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Show STATE OF THE ART Vasculopathies Affecting the Eye Judith E. A. Warner, MD Abstract: The retinal arteries and veins may be involved in isolation or as the result of a systemic vasculitis. This article emphasizes neurologic diseases in which the ocular vasculature is affected. ( JNeuro- Ophthalmol 2004; 24: 164- 169) Vasculopathies that involve the eye may be the result of infectious, hereditary, inflammatory, neoplastic, hypoxic/ ischemic, or idiopathic disorders. In some cases, the vasculopathies are isolated to the eye; in other cases, the involvement is system- wide ( Table 1). INFECTIOUS VASCULOPATHIES In most infectious vasculopathies, the association between infection and vasculopathy is speculative. There are few ophthalmoscopic features of the infectious or parainfectious retinal vasculitides that enable distinction. History and laboratory testing are usually necessary to confirm a diagnosis. Human immunodeficiency virus ( HlV)- associated vasculopathy is often included among infectious vasculopathies but its vascular manifestations may not be mediated by infection. Patients are usually asymptomatic but may have color or contrast sensitivity deficits. On routine examination, they are found to have cotton- wool spots and intra-retinal hemorrhages in the posterior pole, believed to be a manifestation of microvasculopathy of the retina. The cotton- wool spots differ from those seen in diabetes in being more linear, often taking on a boomerang shape ( 1) ( Fig. 1). Lesions resolve spontaneously, usually within two months ( 2). Although the prevalence of HIV- associated vasculopathy increases with decreasing CD4 counts, it can be seen in Department of Ophthalmology and Visual Sciences, University of Utah Health Sciences Center, Salt Lake City, Utah. Address correspondence to Judith E. A. Warner, Department of Ophthalmology and Visual Sciences, John A. Moran Eye Center, 50 North Medical Drive, Salt Lake City, UT 84132; E- mail: Judith. warner@ hsc. utah. edu Supported in part by a grant from Research to Prevent Blindness, Inc., New York, New York, to the Department of Ophthalmology and Visual Sciences, University of Utah. Modified from an oral presentation delivered at the 28th Annual Meeting of the North American Neuro- Ophfhalmology Society, Copper Mountain, Colorado, February 12, 2002. patients whose counts are more than 100 cells/ mm3, a level at which cytomegalovirus ( CMV) retinitis is unlikely. Therefore, the practice in HIV centers is to perform repeated examination on patients who have cotton- wool spots and CD4 counts more than 100 cells/ mm3 ( 3). If the abnormal fundus findings are a result of CMV retinitis, they will worsen within two to three weeks. If they are caused by HIV- associated vasculopathy, the original cotton- wool spots will resolve, although new spots may develop. HIV- associated vasculopathy may be related to the propensity of the virus to infect endothelial cells. Elevated levels of endothelin- 1 immunoreactivity have been found, possibly causing vasoconstrictor activity ( 4). One interesting study ( 5) correlated the presence of HIV- associated retinal vasculopathy with HMPAO- SPECT evidence of reduced cerebral perfusion. The association was not correlated with acquired immune deficiency syndrome staging. The authors speculated that this reduced perfusion might explain neuropsychologic abnormalities experienced by patients with HIV- 1 disease ( 5). When hemorrhages are extensive, anemia should be considered an explanation for the cotton- wool spots. HEREDITARY VASCULOPATHIES In 1988, Grand et al ( 6) described a kindred of patients with variable expression of an inherited cerebroreti-nal vasculopathy. These patients had subtle changes of the vasculature of the posterior pole most suggestive of parafoveal telangiectasia. Vision was relatively preserved, although preretinal hemorrhages occurred late in the disease. On fluorescein angiography, the foveal avascular zone was enlarged with capillary obliteration. Pathologically, there were multiple scattered microinfarctions, but no abnormalities of the retinal capillaries were discovered. Of 18 presumably affected individuals, 10 had brain masses, eight in the frontoparietal region. The masses were typically confined to the white matter and were histologically characterized by vascular abnormalities and coagulation necrosis. The vascular abnormalities were found in the medium and small arteries, and consisted of fibrinoid necrosis of vessel walls. Perivascular adventitial fibrosis was prominent. Since 1988, several cases have been described with similar features ( 7,8). In most cases, a familial feature is evident. 