnesses) and antipsychotic-induced TD that compared benzodiazepines with placebo, no intervention, or any other intervention for the treatment of TD. DATA COLLECTION AND ANALYSIS: We independently extracted data from the included studies and ensured that they were reliably selected, and quality assessed. For homogenous dichotomous data, we calculated random effects, risk ratio (RR), and 95% confidence intervals (CI). We synthesised continuous data from valid scales using mean differences (MD). For continuous outcomes, we preferred endpoint data to change data. We assumed that people who left early had no improvement. MAIN RESULTS: The review now includes four trials (total 75 people, one additional trial since 2006, 21 people) randomising inpatients and outpatients in China and the USA. Risk of bias was mostly unclear as reporting was poor. We are uncertain about all the effects as all evidence was graded at very low quality. We found no significant difference between benzodiazepines and placebo for the outcome of 'no clinically important improvement in TD' (2 RCTs, 32 people, RR 1.12, 95% CI 0.60 to 2.09, very low quality evidence). Significantly fewer participants allocated to clonazepam compared with phenobarbital (as active placebo) experienced no clinically important improvement (RR 0.44, 95% CI 0.20 to 0.96, 1 RCT, 21 people, very low quality evidence). For the outcome 'deterioration of TD symptoms,' we found no clear difference between benzodiazepines and placebo (2 RCTs, 30 people, RR 1.48, 95% CI 0.22 to 9.82, very low quality evidence). All 10 participants allocated to benzodiazepines experienced any adverse event compared with 7/11 allocated to phenobarbital (RR 1.53, 95% CI 0.97 to 2.41, 1 RCT, 21 people, very low quality evidence). There was no clear difference in the incidence of participants leaving the study early for benzodiazepines compared with placebo (3 RCTs, 56 people, RR 2.73, 95% CI 0.15 to 48.04, very low quality evidence) or compared with phenobarbital (as active placebo) (no events, 1 RCT, 21 people, very low quality evidence). No trials reported on social confidence, social inclusion, social networks, or personalised quality of life, which are outcomes designated important by patients. No trials comparing benzodiazepines with placebo or treatment as usual reported on adverse effects. AUTHORS' CONCLUSIONS: There is only evidence of very low quality from a few small and poorly reported trials on the effect of benzodiazepines as an adjunctive treatment for antipsychotic-induced TD. These inconclusive results mean routine clinical use is not indicated and these treatments remain experimental. New and better trials are indicated in this under-researched area; however, as benzodiazepines are addictive, we feel that other techniques or medications should be adequately evaluated before benzodiazepines are chosen.
[Mh] Termos MeSH primário: Ansiolíticos/uso terapêutico
Benzodiazepinas/uso terapêutico
Discinesia Induzida por Medicamentos/tratamento farmacológico
Moduladores GABAérgicos/uso terapêutico
[Mh] Termos MeSH secundário: Antipsicóticos/efeitos adversos
Clonazepam/uso terapêutico
Discinesia Induzida por Medicamentos/etiologia
Seres Humanos
Fenobarbital/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Anti-Anxiety Agents); 0 (Antipsychotic Agents); 0 (GABA Modulators); 12794-10-4 (Benzodiazepines); 5PE9FDE8GB (Clonazepam); YQE403BP4D (Phenobarbital)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD000205.pub3


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[PMID]:29342497
[Au] Autor:El-Sayeh HG; Rathbone J; Soares-Weiser K; Bergman H
[Ad] Endereço:Harrogate District Hospital, Tees, Esk & Wear Valleys NHS Foundation Trust, Briary Wing, Lancaster Park Road, Harrogate, North Yorkshire, UK, HG2 7SX.
[Ti] Título:Non-antipsychotic catecholaminergic drugs for antipsychotic-induced tardive dyskinesia.
