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Rev Neurol Dis. Author manuscript; available in PMC 2012 September 22.
Published in final edited form as: Rev Neurol Dis. 2011 ; 8(1-2): 1–9.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
Hypertension-related eye abnormalities and the risk of stroke
Amanda D. Henderson, M.D.(1), Beau B. Bruce, M.D., M.S.(1),(2), Nancy J. Newman, MD(1),(2), and Valérie Biousse, MD(1),(2) (1)Department of Ophthalmology, Emory University School of Medicine, Atlanta, Georgia
of Neurology, Emory University School of Medicine, Atlanta, Georgia of Neurological Surgery, Emory University School of Medicine, Atlanta, Georgia
Many studies have shown that hypertensive ocular funduscopic abnormalities are clearly related to stroke, even after controlling for level of blood pressure and other vascular risk factors. Retinal abnormalities indicative of a breakdown of the blood-retina barrier confer a greater increase in risk for stroke than sclerotic retinal changes. Similar retinal changes also have a positive relationship with stroke mortality. Hypertensive ocular fundus abnormalities are also reported to be associated with an increased risk for cognitive impairment, cerebral atrophy, progression of MRI-defined white matter lesions, and subclinical infarction. Recent advances in fundus photography allow for improved accuracy and consistency in interpretation of funduscopic lesions, and improve the feasibility of screening for these abnormalities in at-risk patient populations. Evaluating the ocular fundus for signs of hypertensive retinopathy, in combination with an assessment of the presence or absence of other known vascular risk factors, may allow clinicians to further individualize a risk profile for stroke to each individual patient, thus permitting more accurate risk stratification and, potentially, guiding treatment strategies.
Hypertension causes microvascular damage in both the cerebral and retinal circulations (1– 3). Because the retinal and cerebral vessels share embryological and anatomical characteristics, they also may show similar patterns of damage from diseases such as hypertension (3). Thus, it has long been suggested that examination of the ocular fundus could provide a noninvasive view of intracranial vascular pathology (2). Large populationbased studies have confirmed that standardized assessment of ocular fundus photographs provides reliable evaluation of retinal hypertensive abnormalities that have been correlated with a higher risk of cerebrovascular disease (Tables 1 and 2) (2,4–6). The retinal vessel pathology serves as an important marker for stratification of patients’ risk for having or developing cerebrovascular disease (2,4–6). Incorporation of these markers into risk stratification algorithms should enhance the ability to ensure appropriate clinical follow-up and treatment plans for each individual patient. To evaluate the potential value of retinal imaging as a tool to predict stroke risk, we describe the ocular effect of hypertension and review the reported associations between the ocular effects of hypertension and cerebrovascular disease.
Address correspondence to Dr. Valérie Biousse, Neuro-Ophthalmology Unit, Emory Eye Center, 1365-B Clifton Rd. NE, Atlanta, GA 30322. Phone: (404)778-5360. Fax: (404)778-4849. firstname.lastname@example.org. None of the authors have any conflict of interest.
microaneurysms. and increased tortuosity of arterioles. which manifest clinically as vessel attenuation. The most widely used scale for grading hypertensive retinopathy is the Keith. Retinal detachment also may occur in this phase. During this phase. central retinal artery or vein occlusion. often remain.3) (1. during the chronic reparative phase of hypertensive choroidopathy. and Barker classification. The chronic occlusive phase is characterized by extreme narrowing or occlusion of the choroidal capillaries and yellowing and leakage of the retinal pigment epithelium overlying the occluded regions. Page 2 Ocular effects of systemic hypertension Hypertension causes both acute and chronic ocular abnormalities. Degenerative retinal pigment epithelium lesions develop in the macula and peripheral retina and gradually become more extensive. with leakage of plasma and blood products into the vessel wall.Henderson et al. and the retina reattaches. which prevents certain vascular segments from narrowing. Hypertensive choroidopathy can be divided into three phases. The clinical fundus findings during this phase include white areas (a manifestation of retinal pigment epithelium necrosis). Author manuscript. which grades retinopathy from I to IV based on its severity (Table 3) (11). NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Hypertensive choroidopathy occurs as a result of choroidal ischemia.2. arterioles. The effects of this phase lead to many of the classic retinal signs associated with hypertensive retinopathy. Alternatively. This causes vessel dilation and eventual failure of autoregulation (Figure 3). . Severely elevated BP may lead to the exudative phase. available in PMC 2012 September 22. or nonspecific areas of mottling. in vessels with significant arteriosclerosis. hard exudates from the leakage of lipids. which develops because the choroidal vasculature does not possess the autoregulatory capacity of