THE RISK OF NON ARTERITIC

into nerve signals that are sent to the brain.

OPTIC NEUROPATHY IN

It also can damage to the nerves in the eye

HYPERTENSION PEOPLE

(ischemic optic neuropathy) due to poor

Eiffel

(112014090),

(112014102),

Gio

Selley
Vano

Kenanga

Beril

blood flow.

Karel

Method: The literature review is conducted

Naihonam (112014127), Steaffie Eunike

by several major steps such as searching

Cassandra (112014169), Elcha (112014172)

journals and books associated to NAION

pathogenesis according to hypertension, the

ABSTRACT
Introduction:

progression of NAION, and reviewing the

Non

Arteritic

Optic

Neuropathy Anterior is the most common

acute optic neuropathy in people older than
50 years. It is characterized by sudden vision
loss in one eye, usually painless, which can
increase the risk of vision loss in the
contralateral eye. Although definite cause
has not been determined, NAION is thought
to occur following an idiopathic ischemic
event involving the short posterior cilliary
arteries that supply blood to the most
anterior part of the optic nerve. Other factors
that have been hypothesized

to associate

with NAION include high cholesterol,

arteriosclerosis,

stroke,

cardiac

and

intraocular surgery, tobacco use, nocturnal

hypotension,

blood

loss,

glaucoma,

hiperhomocsyteine and sleep apneu. The

most

common

cause

of

NAION

is

risk factor of the hypertension individuals to

NAION.
Results: The sympathetic nervous control
and autoregulatory mechanisms of the
retinal and choroidal vasculatures are briefly
reviewed. In hypertensive choroidopathy
focal occlusion of choriocapillaris leads to
necrosis of retinal pigment epithelium
(Elschnig spots). Hypertensive retinopathy
is described in vasoconstrictive, exudative,
and

sclerotic

complications

phases,
of

the

followed
sclerotic

by

phase.

Hypertensive optic disc edema is influenced

by the blood supply and extracellular tissue
fluid pressure of the optic nerve head. In
baboons with hypertensive disc edema,
accumulation of axoplasmic components is
observed in the optic nerve head.

hypertension. The condition of high blood

Conclusions:

Systemic

hypertension,

pressure can damage to the retina, which can

arteriosclerosis, vasospasm or medications

changes light and images that enter the eye

may reduce the autoregulatory capacity of

the optic disc. Vasoactive substances might

changes, a consequences of endothelial

be released in response to ischemia that

damage and necrosis.

influence the autonomic control of blood

vessels; prove the hypothesis the correlation

METHODS
The objective of this study is to provide

between hypertension with NAAION.

Keyword: NAION, hypertension, optic
neuropathy.

knowledge regarding NA-AION and to

introduce fellow medical students and
people about the risk of NA-AION as a

INTRODUCTION

complication of hypertension.

Hypertension is one of the most common

The method used for this paper is literature

worldwide

humans.

review. This study is conducted by several

Hypertension has been described as the most

major steps such as searching the worldwide

important

for

websites, journals and articles associated to

coronary heart disease, stroke, congestive

NA-AION pathogenesis, identifying the

heart failure, and end stage renal disease.

possible etiological factors of NA-AION,

The prevalence of hypertension in 2003-

looking for the correlation between

2004 was 25,8 % at the 18-39 age group.

AION and hypertension, and reviewing the

Hypertension is usually asymptomatic until

risk

the damaging effects of hypertension.

hypertension.

diseases
modifiable

afflicting
risk

factor

Because of assymptomatic, high blood

pressure is undertreated and underdiagnosed

of

NA-AION

in

people

NAwith

RESULTS

among all races and genders. Beside of

Ischemic optic neuropathies are the most

macrovascular effect, the condition of high

frequent acute optic neuropathies in patients

blood pressure can damage to retina, which

> 50 years of age. Depending on the

can damage to the nerves in the eye

segment of optic nerve affected, they are

(ischemic optic neuropathy). The acute

subdivided into anterior and posterior

elevation of blood pressure typically causes

ischemic optic neuropathies. Optic disc

reversible vasoconstriction in retinal blood

edema from ischemia to the anterior nerve is

pressure, and hypertensive crisis may cause

present

optic disk edema. More prolonged or severe

neuropathy (AION) and absent in posterior

hypertension leads to exudative vascular

ischemic optic neuropathy (PION). AION is

in

anterior

ischemic

optic

much more common than PION, accounting

NA-AION may be mainly recognized as a

for 90% of cases of optic nerve ischemia.1,2

multi-factorial disease, with many risk

AIONs are subdivided into non-arteritic and

arteritic

etiologies.

ischemic

optic

Arteritic

neuropathy

anterior
(AAION),

classically due to Hortons giant cell arteritis

(inflammation of mid-sized arteries), is an
ophthalmologic

emergency,

requiring

prompt recognition and treatment to prevent

devastating blindness. About 9095% cases
of AION are non-arteritic anterior ischemic
optic neuropathy (NAAION). 1-3
Non-arteritic

anterior

ischemic

optic

acute optic neuropathy in patients over the

age of 50 and is the second most common
cause of permanent optic nerve-related

The Risk Factors of NA-AION

collectively contributing to its

pathophysiology.

