Luetic papilledema

Although luetic ocular changes are rarely seen today they should not be neglected in differential diagnosis. Luetic papilledema is extremely rare and neurologic symptoms may be minor. A clinically observed case is described.     

Optic nerve axoplasm and papilledema

A detailed review of optic nerve axoplasm is presented. A number of hypotheses have been postulated for the pathogenesis of papilledema associated with increased intracranial pressure. These hypotheses, mechanical and nonmechanical, are critically evaluated in relation to five essential features of papilledema. Theories, as well as clinical and experimental studies, of axonal transport are reviewed, and a new hypothesis is proposed: Papilledema is primarily a mechanical, nonvascular phenomenon in which an excess amount of extracellular fluid is present in the prelaminar region ofthe optic disc and the accumulation of that fluid results from the leakage of axoplasm from optic nerve fibers which are compressed posterior to the lamina cribrosa of the optic disc. The authors believe that this is the only existing hypothesis consistent with all the known facts about papilledema. Discussions by Drs. J. Terry Ernest, Thomas R. Hedges, and S. S. Hayreh follow the review.     

抗磷脂综合征表现为视乳头水肿1例

目的:报告1例罕见抗磷脂综合征的患者,由于上矢状窦血栓形成而表现为双眼视乳头水肿及右眼第六颅神经麻痹,经抗凝和乙酰唑胺治疗后视乳头水肿恢复。方法:病例报告:一44岁中国男性,主诉为头痛、复视及轻度的视物模糊。临床检查发现右眼第6神经麻痹和双眼视乳头水肿,双眼视野盲点扩大和红绿色觉缺失,计算机断层摄影及核磁共振扫描显示上矢状窦血栓形成,血液学检查证实抗磷脂综合征是其潜在原因。结果:在联合应用抗凝和口服乙酰唑胺治疗3mo后,视乳头水肿恢复至正常的解剖,扩大的视野盲点降至正常水平,双眼红绿色觉恢复正常,伴随右眼视乳头水肿消退和视力改善表明这个患者视功能得以恢复。结论:抗磷脂综合征应与视乳头水肿鉴别诊断;对于顽固性的视乳头水肿,口服乙酰唑胺是抗凝治疗的重要辅助治疗,它可以保护视神经免受有可能导致失明后果的视神经损害。     

Evaluation and treatment of papilledema in pregnancy

Papilledema is defined as optic disk edema that is secondary to increased intracranial pressure. During pregnancy, papilledema poses additional diagnostic and therapeutic challenges. As in the nonpregnant patient, the primary goal is to urgently determine the cause of the papilledema followed by implementing appropriate management for life-threatening conditions in a timely fashion while safeguarding the fetus. Papilledema may occur also in conditions that are not life threatening; in either case, papilledema may cause visual failure. We describe the two most common causes of papilledema during pregnancy, idiopathic intracranial hypertension and cerebral venous thrombosis. In the former, there is no threat to life, while in the latter, depending on the extent of the cerebral venous thrombosis, life-threatening medical issues may dominate the picture. In these conditions, attention to the prevention of visual failure is of major importance; however, treatment options may need to be modified to safeguard the developing fetus. In this article, we review the current diagnostic and treatment options for patients with papilledema, emphasizing special considerations for the pregnant patient, including a chart to help the clinician differentiate between the different conditions causing papilledema. A flow chart suggests an approach as to how to monitor vision function and steps to take to prevent visual loss in these conditions causing papilledema. Drugs that may be considered in the management of papilledema are reviewed, and the FDA information regarding their safety for the fetus is provided.     

Sudden papilledema of unclear origin

A 44-year-old patient with a known history of Crohn??s disease come to our clinic with unilateral vision impairment, orbital pain, and papillary swelling. The patient was treated with methylprednisolone for 5?days. Differential diagnosis excluded ischemic, inflammatory, and tumor-related causes of the papillary swelling, which was more likely to be due to papillitis associated with the known presence of Crohn??s disease. Under steroid treatment visual acuity increased from 0.1 to 0.5, and an evident improvement of the ophthalmological and neurological findings was observed. Papillitis in conjunction with Crohn??s disease is a rare cause of papillary swelling and should be taken into consideration during differential diagnosis. The disorder responds to steroid therapy but does not avoid irreversible damage.