the retinal vasculature (1. boat-shaped hemorrhages. cystoid macular edema. In the vasoconstrictive phase. and vascular remodeling. Arteriovenous nicking describes narrowing of a venule as an arteriole crosses over it. and optic neuropathy (Figures 1. hyaline degeneration of the arteriolar wall. retinopathy. the retinal pigment epithelium heals. causing endothelial damage and disruption of the blood-retina barrier. These changes affect different areas of the eye. particularly in the central region of the macula. Chronic Elschnig spots. including macroaneurysms.7–10). appearing as hyperpigmented areas with surrounding atrophy. and intimal thickening. microaneurysms. and choriocapillaris are recanalized. The sclerotic phase of hypertensive retinopathy occurs in the presence of chronically elevated blood pressure and is characterized by hyperplasia of the tunica media. more focal arteriolar narrowing occurs. Retinal fluorescein angiography shows patches of hypoperfused choriocapillaris. epiretinal membrane formation. Rev Neurol Dis. leading to necrosis of the choriocapillaris and retinal pigment epithelium and the accumulation of exudates in the subretinal space. fluorescein angiography shows underlying choroidal fluorescence (Figure 1). Hypertensive retinopathy describes a spectrum of microvascular abnormalities in people with elevated blood pressure and may be divided into several phases. including flame-shaped hemorrhages in the nerve fiber layer of the retina. which manifests clinically as generalized retinal arteriolar narrowing. an acute rise in blood pressure causes the retinal vessels to increase their vascular tone. Sclerotic changes may lead to long-term complications. During the acute ischemic phase. choroidal arterioles constrict. Increased arteriolar light reflex refers to an increased light reflex from the central portion of the retinal arteriolar surface (Figures 1 and 2). which do not necessarily occur in the order described (1. arteriovenous nicking. Finally.7–10). and cotton wool spots that represent infarctions of the nerve fiber layer (Figure 2). dot and blot hemorrhages.7–10). increased arteriolar light reflex. the occluded choroidal arteries. and focal serous retinal detachment most often involving the macula and peripapillary region. producing three categories of hypertensive ocular change: choroidopathy. Wagener.
Page 3 Hypertensive optic neuropathy results from severely elevated blood pressure.13). With the advent of digital fundus cameras. eventually. although raised intracranial pressure is also posited to play a role. the retinal vasculature must be visualized either via funduscopy or photography. Author manuscript. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Evaluating the ocular effects of hypertension with retinal photography To evaluate hypertensive funduscopic damage. depending on the specific fundus abnormality being evaluated (20). Some blood vessels lose their endothelial cells and pericytes and only retain a basement membrane. Histologic studies showed that fibrous or fibro-hyalinoid thickenings of the retinal arteries near the optic disc reflect intracerebral arterial abnormalities. Several studies show that the use of fundus photography results in more accurate documentation of the signs of retinopathy in the general population. and myelinated axons largely disappear from the retrolaminar optic nerve. confirmed by CT scan (21). vasoconstriction in the prelaminar optic nerve leads to axonal hydropic swelling. chronic optic nerve swelling is progressively replaced by optic atrophy (Figure 3). fundus photography may require pharmacologic pupillary dilation or not. dilated fundus photography may produce higher quality photographs in some patients. Our group recently reported similar findings. Clinically. Depending on the camera used. and only 3% of patients having no photographs of diagnostic value (19). 81% of fundus photographs were deemed adequate for a retinal examination (18). The percentage of patients with a quality dilated fundus photograph in at least one eye ranged from 92% to 98% in the Blue Mountains Eye Study (BMES). lower central retinal artery end-diastolic and mean velocities and higher central retinal artery resistive indices and pulsatility have been associated with cerebral small vessel disease (22). However. degeneration of pericytes. axolemma disruption. Degeneration of endothelial cells and pericytes is evident.Henderson et al. In the atrophic phase. Ocular effects of systemic hypertension and stroke Diverse study types provide evidence for the association between ocular fundus changes and cerebrovascular disease. and glial swelling. In the retrolaminar optic nerve. Vasoconstriction is more severe in the retrolaminar region and leads to endothelial swelling. available in PMC 2012 September 22.7–10). Rev Neurol Dis. vacuolated axons and glial swelling. and. Computerassisted image analysis techniques can be used to make quantitative measurements and to characterize abnormalities of the retinal microvasculature (12. lipid-laden microglia are absent at this stage. This pathologic process occurs secondary to optic nerve ischemia. Additionally. When evaluating non-mydriatic fundus photography for the Atherosclerosis Risk in Communities (ARIC) study. . and is therefore less time consuming. Functional studies