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Pesquisa : paralisia and supranuclear and progressiva [Palavras]
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[PMID]:29373002
[Au] Autor:Franks AM; Guzzo R; Barker S; King-Mallory R
[Ti] Título:Progressive Supranuclear Palsy - A Case Study from the Perspective of a Primary Care Physician Son.
[So] Source:W V Med J;113(1):36-9, 2017 Jan-Feb.
[Is] ISSN:0043-3284
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Progressive Supranuclear Palsy (PSP) is a rare geriatric pathology, from the abnormal deposition of the tau protein, combining the motor tremor and bradykinesia of Parkinson's disease with the cognitive defects of Alzheimer's disease. As physical and mental debilities progressively manifest in PSP, the physician, family, and patient face decisions on how to manage this terminal neurodegenerative disease. Physicians note the outcomes of decisions and often express, either to peers or internally to oneself, how they would handle a similar situation affecting their own family. In this case, we will explore PSP and examine a physician's perspective as his father navigates his journey through it.
[Mh] Termos MeSH primário: Atitude Frente à Saúde
Paralisia Supranuclear Progressiva/psicologia
Paralisia Supranuclear Progressiva/terapia
[Mh] Termos MeSH secundário: Progressão da Doença
Relações Familiares
Evolução Fatal
Seres Humanos
Masculino
Meia-Idade
Paralisia Supranuclear Progressiva/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; PERSONAL NARRATIVES
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE


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[PMID]:28747135
[Au] Autor:Schmotz C; Richinger C; Lorenzl S
[Ad] Endereço:1 Department of Palliative Medicine, University Hospital, LMU Munich, Munich, Germany.
[Ti] Título:High Burden and Depression Among Late-Stage Idiopathic Parkinson Disease and Progressive Supranuclear Palsy Caregivers.
[So] Source:J Geriatr Psychiatry Neurol;30(5):267-272, 2017 Sep.
[Is] ISSN:0891-9887
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Caregivers of patients with late-stage idiopathic Parkinson disease (IPD) and late-stage progressive supranuclear palsy (PSP) often suffer from severe psychological strain themselves. This study investigates the influence of the different kind of symptoms in IPD and PSP on the psychological burden of the caregivers. METHODS: Twenty patients with late-stage IPD and 20 patients with late-stage PSP and their caregivers were investigated. To measure the degree of motor, cognitive, and affective impairment of the patients, the instruments Subscale III of the Unified Rating Scale for Parkinsonism (UPDRS-III), a shortened 24-item version of the Mini-Mental State Examination, and the Geriatric Depression Scale (GDS-30) were used. Psychological burden of the caregivers was determined by using the Beck Depression Inventory (BDI-II) and the Zarit Caregiver Burden Inventory (ZBI). RESULTS: Patients with IPD suffered from a higher level of depression (GDS-30: 15.9 vs 10.2, P = .020), whereas patients with PSP showed greater motor impairment (UPDRS-III: 38.3 vs 29.9, P = .002). Caregivers of both groups reported high psychological burden (ZBI: 36.5 in IPD vs 42.8 in PSP) and symptoms of a depression (BDI-II: 12.5 in IPD vs 15.1 in PSP). No significant influence of motor impairment, cognitive dysfunction, and depressive symptoms of the patient on the burden of the caregiver could be found. CONCLUSIONS: Psychological strain and depression among caregivers seem to become even more relevant in the late stages of IPD and PSP. Further studies will be necessary to investigate the specific determining factors in late-stage parkinsonian syndromes.
[Mh] Termos MeSH primário: Cuidadores/psicologia
Depressão/etiologia
Depressão/psicologia
Doença de Parkinson/psicologia
Paralisia Supranuclear Progressiva/psicologia
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
Masculino
Doença de Parkinson/patologia
Paralisia Supranuclear Progressiva/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1177/0891988717720300


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[PMID]:29187684
[Au] Autor:Watanabe M; Matsumoto Y; Okamoto K; Okuda B; Mizuta I; Mizuno T
[Ad] Endereço:Department of Neurology, Ehime Prefectural Central Hospital.
