Kerala Journal of Ophthalmology 7

MAJOR REVIEW

Neuroretinitis - Review
Dr. Renuka Srinivasan, MS, DO, Professor
Dr. Subashini Kaliaperumal, MS, DNB, FRCS (Glasg), Senior Resident, Department of Ophthalmology, Jawaharlal Institute of
Postgraduate Medical Education and Research, Pondicherry-605 006, India
Address for correspondence:
Dr. Renuka Srinivasan, MS, DO, Professor, Department of Ophthalmology,
Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry-605 006, India
E-mail:[email protected]

Introduction and clinically distinct from other optic neuropathies.

The condition is usually painless but some patients
Neuroretinitis is a particular form of optic neuropathy
complain of eye pain that may worsen with eye
characterised by acute unilateral visual loss in the
movements as seen in optic neuritis. If the neuroretinitis
setting of optic disc swelling and hard exudate arranged
is due to an infectious process, there may be associated
in a star figure around the fovea.1 It affects persons of
fever, malaise or headache. Visual acuity at presentation
all ages, although it occurs more often in the third and
can range from 20/20 to light perception. The degree
fourth decades of life, with no gender predilection.2,3 It
of colour deficit is usually worse than the degree of
is mostly unilateral and may be precipitated by various,
visual loss would suggest. The most common field
known and unknown factors. defect is a cecocentral scotoma, but central scotomas,
Neuroretinitis is a rare clinical entity often confused arcuate defects, and even altitudinal defects may be
with the more common papillitis or papilledema. The present. A relative afferent pupillary defect is present
fundus pictures have several common features and can in most patients, unless the condition is bilateral.
be mistaken for one another by ill-experienced clinicians This is indicative of optic disc involvement. Absence
and sometimes even by ophthalmologists and neurologists. of afferent pupillary defect indicates a primary
However, there are diagnostic features distinctive for macular involvement. 4 The degree of optic disc
neuroretinitis. It is a distinct clinical entity with a swelling ranges from mild to severe, depending in
different etiopathogenesis. Likewise its management and part on the timing of the first examination. In severe
prognosis too differs from fundoscopically similar entities cases, splinter haemorhages may be present.
such as papilledema and papillitis, which are Segmental disc swelling has been reported. A macular
encountered more often in our clinical practice. star figure composed of lipid (hard exudates) may not
Though the term neuroretinitis emphasizes clinical be present when the patient is examined soon after
involvement of both disc and retina, the pathogenic visual symptoms begin, but tends to become more
locus is within the optic nerve head and macula is not prominent as the optic disc swelling resolves. 5
the primary disease locus. Small, discrete, usually white, chorioretinal lesions may
occur in both the symptomatic and asymptomatic eyes.6
Posterior inflammatory signs consisting of vitreous cells
Clinical picture
and venous sheathing as well as occasional cells and
The clinical picture of neuroretinitis is characteristic flare may occur.
8 Kerala Journal of Ophthalmology Vol. XVIII, No. 1

