يعرض 1 - 10 نتائج من 64 نتيجة بحث عن '"Myelooptic neuropathy"', وقت الاستعلام: 0.79s تنقيح النتائج
  1. 1
    دورية أكاديمية

    المؤلفون: Güngör, Olcay, Yılmaz, Sanem, Özgör, Bilge, Dundar, Nihal Olgac, Dursun, Büşra DaÅŸlı, YalnızoÄŸlu, Dilek, Yılmaz, Deniz, AkbaÅŸ, Salih, Ä°pek, Rojan, Güngör, Serdal, BeÅŸen, Åžeyda, Dilber, Cengiz, Kutluk, Gültekin, HaliloÄŸlu, Göknur, Karaca, Nazlı Balcan, Serin, Hepsen Mine, KaradaÄŸ, Meral, Hakkı Akbeyaz, Ä°smail, BektaÅŸ, Ömer, Orgun, Leman Tekin, Keskin, Filiz, Akyüz, Gülcan, Çarman, KürÅŸat Bora, Alıcı, Nurettin, Aksoy, Erhan, Öztürk, Sedef TerzioÄŸlu, Arslan, Mutluay, Deniz, Adnan, Okuyaz, Çetin, Atasoy, Ergin, Bilgin, Neslihan, SarıtaÅŸ, Serdar, Öztoprak, Ãœlkühan, Elitez, Duygu Aykol, Ãœnalp, Aycan, Anlar, Banu, Aykol, Duygu, Yıldız, Edibe Pembegül, Yarar, CoÅŸkun, Kara, Bülent, Acer, Hamit, Yılmaz, Ãœ., Gücüyener, K., Yavuz, M., Öncel, Ä°., Canpolat, M., Saltık, S., Ãœnver, O., Çıtak Kurt, AyÅŸegül NeÅŸe, Tosun, AyÅŸe, Haspolat, Åženay, Ä°ncecik, Faruk, Tan, Hüseyin, Dilek, Tuğçe Damla, TürkdoÄŸan, DilÅŸad, Güleç, Ayten, AyanoÄŸlu, Müge, Kanmaz, Seda, Öztürk, Gülten, Öztürk, Selcan, Yüksel, Deniz, GürkaÅŸ, Esra, KaraoÄŸlu, Pakize, YiÅŸ, Uluç, Polat, Burçin Gönüllü, Okan, Mehmet Sait, Günbey, Ceren, Per, Hüseyin, Gültutan, Pembe, Öztürk, Semra Büyükkorkmaz, Tekgül, Hasan, Kürekçi, Fulya, Kurul, A. Semra Hız, Asadova, Nargis, Alikılıç, Defne, Duman, Özgür, Kömür, Mustafa, Yıldırım, Miraç, Gümüş, Hakan, Polat, Muzaffer, KamaÅŸak, Tülay, KonuÅŸkan, Bahadır, Mert, Gülen Gül, Edizer, Selvinaz, Mıhçı, Filiz, Toker, Rabia Tütüncü, ÅženoÄŸlu, Mine ÇiÄŸdem, Åžahin, Sevim, Gencpinar, Pinar, Yıldırım, Elif, Yüksel, Ersin, Ekici, Arzu, KayılıoÄŸlu, Hülya, Yayici Köken, Özlem, Süt, NurÅŸah Yeniay, Ayça, Senem, Solmaz, Ä°smail, Yetkin, Mehmet Fatih, Atasever, Aslı Kübra, Tekin, Hande Gazeteci, Dokurel, Ä°pek, Özçelik, Aysima, Sarıgeçili, Esra, Aksoy, AyÅŸe, Türköz, AyÅŸe Nur, Koç, Habibe, Cavusoglu, Dilek, Åžahin, Türkan Uygur, Erol, Ä°lknur, Direk, Meltem ÇobanoÄŸulları, Bodur, Muhittin, Teber, Serap, Oktay, Seçil

