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Pesquisa : A08.800.800.720 [Categoria DeCS]
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[PMID]:28729057
[Au] Autor:Hong JR; Choo H; Nam G
[Ad] Endereço:School of Science, University of Science and Technology, Daejeon 305-333, Republic of Korea.
[Ti] Título:Neuropathic pain-alleviating effects of pyrazole-conjugated arylsulfonamides as 5-HT receptor antagonists.
[So] Source:Bioorg Med Chem Lett;27(17):4146-4149, 2017 09 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A novel series of arylsulfonylaminomethyl-3-(1-phenyl-5-isopropyl)pyrazoles was evaluated for serotonin receptor subtype 6 (5-HT R) antagonistic effects in vitro. We also investigated their neuropathic pain-alleviating effects in vivo using a rat spinal nerve ligation (SNL) model. Bicyclic aromatic sulfonamino groups, such as naphthalene and quinolin-substituted derivatives, showed good 5-HT inhibitory activity in vitro. Among them, selected compounds, 12 and 13, having 8-quinoylsulfonamino groups, showed potent neuropathic pain-alleviating effects in the rat model.
[Mh] Termos MeSH primário: Inibidores Enzimáticos/farmacologia
Neuralgia/tratamento farmacológico
Pirazóis/farmacologia
Receptores de Serotonina/metabolismo
Nervos Espinhais/efeitos dos fármacos
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Animais
Sistema Enzimático do Citocromo P-450/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Canais de Potássio Éter-A-Go-Go/antagonistas & inibidores
Canais de Potássio Éter-A-Go-Go/metabolismo
Seres Humanos
Estrutura Molecular
Neuralgia/patologia
Pirazóis/química
Ratos
Ratos Sprague-Dawley
Nervos Espinhais/patologia
Relação Estrutura-Atividade
Sulfonamidas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Ether-A-Go-Go Potassium Channels); 0 (Pyrazoles); 0 (Receptors, Serotonin); 0 (Sulfonamides); 0 (serotonin 6 receptor); 9035-51-2 (Cytochrome P-450 Enzyme System)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


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[PMID]:28715712
[Au] Autor:McCambridge AB; Stinear JW; Peek S; Byblow WD
[Ad] Endereço:Movement Neuroscience Laboratory, Department of Exercise Sciences, and Centre for Brain Research, The University of Auckland, Auckland, New Zealand; Clinical Neurostimulation Laboratory, Graduate School of Health, University of Technology Sydney, Australia.
[Ti] Título:Propriospinal cutaneous-induced EMG suppression is unaltered by anodal tDCS of healthy motor cortex.
[So] Source:Clin Neurophysiol;128(9):1608-1616, 2017 Sep.
[Is] ISSN:1872-8952
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Cervical propriospinal premotoneurons (PN) relay descending motor commands and integrate peripheral afferent feedback. Effects of anodal transcranial direct current stimulation (a-tDCS) on propriospinal excitability in the upper limbs are unknown. METHODS: Healthy right-handed adults received a-tDCS or sham tDCS over primary motor cortex (M1) at 1mA (Experiment 1, n=18) or 2mA current intensity (Experiment 2, n=15). Propriospinal excitability was assessed by suppression of background electromyography (EMG) in extensor carpi radialis (ECR) from electrical stimulation of the superficial radial nerve during bilateral (Experiment 1 and 2) or unilateral (Experiment 2 only) activation of the left and/or right ECR. EMG suppression could be attributed to an early propriospinal component and late cortical component. Motor evoked potentials (MEP) were obtained as a manipulation check. RESULTS: Before tDCS, propriospinal-mediated cutaneous-induced suppression was present in each arm for early and late components. ECR MEP amplitude increased after 1mA, but not 2mA, a-tDCS. Neither 1mA nor 2mA a-tDCS modulated either component of ipsilateral or contralateral propriospinal excitability during bilateral or unilateral tasks. CONCLUSIONS: Propriospinal-mediated cutaneous-induced suppression was not modulated by a-tDCS in healthy adults. SIGNIFICANCE: Reporting non-significant findings is paramount for the development of clinically-relevant tDCS protocols.