Fluorescein angiography 10 days, then remain stable for several weeks before
gradual resolution occurs over 6 to 12 months. Most
Fluorescein angiography in patients with acute
patients ultimately recover good visual acuity, although
neuroretinitis demonstrates diffuse disc swelling and
some complain of persistent metamorphopsia or
leakage of dye from vessels on the surface of the disc.
nonspecific blurred vision from mild disruption of the
The retinal vessels may show staining in the
macular architecture. Most patients do not experience
peripapillary region. But the most important point to
a subsequent attack in the same eye, and only a few
note is the absence of leakage from the macular
patients develop a similar attack in the fellow eye.
vasculature.
Recurrent Idiopathic Neuroretinitis is an uncommon
condition in which repeated acute episodes lead to
Pathogenesis:
progressive and permanent visual loss.4 This disorder
The pathogenesis of neuroretinitis is obscure. It is usually affects young adults and has no predilection
related to direct involvement by an infectious process with regard to sex. The interval between attacks is quite
or inflammation leading to edema of the optic nerve variable ranging from 1 month to 9.8 years. Treatment
and cellular and fluid exudation from the inflamed area of the acute attack with either oral or intravenous
of peripapillary retina. There is abnormal permeability corticosteroids has not appeared to alter the visual
of capillaries deep within the optic disc, with no prognosis of this condition. Although the cause of
abnormality of retinal vasculature. Leakage of lipid-rich recurrent Idiopathic Neuro retinitis has not been
exudates into the adjacent subretinal space and plane elucidated, an autoimmune disorder has been proposed
of the outer plexiform layer results. With reabsorption that involves occlusive vasculitis affecting the optic disc.
of serum, lipid precipitates in a stellate pattern. Long-term immunosuppression has been tried in some
of these patients. 7
Clinical course:
Etiology: (Table 1)
Neuroretinitis is usually a self-limited disorder with
a good visual prognosis. Typically over 6 to 8 weeks, Neuroretinitis is thought to be an infectious or immune-
the optic disc swelling resolves, and the appearance mediated process that may be precipitated by a number
of the disc becomes normal or mildly pale. The macular of different agents. The common infections that cause
exudates appear late and progress over about 7 to neuroretinitis are cat-scratch disease, and the

Table 1. Causative Agents Implicated in Neuroretinitis

Infectious
Viruses- Herpes, Hepatitis B, Mumps, Herpes Zoster, HIV, HBV.
Parasites- Toxoplasma, Toxocara
Fungi- Histoplasmosis
Bacteria- Syphilis, Leptospirosis, Cat scratch disease, Lyme disease, Tuberculosis
Parainfectious (Immune mediated)
Idiopathic
Leber’s stellate neuroretinitis
Differential diagnosis of optic disc edema with macular star
AION
Hypertensive retinopathy
BRVO/CRVO, rarely papillophlebitis
Papilledema
Compressive optic neuropathy
Infiltrative optic neuropathy
Nonspecific uveitis
March 2006 Renuka Srinivasan - Neuroretinitis 9

