DERGİ - g20 istanbul 2015
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DERGİ - g20 istanbul 2015
Uzm.-Op. Umur Kayabaşı - Nörooftalmoloji Toplam A-Puanı B-Puanı 464,1 294,22 169,88 A - DERGİ 28,5 28,5 0B A A- DERGİ Puan Puan Puan SCI ve SCIExp dışındaki 2 / 1. indekslerde Yazar yer alan yurt dışı dergiler Kaynakça: Kayabasi AU, Sergott RC. OCT and FAF in the Early Diagnosis of Alzheimer's Disease. Neurobiology of Aging 2013; 35(4):786-90. Özet: OCT and FAF in the Early Diagnosis of Alzheimer's Disease A. Umur Kayabasi1, Robert C. Sergott2, 1Istanbul University, Istanbul, Turkey; 2Thomas Jefferson University, Department of NeuroOphthalmology, Philadelphia, Pensylvania, USA. Objectives. Optical coherence tomography (OCT) macula- retina exam and fundus autoflorescence (FAF) test give us extremely important clues about neurodegenerative diseases. Since the retina and optic nerve share similar tissues with the brain, any defect detected by OCT and FAF may also be related to a disease of the nervous system. It has been proposed that beta-amyloid, which causes Alzheimer´ s disease (AD) in the brain, may be observed in different tissues of the eye (lens, retina etc.) many years earlier. Methods. We examined 14 patients with a family history of AD and all of whom (except 1 patient with no cognitive defect) had only minor cognitive dysfunction. Results. FAF exam of the retina revealed suspected regions and OCT exam through these retinal lesions revealed plaque deposition in the ganglion layer of the retina. Many plaque deposits colocalized with drusen due to age related macular degeneration. Conclusions. We believe that these deposits can be signs of AD and contain beta-amyloid. They are located in the inner parts of the retina, mostly the ganglion layer and are different from the localization of drusen alone. It is our thought that comprehensive retinal exam should be a part of the neurological exam in AD and similar neurodegenerative diseases . The detection of plaques in the retina may help us with early diagnosis of AD. 30 30 A 0 B A- DERGİ Puan Puan Puan SCI ve SCIExp dışındaki 1 / 1. indekslerde Yazar yer alan yurt dışı dergiler Kaynakça: Kayabasi AU. Different optic neuropathies and novel treatments.Journal of Clinical & Experimental Ophthalmology.Open Access; Published September 23, 2013 Özet: Abstract: The aim of this workshop is to discuss the diagnosis, treatment and follow- up of different optic neuropathies. Meanwhile, images from the new technology devices like OCT and the conventional machines like Perimetry will be shown. Also, MR images of the orbit and brain and images of optic nerve problems will be the subjects of the main topic. There are some new developments in the treatment of the optic neuropathies and different ideas about novel treatments will be shared. OPTİC NEUROPATHİES: - Optic neuritis (demyelination of the optic nerve): Acute, painful vision loss. Occurs mainly in women within the age range of 18-45. Responds well to high dose intravenous steroids. Approximately 1/3 of the cases are seen with disc edema, 2/3 are retrobulber. Retrobulber cases progress to multiple sclerosis (MS) more frequently. The possibility of a woman patient to develop MS after isolated optic neuritis is about 70% in ten years. The progression of optic neuritis to MS can be detected by OCT. - Anterior ischemic optic neuropathy (non-arteritic): Acute, painless visual loss due to a stroke on the optic nerve head. Disc edema is present. Patients usually have hypertension or diabetes. Visual field defect is altitudinal. Cup to disc ratio is small. No definite treatment. Intravitreal injections (triamcinolone and anti- VEGF) may be tried in acute cases. Traumatic optic neuropathy: Occurs after a direct or indirect trauma to the optic nerve. Steroids are not recommended if there is head concussion. Surgery of the optic canal to decompress the nerve may be tried in early stages. There are reports about success with intravenous erythro poietin. - Toxic optic neuropathy: Central, bilateral visual