[So] Source:Cochrane Database Syst Rev;1:CD000458, 2018 01 18.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Tardive dyskinesia (TD) is a disabling movement disorder associated with the prolonged use of antipsychotic medication. Several strategies have been examined in the treatment of TD. Currently, however, there is no clear evidence of the effectiveness of these drugs in TD and they have been associated with many side effects. One particular strategy would be to use pharmaceutical agents which are known to influence the catecholaminergic system at various junctures. OBJECTIVES: 1. To determine the effects of any of the following drugs for antipsychotic-induced TD in people with schizophrenia or other chronic mental illnesses.i. Drugs which influence the noradrenergic system.ii. Dopamine receptor agonists.iii. Dopamine receptor antagonists.iv. Dopamine-depletor drugs.v. Drugs that increase the production or release of dopamine.2. To examine whether any improvement occurred with short periods of intervention (less than 6 weeks) and, if this did occur, whether this effect was maintained at longer periods of follow-up.3. To examine if there was a differential effect for the various compounds.4. To examine whether the use of non-antipsychotic catecholaminergic drugs are most effective in those with more recent onset TD (less than five years). SEARCH METHODS: We retrieved 712 references from searching the Cochrane Schizophrenia Group Trials Register (July 2015 and April 2017). We also inspected references of all identified studies for further trials and contacted authors of trials for additional information. SELECTION CRITERIA: We selected studies if they were randomised controlled trials focusing on people with schizophrenia or other chronic mental illnesses and antipsychotic-induced tardive dyskinesia. We compared the use of catecholaminergic interventions versus placebo, no intervention, or any other intervention for the treatment of antipsychotic-induced tardive dyskinesia. DATA COLLECTION AND ANALYSIS: We independently extracted data from these trials and we estimated risk ratios (RRs) with 95% confidence intervals (CIs). We assumed that people who left the studies early had no improvement. MAIN RESULTS: There are 10 included trials (N = 261) published between 1973 and 2010; eight are new from the 2015 and 2017 update searches. Forty-eight studies are excluded. Participants were mostly chronically mentally ill inpatients in their 50s, and studies were primarily of short (2 to 6 weeks) duration. The overall risk of bias in these studies was unclear, mainly due to poor reporting of allocation concealment and generation of the sequence. Studies were also not clearly blinded and we are unsure if data are incomplete or selectively reported, or if other biases were operating.One small, three-arm trial found that both alpha-methyldopa (N = 20; RR 0.33, 95% CI 0.14 to 0.80; low-quality evidence) and reserpine (N = 20; RR 0.52 95% CI 0.29 to 0.96; low-quality evidence) may lead to a clinically important improvement in tardive dyskinesia symptoms compared with placebo after 2 weeks' treatment, but found no evidence of a difference between alpha-methyldopa and reserpine (N = 20; RR 0.60, 95% CI 0.19 to 1.86; very low quality evidence). Another small trial compared tetrabenazine and haloperidol after 18 weeks' treatment and found no evidence of a difference on clinically important improvement in tardive dyskinesia symptoms (N = 13; RR 0.93, 95% CI 0.45 to 1.95; very low quality evidence). No study reported on adverse events.For remaining outcomes there was no evidence of a difference between any of the interventions: alpha-methyldopa versus placebo for deterioration of tardive dyskinesia symptoms (1 RCT; N = 20; RR 0.33, 95% CI 0.02 to 7.32; very low quality evidence), celiprolol versus placebo for leaving the study early (1 RCT; N = 35; RR 5.28, 95% CI 0.27 to 102.58; very low quality evidence) and quality of life (1 RCT; N = 35; RR 0.87, 95% CI 0.68 to 1.12; very low quality evidence), alpha-methyldopa versus reserpine for deterioration of tardive dyskinesia symptoms (1 RCT; N = 20; not estimable, no reported events; very low quality evidence), reserpine or carbidopa/levodopa versus placebo for deterioration of tardive dyskinesia symptoms (2 RCTs; N = 37; RR 1.18, 95% CI 0.35 to 3.99; very low quality evidence), oxypertine versus placebo for deterioration of mental state (1 RCT; N = 42; RR 2.20, 95% CI 0.22 to 22.45; very low quality evidence), dopaminergic drugs (amantadine, bromocriptine, tiapride, oxypertine, carbidopa/levodopa) versus placebo for leaving the study early (6 RCTs; N = 163; RR 1.29, 95% CI 0.65 to 2.54; very low quality evidence), and tetrabenazine versus haloperidol for deterioration of tardive dyskinesia symptoms (1 RCT; N = 13; RR 1.17, 95% CI 0.09 to 14.92) and leaving the study early (1 RCT; N = 13; RR 0.23, 95% CI 0.01 to 4.00). AUTHORS' CONCLUSIONS: Although there has been a large amount of research in this area, many studies were excluded due to inherent problems in the nature of their cross-over designs. Usually data are not reported before the cross-over and the nature of TD and its likely response to treatments make it imprudent to use this data. The review provides little usable information for service users or providers and more well-designed and well-reported studies are indicated.
