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[PMID]:28631805
[Au] Autor:Warendorf J; Vrancken AF; van Schaik IN; Hughes RA; Notermans NC
[Ad] Endereço:Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Heidelberglaan 100, Utrecht, Netherlands, 3584 CX.
[Ti] Título:Drug therapy for chronic idiopathic axonal polyneuropathy.
[So] Source:Cochrane Database Syst Rev;6:CD003456, 2017 06 20.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chronic idiopathic axonal polyneuropathy (CIAP) is an insidiously progressive sensory or sensorimotor polyneuropathy that affects elderly people. Although severe disability or handicap does not occur, CIAP reduces quality of life. CIAP is diagnosed in 10% to 25% of people referred for evaluation of polyneuropathy. There is a need to gather and review emerging evidence on treatments, as the number of people affected is likely to increase in ageing populations. This is an update of a review first published in 2004 and previously updated in 2006, 2008, 2011 and 2013. OBJECTIVES: To assess the effects of drug therapy for chronic idiopathic axonal polyneuropathy for reducing disability and ameliorating neurological symptoms and associated impairments, and to assess any adverse effects of treatment. SEARCH METHODS: In July 2016, we searched Cochrane Central Register of Controlled Trials and the Cochrane Database of Systematic Reviews in the Cochrane Library, MEDLINE, Embase, and the Web of Science. We searched two trials registries for ongoing trials. We also handsearched the reference lists of relevant articles, reviews and textbooks identified electronically, and we would have contacted authors and other experts in the field to identify additional studies if this seemed useful. SELECTION CRITERIA: We sought all randomised or quasi-randomised (alternate or other systematic treatment allocation) trials that examined the effects of any drug therapy in people with CIAP at least one year after the onset of treatment. People with CIAP had to fulfil the following criteria: age 40 years or older, distal sensory or sensorimotor polyneuropathy, absence of systemic or other neurological disease, chronic clinical course not reaching a nadir in less than two months, exclusion of any recognised cause of the polyneuropathy by medical history taking, clinical or laboratory investigations, and electrophysiological studies in agreement with axonal polyneuropathy, without evidence of demyelinating features. The primary outcome was the proportion of participants with a significant improvement in disability. Secondary outcomes were change in the mean disability score, change in the proportion of participants who make use of walking aids, change in the mean Medical Research Council sum score, degree of pain relief and/or reduction of other positive sensory symptoms, change in the proportion of participants with pain or other positive sensory symptoms, and frequency of adverse effects. DATA COLLECTION AND ANALYSIS: Two review authors independently reviewed the results of the literature search and extracted details of trial methodology and outcome data of all potentially relevant trials. MAIN RESULTS: We identified 39 studies and assessed them for possible inclusion in the review, but we excluded all of them because of insufficient quality or lack of relevance. We summarised evidence from non-randomised studies in the Discussion. AUTHORS' CONCLUSIONS: Even though CIAP has been clearly described and delineated, no adequate randomised or quasi-randomised controlled clinical treatment trials have been performed. In their absence there is no proven efficacious drug therapy.
[Mh] Termos MeSH primário: Perna (Membro)/inervação
Polineuropatias/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Axônios
Doença Crônica
Marcha Atáxica/tratamento farmacológico
Marcha Atáxica/etiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[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:170621
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD003456.pub3


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[PMID]:28369393
[Au] Autor:Castro H; Kul E; Buijsen RAM; Severijnen LWFM; Willemsen R; Hukema RK; Stork O; Santos M
[Ad] Endereço:Department of Genetics and Molecular Neurobiology, Institute of Biology, Otto-von-Guericke University, 39120 Magdeburg, Germany.
[Ti] Título:Selective rescue of heightened anxiety but not gait ataxia in a premutation 90CGG mouse model of Fragile X-associated tremor/ataxia syndrome.