loss. There is a new report about improvement after methanol toxicity with the combination of erythropoietin and steroids. - Radiation optic neuropathy: Bilateral visual loss months or years after radiation therapy of a brain tumor. There are new reports of improvement of vision with intravenous bevacizumab tharapy. - Leber’s optic neuropathy: Painless, bilateral visual loss with central scotomas. Inherited by the maternal mitochondrial DNA mutations: m.11778, m.14484, m.3460. Idebenone treatment in early stage Leber’s disease have been shown to be beneficial. - Chronic relapsing inflammatory optic neuropathy: Steroid sensitive optic neuropathy which recurs after steroid withdrawal. Long term steroids or other immunosuppressive agents are used. There are other optic neuropathies with inflammatory, infectious, etc. etiology which can be discusses, too. 19 19 A 0 B A- DERGİ Puan Puan Puan SCI ve SCIExp dışındaki 2 / 1. indekslerde Yazar yer alan yurt dışı dergiler Kaynakça: Kayabasi AU, Sergott RC. Immunosuppressive therapy in GCA.Int J Biol Med Res.2013;Vol 4,Issue 4:3656-61. Özet: Review Immunosuppressive therapy in giant cell arteritis Umur A. Kayabasi1 , Robert C Sergott2 World Eye Hospital, Istanbul, Turkey Accepted 31 October, 2013 Giant cell arteritis (GCA) is a granulomatous vasculitis of large vessels mostly seen in patients over fifty years of age. Altough GCA causes blindness , stroke and myocardial infarction if left untreated, it has not been clearly shown that life expectancy decreases with it , but for sure the quality of life decreases because of long term use and side effects of drugs, especially steroids. We tried to discuss the treatment of the disease with other drugs, particularly methotrexate to increase the quality of life in patients. Keywords: Methotrexate, Giant cell arteritis, Steroids, Immunosuppression IINTRODUCTION Giant cell arteritis (GCA) is a vasculitis of large vessels generally seen in patients over fifty years of age. The incidence of GCA has been reported as 15-25 / 100.000 and the prevalence as 1/133 over age fifty. After seventyeighty years of age, the incidence increases 20-folds and male / female ratio of patients becomes 2-4 / 1 respectively GCA is more common in white population,who lives in high altitudes and frequently seen in patients with Scandinavian descent. (Beyer et al., 2011) Altough GCA causes blindness , stroke and myocardial infarction if left untreated, it has not been clearly shown that life expectancy decreases with it (Bhatia et al., 2005; Bley et al., 2005). There have been major developments in the diagnosis, treatment and life quality of the patients in the recent years. Methotrexate and other immunosuppressives had been either added to the classical steroid treatment or used alone after a course of steroid treatment (Bhatia et al., 2005). *Corresponding Author E-mail: kayabasi@yahoo.com Tel: 90 532 6129050 Clinical presentation 20 20 A 0 B A- DERGİ Puan Puan Puan SCI ve SCIExp dışındaki 1 / 1. indekslerde Yazar yer alan yurt dışı dergiler Kaynakça: Kayabasi UA. Genetics and treatment of LHON. Comprehensive Research Journal of Medicine and Medical Sciences. October 2013 1(2):18-23 Özet: Genetics and treatment of Leber' s hereditary optic neuropathy (LHON) Umur Ali Kayabasi World Eye Hospital, Istanbul, 34778 Turkey. E-mail: kayabasi@yahoo.com. Article History ABSTRACT Received 09 October, 2013 Received in revised form 17 October, 2013 Accepted 14 November, 2013 Key words: Leber's Hereditary Optic Neuropathy, Mitochondria, Genetics. Article Type: Review The current concepts about Leber's hereditary optic neuropathy (LHON) and mitochondrial connection are very difficult to understand completely. Even after twenty years of clinical studies, it is still difficult to completely explain how LHON mutations cause damage to the optic nerve or why particularly the optic nerve is at risk, and the information about mitochondria, the mitochondrial genome, the metabolism of the optic nerve and the phenotypic variability of LHON are still