of the retinal vasculature show that prolonged retinal arteriovenous passage time is associated with lacunar infarction. Non-mydriatic photography is advantageous because it avoids pupillary dilation. and are associated with an increased risk of both cerebral hemorrhage and cerebral infarction (3). and can also be divided into three phases (Figure 3) (1. Axonal swelling in the prelaminar optic nerve is decreased during the resolution phase. with 83% of patients who had bilateral nonmydriatic fundus photography having a high quality photograph in at least one eye. Additionally. highresolution digital images are easily acquired and quality assessed instantly. axons of the prelaminar optic nerve are replaced by proliferated glial cells. During the acute ischemic phase. when compared with clinical ophthalmoscopy (14– 17). The use of fundus photography for the acquisition of retinal images is a valuable tool for the evaluation of hypertensive ocular changes in patients at risk for cerebrovascular disease (14). disintegrated myelinated axons and lipid-laden microglial cells are present.
but they are also related to stroke. the Cardiovascular Health Study (CHS) (16. in patients with hypertensive retinopathy (20). in the Rotterdam Eye Study. Not only are cerebral white matter lesions related to retinal hypertensive abnormalities. even after controlling for blood pressure (32–35). or retinopathy may be a marker for a more malignant form of cerebral white matter lesions. The BMES demonstrated a higher risk of combined stroke events (defined as incident stroke. using photographs to define retinopathy signs. arteriovenous nicking. these studies did not detect any relationship between retinal arteriolar diameter or focal arteriolar narrowing and cerebrovascular death (4.23–31). In the ARIC study. published in Japan during the 1970s through 1990s. after adjusting for vascular risk factors (27).26. Several studies have focused on the relationship between hypertensive retinopathy and abnormalities detected on brain imaging. Author manuscript. hypertensive retinopathy increased the risk of stroke two. More recent large population-based studies (Table 1). larger retinal venular diameter was associated with marked progression of periventricular white matter lesions and subcortical white matter lesions over time. relationships between other microvascular funduscopic findings and stroke have also been reported in the ARIC study (15. this relationship suggests that funduscopic examination or retinal photography is useful for risk stratification in patients with evidence of cerebral white matter lesions on MRI (34). soft exudates. These findings are consistent with the idea that retinal microvasculature abnormalities likely precede and are harbingers of the development of cerebral white matter lesions.32).to three-fold (23). although generally weaker. Regardless of the reason. focal arteriolar narrowing.24.34). The initial studies examining these relationships. and focal arteriolar narrowing have been associated with cerebral white matter lesions. however. and the Rotterdam Eye Study (17. Interestingly. In addition to subclinical and clinical stroke.20. decreased arteriovenous ratio.25).Henderson et al. the presence of both retinopathy and cerebral white matter lesions has shown a multiplicative effect on the risk for clinical stroke (33. However. . stroke mortality may be related to retinal hypertensive abnormalities. and larger retinal venular caliber have been shown to be associated with increased risk for stroke (4.28.18). blot hemorrhages. hypertensive ocular abnormalities predict stroke risk. transient ischemic attack or cerebrovascular death). flame-shaped hemorrhages. The presence of MRI-defined white matter lesions has been shown to be associated with an increased risk of incident clinical stroke. retinal vessel diameter was not related to the severity of cerebral small vessel disease. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Conclusion and future perspectives The presence of hypertensive funduscopic abnormalities is clearly related to stroke. have provided further support for some of the earlier findings that. reported associations between hypertensive funduscopic findings and subclinical and clinical stroke. Arteriovenous nicking. However. Significant. Retinal changes Rev Neurol Dis. which may have influenced the results (2).27). retinal arteriolar sclerosis. microaneurysms. even after controlling for blood pressure and other vascular risk factors (Table 2). This interaction between retinopathy and white matter lesions may have two possible explanations: microvascular pathology may be more severe in patients with both retinopathy and white matter lesions. even after controlling for level of blood pressure and other vascular risk factors. Retinopathy. The BMES and BDES reported a relationship between retinopathy and cerebrovascular death in patients without diabetes. available in PMC 2012 September 22. and. importantly. many of these studies did not control for blood pressure. Page 4 The strongest evidence supporting the use of hypertensive funduscopic findings in the stratification of patients at risk for cerebrovascular disease comes from longitudinal studies that evaluated the relationships between these ocular findings and cerebrovascular disease (Table 2).