    الوصف: Background: The discovery of anti-myelin oligodendrocyte glycoprotein (MOG)-IgG and anti-aquaporin 4 (AQP4)-IgG and the observation on certain patients previously diagnosed with multiple sclerosis (MS) actually have an antibody-mediated disease mandated re-evaluation of pediatric MS series. Aim: To describe the characteristics of recent pediatric MS cases by age groups and compare with the cohort established before 2015. Method: Data of pediatric MS patients diagnosed between 2015 and 2021 were collected from 44 pediatric neurology centers across Türkiye. Clinical and paraclinical features were compared between patients with disease onset before 12 years (earlier onset) and ≥12 years (later onset) as well as between our current (2015–2021) and previous (2015) cohorts. Results: A total of 634 children (456 girls) were enrolled, 89 (14%) were of earlier onset. The earlier-onset group had lower female/male ratio, more frequent initial diagnosis of acute disseminated encephalomyelitis (ADEM), more frequent brainstem symptoms, longer interval between the first two attacks, less frequent spinal cord involvement on magnetic resonance imaging (MRI), and lower prevalence of cerebrospinal fluid (CSF)-restricted oligoclonal bands (OCBs). The earlier-onset group was less likely to respond to initial disease-modifying treatments. Compared to our previous cohort, the current series had fewer patients with onset 12 years, initial presentation with ADEM-like features, brainstem or cerebellar symptoms, seizures, and spinal lesions on MRI. The female/male ratio, the frequency of sensorial symptoms, and CSF-restricted OCBs were higher than reported in our previous cohort. Conclusion: Pediatric MS starting before 12 years was less common than reported previously, likely due to exclusion of patients with antibody-mediated diseases. The results underline the importance of antibody testing and indicate pediatric MS may be a more homogeneous disorder and more similar to adult-onset MS than previously thought. © 2022 European ...

    العلاقة: European Journal of Paediatric Neurology; Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı; https://doi.org/10.1016/j.ejpn.2022.08.006Test; https://hdl.handle.net/11499/51246Test; 41; 18; 2-s2.0-85143379946

  2. 2
    دورية أكاديمية

    المصدر: Neurology & Clinical Neuroscience. Sep2015, Vol. 3 Issue 5, p173-178. 6p.

    مصطلحات جغرافية: JAPAN

    مستخلص: Background Subacute myelo-optico neuropathy was the first epidemic drug intoxication that affected many people in Japan in the 1970s. Aim More than 40 years later, we assessed the real conditions of subacute myelo-optico neuropathy patients. Methods The present study examined current cognitive and affective functions, activities of daily living, and vascular endothelial function in aged subacute myelo-optico neuropathy patients ( n = 28) compared with age-, sex-, body mass index- and years of schooling-matched normal controls ( n = 141). Results Mini-Mental State Examination, Hasegawa Dementia Scale-Revised, Montreal Cognitive Assessment and Frontal Assessment Battery scores were not significantly lower in subacute myelo-optico neuropathy patients, but the Geriatric Depression Scale was significantly higher without apathy. Computerized touch-panel tests showed poor performance in the flipping cards game, arranging pictures game and beating devils game, whereas activities of daily living and vascular endothelial function were within normal limits. Conclusion The present study shows that subacute myelo-optico neuropathy patients showed essentially normal cognitive function using standard cognitive assessments, although the touch-panel tests detected some decline in subacute myelo-optico neuropathy patients. Subacute myelo-optico neuropathy patients presented a higher depression score without evident apathy, activities of daily living decline or vascular endothelial dysfunction. [ABSTRACT FROM AUTHOR]

  3. 3
    دورية أكاديمية

    المصدر: Focal Points. Sep2014, Vol. 32 Issue 9, p9-14. 6p.