being discussed. We cannot fully explain the incomplete penetrance or the male predominance of LHON, the typical onset in young adults or the bilaterality of visual loss. Evidence points to abnormalities of the mitochondria as the direct or indirect cause of LHON. Primary LHON mutations definitely are not present in every family with the LHON phenotype and multigenerational maternal inheritance. They may be present in only a minority of patients with LHON phenotype without a clear family history. Therefore, the mitochondriaLHON connection needs to be examined more closely and understood better. This is a review that will attempt to provide an update on different aspects of LHON and current novel treatment options. ©2013 BluePen Journals Ltd. All rights reserved INTRODUCTION German ophthalmologist, Theodore Leber (1840-1917), described Leber' s hereditary optic neuropathy (LHON) for the first time (Puomila et al., 2007). LHON is one of the most common inherited optic neuropathies, with an approximate disease prevalence of 1 in 30,000 (Man et al., 2003). LHON is mostly detected between 15 and 35 years of age, but the range of onset can vary between childhood and over 60 years (Nikoskelanien et al., 1996; Howell, 1997). The age of onset is slightly higher in females (19-55 years, average being 31.3 years) than males (15-53 years, average being 24.3) (Leber, 1871; Howell, 1997). LHON affects mostly males, 80% of patients being male (Spruijt et al., 2007). There may be differences in male to female ratio between mutations: 3:1 for m.3460G>A, 6:1 for m.11778G>A and 8:1 for m.14484T>C. The cause of this predominance is still undetermined. Almost one in three cases have no definite family history (Man et al., 2003). Patients present with painless visual loss and both eyes become affected either simultaneously (25% of patients) or sequentially (75 36 36 A 0 B A- DERGİ Puan Puan Puan SCI ve SCIExp 3 / 1. kapsamındaki Yazar dergiler Kaynakça: Curr Opin Ophthalmol. 2012 Nov;23(6):477-84. doi: 10.1097/ICU.0b013e328358c7a6 Özet: Curr Opin Ophthalmol. 2012 Nov;23(6):477-84. doi: 10.1097/ICU.0b013e328358c7a6. Different ophthalmologic manifestations of sarcoidosis. Umur KA, Tayfun B, Oguzhan O. Author information Abstract PURPOSE OF REVIEW: Sarcoidosis can manifest with different ocular findings. Three different cases have been presented, each of which showed different ocular problems. The literature has also been reviewed as to find out other eye signs and treatment strategies of the disease. The diagnosis may be difficult and the treatment may include combination of different immunosuppressors. RECENT FINDINGS: Recent findings include a genetic basis, and certain human leukocyte antigens may affect the course of the disease. Sarcoidosis can influence the eye and the optic nerves in the beginning, and biopsy of the involved tissue may be necessary for the diagnosis. Laboratory investigation may be unyielding. Once the diagnosis is made, steroids are generally started. Other than the classical corticosteroid treatment, other immunosuppressive agents show promise in the atypical cases. SUMMARY: Our cases show different manifestations of the disease like bilateral optic neuropathy, Horner's syndrome, pars planitis, and anterior and posterior uveitis. Patients recovered with steroid treatment, but especially in young patients other agents like methotrexate were needed because of the sideeffects of steroids. PMID: 23014267 [PubMed - indexed for MEDLINE] ALZHEIMER’S DISEASE and LIPOFUSCIN HYPOTHESIS – Accepted for publication in the Next Section of ‘ La Prensa Medica Journal ‘. Summer 2014. Umur Kayabasi, MD World Eye Hospital - Istanbul kayabasi at yahoo.com Professor Robert C. Sergott, MD Wills Eye Hospital -Philadelphia rcs220 at comcast.net Key Words: Curcumin ; FAF ; OCT; Alzheimer’s Disease ABSTRACT: Objective: To demonstrate curcumin’s affinity for AD plaques in retina. Methods: We examined 40 patients with a family history of AD and/or mild cognitive defects. In the patients in whom we found hyper or