. 73 and 74:57–70. Wang JJ. 1986. 1982. et al. 89:1132–1145. 1975. along with the assessment of the presence or absence of other known vascular risk factors. [PubMed: 19808533] 13. [PubMed: 15854064] 6. 2006. cardiovascular disease. Patton N. Arterial blood pressure. [PubMed: 17276782] 2. 2005. Wong TY. Fundus lesions in malignant hypertension. Ophthalmology. This would permit more accurate risk stratification and. 6:263–269. McIntosh R. Stroke. Mitchell P. KL2. Wasserman Merit Award. [PubMed: 15817102] Rev Neurol Dis. microaneurysms and cotton wool spots) seem to confer a greater increase in stroke risk than sclerotic retinal changes (such as generalized and focal retinal arteriolar narrowing and arteriovenous nicking). Ophthalmology. Some different types of essential hypertension: their course and prognosis. Baker ML. [PubMed: 3808599] 10. J Anat. available in PMC 2012 September 22. Lancet. Journal of clinical hypertension (Greenwich. With continuing improvement in retinal photographic techniques and retinal image analysis. References Only very few relevant articles to this review were selected in the list below (there are hundreds of excellent articles relating to this topic). VI. Barker NW. 2001. Wang JJ. 1986. 2005. Retinal vascular imaging: a new tool in microvascular disease research. Marcus DM. Bruce received the American Academy of Neurology Practice Research Fellowship. 2007. Dr. may allow clinicians to further individualize a risk profile for stroke for each patient. Evaluating for these retinal signs. UL1RR025008 (BBB/VB). play a role in guiding treatment strategies. 1939. and mortality. The use of nonmydriatic fundus photography. 3:195–204. Hayreh SS. evaluation of retinal microvascular signs of hypertension from retinal photographs may begin to move from predominately the research arena to clinical practice. 2:156–161. 206:319–348. Keith N. Wong TY. Dr. Retinal signs and stroke: revisiting the link between the eye and brain. 12. potentially. III. Aslam T. Wells JR.Henderson et al. Br Med Bull. Stroke. Servais GE. Jampol LM. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Acknowledgments This study was supported in part by a departmental grant (Department of Ophthalmology) from Research to Prevent Blindness. 46:59–80. et al. 93:1383–1411. Retinal microvascular abnormalities and their relationship with hypertension. Klein R. Servais GE. 11. Katsuki S. 369:425–435. 8:221–223. Virdi PS. Author manuscript. Wong TY. 196:223–229. Ophthalmoscopic findings in malignant hypertension. 2008.. Pathophysiology of hypertensive retinopathy. Retinal vascular image analysis as a potential screening tool for cerebrovascular disease: a rationale based on homology between cerebral and retinal microvasculatures. Wong TY. Mitchell P. 2008. The eye in hypertension. Page 5 indicative of a breakdown of the blood-retina barrier (such as retinal hemorrhages. [PubMed: 3951816] 9. biochemical. core grant P30-EY06360 (Department of Ophthalmology). McIntosh R. Newman is a recipient of the Research to Prevent Blindness Lew R. Hand PJ. 39:1371–1379. 1. Hayreh SS. et al. Circ Cardiovasc Imaging. Fundus lesions in malignant hypertension. Liew G. allows for easy screening for funduscopic abnormalities in the neurologist’s office. Wong TY. Hypertensive retinopathy signs as risk indicators of cardiovascular morbidity and mortality. Surv Ophthalmol. Wagener H. [PubMed: 50653] 4. [PubMed: 18309171] 5. Pathological studies on the intracerebral and retinal arteries in cerebrovascular and noncerebrovascular diseases. Tso MO. Inc. Hypertensive choroidopathy. Hammond S. et al. and fundus changes. K23-EY019341 (BBB). Conn). Goto I. 2005. Ophthalmology. Ikui H. Macgillivray T. 93:45–59. Systemic associations of retinal microvascular signs: a review of recent population-based studies. [PubMed: 16148191] 7. et al. Virdi PS. Am J Med Sci.RR025009 (BBB). Klein BE. [PubMed: 11525792] 3. Wong TY. in particular. Ophthalmic Physiol Opt. and the Knights Templar Eye Foundation (BBB/VB). [PubMed: 7155524] 8.
