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[PMID]:28741230
[Au] Autor:Velayudhan L; Ffytche D; Ballard C; Aarsland D
[Ad] Dirección:Department of Old Age Psychiatry, Institute of Psychiatry, Psychology and Neurosciences, Kings College London, Box PO 70, De Crespigny Park, London, SE5 8AF, UK.
[Ti] Título:New Therapeutic Strategies for Lewy Body Dementias.
[So] Fuente:Curr Neurol Neurosci Rep;17(9):68, 2017 Sep.
[Is] ISSN:1534-6293
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:This article reviews current treatment strategies and recent advances for the Lewy body dementias (LBDs). Current available symptom treatment strategies are based on monoaminergic, cholinergic and glutaminergic neurotransmitter systems. Relatively robust evidence exists for cholinesterase inhibitors for cognitive impairment in LBD and in Parkinson's disease for antidepressants, clozapine and recently pimavanserin for psychosis. interpidine (RVT 101) and nelotanserin are currently under investigation. Non-pharmacological interventions, such as cognitive stimulation, physical exercises and neuromodulation strategies, may be useful in Parkinson's disease but have not yet been tested in dementias. Disease-modifying approaches are aimed at preventing, slowing or ameliorating the production, aggregation and deposition of pathological proteins, including immunotherapy targeting α-synuclein and an ongoing trial using ambroxol which increases glucocerebrosidase activity to lower the levels of the protein alpha-synuclein. Other disease-modifying clinical trials are using agents to augment insulin signalling, stem cell therapy, reducing amyloid pathology and gene therapy.
[Mh] Términos MeSH primario: Manejo de la Enfermedad
Enfermedad por Cuerpos de Lewy/diagnóstico
Enfermedad por Cuerpos de Lewy/terapia
[Mh] Términos MeSH secundario: Inhibidores de la Colinesterasa/uso terapéutico
Terapia Genética/tendencias
Seres Humanos
Enfermedad por Cuerpos de Lewy/inmunología
Enfermedad de Parkinson/diagnóstico
Enfermedad de Parkinson/inmunología
Enfermedad de Parkinson/terapia
Piperidinas/uso terapéutico
Trasplante de Células Madre/tendencias
Urea/análogos & derivados
Urea/uso terapéutico
alfa-Sinucleína/inmunología
[Pt] Tipo de publicación:JOURNAL ARTICLE; REVIEW
[Nm] Nombre de substancia:
0 (Cholinesterase Inhibitors); 0 (Piperidines); 0 (alpha-Synuclein); 8W8T17847W (Urea); JZ963P0DIK (pimavanserin)
[Em] Mes de ingreso:1803
[Cu] Fecha actualización por clase:180306
[Lr] Fecha última revisión:180306
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170726
[St] Status:MEDLINE
[do] DOI:10.1007/s11910-017-0778-2


  2 / 20564 MEDLINE  
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[PMID]:28454042
[Au] Autor:Rajan R; Popa T; Quartarone A; Ghilardi MF; Kishore A
[Ad] Dirección: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] Fuente:Clin Neurophysiol;128(6):992-999, 2017 06.
[Is] ISSN:1872-8952
[Cp] País de publicación:Netherlands
[La] Idioma:eng
[Ab] Resumen: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] Términos MeSH primario: Cerebelo/fisiopatología
Conectoma
Discinesia Inducida por Medicamentos/fisiopatología
Levodopa/uso terapéutico
Plasticidad Neuronal
Enfermedad de Parkinson/fisiopatología
[Mh] Términos MeSH secundario: Cuerpo Estriado/fisiopatología
Discinesia Inducida por Medicamentos/etiología
Seres Humanos
Levodopa/efectos adversos
Corteza Motora/fisiopatología
Enfermedad de Parkinson/tratamiento farmacológico
[Pt] Tipo de publicación:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nombre de substancia:
46627O600J (Levodopa)
[Em] Mes de ingreso:1708
[Cu] Fecha actualización por clase:180306
[Lr] Fecha última revisión:180306
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170429
[St] Status:MEDLINE


  3 / 20564 MEDLINE  
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[PMID]:29390334
[Au] Autor:Lee HD; Chang MC
[Ad] Dirección:Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University, Namku, Daegu, Republic of Korea.