[So] Source:Hum Mol Genet;26(11):2133-2145, 2017 Jun 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A CGG-repeat expansion in the premutation range in the Fragile X mental retardation 1 gene (FMR1) has been identified as the genetic cause of Fragile X-associated tremor/ataxia syndrome (FXTAS), a late-onset neurodegenerative disorder that manifests with action tremor, gait ataxia and cognitive impairments. In this study, we used a bigenic mouse model, in which expression of a 90CGG premutation tract is activated in neural cells upon doxycycline administration-P90CGG mouse model. We, here, demonstrate the behavioural manifestation of clinically relevant features of FXTAS patients and premutation carrier individuals in this inducible mouse model. P90CGG mice display heightened anxiety, deficits in motor coordination and impaired gait and represent the first FXTAS model that exhibits an ataxia phenotype as observed in patients. The behavioural phenotype is accompanied by the formation of ubiquitin/FMRpolyglycine-positive intranuclear inclusions, as another hallmark of FXTAS, in the cerebellum, hippocampus and amygdala. Strikingly, upon cessation of transgene induction the anxiety phenotype of mice recovers along with a reduction of intranuclear inclusions in dentate gyrus and amygdala. In contrast, motor function deteriorates further and no reduction in intranuclear inclusions can be observed in the cerebellum. Our data thus demonstrate that expression of a 90CGG premutation expansion outside of the FMR1 context is sufficient to evoke an FXTAS-like behavioural phenotype. Brain region-specific neuropathology and (partial) behavioural reversibility make the inducible P90CGG a valuable mouse model for testing pathogenic mechanisms and therapeutic intervention methods.
[Mh] Termos MeSH primário: Ataxia/genética
Proteína do X Frágil de Retardo Mental/genética
Síndrome do Cromossomo X Frágil/genética
Tremor/genética
[Mh] Termos MeSH secundário: Animais
Ansiedade/genética
Ansiedade/metabolismo
Ataxia/metabolismo
Encéfalo/patologia
Ataxia Cerebelar/genética
Transtornos Cognitivos/genética
Modelos Animais de Doenças
Proteína do X Frágil de Retardo Mental/metabolismo
Síndrome do Cromossomo X Frágil/metabolismo
Marcha
Marcha Atáxica/genética
Marcha Atáxica/metabolismo
Corpos de Inclusão Intranuclear/genética
Camundongos
Transtornos dos Movimentos/genética
Neurônios/patologia
Tremor/metabolismo
Expansão das Repetições de Trinucleotídeos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fmr1 protein, mouse); 139135-51-6 (Fragile X Mental Retardation Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx108


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[PMID]:28202488
[Au] Autor:Amin OS; Shwani SS
[Ad] Endereço:Department of Medicine, International Medical University School of Medicine, Negeri Sembilan, Malaysia.
[Ti] Título:Opsoclonus.
[So] Source:BMJ Case Rep;2017, 2017 Feb 15.
[Is] ISSN:1757-790X
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Marcha Atáxica/complicações
Mioclonia/complicações
Transtornos da Motilidade Ocular/complicações
[Mh] Termos MeSH secundário: Adolescente
Seres Humanos
Masculino
Transtornos da Motilidade Ocular/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE


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[PMID]:28110629
[Au] Autor:Abkur TM; Kearney H; Hennessy MJ
[Ad] Endereço:1 Neurology registrar, Department of Neurology, University Hospital Galway, Galway, Ireland.
[Ti] Título:CLIPPERS and the need for long-term immunosuppression.
[So] Source:Scott Med J;62(1):28-33, 2017 Feb.
[Is] ISSN:0036-9330
[Cp] País de publicação:Scotland
[La] Idioma:eng
[Ab] Resumo:Chronic Lymphocytic Inflammation with Pontine Perivascular Enhancement Responsive to Steroids (CLIPPERS) is a rare chronic inflammatory disorder of the central nervous system. Herein, we describe the case of a 62-year-old female who presented with right sided facial tingling, gait ataxia and diplopia. Neuroimaging revealed pontine curvilinear enhancing lesions with extension into cerebellar peduncles, characteristic of CLIPPERS. This report discusses the differential diagnosis and the importance of prolonged immunomodulatory treatment for this rare neuro-inflammatory disorder. Long-term immunosuppression appears to be mandatory in order to achieve sustained remission and prevent disability related to atrophy of the structures involved in repeated attacks.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Central/diagnóstico
Diplopia/diagnóstico por imagem
Marcha Atáxica/diagnóstico por imagem
Imunossupressão
Inflamação/diagnóstico
Neuroimagem
Ponte/patologia
[Mh] Termos MeSH secundário: Anti-Inflamatórios/uso terapêutico
Doenças do Sistema Nervoso Central/tratamento farmacológico
Doenças do Sistema Nervoso Central/imunologia
Doenças do Sistema Nervoso Central/fisiopatologia
Diplopia/etiologia
Feminino
Marcha Atáxica/etiologia
Seres Humanos
Inflamação/tratamento farmacológico
Inflamação/imunologia
Inflamação/fisiopatologia
Imagem por Ressonância Magnética
Metilprednisolona/uso terapêutico
Meia-Idade
Punção Espinal
Tomografia Computadorizada por Raios X
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE
[do] DOI:10.1177/0036933016689006


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[PMID]:28058999
[Au] Autor:Tan U
[Ad] Endereço:a Medical School, Department of Physiology , Çukurova University , Adana , Turkey.