164 J Neuro- Ophthalmol, Vol. 24, No. 2, 2004 Vasculopathies Affecting the Eye JNeuro- Ophthalmol, Vol. 24, No. 2, 2004 FIG. 1. HIV- associated vasculopathy. Note the boomerang- shaped cotton- wool spots. ( Courtesy of Paul Zimmerman, MD.) In 1997, Jen et al ( 9) described a family with hereditary endotheliopathy including retinopathy ( Fig. 2), nephropathy, and stroke. In 1998, a Dutch family with hereditary vascular retinopathy associated with Raynaud phenomenon and migraine was described by Terwindt et al ( 10). In 2001, Ophoff et al ( 11) were able to show that these three disparate families had linkage to chromosome 3p21.1- 21.3. Of the various features of the three diseases, the retinopathy was most tightly linked to the same region. Further elucidation of the gene and its encoded protein may be very interesting. INFLAMMATORY VASCULOPATHIES Inflammatory choriocapillaropathies such as multiple evanescent white dot syndrome, acute posterior multifocal placoid pigment epitheliopathy ( APMPPE), multifocal choroiditis, and acute idiopathic blind spot enlargement all manifest focal areas of retinal dysfunction and a weak correlation between funduscopic abnormalities and visual dysfunction. Some observers believe that areas of hy-pofluorescence seen on indocyanine green angiography suggest a vascular abnormality in the choroidal circulation ( 12). In some cases, fluorescein angiography shows retinal vascular staining consistent with vasculitis. APMPPE has been reported in several patients who also have Wegener granulomatosis ( 13) or other autoimmune diseases. APMPPE has also been frequently associated with central nervous system manifestations, including headache, vasculitis, stroke, and sagittal sinus thrombosis ( 14,15). There is a case report of a young woman who developed bilateral central retinal vein occlusions one month after presentation with APMPPE ( 16). Retinal venous sheathing is an infrequent but well-recognized phenomenon in multiple sclerosis ( MS). A careful study from Liverpool in 1996 ( 17) documented the course of retinal venous sheathing in 23 patients with MS folio wed- up over six months. Six of the patients had venous abnormalities, including diffuse or focal sheathing or focal perivenous hemorrhages. One patient had arterial sheathing. For the most part, the venous sheathing/ staining was static over six months, despite ongoing disease activity on enhanced magnetic resonance imaging ( MRI) scans. Two patients showed resolution of retinal angiographic fluorescein leakage over the course of the study. The relationship between retinal vascular abnormalities and the disease course of MS remains to be elucidated. NEOPLASTIC VASCULOPATHIES Neoplasms and their treatments are notorious for producing vasculopathies via hypercoagulable states, radiation injury, or toxic chemotherapeutic regimens. Mild microvascular occlusive changes are seen commonly in association with leukemia. Plasma cell dyscrasias such as multiple myeloma, Waldenstrom macroglobulinemia, and systemic amyloidosis are associated with a variety of ophthalmic manifestations. There is an interesting report ( 18) of a plasma cell dyscrasia resulting in systemic deposition of light chains in the kidney and the eye. In this case, the patient presented with constitutional symptoms, bilateral recent carpal tunnel surgery, and severe retinal nonperfusion. The patient had bilateral intraretinal hemorrhages, cottonwool spots, and neovascularization of the discs. Fluorescein angiography showed capillary nonperfusion, but no venous stasis was reported. Specific staining for light chains revealed extensive deposition in the blood vessels of various biopsy specimens. Testing for hyperviscosity, including cryoglobulins, cryofibrinogen, quantitative immunoglobulins, and serum viscosity, was negative. The well- described carcinoma- associated retinopathy ( CAR) and melanoma- associated retinopathy ( MAR) frequently show severe retinal vascular attenuation. There have been several reports of presumed paraneoplastic retinopathies with diffuse retinal vessel staining on fluorescein angiography, particularly involving veins ( 19,20). Although treatment with corticosteroids resulted in improvement in the vasculitic features, there was no improvement in vision. One patient had melanoma- associated retinal bipolar cell antibodies in his IgG serum fractions ( 19); the other patient had small cell lung cancer and serum reactivity to the 62kd ( rather than the typical 23kd) band of bovine retinal homogenate ( 20). Retinal vasculitis is rare in the CAR/ MAR syndromes, and its presence does not seem to be the major pathologic change. However, vasculitis as a neoplastic and paraneoplastic phenomenon occurs in a wide variety of cancers. 