[Mh] Termos MeSH primário: Eletromiografia/métodos
Potencial Evocado Motor/fisiologia
Córtex Motor/fisiologia
Neurônios Motores/fisiologia
Nervo Radial/fisiologia
Nervos Espinhais/fisiologia
Estimulação Transcraniana por Corrente Contínua/métodos
[Mh] Termos MeSH secundário: Adulto
Idoso
Método Duplo-Cego
Feminino
Seres Humanos
Masculino
Meia-Idade
Medula Espinal/fisiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE


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[PMID]:28634063
[Au] Autor:Keifer OP; Diaz A; Campbell M; Bezchlibnyk YB; Boulis NM
[Ad] Endereço:Department of Neurosurgery, Emory University School of Medicine, Atlanta, Georgia, USA. Electronic address: okeifer@emory.edu.
[Ti] Título:Occipital Nerve Stimulation for the Treatment of Refractory Occipital Neuralgia: A Case Series.
[So] Source:World Neurosurg;105:599-604, 2017 Sep.
[Is] ISSN:1878-8769
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Occipital neuralgia is a chronic pain syndrome characterized by sharp, shooting pains in the distribution of the occipital nerves. Although relatively rare, it associated with extremely debilitating symptoms that drastically affect a patient's quality of life. Furthermore, it is extremely difficult to treat as the symptoms are refractory to traditional treatments, including pharmacologic and procedural interventions. A few previous case studies have established the use of a neurostimulation of the occipital nerves to treat occipital neuralgia. OBJECTIVE: The following expands on that literature by retrospectively reviewing the results of occipital nerve stimulation in a relatively large patient cohort (29 patients). METHODS: A retrospective review of 29 patients undergoing occipital nerve stimulation for occipital neuralgia from 2012 to 2017 at a single institution with a single neurosurgeon. RESULTS: Of those 29 patients, 5 were repair or replacement of previous systems, 4 did not have benefit from trial stimulation, and 20 saw benefit to their trial stage of stimulation and went on to full implantation. Of those 20 patients, even with a history of failed procedures and pharmacological therapies, there was an overall success rate of 85%. The average preoperative 10-point pain score dropped from 7.4 ± 1.7 to a postoperative score of 2.9 ± 1.7. However, as with any peripheral nerve stimulation procedure, there were complications (4 patients), including infection, hardware erosion, loss of effect, and lead migration, which required revision or system removal. CONCLUSION: Despite complications, the results suggest, overall, that occipital nerve stimulation is a safe and effective procedure for refractory occipital neuralgia and should be in the neurosurgical repertoire for occipital neuralgia treatment.
[Mh] Termos MeSH primário: Dor Crônica/terapia
Terapia por Estimulação Elétrica/métodos
Neuralgia/terapia
Manejo da Dor/métodos
Nervos Espinhais
[Mh] Termos MeSH secundário: Adulto
Dor Crônica/diagnóstico por imagem
Estudos de Coortes
Terapia por Estimulação Elétrica/instrumentação
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Neuralgia/diagnóstico por imagem
Manejo da Dor/instrumentação
Estudos Retrospectivos
Nervos Espinhais/diagnóstico por imagem
Estimulação Elétrica Nervosa Transcutânea/instrumentação
Estimulação Elétrica Nervosa Transcutânea/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


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[PMID]:28535568
[Au] Autor:Han SM; Kim YH; Jo HU; Kwak JA; Park HJ
[Ad] Endereço:Department of Anesthesiology and Pain Medicine, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea.
[Ti] Título:Tianeptine Reduces Mechanical Allodynia in Spinal Nerve-ligated and Chemotherapy-induced Neuropathic Mice.
[So] Source:Pain Physician;20(4):E593-E600, 2017 May.