[Ti] Título:[A case of hereditary sensory and autonomic neuropathy type 1E with frontal lobe dysfunction as an initial symptom].
[So] Source:Rinsho Shinkeigaku;57(12):753-758, 2017 Dec 27.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 49-year-old man had developed gradually personality change, gait disturbance, and hearing loss for five years. On admission, he presented with frontal release signs, stuttering, vertical gaze palsy, sensorineural deafness, muscle rigidity, ataxia, and sensory disturbance with areflexia in the lower extremities. Brain MRI demonstrated atrophy in the cerebellum and midbrain tegmentum as well as cerebral atrophy, predominantly in the frontal lobe. He was tentatively diagnosed as progressive supranuclear palsy on the basis of clinical features and imagings. On nerve conduction study, no sensory nerve action potentials were elicited in the upper and lower extremities. Details of family history revealed a hereditary sensory neuropathy with autosomal dominant inheritance in his relatives. Because genetic analysis showed a rare missense mutation (c.1483T>C, p.Y495H) in DNA methyltransferase 1 gene, we diagnosed him as having hereditary sensory and autonomic neuropathy type 1E (HSAN1E). In addition, p.M232R mutation in prion protein gene was detected. It should be kept in mind that there are some patients with HSAN1E presenting with frontal lobe dysfunction as an initial symptom and with clinical features mimicking progressive supranuclear palsy.
[Mh] Termos MeSH primário: Neuropatias Hereditárias Sensoriais e Autônomas/diagnóstico
Neuropatias Hereditárias Sensoriais e Autônomas/genética
[Mh] Termos MeSH secundário: Atrofia
Encéfalo/patologia
DNA (Citosina-5-)-Metiltransferase 1/genética
Diagnóstico Diferencial
Lobo Frontal
Neuropatias Hereditárias Sensoriais e Autônomas/patologia
Neuropatias Hereditárias Sensoriais e Autônomas/fisiopatologia
Seres Humanos
Masculino
Meia-Idade
Mutação
Proteínas Priônicas/genética
Paralisia Supranuclear Progressiva
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Prion Proteins); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNMT1 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001043


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[PMID]:29050386
[Au] Autor:Tong J; Rathitharan G; Meyer JH; Furukawa Y; Ang LC; Boileau I; Guttman M; Hornykiewicz O; Kish SJ
[Ad] Endereço:Preclinical Imaging Unit, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.
[Ti] Título:Brain monoamine oxidase B and A in human parkinsonian dopamine deficiency disorders.
[So] Source:Brain;140(9):2460-2474, 2017 Sep 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:See Jellinger (doi:10.1093/awx190) for a scientific commentary on this article. The enzyme monoamine oxidases (B and A subtypes, encoded by MAOB and MAOA, respectively) are drug targets in the treatment of Parkinson's disease. Inhibitors of MAOB are used clinically in Parkinson's disease for symptomatic purposes whereas the potential disease-modifying effect of monoamine oxidase inhibitors is debated. As astroglial cells express high levels of MAOB, the enzyme has been proposed as a brain imaging marker of astrogliosis, a cellular process possibly involved in Parkinson's disease pathogenesis as elevation of MAOB in astrocytes might be harmful. Since brain monoamine oxidase status in Parkinson's disease is uncertain, our objective was to measure, by quantitative immunoblotting in autopsied brain homogenates, protein levels of both monoamine oxidases in three