[Ti] Título:Sex differences in quadrupedal walking gaits of Uner Tan syndrome cases, healthy humans and nonhuman primates.
[So] Source:Neurol Res;39(3):212-216, 2017 Mar.
[Is] ISSN:1743-1328
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Uner Tan syndrome (UTS) cases with habitual quadrupedal locomotion (QL), impaired intelligence, and dysarthric or no speech predominantly use lateral sequence (LS) gait like nonprimates rather than the predominantly diagonal sequence (DS) gait of nonhuman primates. However, these studies neglected possible sex-related differences in these gait types. OBJECTIVES: (1) To assess the possible sex-related gait types in UTS cases, healthy infants and adults with requested QL, and the nonhuman primates. (2) To test the hypothesis that sex differences may exist in quadrupedal walking gaits in UTS cases, healthy humans, and nonhuman primates. METHODS: The UTS cases were filmed, the other study groups were taken from public open 'youtube' videos, which were used to assess the walking gait types as DS and LS. The right and left hind-limb phase values were calculated separately for males and females to allow a possible sex difference in walking gaits to be determined. RESULTS: Females predominantly used DS gait, contrary to males with predominantly LS gait. CONCLUSIONS: Consistent with the working hypothesis, the results suggested a biological sex-related trend in preferred walking gaits exists in all of the human and nonhuman primates using QL.
[Mh] Termos MeSH primário: Marcha Atáxica/fisiopatologia
Transtornos Neurológicos da Marcha/fisiopatologia
Transtornos dos Movimentos/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Animais
Fenômenos Biomecânicos
Disartria/fisiopatologia
Feminino
Seres Humanos
Lactente
Deficiência Intelectual/fisiopatologia
Masculino
Primatas
Fatores Sexuais
Síndrome
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170227
[Lr] Data última revisão:
170227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.1080/01616412.2016.1275457


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[PMID]:28039539
[Au] Autor:Leonardi L; Aceto MG; Marcotulli C; Arcuria G; Serrao M; Pierelli F; Paone P; Filla A; Roca A; Casali C
[Ad] Endereço:Department of SBMC, Sapienza University Rome, Latina, LT, Italy. leonardi.luca89@gmail.com.
[Ti] Título:A wearable proprioceptive stabilizer for rehabilitation of limb and gait ataxia in hereditary cerebellar ataxias: a pilot open-labeled study.
[So] Source:Neurol Sci;38(3):459-463, 2017 Mar.
[Is] ISSN:1590-3478
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:The aim of this pilot study is to test the feasibility and effectiveness of a wearable proprioceptive stabilizer that emits focal mechanical vibrations in patients affected by hereditary cerebellar ataxias. Eleven adult patients with a confirmed genetic diagnosis of autosomal dominant spinocerebellar ataxia or Friedreich's ataxia were asked to wear an active device for 3 weeks. Assessments were performed at baseline, after the device use (T1), and 3 weeks after (T2). SARA, 9-HPT, PATA, 6MWT, and spatial and temporal gait parameters, measured with a BTS-G-Walk inertial sensor, were used as study endpoints. As expected, no adverse effects were reported. Statistically significant improvements in SARA, 9HPT dominant hand, PATA test, 6MWT, cadence, length cycle, support right/cycle, support left/cycle, flight right/cycle, flight left/cycle, double support right/cycle, double support left/cycle, single support right/cycle, and single support left/cycle were observed between T0 and T1. All parameters improved at T1 did not show statistically significant differences a T2, with the exception of length of cycle. This small open-labeled study shows preliminary evidence that focal mechanical vibration exerted by a wearable proprioceptive stabilizer might improve limb and gait ataxia in patients affected by hereditary cerebellar ataxias.