[Is] ISSN:2150-1149
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Spinal nerve-ligated neuropathy and chemotherapy-induced neuropathy produce a persistent tactile allodynia in mice. Tianeptine is an antidepressant that exhibits structural similarities to tricyclic antidepressants but has distinct neurochemical properties. OBJECTIVE: Here we examined the effects of intraperitoneal (i.p.) tianeptine on allodynia in spinal nerve-ligated and chemotherapy-induced neuropathic mice. STUDY DESIGN: A randomized, experimental trial. SETTING: Laboratory animal study. METHODS: Spinal nerve-ligated neuropathy was induced in a Chung model made by ligating the L5 spinal nerve. Chemotherapy-induced neuropathy was induced by injecting vincristine (0.1 mg/kg/day; i.p.) on the following schedule: 5 days on, 2 days off, for14 days. Tianeptine (10, 30, and 50 mg/kg) and saline were administered, respectively, to both groups of neuropathic mice (n = 5 for each group). We evaluated mechanical allodynia using von Frey hairs prior to drug injections and at 30, 60, 90, 120, 180, and 240 minutes, and 24 hours after injections. We also measured the changes in activate transcription factor 3 (ATF3) level in the dorsal root ganglion (DRG) in each group in order to understand the analgesic mechanism of tianeptine. RESULTS: Both spinal nerve-ligated and chemotherapy-induced neuropathic mice showed prominent allodynia. The control group showed no differences in mechanically induced allodynia compared to the experimental groups. For the tianeptine groups, paw-withdrawal thresholds in response to mechanical stimuli were significantly lower than the pre-administration values and values from the control group (P < 0.05). The increase in DRG ATF3 in neuropathic mice was reduced by tianeptine (P < 0.05). LIMITATIONS: Less is known about the transcription factors that affect inflammation signaling. CONCLUSIONS: Tianeptine administered i.p. reduces mechanical allodynia in spinal nerve-ligated and chemotherapy-induced neuropathic mice models. These effects were confirmed by attenuation of previously increased DRG ATF3.
[Mh] Termos MeSH primário: Analgésicos/uso terapêutico
Hiperalgesia/tratamento farmacológico
Neuralgia/tratamento farmacológico
Tiazepinas/farmacologia
[Mh] Termos MeSH secundário: Fator 3 Ativador da Transcrição/metabolismo
Animais
Modelos Animais de Doenças
Gânglios Espinais/fisiopatologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neuralgia/induzido quimicamente
Ratos Sprague-Dawley
Nervos Espinhais/patologia
Vincristina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activating Transcription Factor 3); 0 (Analgesics); 0 (Atf3 protein, mouse); 0 (Thiazepines); 0T493YFU8O (tianeptine); 5J49Q6B70F (Vincristine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE


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[PMID]:28346321
[Au] Autor:Lai CY; Hsieh MC; Ho YC; Lee AS; Wang HH; Cheng JK; Chau YP; Peng HY
[Ad] Endereço:From the Department of Veterinary Medicine, College of Veterinary Medicine, National Chung-Hsing University, Taichung, Taiwan (C.-Y.L.); Department of Medicine, Mackay Medical College, New Taipei, Taiwan (C.-Y.L., M.-C.H., Y.-C.H., A.-S.L., H.-H.W., J.-K.C., Y.-P.C., H.-Y.P.); Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan (M.-C.H.); and Department of Anesthesiology, Mackay Memorial Hospital, Taipei, Taiwan (J.-K.C.).
[Ti] Título:Growth Arrest and DNA-damage-inducible Protein 45ß-mediated DNA Demethylation of Voltage-dependent T-type Calcium Channel 3.2 Subunit Enhances Neuropathic Allodynia after Nerve Injury in Rats.