hypofluorescent lesions on FAF, OCT was performed through these regions to reveal depositions in the retina. Drusen like spots- dots were noticed in different parts of the retina. All the patients were given curcumin to check for the changes in FAF and OCT. Also, 20 age matched healthy controls were examined. Results: In 32 patiens, we were able to find abnormal deposits in different retinal layers. We believe that these plaque-like lesions are related to neuro- degenerative disease (AD). Curcumin caused patchy hypofluorescent FAF to occur and spots seemed brighter on OCT. Conclusion: We proved that curcumin binds to plaques in retina. This finding may be very important for the early diagnosis of AD. The effects of curcumin on AD plaques need to be examined in detail to find out whether it can shrink these plaques. Journal of Functional Foods in Health and Disease , May 2014 CURCUMIN AS A BIOACTIVE COMPOUND IN ALZHEIMER’S DISEASE Umur Kayabasi, MD World Eye Hospital - Istanbul kayabasi at yahoo.com Professor Robert C. Sergott, MD Wills Eye Hospital -Philadelphia rcs220 at comcast.net Key Words: Curcumin ; FAF ; OCT; Alzheimer’s Disease European Journal of Neurology : Congress abstracts, June, 2014 Retinal plaques in Alzheimer’s disease U.A. Kayabasi1, R.C. Sergott2 1Neuro-Ophthalmology, Dunya Goz Hospital, Istanbul, Turkey, 2Neuro-Ophthalmology, Wills Eye Institute, Philadelphia, PA, United States Objectives: To evaluate the existence of pathologic retinal deposits in patients with possible Alzheimer’s Disease (AD). Methods: We examined 20 patients with mild cognitive impairment, 10 of whom had family history of AD. Also, 10 patients with no complaints were examined. The age range was between 45 and 86. We performed fundus autofluorescence (FAF) test and optical scanning tomography (OCT) test on all of them. The retinal regions with hypofluorescent and hyperfluorescent images were taken into consideration and OCT was also performed through these lesions to detect the layer of the abnormality. Patients with diabetic retinopathy and vascular occlusions were excluded. Results: In 16 patients with mild cognitive defects we were able to find abnormal accumulations in the ganglion layer and nerve fiber layer. Some of the accumulations were hypofluorescent and others were hyperfluorescent on FAF. In the other group of patients who had no complaints , only drusen on the pigment epithelium layer could be seen. Conclusions: We believe that abnormal retinal deposits (possibly containing beta amyloid protein ) can be observed in the ganglion and retinal fiber layers in patients who have high risk for AD. Retinal examination can be very helpful in the evaluation of these patients. Disclosure: Nothing to disclose. NeuroTherapeutics – Dilemmas, Debates, Discussions (DDDN) Accepted to be published in September 2014. RETINA EXAMINATION WITH CURCUMIN FOR THE DIAGNOSIS OF ALZHEIMER’S DISEASE Umur A. Kayabasi 1,*Robert C. Sergott 2 1Neuro- ophthalmology, Istanbul Medical Faculty, Istanbul, Turkey, 2Neuro- ophthalmology, Wills Eye, Philadelphia, United States. Problem statement: To demonstrate Alzheimer’s (AD) plaques in retina .It has been suggested that Beta amyloid starts to accumulate in the retina even before it affects the brain. Some studies even showed amyloid depositions in regions close to age related macular degeneration(AMD) lesions. Methods: Methods We examined 25 patients with a family history of AD and/or mild cognitive defects. All the patients were given oral curcumin for three days before the exam. In the patients in whom we found hyper or hypofluorescent lesions on fundus autofluorescence (FAF), optical coherence tomography (OCT) was performed through these regions to reveal depositions in the ganglion and nerve fiber layers. None of thepatients had retinal vascular disease due to hypertension or diabetes mellitus ; only drusen like spots- dots were noticed in different parts of the retina. Defects on RPE were not taken into consideration so that AMD lesions Conclusion: We stress that all the middle- aged patients who have family history of AD should have thorough medical examinations and retina investigation may be a part of the exam. This is the first study in which AD plaques were shown in the retinas of alive AD patients with FDA approved devices. Disclosure of Interest: None Declared B - KİTAP / E-KİTAP 40 Puan 40 A Puan 0B Puan Orjinal, Türkçe BKİTAP 1 / 1. / EYazar KİTAP Başlık: OCT ve FAF' ın Nörolojik Hastalıklardaki Önemi. Özet: DunyaGoz- Medical Tribune ortak yayın. 