different degenerative parkinsonian disorders: Parkinson's disease (n = 11), multiple system atrophy (n = 11), and progressive supranuclear palsy (n = 16) and in matched controls (n = 16). We hypothesized that if MAOB is 'substantially' localized to astroglial cells, MAOB levels should be generally associated with standard astroglial protein measures (e.g. glial fibrillary acidic protein). MAOB levels were increased in degenerating putamen (+83%) and substantia nigra (+10%, non-significant) in multiple system atrophy; in caudate (+26%), putamen (+27%), frontal cortex (+31%) and substantia nigra (+23%) of progressive supranuclear palsy; and in frontal cortex (+33%), but not in substantia nigra of Parkinson's disease, a region we previously reported no increase in astrocyte protein markers. Although the magnitude of MAOB increase was less than those of standard astrocytic markers, significant positive correlations were observed amongst the astrocyte proteins and MAOB. Despite suggestions that MAOA (versus MAOB) is primarily responsible for metabolism of dopamine in dopamine neurons, there was no loss of the enzyme in the parkinsonian substantia nigra; instead, increased nigral levels of a MAOA fragment and 'turnover' of the enzyme were observed in the conditions. Our findings provide support that MAOB might serve as a biochemical imaging marker, albeit not entirely specific, for astrocyte activation in human brain. The observation that MAOB protein concentration is generally increased in degenerating brain areas in multiple system atrophy (especially putamen) and in progressive supranuclear palsy, but not in the nigra in Parkinson's disease, also distinguishes astrocyte behaviour in Parkinson's disease from that in the two 'Parkinson-plus' conditions. The question remains whether suppression of either MAOB in astrocytes or MAOA in dopamine neurons might influence progression of the parkinsonian disorders.
[Mh] Termos MeSH primário: Encéfalo/enzimologia
Dopamina/deficiência
Monoaminoxidase/metabolismo
Atrofia de Múltiplos Sistemas/metabolismo
Doença de Parkinson/metabolismo
Paralisia Supranuclear Progressiva/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Núcleo Caudado/metabolismo
Feminino
Lobo Frontal/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Isoenzimas/metabolismo
Masculino
Meia-Idade
Atrofia de Múltiplos Sistemas/patologia
Degeneração Neural/patologia
Doença de Parkinson/patologia
Fragmentos de Peptídeos/metabolismo
Fosfopiruvato Hidratase/metabolismo
Putamen/metabolismo
Substância Negra/metabolismo
Paralisia Supranuclear Progressiva/patologia
Tubulina (Proteína)/metabolismo
Adulto Jovem
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 0 (Isoenzymes); 0 (Peptide Fragments); 0 (Tubulin); 0 (alpha-Synuclein); EC 1.4.3.4 (Monoamine Oxidase); EC 4.2.1.11 (Phosphopyruvate Hydratase); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx172


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[PMID]:28987055
[Au] Autor:Sitek EJ; Wieczorek D; Konkel A; Dabrowska M; Slawek J
[Ad] Endereço:Oddzial Neurologii Szpitala Specjalistycznego sw. Wojciecha w Gdansku.
[Ti] Título:The pattern of verbal, visuospatial and procedural learning in Richardson variant of progressive supranuclear palsy in comparison to Parkinson's disease.
[Ti] Título:Specyfika uczenia sie materialu slownego, wzrokowo-przestrzennego oraz proceduralnego w wariancie Richardsona postepujacego porazenia ponadjadrowego w porównaniu z choroba Parkinsona..
[So] Source:Psychiatr Pol;51(4):647-659, 2017 Aug 29.