[Mh] Termos MeSH primário: Antidiscinéticos/uso terapêutico
Antipsicóticos/efeitos adversos
Discinesia Induzida por Medicamentos/tratamento farmacológico
[Mh] Termos MeSH secundário: Inibidores da Captação Adrenérgica/uso terapêutico
Celiprolol/uso terapêutico
Progressão da Doença
Antagonistas de Dopamina/uso terapêutico
Haloperidol/uso terapêutico
Seres Humanos
Metildopa/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Reserpina/uso terapêutico
Tetrabenazina/uso terapêutico
Cloridrato de Tiapamil/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Adrenergic Uptake Inhibitors); 0 (Anti-Dyskinesia Agents); 0 (Antipsychotic Agents); 0 (Dopamine Antagonists); 56LH93261Y (Methyldopa); 8B1QWR724A (Reserpine); DRB57K47QC (Celiprolol); J6292F8L3D (Haloperidol); V824N2T753 (Tiapamil Hydrochloride); Z9O08YRN8O (Tetrabenazine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD000458.pub3


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[PMID]:29381960
[Au] Autor:He ZF; Chen J; Zhou CN; Rao Z; Wang XH
[Ad] Endereço:Department of Pharmacy.
[Ti] Título:Disabling tremor induced by long-term use of sodium valproate and lamotrigine: Case report.
[So] Source:Medicine (Baltimore);96(47):e8711, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Sodium valproate (VPA) and lamotrigine (LTG) are widely used antiepileptic drugs, disabling postural, and action tremors after using LTG with VPA were reported in 1993. However, in this study, we describe a patient in whom disabling resting-type tremor induced by 2-year use of VPA and LTG. PATIENT CONCERNS: A 50-year old man was referred to department of neurology because of involuntary upper limbs resting-type tremor with high amplitude that had begun 6 months previously and progressively worsened, and he could not work on the day of visit. Furthermore, he had been treated with VPA, LTG, and benzhexol for 2 years as he suffered from twitch of eyelids and facial region, and amantadine, monolithic compound preparation (flupentixol and melitracen) were added in the last 2 months because of tremor and anxiety. However, the treatment had no benefit on improving involuntary movements of the patient. DIAGNOSES: Drug-induced disabling tremor was diagnosed. INTERVENTIONS AND OUTCOMES: LTG, amantadine, and VPA were withdrawn, the remaining 2 drugs, benzhexol and compound preparation (flupentixol and melitracen), were continued to use, and the patient improved in 2.5 months after discontinuation of 3 drugs. There was no recurrence at 6 months follow-up. LESSONS: Considering the wide and long-term utilization of VPA and LTG, healthcare providers should be aware of them as a possible cause of tremor. When necessary, an attempt of discontinuing the suspected drugs should be made to confirm the diagnosis, instead of symptomatic treatment, especially when the adverse event was severe and fatal.