[So] Source:Anesthesiology;126(6):1077-1095, 2017 Jun.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Growth arrest and DNA-damage-inducible protein 45ß reactivates methylation-silenced neural plasticity-associated genes through DNA demethylation. However, growth arrest and DNA-damage-inducible protein 45ß-dependent demethylation contributes to neuropathic allodynia-associated spinal plasticity remains unclear. METHODS: Adult male Sprague-Dawley rats (654 out of 659) received a spinal nerve ligation or a sham operation with or without intrathecal application of one of the following: growth arrest and DNA-damage-inducible protein 45ß messenger RNA-targeted small interfering RNA, lentiviral vector expressing growth arrest and DNA-damage-inducible protein 45ß, Ro 25-6981 (an NR2B-bearing N-methyl-D-aspartate receptor antagonist), or KN-93 (a calmodulin-dependent protein kinase II antagonist) were used for behavioral measurements, Western blotting, immunofluorescence, dot blots, detection of unmodified cytosine enrichment at cytosine-phosphate-guanine site, chromatin immunoprecipitation quantitative polymerase chain reaction analysis, and slice recordings. RESULTS: Nerve ligation-enhanced growth arrest and DNA-damage-inducible protein 45ß expression (n = 6) in ipsilateral dorsal horn neurons accompanied with behavioral allodynia (n = 7). Focal knockdown of growth arrest and DNA-damage-inducible protein 45ß expression attenuated ligation-induced allodynia (n = 7) by reducing the binding of growth arrest and DNA-damage-inducible protein 45ß to the voltage-dependent T-type calcium channel 3.2 subunit promoter (n = 6) that decreased expression of and current mediated by the voltage-dependent T-type calcium channel 3.2 subunit (both n = 6). In addition, NR2B-bearing N-methyl-D-aspartate receptors and calmodulin-dependent protein kinase II act in an upstream cascade to increase growth arrest and DNA-damage-inducible protein 45ß expression, hence enhancing demethylation at the voltage-dependent T-type calcium channel 3.2 subunit promoter and up-regulating voltage-dependent T-type calcium channel 3.2 subunit expression. Intrathecal administration of Ro 25-6981, KN-93, or a growth arrest and DNA-damage-inducible protein 45ß-targeting small interfering RNA (n = 6) reversed the ligation-induced enrichment of unmodified cytosine at the voltage-dependent T-type calcium channel 3.2 subunit promoter by increasing the associated 5-formylcytosine and 5-carboxylcytosine levels. CONCLUSIONS: By converting 5-formylcytosine or 5-carboxylcytosine to unmodified cytosine, the NR2B-bearing N-methyl-D-aspartate receptor, calmodulin-dependent protein kinase II, or growth arrest and DNA-damage-inducible protein 45ß pathway facilitates voltage-dependent T-type calcium channel 3.2 subunit gene demethylation to mediate neuropathic allodynia.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/metabolismo
Canais de Cálcio Tipo T/metabolismo
Metilação de DNA
Hiperalgesia/metabolismo
Neuralgia/metabolismo
Nervos Espinhais/lesões
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação/genética
Western Blotting
Canais de Cálcio Tipo T/genética
Modelos Animais de Doenças
Imunofluorescência
Hiperalgesia/genética
Masculino
Neuralgia/genética
Reação em Cadeia da Polimerase
Ratos
Ratos Sprague-Dawley
Nervos Espinhais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (Calcium Channels, T-Type); 0 (Gadd45b protein, rat)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001610


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[PMID]:28302538
[Au] Autor:Wang YW; Zhang X; Chen CL; Liu QZ; Xu JW; Qian QQ; Li WY; Qian YN
[Ad] Endereço:Department of Anesthesiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210002, PR China.
[Ti] Título:Protective effects of Garcinol against neuropathic pain - Evidence from in vivo and in vitro studies.