[Is] ISSN:2391-5854
[Cp] País de publicação:Poland
[La] Idioma:eng; pol
[Ab] Resumo:OBJECTIVES: Progressive supranuclear palsy (PSP) is regarded either within spectrum of atypical parkinsonian syndromes or frontotemporal lobar degeneration. We compared the verbal, visuospatial and procedural learning profiles in patients with PSP and Parkinson's disease (PD). Furthermore, the relationship between executive factors (initiation and inhibition) and learning outcomes was analyzed. METHODS: Thirty-three patients with the clinical diagnosis of PSP-Richardson's syndrome (PSP-RS), 39 patients with PD and 29 age -and education -matched controls were administered Mini-Mental State Examination (MMSE), phonemic and semantic fluency tasks, Auditory Verbal Learning Test (AVLT), Visual Learning and Memory Test for Neuropsychological Assessment by Lamberti and Weidlich (Diagnosticum für Cerebralschädigung, DCS), Tower of Toronto (ToT) and two motor sequencing tasks. Patients with PSP-RS and PD were matched in terms of MMSE scores and mood. RESULTS: Performance on DCS was lower in PSP-RS than in PD. AVLT delayed recall was better in PSP-RS than PD. Motor sequencing task did not differentiate between patients. Scores on AVLT correlated positively with phonemic fluency scores in both PSP-RS and PD. ToT rule violation scores were negatively associated with DCS performance in PSP-RS and PD as well as with AVLT performance in PD. CONCLUSIONS: Global memory performance is relatively similar in PSP-RS and PD. Executive factors (initiation and inhibition) are closely related to memory performance in PSP-RS and PD. Visuospatial learning impairment in PSP-RS is possibly linked to impulsivity and failure to inhibit automatic responses.
[Mh] Termos MeSH primário: Cognição/fisiologia
Transtornos Parkinsonianos/psicologia
Paralisia Supranuclear Progressiva/psicologia
[Mh] Termos MeSH secundário: Adulto
Atenção/fisiologia
Seres Humanos
Masculino
Meia-Idade
Testes Neuropsicológicos
Percepção Espacial/fisiologia
Comportamento Verbal/fisiologia
Percepção Visual/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171008
[St] Status:MEDLINE


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[PMID]:28980714
[Au] Autor:Schonhaut DR; McMillan CT; Spina S; Dickerson BC; Siderowf A; Devous MD; Tsai R; Winer J; Russell DS; Litvan I; Roberson ED; Seeley WW; Grinberg LT; Kramer JH; Miller BL; Pressman P; Nasrallah I; Baker SL; Gomperts SN; Johnson KA; Grossman M; Jagust WJ; Boxer AL; Rabinovici GD
[Ad] Endereço:Memory and Aging Center, University of California, San Francisco, San Francisco, CA.
[Ti] Título: F-flortaucipir tau positron emission tomography distinguishes established progressive supranuclear palsy from controls and Parkinson disease: A multicenter study.
[So] Source:Ann Neurol;82(4):622-634, 2017 Oct.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: F-flortaucipir (formerly F-AV1451 or F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue studies assessing binding to tau aggregates in progressive supranuclear palsy (PSP) have yielded mixed results. We compared in vivo F-flortaucipir uptake in patients meeting clinical research criteria for PSP (n = 33) to normal controls (n = 46) and patients meeting criteria for Parkinson disease (PD; n = 26). METHODS: Participants underwent magnetic resonance imaging and positron emission tomography for amyloid-ß ( C-PiB or F-florbetapir) and tau ( F-flortaucipir). F-flortaucipir standardized uptake value ratios were calculated (t = 80-100 minutes, cerebellum gray matter reference). Voxelwise and region-of-interest group comparisons were performed in template space, with receiver operating characteristic curve analyses to assess single-subject discrimination. Qualitative comparisons with postmortem tau are reported in 1 patient who died 9 months after F-flortaucipir. RESULTS: Clinical PSP patients showed bilaterally elevated F-flortaucipir uptake in globus pallidus, putamen, subthalamic nucleus, midbrain, and dentate nucleus relative to controls and PD patients (voxelwise p < 0.05 family wise error corrected). Globus pallidus binding best distinguished PSP patients from controls and PD (area under the curve [AUC] = 0.872 vs controls, AUC = 0.893 vs PD). PSP clinical severity did not correlate with F-flortaucipir in any region. A patient with clinical PSP and pathological diagnosis of corticobasal degeneration had severe tau pathology in PSP-related brain structures with good correspondence between in vivo F-flortaucipir and postmortem tau neuropathology. INTERPRETATION: F-flortaucipir uptake was elevated in PSP versus controls and PD patients in a pattern consistent with the expected distribution of tau pathology. Ann Neurol 2017;82:622-634.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Carbolinas/farmacocinética