[Mh] Termos MeSH primário: Anticonvulsivantes/efeitos adversos
Discinesia Induzida por Medicamentos/diagnóstico
Triazinas/efeitos adversos
Ácido Valproico/efeitos adversos
[Mh] Termos MeSH secundário: Amantadina/uso terapêutico
Anticonvulsivantes/uso terapêutico
Antiparkinsonianos/uso terapêutico
Discinesia Induzida por Medicamentos/tratamento farmacológico
Discinesias/tratamento farmacológico
Seres Humanos
Masculino
Meia-Idade
Triazinas/uso terapêutico
Triexifenidil/uso terapêutico
Ácido Valproico/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Antiparkinson Agents); 0 (Triazines); 614OI1Z5WI (Valproic Acid); 6RC5V8B7PO (Trihexyphenidyl); BF4C9Z1J53 (Amantadine); U3H27498KS (lamotrigine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008711


  7 / 6561 MEDLINE  
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[PMID]:29233065
[Au] Autor:Choi H; Koh SH
[Ad] Endereço:a Department of Neurology , Hanyang University College of Medicine , Seoul , South Korea.
[Ti] Título:Understanding the role of glycogen synthase kinase-3 in L-DOPA-induced dyskinesia in Parkinson's disease.
[So] Source:Expert Opin Drug Metab Toxicol;14(1):83-90, 2018 Jan.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Levodopa (L-DOPA) is the most commonly used drug for Parkinson's disease (PD), but its long-term use is associated with various complications, including L-DOPA-induced dyskinesia (LID). Many studies have suggested that L-DOPA neurotoxicity and LID are associated with glycogen synthase kinase-3 (GSK-3) activation. Areas covered: LID is caused by striatal dopamine (DA) denervation in PD and pulsatile L-DOPA treatment. These factors lead to dysregulated DA transmission, abnormal intracellular signaling and transcription factors in striatal neurons, and altered gene expression and plasticity at corticostriatal synapses. The mechanisms of L-DOPA toxicity involve oxidative stress, L-DOPA oxidation to quinone, mitochondrial dysfunction, and α-synuclein. GSK-3 has been suggested to play key roles in all the mechanisms associated of L-DOPA toxicity and LID in PD. Expert opinion: GSK-3 plays critical roles in L-DOPA-induced neurotoxicity, and the development of specific methods to inhibit GSK-3 function may help prevent L-DOPA neurotoxicity and LID in PD. However, balanced GSK-3 inhibition and less ß-catenin degradation is essential for preventing LID, because too much GSK-3 inhibition increases ß-catenin levels, which is related to cancers.
[Mh] Termos MeSH primário: Antiparkinsonianos/efeitos adversos
Discinesia Induzida por Medicamentos/etiologia
Quinase 3 da Glicogênio Sintase/metabolismo
Levodopa/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Antiparkinsonianos/administração & dosagem
Dopamina/metabolismo
Discinesia Induzida por Medicamentos/enzimologia
Discinesia Induzida por Medicamentos/prevenção & controle
Quinase 3 da Glicogênio Sintase/antagonistas & inibidores
Seres Humanos
Levodopa/administração & dosagem
Síndromes Neurotóxicas/enzimologia
Síndromes Neurotóxicas/etiologia
Estresse Oxidativo/efeitos dos fármacos
Doença de Parkinson/tratamento farmacológico
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (beta Catenin); 46627O600J (Levodopa); EC 2.7.11.26 (Glycogen Synthase Kinase 3); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1417387


  8 / 6561 MEDLINE  
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[PMID]:27771532
[Au] Autor:Han C; Nie S; Chen G; Ma K; Xiong N; Zhang Z; Xu Y; Wang T; Papa SM; Cao X
[Ad] Endereço:Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
[Ti] Título:Intrastriatal injection of ionomycin profoundly changes motor response to l-DOPA and its underlying molecular mechanisms.