[Ti] Título:Degeneration of the corticofugal tract from the secondary motor area in a Parkinson's disease patient with limb-kinetic apraxia: A case report.
[So] Fuente:Medicine (Baltimore);96(50):e9195, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:RATIONALE: In this case report, we describe a Parkinson's disease (PD) patient with limb-kinetic apraxia (LKA) in whom degeneration of the corticofugal tract (CFT) from the supplementary motor area (SMA) was observed in diffusion tensor tractography (DTT). PATIENT CONCERNS: A 63-year-old woman presented with a loss of dexterity in both upper extremities, which indicated LKA, and typical PD-related symptoms, including a gait disturbance with a short step, resting tremor in both upper extremities, and rigidity, and these symptoms had been present for 2 years. The F-florinated-N-3-fluoropropyl-2-ß-carboxymethoxy-3-ß-(4-lodophenyl) nortropane positron emission tomography scanning findings were consistent with PD. Based on the clinical symptoms and imaging findings, we diagnosed the patient with PD. In a coin-rotation test that was used to evaluate the severity of the LKA, the patient's results significantly decreased compared to the results of the normal controls. DIAGNOSES: The DTT showed that the CFTs from the SMAs in both hemispheres were partially torn and thinned. The fractional anisotropy values and CFT volumes in both SMAs were >2 standard deviations lower than those of the normal controls. INTERVENTIONS: The patient was treated with an initial dose of 150/37.5 mg/day of levodopa/benserazide, and the dose was gradually increased to 400/100 mg/day. OUTCOMES: After treatment, although the bradykinesia, rigidity, and resting tremor of the patient significantly decreased, the dexterity of the patient's hands did not improve. LESSONS: These observations indicated degeneration of the CFTs from the SMAs in both hemispheres in the patient. This degeneration might have, at least in part, contributed to the patient's LKA. The results of this study suggest that CFT degeneration could be one of the pathological mechanisms underlying LKA in patients with PD.
[Mh] Términos MeSH primario: Corteza Motora/patología
Enfermedad de Parkinson/patología
[Mh] Términos MeSH secundario: Anisotropía
Antiparkinsonianos/uso terapéutico
Benserazida/uso terapéutico
Imagen de Difusión Tensora
Combinación de Medicamentos
Femenino
Seres Humanos
Levodopa/uso terapéutico
Mediana Edad
Corteza Motora/diagnóstico por imagen
Rigidez Muscular/diagnóstico por imagen
Rigidez Muscular/tratamiento farmacológico
Rigidez Muscular/patología
Atrofia Muscular Espinal/diagnóstico por imagen
Atrofia Muscular Espinal/tratamiento farmacológico
Atrofia Muscular Espinal/patología
Enfermedad de Parkinson/diagnóstico por imagen
Enfermedad de Parkinson/tratamiento farmacológico
Tomografía de Emisión de Positrones
Temblor/diagnóstico por imagen
Temblor/tratamiento farmacológico
Temblor/patología
[Pt] Tipo de publicación:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nombre de substancia:
0 (Antiparkinson Agents); 0 (Drug Combinations); 0 (benserazide, levodopa drug combination); 46627O600J (Levodopa); 762OS3ZEJU (Benserazide)
[Em] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180301
[Lr] Fecha última revisión:180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009195


  4 / 20564 MEDLINE  
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[PMID]:29364897
[Au] Autor:Jehangir N; Yu CY; Song J; Shariati MA; Binder S; Beyer J; Santini V; Poston K; Liao YJ
[Ad] Dirección:Department of Ophthalmology, Stanford University School of Medicine, Stanford, California, United States of America.
[Ti] Título:Slower saccadic reading in Parkinson's disease.