Doença de Parkinson/diagnóstico por imagem
Tomografia por Emissão de Pósitrons
Paralisia Supranuclear Progressiva/diagnóstico por imagem
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Idoso
Compostos de Anilina/farmacocinética
Mapeamento Encefálico
Estudos de Casos e Controles
Transtornos Cognitivos/diagnóstico
Transtornos Cognitivos/etiologia
Diagnóstico
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Testes Neuropsicológicos
Doença de Parkinson/complicações
Índice de Gravidade de Doença
Paralisia Supranuclear Progressiva/complicações
Tiazóis/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole); 0 (7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole); 0 (Aniline Compounds); 0 (Carbolines); 0 (Thiazoles); 0 (tau Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1002/ana.25060


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[PMID]:28829981
[Au] Autor:Avenali M; Tassorelli C; De Icco R; Perrotta A; Serrao M; Fresia M; Pacchetti C; Sandrini G
[Ad] Endereço:Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; Department of Neurology and Neurorehabilitation, C. Mondino National Neurological Institute, Pavia, Italy. Electronic address: avenali.micol87@gmail.com.
[Ti] Título:Pain processing in atypical Parkinsonisms and Parkinson disease: A comparative neurophysiological study.
[So] Source:Clin Neurophysiol;128(10):1978-1984, 2017 Oct.
[Is] ISSN:1872-8952
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Pain is a frequent non-motor feature in Parkinsonism but mechanistic data on the alteration of pain processing are insufficient to understand the possible causes and to define specifically-targeted treatments. METHODS: we investigated spinal nociception through the neurophysiological measure of the threshold (TR) of nociceptive withdrawal reflex (NWR) and its temporal summation threshold (TST) comparatively in 12 Progressive Supranuclear Palsy (PSP) subjects, 11 Multiple System Atrophy (MSA) patients, 15 Parkinson's disease (PD) subjects and 24 healthy controls (HC). We also investigated the modulatory effect of L-Dopa in these three parkinsonian groups. RESULTS: We found a significant reduction in the TR of NWR and in the TST of NWR in PSP, MSA and PD patients compared with HC. L-Dopa induced an increase in the TR of NWR in the PSP group while TST of NWR increased in both PSP and PD. CONCLUSIONS: Our neurophysiological findings identify a facilitation of nociceptive processing in PSP that is broadly similar to that observed in MSA and PD. Specific peculiarities have emerged for PSP. SIGNIFICANCE: Our data advance the knowledge of the neurophysiology of nociception in the advanced phases of parkinsonian syndromes and on the role of dopaminergic pathways in the control on pain processing.
[Mh] Termos MeSH primário: Medição da Dor/métodos
Dor/diagnóstico
Dor/fisiopatologia
Doença de Parkinson/diagnóstico
Doença de Parkinson/fisiopatologia
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
Levodopa/administração & dosagem
Masculino
Meia-Idade
Atrofia de Múltiplos Sistemas/diagnóstico
Atrofia de Múltiplos Sistemas/tratamento farmacológico
Atrofia de Múltiplos Sistemas/fisiopatologia
Dor/tratamento farmacológico
Medição da Dor/efeitos dos fármacos
Doença de Parkinson/tratamento farmacológico
Transtornos Parkinsonianos/diagnóstico
Transtornos Parkinsonianos/tratamento farmacológico
Transtornos Parkinsonianos/fisiopatologia
Paralisia Supranuclear Progressiva/diagnóstico
Paralisia Supranuclear Progressiva/tratamento farmacológico
Paralisia Supranuclear Progressiva/fisiopatologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
46627O600J (Levodopa)
[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:170823
[St] Status:MEDLINE


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[PMID]:28754841
[Au] Autor:Smith R; Schöll M; Widner H; van Westen D; Svenningsson P; Hägerström D; Ohlsson T; Jögi J; Nilsson C; Hansson O
[Ad] Endereço:From the Departments of Neurology (R.S., H.W., C.N.), Clinical Neurophysiology (D.H.), Radiation Physics (T.O.), and Clinical Physiology and Nuclear Medicine (J.J.), Skåne University Hospital (D.v.W.), Lund; Clinical Memory Research Unit (R.S., M.S., C.N., O.H.), Department of Clinical Sciences (D.v
[Ti] Título:In vivo retention of F-AV-1451 in corticobasal syndrome.