[So] Source:Neuroscience;340:23-33, 2017 Jan 06.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long-term l-DOPA treatment of Parkinson's disease is accompanied with fluctuations of motor responses and l-DOPA-induced dyskinesia (LID). Phosphorylation of the dopamine and c-AMP regulated phosphoprotein of 32kDa (DARPP-32) plays a role in the pathogenesis of LID, and thus dephosphorylation of this protein by activated calcineurin may help reduce LID. One important activator of calcineurin is the Ca ionophore ionomycin. Here, we investigated whether intrastriatal injection of ionomycin to hemiparkinsonian rats produced changes in l-DOPA responses including LID. We also analyzed the effects of ionomycin on key molecular mediators of LID. Results confirmed our hypothesis that ionomycin could downregulate the phosphorylation of DARPP32 at Thr-34 and reduce LID. Besides, ionomycin decreased two established molecular markers of LID, FosB/ΔFosB and phosphorylated ERK1/2. Ionomycin also decreased the phosphorylation of three main subunits of the NMDA receptor, NR1 phosphorylated at ser896, NR2A phosphorylated at Tyr-1325, and NR2B phosphorylated at Tyr-1472. Furthermore, the anti-LID effect of striatally injected ionomycin was not accompanied by reduction of the antiparkinsonian action of l-DOPA. These data indicate that ionomycin largely interacts with striatal mechanisms that are critical to the l-DOPA motor response highlighting the role of protein dephosphorylation by calcineurin.
[Mh] Termos MeSH primário: Antiparkinsonianos/farmacologia
Ionóforos de Cálcio/farmacologia
Discinesia Induzida por Medicamentos/tratamento farmacológico
Ionomicina/farmacologia
Levodopa/efeitos adversos
Transtornos Parkinsonianos/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antiparkinsonianos/efeitos adversos
Calcineurina/metabolismo
Corpo Estriado/efeitos dos fármacos
Corpo Estriado/metabolismo
Dopamina/metabolismo
Fosfoproteína 32 Regulada por cAMP e Dopamina/metabolismo
Discinesia Induzida por Medicamentos/metabolismo
Ácido Glutâmico/metabolismo
Levodopa/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/fisiologia
Masculino
Transtornos Parkinsonianos/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-fos/metabolismo
Distribuição Aleatória
Ratos Sprague-Dawley
Receptores de N-Metil-D-Aspartato/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (Calcium Ionophores); 0 (Dopamine and cAMP-Regulated Phosphoprotein 32); 0 (Fosb protein, rat); 0 (N-methyl D-aspartate receptor subtype 2A); 0 (NMDA receptor A1); 0 (NR2B NMDA receptor); 0 (Ppp1r1b protein, rat); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, N-Methyl-D-Aspartate); 3KX376GY7L (Glutamic Acid); 46627O600J (Levodopa); 56092-81-0 (Ionomycin); EC 3.1.3.16 (Calcineurin); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171224
[Lr] Data última revisão:
171224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28854243
[Au] Autor:Michel A; Nicolas JM; Rose S; Jackson M; Colman P; Briône W; Sciberras D; Muglia P; Scheller DK; Citron M; Downey P
[Ad] Endereço:UCB BioPharma, Braine L'Alleud, Belgium.
[Ti] Título:Antiparkinsonian effects of the "Radiprodil and Tozadenant" combination in MPTP-treated marmosets.
[So] Source:PLoS One;12(8):e0182887, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Investigate a combination of two clinically tested drugs, the NR2B antagonist Radiprodil and the A2A antagonist Tozadenant in the MPTP-treated marmoset model of Parkinson's Disease (PD). BACKGROUND: In PD, there remains a need for the development of non-dopaminergic drugs to effectively treat the motor symptoms without the induction of L-Dopa-induced motor complications. METHODS: Clinically relevant doses of Radiprodil and Tozadenant were given both alone and in combination without the addition of L-Dopa, and the antiparkinsonian efficacy of the treatments was assessed in a primate model of PD. RESULTS: When compared to the drugs tested alone, the drug combination led to a significant increase of motor activity and an improvement of motor disability in MPTP-treated marmosets. In addition, the motor restoration brought about by the combination was almost completely devoid of dyskinesia. Interestingly, treated primates were not overstimulated, but were able to move normally when motivated by the exploration of novel objects. CONCLUSION: We have demonstrated in a primate model that, the "Radiprodil/Tozadenant" combination significantly improves motor activity, extending previous results obtained in unilaterally lesioned 6-OHDA-rats. The strength of the preclinical data accumulated so far suggests that the use of such an A2A and NR2B antagonist combination could bring significant motor improvement to PD patients, without inducing the motor complications induced by L-Dopa therapy. Although encouraging, these preclinical data need to be confirmed in the clinic.