[So] Fuente:PLoS One;13(1):e0191005, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Idiopathic Parkinson's Disease (PD) is characterized by degeneration of dopaminergic and other neurons, leading to motor and non-motor deficits. Abnormal eye movements in PD, including fixations, saccades, and convergence, are well described. However, saccadic reading, which requires serial and alternating saccades and fixations, is not well studied, despite its obvious impact on the quality of life. In this study, we assessed saccadic reading using variations of the King-Devick (KD) test, a rapid single digit number naming test, as a way to assess the ability to make serial left-to-right ocular motor movements necessary for reading. We recruited 42 treated PD patients and 80 age-matched controls and compared their reading times with a variety of measures, including age, duration of disease, Unified Parkinson's Disease Rating Scale (UPDRS), the National Eye Institute 25-Item Visual Functioning Questionnaire 25 (VFQ-25), and Montreal Cognitive assessment (MoCA) test. The subjects performed 4 trials of reading 120 single digit numbers aloud as fast as possible without making errors. In each trial, they read 3 pages (KD1, KD2, and KD3), and each page contained 40 numbers per page in 8 lines with 5 numbers/line. We found that PD patients read about 20% slower than controls on all tests (KD1, 2, and 3 tests) (p < 0.02), and both groups read irregularly spaced numbers slower than regularly spaced numbers. Having lines between numbers to guide reading (KD1 tests) did not impact reading time in both PD and controls, but increased visual crowding as a result of decreased spacing between numbers (KD3 tests) was associated with significantly slower reading times in both PD and control groups. Our study revealed that saccadic reading is slower in PD, but controls and PD patients are both impacted by visuospatial planning challenges posed by increased visual crowding and irregularity of number spacing. Reading time did not correlate with UPDRS or MoCA scores in PD patients but significantly correlated with age, duration of disease, and VFQ-25 scores. The presence of convergence insufficiency did not significantly correlate with reading time in PD patients, although on average there was slower reading time in those with convergence insufficiency by 8 s (p = 0.2613). We propose that a simple reading task using 120 single-digit numbers can be used as a screening tool in the clinical setting to assess functional ocular motor difficulties in Parkinson's disease that can have a profound impact on quality of life.
[Mh] Términos MeSH primario: Enfermedad de Parkinson/fisiopatología
Lectura
Movimientos Sacádicos
[Mh] Términos MeSH secundario: Adulto
Anciano
Estudios de Casos y Controles
Femenino
Seres Humanos
Masculino
Mediana Edad
Adulto Joven
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180226
[Lr] Fecha última revisión:180226
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191005


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[PMID]:28453723
[Au] Autor:Blanca Ramírez M; Lara Ordóñez AJ; Fdez E; Madero-Pérez J; Gonnelli A; Drouyer M; Chartier-Harlin MC; Taymans JM; Bubacco L; Greggio E; Hilfiker S
[Ad] Dirección:Institute of Parasitology and Biomedicine 'López-Neyra', Consejo Superior de Investigaciones Científicas (CSIC), 18016 Granada, Spain.
[Ti] Título:GTP binding regulates cellular localization of Parkinson's disease-associated LRRK2.
[So] Fuente:Hum Mol Genet;26(14):2747-2767, 2017 07 15.
[Is] ISSN:1460-2083
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:Mutations in leucine-rich repeat kinase 2 (LRRK2) comprise the most common cause of familial Parkinson's disease (PD), and sequence variants modify risk for sporadic PD. Previous studies indicate that LRRK2 interacts with microtubules (MTs) and alters MT-mediated vesicular transport processes. However, the molecular determinants within LRRK2 required for such interactions have remained unknown. Here, we report that most pathogenic LRRK2 mutants cause relocalization of LRRK2 to filamentous structures which colocalize with a subset of MTs, and an identical relocalization is seen upon pharmacological LRRK2 kinase inhibition. The pronounced colocalization with MTs does not correlate with alterations in LRRK2 kinase activity, but rather with increased GTP binding. Synthetic mutations which impair GTP binding, as well as LRRK2 GTP-binding inhibitors profoundly interfere with the abnormal localization of both pathogenic mutant as well as kinase-inhibited LRRK2. Conversely, addition of a non-hydrolyzable GTP analog to permeabilized cells enhances the association of pathogenic or kinase-inhibited LRRK2 with MTs. Our data elucidate the mechanism underlying the increased MT association of select pathogenic LRRK2 mutants or of pharmacologically kinase-inhibited LRRK2, with implications for downstream MT-mediated transport events.