[So] Source:Neurology;89(8):845-853, 2017 Aug 22.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To study the usefulness of F-AV-1451 PET in patients with corticobasal syndrome (CBS). METHODS: We recruited 8 patients with CBS, 17 controls, 31 patients with Alzheimer disease (AD), and 11 patients with progressive supranuclear palsy (PSP) from the Swedish BioFINDER study. All patients underwent clinical assessment, F-AV-1451 PET, MRI, and quantification of ß-amyloid pathology. A subset of participants also underwent F-FDG-PET. RESULTS: In the 8 patients with CBS, 6 had imaging findings compatible with the corticobasal degeneration pathology and 2 with typical AD pathology. In the 6 patients with CBS without typical AD pathology, there were substantial retentions of F-AV-1451 in the motor cortex, corticospinal tract, and basal ganglia contralateral to the most affected body side. These patients could be clearly distinguished from patients with AD dementia or PSP using F-AV-1451. However, cortical atrophy was more widespread than the cortical retention of F-AV1451 in these CBS cases, and cortical AV-1451 uptake did not correlate with cortical thickness or glucose hypometabolism. These results are in sharp contrast to AD dementia, where F-AV-1451 retention was more widespread than cortical atrophy, and correlated well with cortical thickness and hypometabolism. CONCLUSIONS: Patients with CBS without typical AD pathology exhibited AV-1451 retention in the motor cortex, corticospinal tract, and basal ganglia contralateral to the affected body side, clearly different from controls and patients with AD dementia or PSP. However, cortical atrophy measured with MRI and decreased F-fluorodeoxyglucose uptake were more widespread than F-AV-1451 uptake and probably represent earlier, yet less specific, markers of CBS. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that F-AV-1451 PET distinguishes between CBS and AD or PSP.
[Mh] Termos MeSH primário: Doenças dos Gânglios da Base/diagnóstico por imagem
Encéfalo/diagnóstico por imagem
Carbolinas/farmacocinética
Tomografia por Emissão de Pósitrons
Compostos Radiofarmacêuticos/farmacocinética
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/diagnóstico por imagem
Doença de Alzheimer/metabolismo
Doenças dos Gânglios da Base/metabolismo
Encéfalo/metabolismo
Mapeamento Encefálico
Diagnóstico Diferencial
Seres Humanos
Imagem por Ressonância Magnética
Meia-Idade
Tratos Piramidais/diagnóstico por imagem
Tratos Piramidais/metabolismo
Paralisia Supranuclear Progressiva/diagnóstico por imagem
Paralisia Supranuclear Progressiva/metabolismo
Suécia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole); 0 (Carbolines); 0 (Radiopharmaceuticals)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170910
[Lr] Data última revisão:
170910
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004264


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[PMID]:28704733
[Au] Autor:Bologna M; Bertram K; Paparella G; Papi C; Belvisi D; Conte A; Suppa A; Williams DR; Berardelli A
[Ad] Endereço:Department of Neurology and Psychiatry, Sapienza University of Rome, Italy; Neuromed Institute IRCCS, Pozzilli, IS, Italy.
[Ti] Título:Reversal of long term potentiation-like plasticity in primary motor cortex in patients with progressive supranuclear palsy.
[So] Source:Clin Neurophysiol;128(9):1547-1552, 2017 Sep.