[Mh] Termos MeSH primário: Antiparkinsonianos/farmacologia
Benzotiazóis/farmacologia
Intoxicação por MPTP/tratamento farmacológico
Atividade Motora/efeitos dos fármacos
Receptores A2 de Adenosina/genética
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Callithrix
Esquema de Medicação
Combinação de Medicamentos
Avaliação Pré-Clínica de Medicamentos
Sinergismo Farmacológico
Discinesia Induzida por Medicamentos/prevenção & controle
Feminino
Expressão Gênica
Intoxicação por MPTP/genética
Intoxicação por MPTP/metabolismo
Intoxicação por MPTP/fisiopatologia
Masculino
Atividade Motora/fisiologia
Receptores A2 de Adenosina/metabolismo
Receptores de N-Metil-D-Aspartato/genética
Receptores de N-Metil-D-Aspartato/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (Benzothiazoles); 0 (Drug Combinations); 0 (NR2B NMDA receptor); 0 (Receptors, Adenosine A2); 0 (Receptors, N-Methyl-D-Aspartate); D9K857J81I (tozadenant)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182887


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[PMID]:28757258
[Au] Autor:Tronci E; Napolitano F; Muñoz A; Fidalgo C; Rossi F; Björklund A; Usiello A; Carta M
[Ad] Endereço:Department of Biomedical Sciences, Cagliari University, Cagliari 09042, Italy.
[Ti] Título:BDNF over-expression induces striatal serotonin fiber sprouting and increases the susceptibility to l-DOPA-induced dyskinesia in 6-OHDA-lesioned rats.
[So] Source:Exp Neurol;297:73-81, 2017 Nov.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In addition to its role in neuronal survival, the brain neurotrophic factor (BDNF) has been shown to influence serotonin transmission and synaptic plasticity, events strongly implicated in the appearance of l-DOPA-induced dyskinesia (LID), a motor complication occurring in parkinsonian patients after long-term treatment with the dopamine precursor. In order to evaluate a possible influence of BDNF in the appearance of LID, 6-OHDA-lesioned rats received a striatal injection of different concentrations of an adeno-associated viral (AAV) vector over-expressing either BDNF or GFP, as control vector. Eight weeks later, animals started to receive a daily treatment with l-DOPA (4-6mg/kg plus benserazide 4-6mg/kg, s.c.) or saline, and dyskinesias, as well as l-DOPA-induced rotations, were evaluated at several time-points. Moreover, molecular changes in striatal D1 receptor-dependent cAMP/PKA and ERK/mTORC signaling pathways, as well as, sprouting of striatal serotonin axons, were measured. Results showed that the AAV-BDNF vector injection induced striatal over-expression of BDNF, as well as striatal and pallidal serotonin axon hyperinnervation. Moreover, rats that over-expressed BDNF were more prone to develop LID and l-DOPA-induced rotations, compared to the GFP-treated control group. Finally, rats that over-expressed BDNF showed increased levels of striatal D1R-dependent signaling phospho-proteins in response to l-DOPA administration. This study suggests that BDNF over-expression, by inducing changes in pre-synaptic serotonin axonal trophism, is able to exacerbate maladaptive responses to l-DOPA administration.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado do Encéfalo/biossíntese
Corpo Estriado/metabolismo
Discinesia Induzida por Medicamentos/metabolismo
Levodopa/toxicidade
Oxidopamina/toxicidade
Neurônios Serotoninérgicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antiparkinsonianos/toxicidade
Fator Neurotrófico Derivado do Encéfalo/genética
Corpo Estriado/efeitos dos fármacos
Corpo Estriado/patologia
Discinesia Induzida por Medicamentos/patologia
Expressão Gênica
Células HEK293
Seres Humanos
Masculino
Ratos
Ratos Sprague-Dawley
Neurônios Serotoninérgicos/efeitos dos fármacos
Neurônios Serotoninérgicos/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (Brain-Derived Neurotrophic Factor); 46627O600J (Levodopa); 8HW4YBZ748 (Oxidopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE



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