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By: Z. Surus, M.S., Ph.D.
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Decreased acuity, impaired color perception, an altitudinal field defect, usually inferior, and pallid disc edema are the typical findings acutely; evolving subsequently into optic atrophy. A history of headache, jaw claudication, malaise, weight loss, arthralgias and myalgias, and scalp tenderness is very suspicious. Predictive physical findings included temporal artery beading, prominence and tenderness; the absence of any temporal artery abnormality was the only clinical factor that modestly reduced the likelihood of disease. Involvement of the opposite eye occurs in approximately 15% ofPthomegroup patients within 5 years. While no treatment affects the outcome in the involved eye, recognition and management of underlying vasculitis may prevent a future attack in the opposite eye. Some cases are due to impaired microvascular perfusion related to system hypotension or increased intraocular pressure. There is a syndrome of posterior ischemic optic neuropathy, lacking disc edema, but it is rare and much less well defined than the anterior ischemic syndromes. Other Optic Neuropathies Numerous other conditions may affect the optic nerve head, causing visual loss and disc abnormalities. Dysthyroid optic neuropathy occurs as a late complication of thyroid orbitopathy when enlarged ocular muscles compress the nerve at the orbital apex. One characteristic feature of compressive optic neuropathy is that the condition continues to progress, often insidiously. Large, abnormal-appearing veins on the disc surface due to collateral venous drainage between the retinal and ciliary venous systems (optociliary shunt vessels) may provide a telltale clue to a compressive lesion. The triad of progressive visual loss, optic atrophy, and optociliary shunt vessels is highly suggestive. Pseudopapilledema Some conditions affecting the nerve head cause striking disc changes of little or no clinical import. This circumstance arises frequently when routine ophthalmoscopy unexpectedly reveals an abnormal- appearing disc in a patient with migraine or some seemingly benign neurologic complaint. Common causes of pseudopapilledema include optic nerve drusen and myelinated nerve fibers. Optic nerve drusen, or hyaloid bodies, are acellular, calcified hyaline deposits within the optic nerve that may elevate and distort the disc (Figure 13. They are familial, inherited as an irregular dominant with incomplete penetrance, and occur almost exclusively in Caucasians. But when buried beneath the surface, drusen may produce only disc elevation and blurred margins, causing confusion with papilledema. Optic nerve drusen are not to be confused with retinal drusen, which are an age-related abnormality consisting of yellowish-white, round spots of variable size concentrated at the posterior pole. Myelinated nerve fibers occasionally extend beyond the disc margin into the retina, which causes a very striking disc picture but signifies nothing (Figure 13.
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Therefore, it is not surprising that these quently deposition of type 1 collagen, most likely via repres- disorders as a result of diabetes are named complications, sion of Smad7 signaling (107). Indeed, Indeed, we have a difficult task ahead to address the current more research should be targeted toward elucidating the and future disease burden of these predominantly vascular initial functional and structural patterns altered by the in- complications. Diligent control of glycemia and blood pres- evitable but common changes in glucose uptake and traf- sure (693) have stabilized the level of morbidity and mor- ficking that occur at sites of diabetes complications. Hence, (203, 454) and may in fact increase the risk of adverse identification of why certain persons with diabetes progress events (695). In particular, the concern is that a vast number to complications whereas others remain remarkably resis- of new cases of diabetes are now originating from develop- tant to developing these vascular disorders is of paramount ing nations (129), and hence, it is likely that less stringent importance. This puzzle is likely to be solved using the management in these nations due to resource issues may combined approaches of genetics, epidemiology, physiol- result in a greater incidence of vascular complications ogy, and biochemistry. Association of estimated glomerular filtration rate, and albuminuria with all-cause and seen within animal models, however, must be interpreted cardiovascular mortality in general population cohorts: a collaborative meta-analysis. Effect of intensive blood-glucose control with metformin on complications in over- weight patients with type 2 diabetes (U. Tight blood pressure control, and risk of macrovascular and microvascular complica- nal impairment seems a worthwhile strategy, since this is a tions in type 2 diabetes: U. Four-weekadministrationofnimesulide,acyclo- oxygenase-2inhibitor,improvesendothelialdysfunctioninthehindlimbvasculatureof shown reduced efficacy of the various interventions, once streptozotocin-induced diabetic rats. Long-term administration of the histone deacetylase inhibi- type 2 diabetes who have inadequate glycaemic control with metformin: a ran- tor vorinostat attenuates renal injury in experimental diabetes through an endothelial domised, double-blind, placebo-controlled trial. Drug intervention can correct subnormal retinal oxygenation response in exper- Diminished superoxide generation is associated with respiratory chain dysfunction imental diabetic retinopathy. Cardiovascular outcomes in the Irbesartan Diabetic Ne- closureusingtheAmplatzerseptaloccluder:riskfactorsandrecommendations. A double-blind, randomized, placebo-controlled clinical trial on benfotiamine treatment in patients with diabetic 41. Bianchi R, Buyukakilli B, Brines M, Savino C, Cavaletti G, Oggioni N, Lauria G, Borgna 23. Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 43. Cholesterol-independent effects of statins in infiam- Luther T, Henle T, Kloting I, Morcos M, Hofmann M, Tritschler H, Weigle B, Kasper mation,immunomodulationandatherosclerosis. Diabetes-associated sustained activation of the transcription factor nuclear factor- kappaB.
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Further thanks go to my heads at Uppsala University Hospital, Marianne Christensen and Eva Sandin, who released me from my clinical duties and with enthusiasm supported my choice for further education. Our monthly meetings, your encouraging questions and comments, your precious help 85 with finding suitable study participants, and your own participation in a pilot study have been of unspeakable value. In addition, I would like to thank all the rest of my colleagues and fellow workers at the Departments of Regional Logopedics and Rehabilitation Medicine at Uppsala University Hospital for your interest in my work and encouraging comments. Speaking of colleagues, a special thanks to all my speech-language pa- thologist colleagues throughout Sweden who assisted me in distributing questionnaires to significant others of your patients with aphasia. Thank you very much also for collegial support and joy during national and interna- tional conferences and courses. In particular, I want to mention Eva Tures- son Muhrman and Maryse Poisson to whom I felt especially close. Special thanks go to Eric Lindstrom and Rebecka Jakobsson, who assisted with assessments of video-recorded conversations. I also received much help with recruitment of study participants and inter- view arrangements from the Stockholm Aphasia Association. I would also like to thank Karin Sagren at the Uppsala Aphasia Associa- tion who was most helpful during the preparation of study I. I also thank all of you at different local aphasia associations who helped with the distribution of questionnaires to significant others of persons with aphasia: Magnus Gustafsson, Lisbeth Nilsson, Hildur Lindqvist, Torgny Wahrenberg and Ellinor Berntsson. I would like to express my gratitude to all the members of the research group Disability and Habilitation at the Department of Public Health and Caring Sciences at Uppsala University: Karin Sonnander, Helena Lindstedt, Oie Umb-Carlsson, Mia Pless, Gerth Hedov, Kjerstin Larsson, Gunilla Eriksson, Helene Lidstrom, Gunnel Janeslatt, Johan Glad, Annika Terner and, most recently, Helena Wandin. Your knowledge and support and patient correc- tions of my repeated errors have been of immense value. Thank you for your patience, your generous sharing of knowledge, and for never letting me feel inferior to you! Most of all, I want to thank Johan and Annika, my fellow PhD students in the research group. I would also like to thank Paivi Adolfsson and Karin Joreskog at the Cen- tre for Disability Research at Uppsala University who are situated in the 86 room next to me. Thanks for your friendship, laughs, celebrations, offered cookies, washing nuts, and our wonderful daily chats! The administrative staffs at the Department of Public Health and Caring Sciences at Uppsala University have been extremely helpful. I especially want to mention Catarina Olsson, Hakan Jansson, Soren Jonasson, Rose- Marie Marcusson, Karin Torbratt, and Helene Eriksson. You have always been there when computers and other technical devices caused problems or when incomprehensible forms needed to be completed. Always with a smile, you have been of help when I disturbed you with yet another question.
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