[Is] ISSN:1872-8952
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Abnormal primary motor cortex plasticity might be involved in the pathophysiology of progressive supranuclear palsy. In the present study we aimed to investigate possible abnormalities of depotentiation, a mechanism involved in plasticity regulation, in this condition. METHODS: Primary motor cortex excitability, investigated with single and paired-pulse transcranial magnetic stimulation, as well as long-term potentiation-like plasticity and its reversibility, were studied using theta burst stimulation in 15 patients with progressive supranuclear palsy and 11 healthy controls. Participants underwent two sessions using (1) the intermittent theta-burst stimulation (potentiation protocol) and (2) intermittent theta-burst stimulation combined with a depotentiation protocol (a short continuous theta-burst stimulation). RESULTS: Patients with PSP had higher corticospinal excitability and lower intracortical inhibition than healthy controls. Intermittent theta-burst stimulation elicited an abnormally increased long term potentiation-like effect in patients in comparison to healthy subjects. However, the depotentiation protocol was able to reverse the effects intermittent theta-burst stimulation on motor cortex excitability both in patients and in healthy controls. CONCLUSIONS: Altered primary motor cortex plasticity in patients with PSP does not reflect an abnormality of depotentiation. SIGNIFICANCE: This study provides information for a deeper understanding of the possible pathophysiological mechanisms underlying the altered M1 plasticity in PSP.
[Mh] Termos MeSH primário: Potencial Evocado Motor/fisiologia
Potenciação de Longa Duração/fisiologia
Córtex Motor/fisiologia
Plasticidade Neuronal/fisiologia
Paralisia Supranuclear Progressiva/fisiopatologia
[Mh] Termos MeSH secundário: Idoso
Eletromiografia/métodos
Feminino
Seres Humanos
Masculino
Meia-Idade
Paralisia Supranuclear Progressiva/diagnóstico
Estimulação Magnética Transcraniana/métodos
[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:170714
[St] Status:MEDLINE


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[PMID]:28653647
[Au] Autor:Boxer AL; Yu JT; Golbe LI; Litvan I; Lang AE; Höglinger GU
[Ad] Endereço:Department of Neurology, Memory and Aging Center, University of California, San Francisco, CA, USA. Electronic address: adam.boxer@ucsf.edu.
[Ti] Título:Advances in progressive supranuclear palsy: new diagnostic criteria, biomarkers, and therapeutic approaches.
[So] Source:Lancet Neurol;16(7):552-563, 2017 Jul.
[Is] ISSN:1474-4465
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Progressive supranuclear palsy (PSP), previously believed to be a common cause of atypical parkinsonism, is now recognised as a range of motor and behavioural syndromes that are associated with a characteristic 4-repeat tau neuropathology. New research criteria that recognise early presentations of PSP and operationalise diagnosis of the full spectrum of clinical phenotypes have been reported. The Movement Disorders Society PSP diagnostic criteria include syndromes with few or mild symptoms that are suggestive of underlying PSP pathology and could provide an opportunity for earlier therapeutic interventions in the future. These criteria also include definitions for variant PSP syndromes with different patterns of movement, language, or behavioural features than have been conclusively associated with PSP pathology. Data from new diagnostic biomarkers can be combined with the clinical features of disease to increase the specificity of the new criteria for underlying PSP pathology. Because PSP is associated with tau protein abnormalities, there is growing interest in clinical trials of new tau-directed therapies. These therapies are hypothesised to have disease-modifying effects by reducing the concentration of toxic forms of tau in the brain or by compensating for loss of tau function. Since tau pathology is also central to Alzheimer's disease and chronic traumatic encephalopathy, a successful tau therapeutic for PSP might inform treatment of other neurodegenerative diseases.
[Mh] Termos MeSH primário: Biomarcadores
Paralisia Supranuclear Progressiva/diagnóstico
Paralisia Supranuclear Progressiva/terapia
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE



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