[Mh] Termos MeSH primário: Retroalimentação Sensorial
Ataxia de Friedreich/reabilitação
Modalidades de Fisioterapia/instrumentação
Ataxias Espinocerebelares/reabilitação
[Mh] Termos MeSH secundário: Feminino
Marcha Atáxica/etiologia
Marcha Atáxica/reabilitação
Seres Humanos
Masculino
Projetos Piloto
Vibração
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170101
[St] Status:MEDLINE
[do] DOI:10.1007/s10072-016-2800-x


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[PMID]:27898636
[Au] Autor:Regina A; Lee D; Sud P; Crevi D
[Ad] Endereço:Department of Emergency Medicine and Medical Toxicology, North Shore University Hospital, Manhasset, NY AReginaTox@gmail.com. Department of Emergency Medicine and Medical Toxicology, North Shore University Hospital, Manhasset, NY. Department of Emergency Medicine and Medical Toxicology, Long Island Jewish Medical Center, New Hyde Park, NY. Department of Pediatric Emergency Medicine, Cohen's Children's Medical Center, New Hyde Park, NY.
[Ti] Título:Flumazenil Use for Isolated Ataxia in a Child.
[So] Source:Pediatr Emerg Care;32(12):e13, 2016 Dec.
[Is] ISSN:1535-1815
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Alprazolam/envenenamento
Antídotos/administração & dosagem
Flumazenil/administração & dosagem
Marcha Atáxica/tratamento farmacológico
[Mh] Termos MeSH secundário: Pré-Escolar
Feminino
Marcha Atáxica/induzido quimicamente
Seres Humanos
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Antidotes); 40P7XK9392 (Flumazenil); YU55MQ3IZY (Alprazolam)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE


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[PMID]:27806235
[Au] Autor:Kerbrat A; Ferré JC; Fillatre P; Ronzière T; Vannier S; Carsin-Nicol B; Lavoué S; Vérin M; Gauvrit JY; Le Tulzo Y; Edan G
[Ad] Endereço:From the Departments of Neurology (A.K., T.R., S.V., M.V., G.E.), Radiology (J.-C.F., B.C.-N., J.-Y.G.), and Infectious Diseases and Medical Intensive Care (P.F., S.L., Y.L.T.), Centre d'Investigation Clinique-Plurithématique, INSERM 1414 (P.F., Y.L.T., G.E.), and EA 4712 Comportement et Noyaux Gris
[Ti] Título:Acute Neurologic Disorder from an Inhibitor of Fatty Acid Amide Hydrolase.
[So] Source:N Engl J Med;375(18):1717-1725, 2016 11 03.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: A decrease in fatty acid amide hydrolase (FAAH) activity increases the levels of endogenous analogues of cannabinoids, or endocannabinoids. FAAH inhibitors have shown analgesic and antiinflammatory activity in animal models, and some have been tested in phase 1 and 2 studies. In a phase 1 study, BIA 10-2474, an orally administered reversible FAAH inhibitor, was given to healthy volunteers to assess safety. METHODS: Single doses (0.25 to 100 mg) and repeated oral doses (2.5 to 20 mg for 10 days) of BIA 10-2474 had been administered to 84 healthy volunteers in sequential cohorts; no severe adverse events had been reported. Another cohort of participants was then assigned to placebo (2 participants) or 50 mg of BIA 10-2474 per day (6 participants). This report focuses on neurologic adverse events in participants in this final cohort. A total of 4 of the 6 participants who received active treatment consented to have their clinical and radiologic data included in this report. RESULTS: An acute and rapidly progressive neurologic syndrome developed in three of the four participants starting on the fifth day of drug administration. The main clinical features were headache, a cerebellar syndrome, memory impairment, and altered consciousness. Magnetic resonance imaging showed bilateral and symmetric cerebral lesions, including microhemorrhages and hyperintensities on fluid-attenuated inversion recovery and diffusion-weighted imaging sequences predominantly involving the pons and hippocampi. One patient became brain dead; the condition of two patients subsequently improved, but one patient had residual memory impairment, and the other patient had a residual cerebellar syndrome. One patient remained asymptomatic. CONCLUSIONS: An unanticipated severe neurologic disorder occurred after ingestion of BIA 10-2474 at the highest dose level used in a phase 1 trial. The underlying mechanism of this toxic cerebral syndrome remains unknown.