[So] Source:Neurosci Lett;647:85-90, 2017 Apr 24.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Neuroinflammatory processes have a vital role in the pathogenesis of neuropathic pain. Garcinol, harvested from Garcinia indica, is known to exert potent anti-inflammatory properties. Recent studies have indicated that Garcinol may inhibit activation of nuclear factor-κB (NF-κB) by inhibiting NF-κB/p65 acetylation. These findings prompted us to evaluate the protective effects of Garcinol in the lumbar fifth spinal nerve ligation (SNL)-induced rat model of neuropathic pain and Lipopolysaccharide(LPS)-stimulated primary cultured microglia. In the present study, we found that intrathecal administration of Garcinol significantly attenuated SNL-induced nociceptive behaviors. Garcinol suppressed microglial activation as well as the expression of interleukin (IL)-1ß, IL-6, inducible nitric oxide synthase (iNOS)/nitric oxide (NO), and cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) in the spinal cord of SNL rats. It also reduced the nuclear translocation of NF-κB by decreasing acetyl-p65 protein expression. Similarly, in the in vitro study, Garcinol decreased the production of NO/iNOS, PGE2/COX-2, and proinflammatory cytokines in LPS-exposed microglia. Likewise, Garcinol inhibited the NF-κB signaling pathway by downregulating acetyl-p65 levels in LPS-challenged microglia. Our findings suggest that Garcinol may have protective effects against neuropathic pain that are associated with the inhibition of neuroinflammation in microglia. Therefore, Garcinol could be a promising agent in the treatment of neuropathic pain.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Microglia/efeitos dos fármacos
Neuralgia/tratamento farmacológico
Terpenos/uso terapêutico
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Animais
Anti-Inflamatórios não Esteroides/farmacologia
Núcleo Celular/metabolismo
Células Cultivadas
Ciclo-Oxigenase 2/metabolismo
Citocinas/metabolismo
Dinoprostona/metabolismo
Hiperalgesia/tratamento farmacológico
Hiperalgesia/fisiopatologia
Inflamação/tratamento farmacológico
Inflamação/metabolismo
Lipopolissacarídeos/farmacologia
Masculino
Microglia/metabolismo
NF-kappa B/metabolismo
Neuralgia/metabolismo
Neuralgia/fisiopatologia
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo II/metabolismo
Cultura Primária de Células
Ratos Sprague-Dawley
Medula Espinal/efeitos dos fármacos
Medula Espinal/metabolismo
Nervos Espinhais/lesões
Terpenos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cytokines); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Terpenes); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); EC 1.14.99.1 (Cyclooxygenase 2); K7Q1JQR04M (Dinoprostone); TR1VR1V71B (garcinol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE


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[PMID]:28236051
[Au] Autor:Yu A; Wang S; Cheng X; Liang W; Bai R; Xue Y; Li W
[Ad] Endereço:Department of Radiology, Beijing Jishuitan Hospital, The 4th Medical College of Peking University, 31 Xinjiekou E Rd, Xicheng Qu, Beijing, 100035, China. imaging2008@sina.com.
[Ti] Título:Functional connectivity of motor cortical network in patients with brachial plexus avulsion injury after contralateral cervical nerve transfer: a resting-state fMRI study.
[So] Source:Neuroradiology;59(3):247-253, 2017 Mar.
[Is] ISSN:1432-1920
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The purpose of this study is to assess the functional connectivity of the motor cortical network in patients with brachial plexus avulsion injury (BPAI) after contralateral C7 nerve transfer, using resting-state functional magnetic resonance imaging (RS-fMRI). METHODS: Twelve patients with total brachial plexus root avulsion underwent RS-fMRI after contralateral C7 nerve transfer. Seventeen healthy volunteers were also included in this fMRI study as controls. The hand motor seed regions were defined as region of interests in the bilateral hemispheres. The seed-based functional connectivity was calculated in all the subjects. Differences in functional connectivity of the motor cortical network between patients and healthy controls were compared. RESULTS: The inter-hemispheric functional connectivity of the M1 areas was increased in patients with BPAI compared with the controls. The inter-hemispheric functional connectivity between the supplementary motor areas was reduced bilaterally. CONCLUSIONS: The resting-state inter-hemispheric functional connectivity of the bilateral M1 areas is altered in patients after contralateral C7 nerve transfer, suggesting a functional reorganization of cerebral cortex.