The most commonly

proposed pathogenic theory involves an

insufficiency of the optic disc circulation,
exacerbated by structural crowding of
nerve fibers and supporting structures at the
nerve

head,

resulting

in

inadequate

oxygenation, ischemia and swelling of the

disc. 4,5
NA-AION could be caused by several

neuropathy (NAION) is the most common

visual loss in adults after glaucoma.3

factors

combined factors which is the increasing

blood flow resistance, arterial hypotension,
and

reduction

of

perfusion

pressure.

Increasing blow flow due to systemic and

local causes including aging processes,
arterial hypertension,
atherosclerosis,
increased

diabetes

mellitus,

hypercholesterolemia

blood

viscosity

due

or
to

haematologic disorder. Arterial hypotension

mainly

caused

by

nocturnal

arterial

hypotension during sleep or by intensive

antihypertensive medication. Reduction of
perfusion pressure intended as the
difference between the mean systemic blood
pressure and the intraocular pressure (IOP)
which may be due to arterial hypotension
but also to a relevant rise of the IOP. Thus,
according

to

the

available

evidence,

ischemic optic neuropathy, and particularly

the NA-AION, is a multifactorial disease:

this means that each patient may have a
special combination of systemic and local
factors that all together may have caused
it.4,5
NAION typically presents with rapid onset,
stable course, unilateral loss of visual acuity

Figure 1. Typical inferior altitudinal/arcuate visual

and/or field and generally poor recovery.

field defect in NAION.5

The visual loss in NAION is commonly first

noted upon awakening, and may progress
over several hours to days, and rarely even
weeks. Visual acuity may range from 20/15
to no light perception, though severe visual
loss may prompt investigation for alternative
types of optic neuropathy such as AAION or
optic neuritis. Patients also tend to have mild
to moderate dyschromatopsia consistent
with the degree of acuity loss.6

Fundus examination of the optic nerve may

reveal

disc

edema

with

possible

peripapillary hemorrhaging. The end stage

finding is pallor of the nerve head which can
be diffuse or sectoral depending on the
amount of initial edema. Examination of the
fellow eye may show a disc at risk.. This
term is used to describe the appearance of
the fellow nerve, which is small and
crowded with blood vessels, with minimal to

With respect to the visual field defect in

no

cup-to-disc

NAION, though any pattern of loss may

presentation is thought to compromise the

develop, the most common are an inferior

blood supply to the optic nerve, leaving it at

altitudinal or arcuate defect. Visual field

risk

patterns in NAION resemble the nerve fiber

NAION is a diagnosis of exclusion and A-

bundle defects of glaucoma and typically

AION should be ruled out. Test results show

obey the horizontal midline. An altitudinal

a normal ESR and CRP as the condition is

field defect, usually involving the inferior

not inflammatory but vascular in nature.

field, is most common, but generalized

Also, patients will rarely have episodes of

depression, broad arcuate scotomas, and

amaurosis fugax, or systemic symptoms

cecocentral defects also are seen.6

suggesting GCA. If a temporal artery biopsy

for

ratio.

possible

This

future

anatomical

involvement.

is performed, it will also be negative.6

Hypertension
Hypertension is a chronic elevation of blood
pressure that, in the long term ,causes endorgan damage and results in increase
morbidity and mortality. Blood pressure is
Figure 2. Appearance of affected and unaffected optic
discs in a patient with NAION. a, optic disc in eye
with NAION is swollen and hyperaemic. Note
several peripapillary flame-shaped haemorrhages. b,
optic disc in unaffected eye is small and has no cup.5

the product of cardiac output and systemic

vascular resistance. It follows that patients
with arterial hypertension may have an
increase in cardiac output, an increase in
systemic vascular resistance, or both. In the

