Rivista di neurologia最新文献_第3页

[Anoxic-ischemic encephalopathy and myoclonic status epilepticus]. [缺氧缺血性脑病和肌阵挛性癫痫持续状态]。

Rivista di neurologia Pub Date : 1991-09-01

W Borsini, P Lambruschini, S Pappagallo, G Gianni, C Maltinti, G Giannoni, G Marcacci

引用次数: 0

[Miller Fisher syndrome: review of the literature and presentation of 2 cases]. [Miller Fisher综合征:文献回顾及2例报告]。

Rivista di neurologia Pub Date : 1991-07-01

C Scoppetta, M Fontana, R Quadrini, I La Cesa, R Di Lello, A Peppe, V S Tolli, C Casali

{"title":"[Miller Fisher syndrome: review of the literature and presentation of 2 cases].","authors":"C Scoppetta, M Fontana, R Quadrini, I La Cesa, R Di Lello, A Peppe, V S Tolli, C Casali","doi":"","DOIUrl":"","url":null,"abstract":"Miller Fisher Syndrome (MFS), which is characterized by ophthalmoplegia, ataxia and tendon areflexia, is generally considered as a clinical variant of Guillain-Barré Syndrome. However some features of the disease are still debated, particularly regarding possible central nervous system involvement. After presenting two new cases of MFS, the authors provide a critical review of the literature and discuss the nosographical position of the disease. The main conclusions can be summarized as follows: MFS is a predominantly axonal inflammatory neuropathy with prevailing involvement of oculomotor nerves. It is associated to spinal multi or polyneuropathy, which in mildly affected cases is manifested by areflexia, while in severe ones it can be responsible of sense and/or motor impairment. In addition to peripheral neuropathy CNS involvement, exclusive or more marked in posterior fossa, occurs not infrequently. The prognosis of the disease is often benign, but disabling or even fatal outcome is possible. Corticosteroid treatment, possibly because of antiinflammatory and/or immunosuppressive action, could be effective in some patients. Finally, in spite of some similarities with GBS, MFS should be considered as a separate entity with its own nosographical position.","PeriodicalId":76494,"journal":{"name":"Rivista di neurologia","volume":"61 4","pages":"137-44"},"PeriodicalIF":0.0,"publicationDate":"1991-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12833146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Expression of a defect in the respiratory chain in cultured human cells]. [在培养的人类细胞中呼吸链缺陷的表达]。

Rivista di neurologia Pub Date : 1991-07-01

G Meola, G Rotondo, M Velicogna, R Toppi, V Sansone, N Bresolin, G Comi, A Bordoni, P Amati, C Ausenda

{"title":"[Expression of a defect in the respiratory chain in cultured human cells].","authors":"G Meola, G Rotondo, M Velicogna, R Toppi, V Sansone, N Bresolin, G Comi, A Bordoni, P Amati, C Ausenda","doi":"","DOIUrl":"","url":null,"abstract":"Large scale deletions of mitochondrial DNA (mtDNA) or altered inter-genomic regulation in skeletal muscle have been demonstrated in patients with mitochondrial encephalomyopathies due to Cytochrome C oxidase (COx) deficiency. We have analyzed by Southern blotting and Polymerase Chain Reaction (PCR) the mtDNA in primary muscle cultures (myoblast-myotube stages and at clonal densities) and in fibrogenic subclones obtained from 9 patients with partial COx deficiency who had in their muscle biopsy a subpopulation of mtDNA showing deletions of variable size (between 2.1 and 6.5 Kb). Only in the cultures from one patient, southern analysis revealed in myoblasts and myotubes a mtDNA almost identical to that found in the original muscle biopsy and persistence of deletion in muscle cells grown at clonal densities. The deletion was detectable in fibrogenic lineage only by PCR amplification. The deleted mtDNA molecules were detectable in myogenic or fibrogenic cultures from other patients only by PCR amplification. The different amounts of deleted mtDNA in the various tissues could be due either to an unequal distribution of the altered mtDNA during embryogenesis with amplification of deleted molecules in myogenic lineage or could result from negative selection against the altered mtDNA in rapidly proliferating cells, such as fibroblasts.","PeriodicalId":76494,"journal":{"name":"Rivista di neurologia","volume":"61 4","pages":"122-34"},"PeriodicalIF":0.0,"publicationDate":"1991-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12833147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Femoral neuropathy, diabetes mellitus, reduced glucose tolerance. Possible correlations]. [股神经病变，糖尿病，糖耐量降低。]可能的相关性)。

Rivista di neurologia Pub Date : 1991-07-01

L G Lazzarino, A Nicolai, D Toppari

引用次数: 0

[Gilles de la Tourette disease: review of the literature]. [Gilles de la Tourette病:文献综述]。

Rivista di neurologia Pub Date : 1991-07-01

M Raffaele, R Silvestri, P De Domenico, R Di Perri

引用次数: 0

Recent results in ataxia research. 共济失调研究的最新成果。

Rivista di neurologia Pub Date : 1991-07-01

P Giunti, M Spadaro, G B Colazza, C Morocutti