spirochetoses especially syphilis8, Lyme disease, and Lyme disease

leptospirosis.2 Cat-scratch disease accounts for two
Neuroretinitis in Lyme disease may be unilateral or
thirds of cases. 9,10 Additional causes include
bilateral, but when bilateral is usually simultaneous and
toxoplasmosis,11 mumps,12 salmonella,13 tuberculosis,14
symmetric.18 The patients usually live or work in an
and histoplasmosis. Rarely, a toxocaral granuloma
endemic area and may give a history of a tick bite
within the optic nerve head produces a similar
within the last 6 months. They often have cutaneous,
ophthalmoscopic picture.15 Despite thorough evaluation,
approximately one quarter of cases remain idiopathic. cardiac and neurological manifestations. Cardiac
manifestations include atrioventricular block,
Neuroretinitis is commonly associated with an antecedent
myocarditis, cardiomyopathy, and pericarditis.
viral syndrome, suggesting a possible viral etiology for
Neurological manifestations include meningitis,
upto 50% of the cases; however viruses are rarely
myelitis, encephalitis, cranial and peripheral
cultured from the CSF of such patients, and serological
neuropathies. Although ocular manifestations of Lyme
evidence of a concomittant viral infection is usually
disease have long been noted, they remain a rare feature
lacking. Proposed causative viral agents include herpes
of the disease. The spirochete invades the eye early and
simplex, hepatitis B, mumps, and the herpes viruses
remains dormant, accounting for both early and late
associated with the acute retinal necrosis syndrome.
ocular manifestations. A nonspecific follicular
HIV with opportunistic infections especially syphilis and
conjunctivitis occurs in approximately 10% of patients
hepatitis viruses have been implicated in neuroretinitis.16
with early Lyme disease. Keratitis is characterized by
nummular nonstaining opacities. Inflammatory
Cat scratch disease syndromes, such as vitritis and uveitis, have been
Cat- scratch disease, a systemic infection caused by the reported; in some cases, a vitreous tap is required for
pleomorphic gram-negative bacillus Bartonella diagnosis. Neuro-ophthalmic manifestations include
henselae, is the most common infectious process neuroretinitis, multiple cranial nerves involvement and
associated with neuroretinitis. Patients present optic atrophy. Criteria for establishing that eye findings
following cat exposure with fever, malaise, headache, can be attributed to Lyme disease include the lack of
eye pain and blurred vision. Examination typically evidence of other disease, other clinical findings
reveals local lymphadenopathy. Some patients also have consistent with Lyme disease, occurrence in patients
symptoms of arthritis, hepatitis, meningitis, or living in an endemic area, positive serology, and, in most
encephalitis. Decreased visual acuity (ranging from cases, response to treatment. Management of ocular
20/40 to counting fingers) is often associated with manifestations often requires intravenous therapy. 18
dyschromatopsia and afferent pupillary defects.
Ophthalmoscopic findings include neuroretinitis, Leber’s stellate retinopathy
cottonwool spots, multiple discrete lesions in the deep
retina, and stellate macular exudates. B. henselae When there is no proven etiology to the disease, a
infection is confirmed with positive blood cultures or diagnosis of Leber’s idiopathic stellate retinopathy is
elevated immunofluorescent antibody titers or both. made.19 Thus; it is a diagnosis of exclusion made after
Therapy is aimed to promote resolution of other known causes of neuroretinitis are ruled out.
neuroretinitis, restoration of visual acuity, and clearance It usually affects children or young adults. This diagnosis
of bacteremia.9 Electrophysiologic studies show that is mostly not assigned to patients aged more than
when compared to the fellow eye, affected eyes have 50 years until treatable causes of neuroretinitis or a
subnormal contrast sensitivity, abnormal color vision, macular star have been excluded. Most cases are
and abnormal visually evoked potentials. However unilateral. The incidence is equal in both sexes. Patients
electroretinograms may be normal. Recently present with acute loss of vision with or without ocular
polymerase chain reaction has been found to be a pain. A nonspecific viral illness precedes or accompanies
valuable method of diagnosing cat-scratch disease when the visual loss. Presenting visual acuity may be 20/20
serology is considered negative or borderline.17 to LP. But, most cases are in the 20/40 to 20/200 range.
10 Kerala Journal of Ophthalmology Vol. XVIII, No. 1