[Mh] Términos MeSH primario: Guanosina Trifosfato/metabolismo
Proteína 2 Quinasa Serina-Treonina Rica en Repeticiones de Leucina/metabolismo
Enfermedad de Parkinson/metabolismo
[Mh] Términos MeSH secundario: GTP Fosfohidrolasas/metabolismo
Proteínas de Unión al GTP/genética
Proteínas de Unión al GTP/metabolismo
Variación Genética
Guanosina Trifosfato/genética
Células HEK293
Seres Humanos
Proteína 2 Quinasa Serina-Treonina Rica en Repeticiones de Leucina/antagonistas & inhibidores
Proteína 2 Quinasa Serina-Treonina Rica en Repeticiones de Leucina/genética
Microtúbulos/genética
Microtúbulos/metabolismo
Mutación
Enfermedad de Parkinson/genética
Fosforilación
Inhibidores de Proteínas Quinasas/farmacología
Transducción de Señales
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Protein Kinase Inhibitors); 86-01-1 (Guanosine Triphosphate); EC 2.7.11.1 (LRRK2 protein, human); EC 2.7.11.1 (Leucine-Rich Repeat Serine-Threonine Protein Kinase-2); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mes de ingreso:1801
[Cu] Fecha actualización por clase:180225
[Lr] Fecha última revisión:180225
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx161


  6 / 20564 MEDLINE  
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[PMID]:29287724
[Au] Autor:Kang H; Jo A; Kim H; Khang R; Lee JY; Kim H; Park CH; Choi JY; Lee Y; Shin JH
[Ad] Dirección:Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea.
[Ti] Título:PARIS reprograms glucose metabolism by HIF-1α induction in dopaminergic neurodegeneration.
[So] Fuente:Biochem Biophys Res Commun;495(4):2498-2504, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Our previous study found that PARIS (ZNF746) transcriptionally suppressed transketolase (TKT), a key enzyme in pentose phosphate pathway (PPP) in the substantia nigra (SN) of AAV-PARIS injected mice. In this study, we revealed that PARIS overexpression reprogrammed glucose metabolic pathway, leading to the increment of glycolytic proteins along with TKT reduction in the SN of AAV-PARIS injected mice. Knock-down of TKT in differentiated SH-SY5Y cells led to an increase of glycolytic enzymes and decrease of PPP-related enzymes whereas overexpression of TKT restored PARIS-mediated glucose metabolic shift, suggesting that glucose metabolic alteration by PARIS is TKT-dependent. Inhibition of PPP by either PARIS overexpression or TKT knock-down elevated the level of H O , and diminished NADPH and GSH levels, ultimately triggering the induction of HIF-1α, a master activator of glycolysis. In addition, TKT inhibition by stereotaxic injection of oxythiamine demonstrated slight decrement of dopaminergic neurons (DNs) in SN but not cortical neurons in the cortex, suggesting that TKT might be a survival factor of DNs. In differentiated SH-SY5Y, cell toxicity by GFP-PARIS was partially restored by introduction of Flag-TKT and siRNA-HIF-1α. We also observed the increase of HIF-1α and glycolytic hexokinase 2 in the SN of Parkinson's disease patients. Taken together, these results suggest that PARIS accumulation might distort the balance of glucose metabolism, providing clues for understanding mechanism underlying selective DNs death by PARIS.