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even after controlling for level of blood pressure and other vascular risk factors. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript • • • Rev Neurol Dis. microaneurysms and cotton wool spots) seem to confer a greater increase in stroke risk than sclerotic retinal changes (such as generalized and focal retinal arteriolar narrowing and arteriovenous nicking). potentially. . Retinal changes indicative of a breakdown of the blood-retina barrier (such as retinal hemorrhages. With continuing improvement in retinal photographic techniques and automated retinal image analysis. Evaluation for signs of hypertensive retinopathy. Author manuscript. Page 7 Main points • The presence of hypertensive funduscopic abnormalities is clearly related to stroke. evaluation of retinal microvascular signs of hypertension from retinal photographs may begin to move from predominately the research arena to clinical practice. along with the assessment of the presence or absence of other known vascular risk factors. guiding treatment strategies.Henderson et al. available in PMC 2012 September 22. may allow clinicians to further individualize a risk profile for stroke for each patient. thus permitting more accurate risk stratification and.
which explains the decreased visual acuity. available in PMC 2012 September 22. . dilation of the veins. Note the improvement of macular edema and the increased hard exudates. Third row of photographs: Retinal appearance two weeks later (after normalization of blood pressure). Top row of photographs: Acutely. Note the attenuation of retinal arteries. hard exudates (white arrow).Henderson et al. cotton wool spots (soft exudates) (white circle). There is macular edema bilaterally. and Elschnig spots (star). Page 8 NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Figure 1. Evolution of severe bilateral hypertensive retinopathy and choroidopathy over time (the right eye is on the left and the left eye is on the right). Second row of photographs: Retinal fluorescein angiography showing hyperfluorescence at the level of the Elschnig spots (star). Author manuscript. flame shaped hemorrhages (white arrowheads). the patient complains of mild bilateral visual loss and blood pressure is 224/68 mmHg. Rev Neurol Dis. and microaneurysms (white arrows).
Page 9 Bottom row of photographs: Three months later. . Both optic nerves have become slightly pale. The arterial attenuation persists.Henderson et al. and the veins are less dilated. the cotton wool spots and retinal hemorrhages have resolved. Author manuscript. available in PMC 2012 September 22. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Rev Neurol Dis.
Note the arteriovenous nicking (white arrows). Author manuscript. available in PMC 2012 September 22. There is mild bilateral optic nerve edema. the flame hemorrhage (white arrowhead). Stage III/IV hypertensive retinopathy (the right eye is on the left and the left eye is on the right).Henderson et al. and the arteriolar narrowing (black arrows). Page 10 NIH-PA Author Manuscript Figure 2. the boat-shaped hemorrhage (star). . NIH-PA Author Manuscript NIH-PA Author Manuscript Rev Neurol Dis.
Figure 3. Page 11 NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Rev Neurol Dis. there is severe bilateral optic nerve head edema with dilated and tortuous veins and exudates. Bottom row of photographs: Three months after treatment of hypertension.Henderson et al. but the patient has developed severe bilateral optic nerve atrophy. the optic nerve edema has resolved. Top row of photographs: Acutely. . available in PMC 2012 September 22. Author manuscript. Severe stage IV hypertensive retinopathy with bilateral optic nerve head edema in the setting of malignant hypertension (the right eye is on the left and the left eye is on the right).