[Mh] Termos MeSH primário: Amidoidrolases/antagonistas & inibidores
Doenças Cerebelares/induzido quimicamente
Transtornos da Consciência/induzido quimicamente
Óxidos N-Cíclicos/efeitos adversos
Hipocampo/patologia
Transtornos da Memória/induzido quimicamente
Ponte/patologia
Piridinas/efeitos adversos
[Mh] Termos MeSH secundário: Doença Aguda
Administração Oral
Adulto
Morte Encefálica
Cerebelo/patologia
Hemorragia Cerebral/induzido quimicamente
Hemorragia Cerebral/diagnóstico
Óxidos N-Cíclicos/administração & dosagem
Método Duplo-Cego
Marcha Atáxica/induzido quimicamente
Cefaleia/induzido quimicamente
Voluntários Saudáveis
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Piridinas/administração & dosagem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (BIA 10-2474); 0 (Cyclic N-Oxides); 0 (Pyridines); EC 3.5.- (Amidohydrolases); EC 3.5.1.- (fatty-acid amide hydrolase)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE


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[PMID]:27658421
[Au] Autor:Reich MM; Brumberg J; Pozzi NG; Marotta G; Roothans J; Åström M; Musacchio T; Lopiano L; Lanotte M; Lehrke R; Buck AK; Volkmann J; Isaias IU
[Ad] Endereço:Department of Neurology, University Hospital and Julius-Maximilian-University, Wuerzburg, Germany.
[Ti] Título:Progressive gait ataxia following deep brain stimulation for essential tremor: adverse effect or lack of efficacy?
[So] Source:Brain;139(11):2948-2956, 2016 Nov 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Thalamic deep brain stimulation is a mainstay treatment for severe and drug-refractory essential tremor, but postoperative management may be complicated in some patients by a progressive cerebellar syndrome including gait ataxia, dysmetria, worsening of intention tremor and dysarthria. Typically, this syndrome manifests several months after an initially effective therapy and necessitates frequent adjustments in stimulation parameters. There is an ongoing debate as to whether progressive ataxia reflects a delayed therapeutic failure due to disease progression or an adverse effect related to repeated increases of stimulation intensity. In this study we used a multimodal approach comparing clinical stimulation responses, modelling of volume of tissue activated and metabolic brain maps in essential tremor patients with and without progressive ataxia to disentangle a disease-related from a stimulation-induced aetiology. Ten subjects with stable and effective bilateral thalamic stimulation were stratified according to the presence (five subjects) of severe chronic-progressive gait ataxia. We quantified stimulated brain areas and identified the stimulation-induced brain metabolic changes by multiple 18 F-fluorodeoxyglucose positron emission tomography performed with and without active neurostimulation. Three days after deactivating thalamic stimulation and following an initial rebound of symptom severity, gait ataxia had dramatically improved in all affected patients, while tremor had worsened to the presurgical severity, thus indicating a stimulation rather than disease-related phenomenon. Models of the volume of tissue activated revealed a more ventrocaudal stimulation in the (sub)thalamic area of patients with progressive gait ataxia. Metabolic maps of both patient groups differed by an increased glucose uptake in the cerebellar nodule of patients with gait ataxia. Our data suggest that chronic progressive gait ataxia in essential tremor is a reversible cerebellar syndrome caused by a maladaptive response to neurostimulation of the (sub)thalamic area. The metabolic signature of progressive gait ataxia is an activation of the cerebellar nodule, which may be caused by inadvertent current spread and antidromic stimulation of a cerebellar outflow pathway originating in the vermis. An anatomical candidate could be the ascending limb of the uncinate tract in the subthalamic area. Adjustments in programming and precise placement of the electrode may prevent this adverse effect and help fine-tuning deep brain stimulation to ameliorate tremor without negative cerebellar signs.