[Mh] Términos MeSH primario: Encéfalo/metabolismo
Neuronas Dopaminérgicas/metabolismo
Glucosa/metabolismo
Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo
Enfermedad de Parkinson/metabolismo
Proteínas Represoras/metabolismo
Transcetolasa/metabolismo
[Mh] Términos MeSH secundario: Animales
Apoptosis
Encéfalo/patología
Línea Celular
Neuronas Dopaminérgicas/patología
Glucólisis
Masculino
Ratones
Ratones Consanguíneos C57BL
Enfermedad de Parkinson/patología
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Hif1a protein, mouse); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Repressor Proteins); 0 (ZNF746 protein, mouse); EC 2.2.1.1 (Transketolase); IY9XDZ35W2 (Glucose)
[Em] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180222
[Lr] Fecha última revisión:180222
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:171231
[St] Status:MEDLINE


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[PMID]:28449889
[Au] Autor:Terzaghi M; Spelta L; Minafra B; Rustioni V; Zangaglia R; Pacchetti C; Manni R
[Ad] Dirección:Unit of Sleep Medicine and Epilepsy, C. Mondino National Neurological Institute, Pavia, Italy. Electronic address: michele.terzaghi@mondino.it.
[Ti] Título:Treating sleep apnea in Parkinson's disease with C-PAP: feasibility concerns and effects on cognition and alertness.
[So] Fuente:Sleep Med;33:114-118, 2017 May.
[Is] ISSN:1878-5506
[Cp] País de publicación:Netherlands
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: Obstructive sleep apnea (OSA) is highly prevalent in Parkinson disease (PD) and is known to contribute to cognitive impairment and daytime sleepiness. We investigated feasibility of continuous positive airway pressure treatment (CPAP) and its effects on subjective daytime sleepiness and cognitive profile in PD plus OSA subjects in a longitudinal three months follow up study. METHODS: Seventy (age 71.7 ± 7.6, disease duration 9.9 ± 12.3, UPDRS-III 33.7 ± 12.5, MMSE 25.3 ± 3.6; years of education 7.7 ± 3.2) out of 228 consecutive PD patients undergoing in-lab video-polysomnography were found to have obstructive sleep apnea. Thirty-six subjects accepted to titrate therapeutic CPAP. Video-polysomnography, neuropsychological battery evaluating different cognitive domains and subjective scales for daytime sleepiness were scheduled at baseline and after three months. All the patients were given educational informations relative to diagnosis of OSA and benefits of OSA treatment, and an individualized training with CPAP. RESULTS: Twenty-seven (75%) subjects dropped out of the study due to CPAP intolerance. No demographic or disease-related variables (in particular, severity of OSA), could be found between subjects who completed the study versus those who dropped out. Nine subjects completed the three-month follow up, and there were no significant changes in subjective sleepiness, neuropsychological scores and sleep structure (except for reduction in apnea/hypopnea index and a trend toward increase in stage N3 sleep). CONCLUSION: Our data show that feasibility of CPAP treatment can be significantly threatened by overall attrition rates. Further studies should consider well-structured adherence promoting interventions. The actual role of OSA as a determinant of the profile of subjective daytime sleepiness and cognition in PD, and the effects of CPAP in PD need to be further studied.
[Mh] Términos MeSH primario: Atención/fisiología
Cognición/fisiología
Disfunción Cognitiva/complicaciones
Presión de las Vías Aéreas Positiva Contínua/métodos
Estudios de Factibilidad
Enfermedad de Parkinson/complicaciones
Síndromes de la Apnea del Sueño/terapia
Apnea Obstructiva del Sueño/terapia
[Mh] Términos MeSH secundario: Anciano
Disfunción Cognitiva/epidemiología
Disfunción Cognitiva/fisiopatología
Femenino
Estudios de Seguimiento
Seres Humanos
Masculino
Mediana Edad
Pruebas Neuropsicológicas/normas
Enfermedad de Parkinson/epidemiología
Enfermedad de Parkinson/terapia
Cooperación del Paciente
Polisomnografía/métodos
Síndromes de la Apnea del Sueño/complicaciones
Síndromes de la Apnea del Sueño/fisiopatología
Apnea Obstructiva del Sueño/complicaciones
Apnea Obstructiva del Sueño/epidemiología
Apnea Obstructiva del Sueño/fisiopatología
Fases del Sueño/fisiología
Resultado del Tratamiento
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180216
[Lr] Fecha última revisión:180216
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170429
[St] Status:MEDLINE


  8 / 20564 MEDLINE  
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[PMID]:27771287
[Au] Autor:Casula EP; Stampanoni Bassi M; Pellicciari MC; Ponzo V; Veniero D; Peppe A; Brusa L; Stanzione P; Caltagirone C; Stefani A; Koch G
[Ad] Dirección:Non-Invasive Brain Stimulation Unit, Neurologia Clinica e Comportamentale, Fondazione Santa Lucia IRCCS, Rome, Italy.