including 5201 at 4 US field centers (Forsyth County. Sacramento County. 4926 participated in the baseline examination between March 1.up examination between March 1. the northwestern suburbs of Minneapolis. Maryland.792 45–64 Population samples were selected by probability sampling methods in 1987–1989 from 4 US communities: Forsyth County. 3684 of those surviving (81. resident in two postcode areas in the Blue Mountains region. Australia. Beaver Dam Eye Study (BDES) 3654 14. 1990. and Allegheny County. 1987 to May 4.Table 1 Recent large population-based studies evaluating the relationships between ocular effects of hypertension and cerebrovascular disease Henderson et al. Minnesota (n = 4.035).institutionalized. As of 2008.020). Author manuscript.1%) participated in the 5-year follow. Atherosclerosis Risk in Communities (ARIC) study 15. who were 43 to 84 years of age. Of the 5924 eligible individuals. 1988 to identify all residents in the city or township of Beaver Dam.009).926 >45 49–97 4926 43–84 A private census of the population of Beaver Dam. Blue Mountains Eye Study (BMES) Rev Neurol Dis. and Washington County.728). non. and an additional 687 African-American participants in 1992–93 at 3 of the 4 sites. 1993 and June 14. Study name or Number of Age range in years Cardiovascular Health Study (CHS) 5888 65–97 Prospective cohort study based on sampling from Medicare eligibility lists. Wisconsin. Population-based survey of vision and eye disease in an urban population aged 49 years or older. Jackson. 14. Maryland (n = 4. n = 3. North Carolina. west of Sydney. 1995. Prospective cohort study ongoing since 1990 in the city of Rotterdam in The Netherlands. ambulatory men and women age 65 and older were enrolled. 1988 and September 14. Rotterdam Eye Study NIH-PA Author Manuscript Page 12 NIH-PA Author Manuscript NIH-PA Author Manuscript .926 subjects aged 45 years or over comprise the Rotterdam Study cohort. North Carolina (n = 4. Washington County. available in PMC 2012 September 22. Pennsylvania) in 1989–90. Wisconsin (US) was performed from September 15. Mississippi (blacks only. California.
Author manuscript. . available in PMC 2012 September 22.Henderson et al. Page 13 Table 2 Association of hypertensive retinal microvascular changes and neurologic and cardiovascular complications in recent large population-based studies Retinal microvascular changes Retinal hemorrhages Microaneurysms Cotton wool spots Associations Current blood pressure Carotid artery disease Incident clinical stroke Subclinical cerebral disease (MRI) Cognitive impairment Cardiovascular mortality Renal dysfunction Arterio-venous nicking Current blood pressure Past blood pressure Incident clinical stroke Subclinical cerebral disease (MRI) Renal dysfunction Metabolic syndrome Focal arteriolar narrowing Current blood pressure Incident hypertension Metabolic syndrome Generalized arteriolar narrowing Current blood pressure Past blood pressure Incident hypertension Incident clinical stroke Carotid atherosclerosis Incident heart disease Cardiovascular mortality Metabolic syndrome Larger retinal venular caliber Incident clinical stroke Cardiovascular mortality Associations Stroke Ischemic heart disease Grade III hypertensive retinopathy Stroke Cognitive impairment Cardiovascular mortality Renal dysfunction Grade IV hypertensive retinopathy Mortality Strength of association* +++ +++ +++ +++ +++ +++ +++ +++ +++ ++ ++ + + +++ + NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript +++ +++ ++ + ++ ++ + + ++ Severity of hypertensive retinopathy (See Table 3) Grade I/II hypertensive retinopathy Strength of association* +/++ +/++ +++ +++ +++ +++ +++ Rev Neurol Dis.
available in PMC 2012 September 22. .5–2.5) NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Rev Neurol Dis.0). + (relative risk/odds ratio <1. * Page 14 Strength of association: +++ (relative risk/odds ratio >2. Author manuscript. ++ (relative risk/odds ratio 1.Henderson et al.0).
with an arteriovenous ratio of ≥1:2 Modest to severe narrowing of retinal arterioles with an arteriovenous ratio <1:2 or arteriovenous nicking Soft exudates or flame-shaped hemorrhages Bilateral optic nerve edema NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript Rev Neurol Dis. Page 15 Table 3 Keith. available in PMC 2012 September 22.Henderson et al. Author manuscript. . Wagener. and Barker classification of hypertensive retinopathy. which grades retinopathy from I to IV based on its severity (11) Grade I Grade II Grade III Grade IV Slight or modest narrowing of the retinal arterioles.
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