[Mh] Termos MeSH primário: Neuropatias do Plexo Braquial/cirurgia
Mapeamento Encefálico/métodos
Córtex Motor/diagnóstico por imagem
Córtex Motor/fisiopatologia
Transferência de Nervo/métodos
Vias Neurais/diagnóstico por imagem
Vias Neurais/fisiopatologia
Nervos Espinhais/transplante
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Vértebras Cervicais
Feminino
Seres Humanos
Masculino
Meia-Idade
Plasticidade Neuronal
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170226
[St] Status:MEDLINE
[do] DOI:10.1007/s00234-017-1796-0


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[PMID]:28215303
[Au] Autor:Hodgetts SI; Harvey AR
[Ad] Endereço:School of Anatomy, Physiology and Human Biology, The University of Western Australia, Perth, WA, Australia; Western Australian Neuroscience Research Institute, Perth, WA, Australia. Electronic address: stuart.hodgetts@uwa.edu.au.
[Ti] Título:Neurotrophic Factors Used to Treat Spinal Cord Injury.
[So] Source:Vitam Horm;104:405-457, 2017.
[Is] ISSN:0083-6729
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The application of neurotrophic factors as a therapy to improve morphological and behavioral outcomes after experimental spinal cord injury (SCI) has been the focus of many studies. These studies vary markedly in the type of neurotrophic factor that is delivered, the mode of administration, and the location, timing, and duration of the treatment. Generally, the majority of studies have had significant success if neurotrophic factors are applied in or close to the lesion site during the acute or the subacute phase after SCI. Comparatively fewer studies have administered neurotrophic factors in order to directly target the somata of injured neurons. The mode of delivery varies between acute injection of recombinant proteins, subacute or chronic delivery using a variety of strategies including osmotic minipumps, cell-mediated delivery, delivery using polymer release vehicles or supporting bridges of some sort, or the use of gene therapy to modify neurons, glial cells, or precursor/stem cells. In this brief review, we summarize the state of play of many of the therapies using these factors, most of which have been undertaken in rodent models of SCI.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Drogas em Investigação/uso terapêutico
Fatores de Crescimento Neural/uso terapêutico
Neurogênese/efeitos dos fármacos
Traumatismos da Medula Espinal/tratamento farmacológico
Nervos Espinhais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Fator Neurotrófico Derivado do Encéfalo/administração & dosagem
Fator Neurotrófico Derivado do Encéfalo/genética
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Fator Neurotrófico Derivado do Encéfalo/uso terapêutico
Terapia Combinada/efeitos adversos
Drogas em Investigação/administração & dosagem
Drogas em Investigação/efeitos adversos
Drogas em Investigação/metabolismo
Seres Humanos
Fatores de Crescimento Neural/administração & dosagem
Fatores de Crescimento Neural/genética
Fatores de Crescimento Neural/metabolismo
Neuroproteção/efeitos dos fármacos
Fármacos Neuroprotetores/administração & dosagem
Fármacos Neuroprotetores/efeitos adversos
Fármacos Neuroprotetores/metabolismo
Fármacos Neuroprotetores/uso terapêutico
Proteínas Recombinantes/administração & dosagem
Proteínas Recombinantes/efeitos adversos
Proteínas Recombinantes/metabolismo
Proteínas Recombinantes/uso terapêutico
Traumatismos da Medula Espinal/metabolismo
Traumatismos da Medula Espinal/patologia
Traumatismos da Medula Espinal/terapia
Nervos Espinhais/metabolismo
Nervos Espinhais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Drugs, Investigational); 0 (Nerve Growth Factors); 0 (Neuroprotective Agents); 0 (Recombinant Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE


  9 / 4819 MEDLINE  
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[PMID]:28197545
[Au] Autor:Xie W; Strong JA; Zhang JM
[Ad] Endereço:Pain Research Center, Department of Anesthesiology, University of Cincinnati College of Medicine , Cincinnati, Ohio 45267.
[Ti] Título:Active Nerve Regeneration with Failed Target Reinnervation Drives Persistent Neuropathic Pain.