40 Puan 40 A Puan 0B Puan Orjinal BKİTAP 1 / 1. / EYazar KİTAP Başlık: Optik Nöropatiler Özet: Dunya Goz Yayınları. 25 Puan 25 A Puan 0B Puan Orjinal, Türkçe BKİTAP 1 / 1. / EYazar KİTAP Başlık: MS ve optik nöropatiler. Özet: Dünya Göz: Göz Hastalıkları Nöro-oftalmoloji chapter'ı. 25 Puan 25 A Puan 0B Puan Çeviri Başlık: Non-organik hastalıklar Özet: Walsh ve Hoyt Esaslar SERBEST SUNU KABULLERİ My Schedule Friday - 12 September 2014 Free paper BKİTAP 1 / 1. / EYazar KİTAP Session ID Title Room Start Time End Time Main Session Start Main Session End FP2751 Retina examination with examination with curcumin for the diagnosis of Alzheimer's disease Boulevard C. 17:42 17:50 16:30 18:00 © 2014 EURETINA Rome - December 12 -13, 2014 International Congress on "En Face" OCT imaging New Developments in OCT, OCT Angiography 13.30 – 14.30 LUNCH BREAK Audrey Giocanti (Paris, France) - Predictive value of outer retina “En face” OCT imaging in geographic atrophy progression Anita Leys (Leuven, Belgium) - “En face” OCT in familial pattern dystrophy Thomas Jouffroy (Paris, France) - "En face" imaging in retinal detachment Andrea Sodi (Florence, Italy) - “En face” OCT in Stargardt disease Claire Scemama(Paris, France) - OCT “En face” in choroidal focal folds Amani Fawzi (Chicago, USA) - “En face” to predict vision after recovery in uveitic CME Umur A. Kayabasi (Istanbul, Turkey), Robert C. Sergott (Philadelphia, USA) - Differential diagnosis of Alzheimer’s disease by OCT-FAF Ioannis Theocharis (Athens, Greece) – “En face” 3D-SDOCT images and the saltmarshes sign C - EĞİTİM VE DİPLOMALAR 50 Puan 10 A Puan 0B Puan C- EĞİTİM VE DİPLOMALAR Wills Eye. 2005 C- EĞİTİM VE DİPLOMALAR Michigan State University 1995 Detay: Fellowship Başlık: Adjustable sutures. 50 Puan 10 A Puan 0B Puan Detay: NO Clinical Fellowship Başlık: MRI in NO. ESKİ YAYINLAR: Yurtdışı : Eggenberger E, Kayabaşı AU. Hering’ s law for the Neurology: November, 1996 ; 55 ( 11 ) : 1105- 08. eyelids. Manrique C, Kayabaşı U, Varadarajan J et al. MRI enhancement of the optic nerve. Journal of N- O, December 1997 ; 17 ( 4 ) : 240- 2. Kayabaşı U, Eggenberger E. Lid signs in Miller- Fisher syndrome. Neurology, 2000 ; 54 : 2039- 2042. Yurtiçi yayınlar: Kayabaşı U, Kaufman D. Temporal kresent defekti. Türk oftalmoloji gazetesi 2003; 33 ( 5 ) : 682- 685. Kayabaşı U, Kandemir B, Doğan ÖK . Tolosa- Hunt sendromu. Türk oftalmoloji gazetesi 2004 ; 34 (4 ) : 413- 416. 1997-2012 arasında, Türk oftalmoloji derneği kongre toplantılarında, poster sunumları ve panel konuşmaları. ve D2 – TOPLANTILARDA BİLİMSEL FAALİYETLER 3,6 Puan 0,72 A 2,88 B - Sözel Dunyagoz Noro-oftalmoloji 2012 Puan Puan sunum 1 / 1. Yazar Başlık: Non-organik gorme kaybı Özet: www.dunyagoz.com Oturum Başkanı 1,5 0,3 A 1,2 B (Konferans Dunyagoz Noro-oftalmoloji Puan Puan Puan ve bildiri seansları) / 0. Yazar Başlık: Diplopi Özet: www.dunyagoz.com 11,4 Puan 2,28 A 9,12 B - Sözel 1.retina gunleri Aralık 2013 Puan Puan sunum 2 / 1. Yazar Başlık: Alzheimer H.da FAF ve OCT Özet: www.todnet.org 17,1 Puan 3,42 A 13,68 - Sözel International OCT en face, Rome Puan B Puan sunum Başlık: OCT in AD. Özet: www.symposiacongressi.eu 2 / 1. Yazar E - ÖDÜLLER 20 Puan 4A Puan 16 B Puan E- ÖDÜLLER Kızılay Dernegi odulu 1997 Detay: 1997 Kızılay Uluslararası NO Kongresi Adres: www.kizilay.com.tr Akademik Unvan: Klinik Nöro-oftalmoloji Fellowship - Michigan State UniversityWills Eye Hospital. Ameliyat tecrübesi: Intravitreal Enjeksiyon ( 5 yıldır yapılıyor. ) Extraorbital kas Botox Enjek. ( 3 yıldır yapılıyor ) DGH çalışma süresi: 4 yıl