  4. 4

    المؤلفون: Ünsal Yılmaz, Kıvılcım Gücüyener, Merve Yavuz, İbrahim Öncel, Mehmet Canpolat, Sema Saltık, Olcay Ünver, Ayşegül Neşe Çıtak Kurt, Ayşe Tosun, Sanem Yılmaz, Bilge Özgör, İlknur Erol, Ülkühan Öztoprak, Duygu Aykol Elitez, Meltem Çobanoğulları Direk, Muhittin Bodur, Serap Teber, Banu Anlar, Sema Saltik, Duygu Aykol, Edibe Pembegül Yıldız, Coşkun Yarar, Bülent Kara, Şenay Haspolat, Faruk İncecik, Gültekin Kutluk, Cengiz Dilber, Nihal Olgac Dundar, Hüseyin Tan, Ercan Demir, Büşra Daşlı Dursun, Tuğçe Damla Dilek, Dilşad Türkdoğan, Dilek Yalnızoğlu, Salih Akbaş, Ayten Güleç, Deniz Yılmaz, Müge Ayanoğlu, Seda Kanmaz, Serdal Güngör, Gülten Öztürk, Şeyda Beşen, Göknur Haliloğlu, Nazlı Balcan Karaca, Selcan Öztürk, Deniz Yüksel, Esra Gürkaş, Seçil Oktay, Hepsen Mine Serin, Meral Karadağ, İsmail Hakkı Akbeyaz, Uluç Yiş, Burçin Gönüllü Polat, Mehmet Sait Okan, Ömer Bektaş, Leman Tekin Orgun, Ceren Günbey, Hüseyin Per, Pembe Gültutan, Semra Büyükkorkmaz Öztürk, Erhan Aksoy, Gülcan Akyüz, Hasan Tekgül, Fulya Kürekçi, A. Semra Hız Kurul, Kürşat Bora Çarman, Defne Alikılıç, Özgür Duman, Mustafa Kömür, Miraç Yıldırım, Nurettin Alıcı, Hakan Gümüş, Muzaffer Polat, Bahadır Konuşkan, Olcay Güngör, Gülen Gül Mert, Selvinaz Edizer, Filiz Mıhçı, Sedef Terzioğlu Öztürk, Rabia Tütüncü Toker, Mutluay Arslan, Sevim Şahin, Pinar Gencpinar, Elif Yıldırım, Ersin Yüksel, Arzu Ekici, Adnan Deniz, Özlem Yayici Köken, Çetin Okuyaz, Nurşah Yeniay Süt, Ergin Atasoy, İsmail Solmaz, Mehmet Fatih Yetkin, Neslihan Bilgin, Aslı Kübra Atasever, Hande Gazeteci Tekin, İpek Dokurel, Aysima Özçelik, Ayşe Aksoy, Ayşe Nur Türköz, Dilek Cavusoglu, Mehbare Özkan, Emine Tekin, Türkan Uygur Şahin, Aycan Ünalp, Habibe Koç, Esra Sarıgeçili, Serdar Sarıtaş, Senem Ayça, Hülya Kayılıoğlu, Mine Çiğdem Şenoğlu, Tülay Kamaşak, Nargis Asadova, Filiz Keskin, Pakize Karaoğlu, Rojan İpek, Hamit Acer

    الوصف: Background: The discovery of anti-myelin oligodendrocyte glycoprotein (MOG)-IgG and anti-aquaporin 4 (AQP4)-IgG and the observation on certain patients previously diagnosed with multiple sclerosis (MS) actually have an antibody-mediated disease mandated re-evaluation of pediatric MS series. Aim: To describe the characteristics of recent pediatric MS cases by age groups and compare with the cohort established before 2015. Method: Data of pediatric MS patients diagnosed between 2015 and 2021 were collected from 44 pediatric neurology centers across Türkiye. Clinical and paraclinical features were compared between patients with disease onset before 12 years (earlier onset) and ≥12 years (later onset) as well as between our current (2015–2021) and previous (

  5. 5
    دورية أكاديمية

    المؤلفون: Chung Reen Kim1, Min Ho Chun1, Eun Young Han1

    المصدر: American Journal of Physical Medicine & Rehabilitation. Apr2010, Vol. 89 Issue 4, p315-322. 8p. 3 Charts.

    مستخلص: The article presents a study which examines the impact of hypnotics to the sleep patterns and recovery of subacute stroke patients. Subacute stroke patients were divided in two groups according to sleep patterns and those group with insomnia was treated with hypnotics. The study founds that administration of hypnotics improve the sleep patterns of the insomnia group and no significant difference in functional and cognitive status were observed between the two group.