[So] Source:eNeuro;4(1), 2017 Jan-Feb.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peripheral nerves can regenerate and, when injured, may cause neuropathic pain. We propose that the active regeneration process plays a pivotal role in the maintenance of neuropathic pain. In one commonly used rodent neuropathic pain model, pronounced pain behaviors follow ligation and cutting of the L5 spinal nerve. We found that the injured nerve regenerates into the sciatic nerve and functionally reinnervates target tissues: the regenerated nerve conducts electrical signals, mechanical responses, and tracers between the leg/hindpaw and axotomized sensory ganglion. The regenerating nerve is the primary source of abnormal spontaneous activity detected . Disrupting the regeneration inhibited pain. First, semaphorin 3A, an inhibitory axonal guidance molecule, reduced functional regeneration, spontaneous activity, and pain behaviors when applied to the injury site . Second, knockdown of the upregulated growth-associated protein 43 (GAP43) with siRNA injected into the axotomized sensory ganglion reduced pain behaviors. We next examined the spared nerve injury model, in which pain behaviors are essentially permanent. The regeneration resulted in tangled GAP43-positive neuromas at the nerve injury site without target reinnervation. Perfusing the nerve stump with semaphorin 3A, but not removing the tangled fibers, prevented or reversed pain behaviors. This effect far outlasted the semaphorin 3A perfusion. Hence, in this model the long-lasting chronic pain may reflect the anatomical inability of regenerating nerves to successfully reinnervate target tissues, resulting in an ongoing futile regeneration process. We propose that specifically targeting the regeneration process may provide effective long-lasting pain relief in patients when functional reinnervation becomes impossible.
[Mh] Termos MeSH primário: Dor Crônica/fisiopatologia
Regeneração Nervosa/fisiologia
Neuralgia/fisiopatologia
Nervos Espinhais/lesões
Nervos Espinhais/fisiopatologia
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Animais
Dor Crônica/patologia
Modelos Animais de Doenças
Feminino
Proteína GAP-43/antagonistas & inibidores
Proteína GAP-43/genética
Proteína GAP-43/metabolismo
Gânglios Espinais/patologia
Gânglios Espinais/fisiopatologia
Masculino
Neuralgia/patologia
Distribuição Aleatória
Ratos Sprague-Dawley
Semaforina-3A/administração & dosagem
Semaforina-3A/metabolismo
Nervos Espinhais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GAP-43 Protein); 0 (Semaphorin-3A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE


  10 / 4819 MEDLINE  
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[PMID]:28165638
[Au] Autor:Maddali P; Moisi M; Page J; Chamiraju P; Fisahn C; Oskouian R; Tubbs RS
[Ad] Endereço:Department of Neurosurgery, Wayne State University, Detroit, MI.
[Ti] Título:Anatomical complications of epidural anesthesia: A comprehensive review.
[So] Source:Clin Anat;30(3):342-346, 2017 Apr.
[Is] ISSN:1098-2353
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidural anesthesia is a versatile technique widely used in treating lumbar spinal pain syndromes. Complications during these procedures can arise either from needle placement or from administration of medication. Potential risks include infection, hematoma, intravascular or subdural injections of medication, direct nerve trauma, air embolism, entry into a disc space, urinary retention, radiation exposure, and hypersensitivity reactions. The objective of this article is to review the complications of lumbar epidural injections and discuss the potential pitfalls related to these procedures. We searched Medline comprehensively for relevant case reports, clinical trials, and review articles. Complications from lumbar epidural injections are extremely rare. Most if not all of them can be avoided by careful techniques with accurate needle placement, sterile precautions, and a thorough understanding of the relevant anatomy and contrast patterns on fluoroscopic imaging. Clin. Anat. 30:342-346, 2017. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Anestesia Epidural/efeitos adversos
Anestésicos Locais/efeitos adversos
Embolia Aérea/etiologia
Hematoma/etiologia
Injeções Epidurais/métodos
Nervos Espinhais/lesões
[Mh] Termos MeSH secundário: Anestésicos Locais/administração & dosagem
Bupivacaína/administração & dosagem
Embolia Aérea/prevenção & controle
Hematoma/prevenção & controle
Seres Humanos
Injeções Epidurais/efeitos adversos
Lidocaína/administração & dosagem
Lidocaína/efeitos adversos
Dor Lombar/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anesthetics, Local); 98PI200987 (Lidocaine); Y8335394RO (Bupivacaine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE
[do] DOI:10.1002/ca.22831



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