[Ti] Título:Subthalamic stimulation and levodopa modulate cortical reactivity in Parkinson's patients.
[So] Fuente:Parkinsonism Relat Disord;34:31-37, 2017 Jan.
[Is] ISSN:1873-5126
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: The effects of deep brain stimulation of the subthalamic nucleus (DBS-STN) and L-dopa (LD) on cortical activity in Parkinson's disease (PD) are poorly understood. OBJECTIVES: By combining transcranial magnetic stimulation (TMS) and electroencephalography (EEG) we explored the effects of STN-DBS, either alone or in combination with L-Dopa (LD), on TMS-evoked cortical activity in a sample of implanted PD patients. METHODS: PD patients were tested in three clinical conditions: i) LD therapy with STN-DBS turned on (ON/ON condition); ii) without LD therapy with STN-DBS turned on (OFF/ON condition); iii) without LD therapy with STN-DBS turned off (OFF/OFF condition). TMS pulses were delivered over left M1 while simultaneously acquiring EEG. Eight age-matched healthy volunteers (HC) were tested as a control group. RESULTS: STN-DBS enhanced early global TMS-evoked activity (∼45-80ms) and high-alpha TMS-evoked oscillations (11-13 Hz) as compared to OFF/OFF condition, independently from concomitant LD therapy. LD intake (ON/ON condition) produced a further increase of late TMS-evoked activity (∼80-130ms) and beta TMS-evoked oscillations (13-30 Hz), as compared to OFF/OFF and OFF/ON conditions, that normalized reactivity as compared to HC range of values. CONCLUSIONS: Our data reveal that bilateral STN-DBS and LD therapy induce a modulation of specific cortical components and specific ranges of frequency. These findings demonstrate that STN-DBS and LD therapy may have synergistic effects on motor cortical activity.
[Mh] Términos MeSH primario: Corteza Cerebral/efectos de los fármacos
Estimulación Encefálica Profunda
Levodopa/farmacología
Levodopa/uso terapéutico
Enfermedad de Parkinson/terapia
Núcleo Subtalámico/fisiología
[Mh] Términos MeSH secundario: Anciano
Antiparkinsonianos/farmacología
Antiparkinsonianos/uso terapéutico
Mapeo Encefálico
Estudios de Casos y Controles
Corteza Cerebral/fisiopatología
Electroencefalografía
Potenciales Evocados/efectos de los fármacos
Potenciales Evocados/fisiología
Femenino
Seres Humanos
Masculino
Mediana Edad
Enfermedad de Parkinson/tratamiento farmacológico
Enfermedad de Parkinson/patología
Índice de Severidad de la Enfermedad
Análisis Espectral
Estimulación Magnética Transcraneal
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
0 (Antiparkinson Agents); 46627O600J (Levodopa)
[Em] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180215
[Lr] Fecha última revisión:180215
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:161025
[St] Status:MEDLINE


  9 / 20564 MEDLINE  
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Fotocopia
Texto completo
[PMID]:29419682
[Au] Autor:Kim JI; Choi TY; Jun JH; Kang H; Lee MS
[Ad] Dirección:Division of Acupuncture & Moxibustion Medicine, Kyung Hee Korean Medicine Hospital, Kyung Hee University, Seoul.
[Ti] Título:Acupuncture for management of lower urinary tract symptoms in Parkinson's disease: A protocol for the systematic review of randomized controlled trials.