  6. 6
    دورية أكاديمية

    المؤلفون: Yan-Ming Chen, Chih-Chao Yang1, I-Hua Wang2, Fung-Rong Hu3, Jieh-Ren Jou3 louice1070@yahoo.com.tw

    المصدر: Graefe's Archive of Clinical & Experimental Ophthalmology. Feb2010, Vol. 248 Issue 2, p231-235. 5p. 1 Chart, 2 Graphs.

    مستخلص: To evaluate the clinical effect of interferon β-1a on optic neuritis (ON) relapse in patients with multiple sclerosis (MS) in Taiwan. Data were collected from 23 MS patients with ON at National Taiwan University Hospital between January 1, 1993 and February 1, 2007. Twenty-three MS patients with ON received interferon β-1a (Rebif) 44 µg via subcutaneous injection three times weekly. All patients received corticosteroids pulse therapy followed by oral prednisolone for acute ON. The annual relapse rate (ARR) of ON in these MS patients before and after the use of interferon β-1a (Rebif) was the main clinical parameter of outcome in this study. The ARR of ON was lower in the posttreatment period than in the pretreatment period ( P = 0.0068). Thirteen patients (56.5%) had improved final visual acuity (>2 lines), and the other ten patients (43.5%) had stable final visual outcome (−2 lines < X < 2 lines). In addition, no recurrence of ON was noted in 15 patients (65.2%) during the posttreatment period. The use of interferon β-1a 44 µg via subcutaneous injection three times weekly did not increase the ON attacks in MS patients receiving this treatment. In addition, beneficial effects were found with the use of interferon β-1a on these patients. [ABSTRACT FROM AUTHOR]

  7. 7
    دورية أكاديمية

    المؤلفون: Asakura, Kunihiko kasakura@fujita-hu.ac.jp, Ueda, Akihiro1, Kawamura, Naoki1, Ueda, Madoka1, Mihara, Takateru1, Mutoh, Tatsuro1

    المصدر: Brain Research. Nov2009, Vol. 1301, p110-115. 6p.

    مستخلص: Abstract: Clioquinol is considered to be a causative agent of subacute myelo-optico neuropathy (SMON), although the pathogenesis of SMON is yet to be elucidated. To investigate the mechanism of neurotoxicity of clioquinol, we used PC12 cell line and focused on nerve growth factor (NGF) signaling through Trk receptor, which is essential for survival and differentiation of neuronal cells. Clioquinol inhibited NGF-induced Trk autophosphorylation in a dose-dependent manner. This inhibitory activity was further confirmed by the data of the inhibition of NGF-induced mitogen-activated protein kinase (MAPK) phosphorylation, which is located in the down stream of NGF-Trk intracellular signaling pathway. Clioquinol also caused neurite retraction induced by NGF and cell death. NGF-stimulated (differentiated) cells were more vulnerable than naïve cells. These results strongly suggest that clioquinol may cause the perturbation of the intracellular survival pathway by inhibiting Trk-initiated signaling pathway. [Copyright &y& Elsevier]

  8. 8
    دورية أكاديمية

    المؤلفون: Costello, F.1 fiona.costello@calgaryhealthregion.ca, Hodge, W.2, Pan, Y. I.2, Eggenberger, E.3, Coupland, S.2, Kardon, R. H.4

    المصدر: Multiple Sclerosis (13524585). Aug2008, Vol. 14 Issue 7, p893-905. 13p. 9 Charts, 2 Graphs.