165 JNeuro- Ophthalmol, Vol. 24, No. 2, 2004 Warner TABLE 1. Vasculopathies affecting the eye Hereditary Retinitis pigmentosa- associated ( 28) Cerebroretinal vasculopathy with brain masses ( Grand syndrome) ( 6,7,8) Hereditary endotheliopathy with retinopathy, nephropathy, and stroke ( HERNS) ( 9) Hereditary vascular retinopathy with migraine and Raynaud phenomenon ( 10) Inherited retinal arteriolar tortuosity ( 29) Amyloidosis ( 30) Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy CADASIL ( 31) Inflammatory Birdshot retinochoroidopathy ( 32) Sarcoidosis ( 33) Multiple sclerosis ( 17) Multiple evanescent white dot syndrome Acute posterior multifocal placoid pigment epitheliopathy ( 14,15) Acute idiopathic blind spot enlargement ( 34) Behcet disease ( 35,36) Wegener granulomatosis ( 13) Inflammatory bowel disease ( 37,38) Giant cell arteritis ( 39) Systemic lupus erythematosus ( 40) Rheumatoid arthritis ( 41,42) Polyarteritis nodosa ( 43) Churg- Strauss syndrome ( 44,45) Infectious Human immunodeficiency virus ( 1- 5) Herpes viruses Progressive outer retinal necrosis ( 46,47) Vasculopathy of herpes zoster ophthalmicus ( 48) Tuberculosis ( 49) Lyme disease ( 50) Cat- scratch disease ( 51) Leptospirosis ( 52) Cytomegalovirus ( 53,54) Cryptococcosis ( 55) Rubella ( 56) Measles/ SSPE ( 57) Wuchereria bancrofti ( filariasis) ( 58) Neoplastic Acute lymphocytic leukemia ( 59) Hairy cell leukemia ( 60) Systemic light chain disease ( 18) Hyperimmunoglobulin D ( 61) Carcinoma- associated retinopathy ( 20) Melanoma- associated retinopathy ( 19) 166 TABLE 1. Continued Hypoxic/ Ischemic Ocular ischemic syndrome ( 62,63) Exfoliation syndrome ( 21,64) Takayasu arteritis ( 65,66) Toxic Ergot alkaloids ( 67) Cranial/ orbital irradiation ( 68,69) Idiopathic Eales disease ( 27) Idiopathic polypoidal choroidal vasculopathy ( 70) Idiopathic retinal vasculitis, aneurysms, and neuro- retinitis ( 71) Parafoveal telangiectasia ( 72) Idiopathic recurrent branch retinal artery occlusions ( 26) Susac syndrome ( 22- 25) HYPOXIC/ ISCHEMIC VASCULOPATHIES Neovascularization is an abnormal vascular proliferation in response to hypoxia. It is a well- recognized late effect of ocular ischemic syndrome caused by carotid disease, diabetes, hypertension, or after central retinal vein occlusion. Neovascular vessels can occur in various structures of the eye, including retina, optic nerve head, and iris. Iris vasculopathy is a feature of exfoliation syndrome. In this case, the stimulus for micro- neovascularization appears to be deposition of exfoliation material in vessels progressing from the adventitia to the endothelium, resulting in obliteration of the lumen and consequent anterior chamber hypoxia ( 21). IDIOPATHIC VASCULOPATHIES Among the idiopathic vasculopathies is Susac syndrome, or retinocochleocerebral microangiopathy of the brain and retina. Originally reported by Susac in 1979 ( 22), and later elaborated by O'Halloran ( 23), among others, it is a perplexing condition typically affecting young women. Patients have multiple, usually bilateral, branch retinal artery occlusions ( Fig. 3), hearing loss attributed to cochlear arterial occlusion, and central nervous system abnormalities characterized as encephalopathy, memory loss, and headache. MRIs usually show lesions within the corpus cal-losum and cerebral gray matter. The CSF shows elevated protein and often mononuclear cells. Brain biopsies have shown microinfarcts, some with evidence of perivascular inflammatory infiltrates. Petty et al ( 24) found sparse peri-arteriolar inflammatory cells on muscle biopsies in three of five patients. In one specimen, swollen vascular endothelium nearly occluded some small arterioles. The disease can remain active for several months to several years, and may remit spontaneously. However, a recently re- © 2004 Lippincott Williams & Wilkins Vasculopathies Affecting the Eye JNeuro- Ophthalmol, Vol. 24, No. 2, 2004 FIG. 2. Hereditary endotheliopathy including retinopathy, nephropathy, and stroke. Fluorescein angiogram shows parafoveal telangiectasia, microaneurysms, and capillary dropout. ( Courtesy of R. W. Baloh, MD.) ported case documented recrudescence after a hiatus of 18 years ( 25). In 1986, Gass et al ( 26) reported a small series of patients with idiopathic recurrent branch retinal artery occlusions. There were nine patients, seven of whom were men, with recurrent arterial occlusions, no uveitis, and in whom systemic evaluation was unrevealing. There was no evidence of embolic material. Again, the features on fluorescein angiography were retinal arterial/ venous staining with FIG. 3. Susac syndrome. Fluorescein angiogram shows multiple branch retinal artery occlusions. ( Courtesy of H. O'Halloran, MD.) FIG. 4. Eales disease. Fluorescein angiogram shows hyper-fluorescence of peripheral veins. ( Courtesy of Paul S. Bernstein, MD, PhD.) capillary non- perfusion. Three patients ( one woman and two men) had auditory complaints ( auditory hallucinations 1, tinnitus 2). Perhaps they represent a forme fruste of Susac syndrome. Eales disease is a noninflammatory occlusive disorder of the retinal vasculature that causes recurrent hemorrhages in the retina and vitreous and ischemic changes in the eye. Most patients are men in the fourth decade of life. 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