[So] Fuente:Medicine (Baltimore);97(6):e9821, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: Acupuncture is claimed to improve the lower urinary tract symptoms (LUTS). Currently, no systematic reviews are performed for acupuncture on LUTS in patients with Parkinson's diseases (PD). This review aims to evaluate the current evidence on the efficacy of acupuncture for the management of LUTS in PD. METHODS AND ANALYSES: Eleven databases will be searched from their inception. These include PubMed, AMED, EMBASE, the Cochrane Library, 6 Korean medical databases, and 1 Chinese medical database. Study selection, data extraction, and assessment will be performed independently by 2 researchers. Risk of bias will be assessed with the Cochrane risk of bias assessment tool. ETHICS AND DISSEMINATION: Ethical approval will not be required, given that this protocol is for a systematic review. The systematic review will be published in a peer-reviewed journal and disseminated both electronically and in print. The review will be updated to inform and guide healthcare practice and policy. TRIAL REGISTRATION NUMBER: PROSPERO 2018 CRD42018083857.
[Mh] Términos MeSH primario: Terapia por Acupuntura/métodos
Síntomas del Sistema Urinario Inferior
Enfermedad de Parkinson/complicaciones
Ensayos Clínicos Controlados Aleatorios como Asunto
[Mh] Términos MeSH secundario: Seres Humanos
Síntomas del Sistema Urinario Inferior/etiología
Síntomas del Sistema Urinario Inferior/terapia
Metaanálisis como Asunto
Proyectos de Investigación
[Pt] Tipo de publicación:JOURNAL ARTICLE; REVIEW
[Em] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180214
[Lr] Fecha última revisión:180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:180209
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009821


  10 / 20564 MEDLINE  
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Barbosa, Egberto Reis
Texto completo
[PMID]:28747137
[Au] Autor:Almeida KJ; de Macêdo LP; Lemos de Melo Lobo Jofili Lopes J; Bor-Seng-Shu E; Campos-Sousa RN; Barbosa ER
[Ad] Dirección:1 Department of Neurology, University of São Paulo, Sao Paulo, Brazil.
[Ti] Título:Modified Pfeffer Questionnaire for Functional Assessment in Parkinson Disease.
[So] Fuente:J Geriatr Psychiatry Neurol;30(5):261-266, 2017 Sep.
[Is] ISSN:0891-9887
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:INTRODUCTION: It was proposed to modify the Pfeffer questionnaire (PQ) for functional assessment in patients with Parkinson disease (PD). AIM: To determine the cutoff score for diagnosis of functional impairment in patients with PD by modified PQ (mPQ). METHODS: A total of 110 patients with PD were enrolled into the study, and a neuropsychological test battery was performed to assess their cognitive status. Regarding functional assessment, the mPQ has been applied, and their results were compared to the functional assessment by Informant Questionnaire on Cognitive Decline in the Elderly adapted for use in Brazil (IQCODE-BR). The statistical analysis was accomplished through receiver operating characteristic (ROC) curve with evaluation of the area under the curve, sensitivity, and specificity of the new cutoff point. RESULTS: Eighty-nine patients with PD were evaluated with a mean age of 63.69 ± 9.14 years. Cognitive status categorization was 28.10% as normal, 44.94% as mild cognitive impairment, and 26.96% of patients as dementia associated with PD. The average score on PQ was 3.49 ± 4.79 and on the mPQ 2.56 ± 3.49. In IQCODE-BR, the average score was 6.75 ± 32.72. The ROC curve for the new cutoff point presented 47.4% sensitivity, 88.10% specificity, and 0.757 of area under the curve, with a standard deviation of 0.055 (95% confidence interval: 0.650-0.864). CONCLUSION: 3.5 is proposed as the cutoff point to define functional impairment in patients with PD by mPQ.
[Mh] Términos MeSH primario: Trastornos del Conocimiento/psicología
Pruebas Neuropsicológicas/normas
Enfermedad de Parkinson/psicología
[Mh] Términos MeSH secundario: Trastornos del Conocimiento/patología
Femenino
Seres Humanos
Masculino
Mediana Edad
Enfermedad de Parkinson/patología
Encuestas y Cuestionarios
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1802
[Cu] Fecha actualización por clase:180214
[Lr] Fecha última revisión:180214
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170728
[St] Status:MEDLINE
[do] DOI:10.1177/0891988717720298



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