[Mh] Termos MeSH primário: Estimulação Encefálica Profunda/efeitos adversos
Marcha Atáxica/etiologia
Tálamo/fisiologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Biofísica
Tremor Essencial/diagnóstico por imagem
Tremor Essencial/terapia
Feminino
Fluordesoxiglucose F18/metabolismo
Marcha Atáxica/diagnóstico por imagem
Seres Humanos
Imagem Tridimensional
Imagem por Ressonância Magnética
Masculino
Tomografia por Emissão de Pósitrons
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0Z5B2CJX4D (Fluorodeoxyglucose F18)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160924
[St] Status:MEDLINE
[do] DOI:10.1093/brain/aww223


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[PMID]:27565146
[Au] Autor:Simon-O'Brien E; Gauthier D; Riban V; Verleye M
[Ad] Endereço:Pharmacology Department, Biocodex, Chemin d'Armancourt, 60200, Compiègne, France. e.simonobrien@biocodex.fr.
[Ti] Título:Etifoxine improves sensorimotor deficits and reduces glial activation, neuronal degeneration, and neuroinflammation in a rat model of traumatic brain injury.
[So] Source:J Neuroinflammation;13(1):203, 2016 Aug 26.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Traumatic brain injury (TBI) results in important neurological impairments which occur through a cascade of deleterious physiological events over time. There are currently no effective treatments to prevent these consequences. TBI is followed not only by an inflammatory response but also by a profound reorganization of the GABAergic system and a dysregulation of translocator protein 18 kDa (TSPO). Etifoxine is an anxiolytic compound that belongs to the benzoxazine family. It potentiates GABAergic neurotransmission, either through a positive allosteric effect or indirectly, involving the activation of TSPO that leads to an increase in neurosteroids synthesis. In several models of peripheral nerve injury, etifoxine has been demonstrated to display potent regenerative and anti-inflammatory properties and to promote functional recovery. Prior study also showed etifoxine efficacy in reducing brain edema in rats. In light of these positive results, we used a rat model of TBI to explore etifoxine treatment effects in a central nervous system injury, from functional outcomes to the underlying mechanisms. METHODS: Male Sprague-Dawley rats received contusion (n = 18) or sham (n = 19) injuries centered laterally to bregma over the left sensorimotor cortex. They were treated with etifoxine (50 mg/kg, i.p.) or its vehicle 30 min following injury and every day during 7 days. Rats underwent behavioral testing to assess sensorimotor function. In another experiment, injured rats (n = 10) or sham rats (n = 10) received etifoxine (EFX) (50 mg/kg, i.p.) or its vehicle 30 min post-surgery. Brains were then dissected for analysis of neuroinflammation markers, glial activation, and neuronal degeneration. RESULTS: Brain-injured rats exhibited significant sensorimotor function deficits compared to sham-injured rats in the bilateral tactile adhesive removal test, the beam walking test, and the limb-use asymmetry test. After 2 days of etifoxine treatment, behavioral impairments were significantly reduced. Etifoxine treatment reduced pro-inflammatory cytokines levels without affecting anti-inflammatory cytokines levels in injured rats, reduced macrophages and glial activation, and reduced neuronal degeneration. CONCLUSIONS: Our results showed that post-injury treatment with etifoxine improved functional recovery and reduced neuroinflammation in a rat model of TBI. These findings suggest that etifoxine may have a therapeutic potential in the treatment of TBI.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Encefalite/tratamento farmacológico
Marcha Atáxica/tratamento farmacológico
Degeneração Neural/tratamento farmacológico
Neuroglia/efeitos dos fármacos
Oxazinas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Lesões Encefálicas Traumáticas/complicações
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalite/etiologia
Lateralidade Funcional/efeitos dos fármacos
Marcha Atáxica/etiologia
Proteína Glial Fibrilar Ácida/metabolismo
Locomoção/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Masculino
Degeneração Neural/etiologia
Desempenho Psicomotor/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Recuperação de Função Fisiológica/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 antigen, human); 0 (Cytokines); 0 (Glial Fibrillary Acidic Protein); 0 (Oxazines); X24X82MX4X (etifoxine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160828
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-016-0687-3



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