    مستخلص: Introduction Optic neuritis causes retinal nerve fiber layer damage, which can be quantified with optical coherence tomography. Optical coherence tomography may be used to track nerve fiber layer changes and to establish a time-dependent relationship between retinal nerve fiber layer thickness and visual function after optic neuritis. Methods This prospective case series included 78 patients with optic neuritis, who underwent optical coherence tomography and visual testing over a mean period of 28 months. The main outcome measures included comparing inter-eye differences in retinal nerve fiber layer thickness between clinically affected and non-affected eyes over time; establishing when RNFL thinning stabilized after optic neuritis; and correlating retinal nerve fiber layer thickness and visual function. Results The earliest significant inter-eye differences manifested 2-months after optic neuritis, in the temporal retinal nerve fiber layer. Inter-eye comparisons revealed significant retinal nerve fiber layer thinning in clinically affected eyes, which persisted for greater than 24 months. Retinal nerve fiber thinning manifested within 6 months and then stabilized from 7 to 12 months after optic neuritis. Regression analyses demonstrated a threshold of nerve fiber layer thickness (75μm), which predicted visual recovery after optic neuritis. Conclusions Retinal nerve fiber layer changes may be tracked and correlated with visual function within 12 months of an optic neuritis event. [ABSTRACT FROM AUTHOR]

  9. 9
    دورية أكاديمية

    المؤلفون: Tateishi, Jun1

    المصدر: Neuropathology. Sep2000 Supplement, Vol. 20, pS20-S24. 5p.

    مصطلحات جغرافية: JAPAN

    مستخلص: It remains a tragic event that some 10000 individuals in Japan developed a unique neurologic disease, subacute myelo-optico-neuropathy (SMON). Many of the affected patients still suffer serious sequelae, such as dysesthesia and muscle weakness in the lower extremities, and loss or deficits in visual acuity. Neuropathologic studies on SMON patients and experimental reproduction of the disease in animals which had been administered clioquinol helped resolve the etiology of this disease. Common pathologic features seen in SMON patients and in dogs and cats chronically intoxicated with clioquinol were distal dominant axonopathy, mainly in the spinal long tracts and optic tracts. Particular abdominal symptoms present in patients after clioquinol ingestion could also be reproduced experimentally in dogs. SMON research in Japan may be worth reviewing for determining the etiology and preventing similar neurotoxic diseases in the future. [ABSTRACT FROM AUTHOR]

  10. 10
    مؤتمر

    المصدر: Berg , C , Khorooshi , R , Asgari , N , Linington , C , Morgan , P B & Owens , T 2015 , ' Antibody and complement-mediated glial response and demyelination ' , Glia , vol. 63 , no. S1 , T12-06B , pp. E361-E362 . < https://doi.org/10.1002/glia.22870Test >

    الوصف: Multiple Sclerosis (MS) is a CNS disease driven by inflammatory and neurodegenerative components. Although MS is thought to be a T cell-mediated disease, many MS lesions show deposition of immunoglobulin and activated complement (C). Detection of oligoclonal bands in cerebrospinal fluid, a sign of intrathecally-synthesized IgG, is characteristic of MS. B cells and antibody-producing plasma cells are also present in the meninges and perivascular space. Myelin oligodendrocyte glycoprotein (MOG) is a candidate autoantigen in MS . Injection of anti-MOG into rats with pre-established experimental allergic encephalomyelitis (EAE) increased disease severity and demyelination. The related disease Neuromyelitis Optica (NMO) is known to be mediated by antibodies, and pathology can be transferred to mice by intrathecal injection of NMO IgG + C. Mice lacking the C regulator CD59a develop more severe demyelination and axonal damage in NMO and EAE. This indicates that C regulation plays an important role in controlling CNS pathology. We hypothesized that anti-MOG antibodies could induce C-dependent demyelinating pathology. In this study, we investigated the role of C and antibodies in CNS demyelination. Injection of anti-MOG Mab with C into corpus callosum of C57BL/6 mice induced demyelination after 2 days. Demyelination was enhanced by CD59a blockade using a specific Mab. In the absence of exogenous complement, but with CD59a blockade, demyelination was still detectable though reduced. Control Mabs did not induce demyelination. Antibody-mediated damage was accompanied by an inflammatory response involving activation of astrocytes and microglia. Astrocyte response (shown by staining with anti-GFAP) was C-dependent, varied with dose of anti-MOG, and was not enhanced by CD59a blockade. By contrast, microglial response (shown by staining with anti-Iba1) was independent of dose of anti-MOG, and was also induced by anti-CD59a + C. Studies are ongoing to determine whether CD59a expression by microglia plays any role in their ...