NA-AION Current Management

younger age group, the cardiac output is

There are no accepted treatment guidelines

often elevated, while in older patients

although numerous surgical and medical

increased systemic vascular resistance and

therapies have been proposed including:

increased stiffness of the vasculature play a

optic nerve decompression, aspirin, anti-

dominant role. Vascular tone may be

coagulants,

elevated

agents,

thrombolytics,

systemic

vasodilating

steroids,

intravitreal

because

adrenoceptor

of

stimulation

increased
or

increased

triamcinolone, anti- vegf agents, levodopa,

release of peptides such as angiotensin or

diphenylhydantoin and hyperbaric oxygen.

endothelins. The final pathway is an

Literature on these treatments, however, is

increase in cytosolic calcium in vascular

mostly of retrospective or prospective case

smooth muscle causing vasoconstriction.

series with the largest study on NA-AION

treatment, the Ischemic Optic Neuropathy
Decompression Trial, showed that treatment
actually exacerbated the condition. The
general consensus among clinicians is that
the

systemic

vascular

diseases

that

precipitate the condition should be well

managed in hopes of averting or delaying
bilateral ocular involvement and further
systemic involvement.6,7

Table 1. JNC 7: Hypertension Classification.8

Hypertension can effect the retina, choroid,

Certain vascular anatomic factors, some still

and optic nerve of the eye, particularly with

unknown, may render this region especially

stage 2 hypertension. These changes can be

vulnerable

appreciated with inspection of the retinal

properties of the disk vasculature may also

vessels

play a role in this vulnerability.8,9

by

direct

ophthalmoscopy,

photography, or angiography. In acute or

advanced

hypertension,

the

retinal

vasculature may be injured sufficiently to

cause occlusion or leakage. These changes
may be manifested as nerve fiber layer
infarcts
patches),

(soft exudates
extravascular

or cotton-wool
edema

(hard

exudates), intra retinal hemorrhages, and

retinal arterial macroaneurysms.8,9
DISSCUSION
The pathogenesis of NAAION is clearly
multifactorial; acute blood loss, migraine,
periarteritis nodosa, and other vascular
disorders predispose patients to ischemic
optic neuropathy on less frequent occasions.
Several observers have found focal areas of
infarction, post mortem, in the retrolaminar
region of the optic nerve in patients with
ischemic optic neuropathy. The almost
invariably anterior location of the infarction
produces disk edema, not only through
ischemia, but also by compromise of venous
and perhaps axoplasmic flow through the
inexpansile scleral canal with its rigid
supporting network, the lamina cribrosa.

to

infarction.

Functional

Loss of blood supply within the posterior

cilliary arteries deprives the optic nerve
tissue of oxygen and results in damage to
part or all of the optic nerve. This is a small
"stroke" in the optic nerve but unlike other
strokes is unassociated with weakness,
numbness, or loss of speech, nor is there an
increased risk of a classic stroke later. It is
also not associated with pain. Patients may
become aware of decreased vision or
difficulty seeing above or below the center
of gaze. Loss of the blood supply results in
swelling of the optic disc, often associated
with hemorrhages. The hemorrhages and
swelling will go away within several weeks
leading to the development of a pale disc
(optic atrophy). As the swelling resolves,
some of the affected portion of the nerve
fiber layer disappears from the surface of the
retina and the axons will be permanently
lost.8,9
CONCLUSION
1. Non-Arteritic Anterior Ischemic Optic
Neuropathy (NAAION) is the leading
cause optic neuropathy in persons over

age

50

and

hypertension.
2. Main
proccess

associated

with

on demographics, clinical presentation,

pathophysiology,

in

NAAION

pathogenesis is insufficiency of the

animal

models,

prognosis, and treatment. J Clin Exp

optic disc circulation, exacerbated by

Ophthalmol S3: 004.

3. Lin MC, Hsu FM, Sheu SJ. (2007).

structural crowding of nerve fibers

Nonarteritic ischemic optic neuropathy.

and supporting structures at the nerve

J Chin Med Assoc 70:2.

4. Brouzas D, Charakidas A, Ladas I,

head,

resulting

in

inadequate

oxygenation, ischemia and swelling of

the disc.
3. Hypertension can effect the retina,

Apostolopolous M. (2009). Nonarteritic

anterior ischemic optic neuropathy
associated with chronic anemia: a case

choroid, and optic nerve of the eye,

series of myelodysplastic syndrome

particularly with stage 2 hypertension.

patients.

The retinal vasculature may be injured

sufficiently to cause occlusion or
leakage. Loss of blood supply within
the posterior cilliary arteries deprives
the optic nerve tissue of oxygen and
results in damage to part or all of the
optic nerve; prove the hypothesis that
people with hypertension have a higher
risk of NAAION.
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