In children, Leber’s neuroretinitis must be distinguished syndrome is primarily unilateral, although bilateral
from anterior optic neuritis and papillitis, since multiple cases have occurred. The ocular findings include visual
sclerosis occasionally develops in children with these loss, vitreous cells, optic disc inflammation and leakage,
diseases.20 A distinguishing feature is the development and transient recurrent crops of gray-white outer retinal
of macular star. In Leber’s disease, the target tissue as lesions.23 Stationary or migrating nematodes have been
suggested by Gass 21 is vascular whereas in anterior identified deep in the retina or in the subretinal space.
optic neuritis caused by demyelinating disease, the DUSN is a condition in which prompt identification and
target tissue is primarily neural. Leber’s neuroretinitis destruction of the infecting nematode can result in the
usually resolves without treatment within 6-12 weeks.19 cessation of symptoms and the preservation of good
However the macular star may persist beyond this visual acuity. If untreated, the disease progressively
period. Most patients recover good visual acuity with damages the retina and the optic nerve leading to severe
over 90% returning to 20/50 or better. Recurrences are visual loss. Laser photocoagulation of the nematode is
very rare although in bilateral cases, involvement of the treatment of choice.24 Visual acuity may not improve
the fellow eye may follow the first. Fluorescein study significantly unless the worm is killed soon after onset
demonstrates intense hyperfluorescence due to leakage of visual loss. It has been found that thiabendazole is
from capillaries within the disc. There is no leakage effective in the treatment of some patients when the
from the retinal vessels in the macula. worm cannot be found and when DUSN is accompanied
by a moderate degree of vitritis that is associated with
Idiopathic retinal vasculitis aneurysms a breakdown in the blood-retinal barrier.25 But by and
and neuroretinitis (IRVAN) large, antihelminthics have not been found to be that
effective in confirmed cases of DUSN.26 Regardless of
IRVAN syndrome is the acronym for idiopathic retinal the nature of the causative nematode, DUSN should
vasculitis, aneurysms and neuroretinitis. This syndrome always be suspected in healthy patients with unilateral
typically affects young, healthy individuals; it has a ocular signs of persistent vitritis associated with
female predominance, is usually bilateral and is not papillitis, retinal vasculitis, and multifocal lesions
associated with any systemic abnormalities. The most involving the outer retinal layers.
characteristic feature is the presence of macroaneurysms
seen as dilatations of the retinal and optic nerve head
Mutiple sclerosis
arterioles. Exudative retinopathy and capillary non-
perfusion is usually seen adjacent to retinal and optic Multiple sclerosis is one condition that is not associated
nerve head aneurysms and is concentrated in the with neuroretinitis.2 It is a well known fact that patients
peripapillary location. This condition is not a true who develop typical optic neuritis are prone to develop
neuroretinitis as there is no clinically evident multiple sclerosis but there is no similar increased
neuropathy but only late diffuse staining of the optic tendency for patients who experience an attack of
nerve head due to local vascular changes. There is little neuroretinitis.27 Thus, when a diagnosis of an attack of
role of steroids and panretinal photocoagulation is acute optic neuropathy as an episode of neuroretinitis
advocated if retinal neovascularisation occurs.22 Central rather than anterior optic neuritis is made, it
retinal vein occlusion and hypertensive retinopathy may substantially alters the neurologic prognosis in the
also have disc edema and macular star figure but have patient being evaluated. Nevertheless, there have been
associated multiple flame-shaped haemorrhages and anecdotal reports of patients with multiple sclerosis who
soft exudates. developed neuroretinitis .28

Diffuse unilateral subacute neuroretinitis Conditions mimicking neuroretinitis

(DUSN) (Table 2)

DUSN is a progressive parasitic disease affecting the Certain noninfectious and noninflammatory conditions
outer retina and retinal pigment epithelium (RPE). This mimick neuroretinitis as they are characterised by optic
March 2006 Renuka Srinivasan - Neuroretinitis 11

Table 2. Differentiating features between Neuroretinitis and other closely resembling entities.
Neuroretinitis Papillitis Papilledema CRVO AION
VA 6/60-6/12 Light perception No visual loss Moderate to severe Moderate to severe
to 6/12 visual loss impairment
Pupillary reactions Relative afferent RAPD+ Normal Normal/RAPD+ RAPD+
pupillary defect
(RAPD+)
Laterality Unilateral, Unilateral/bilateral Always bilateral Unilateral Typically unilateral
rarely bilateral
Eye pain Nil Pain especially Nil painless painless
on upgaze
Visual fields Centrocaecal Central/ Enlarged Normal Altitudinal field
scotoma centrocaecal blind spot defects
scotoma
Color vision Severely impaired, Severely impaired, Normal Normal Diminished in
disproportionate disproportionate proportion to
to visual loss to visual loss level of v/a
Systemic symptoms Fever, rash Weakness of limbs Headache, - Headache,
vomiting jaw claudication,
polymyalgia
rheumatica
Fundus findings Disc swelling of Disc swelling rarely Disc swelling Disc edema, Pale disc edema
2D,hyperemic above 2D, venous frequently higher, macular star along
with macular star engorgement and upto 8-9D, with haemorrhages
figure haemorrhages less more venous and soft exudates
marked engorgement,
macular star may
develop
Fluorescein Leakage from disc Leakage from disc Leakage from disc Shows areas of Unequal choroidal
Angiography and peripapillary and peripapillary and peripapillary capillary non- filling in arterial
retina retina retina perfusion phase
VEP Decrease in Decrease in Normal - Decrease in
amplitude, amplitude, amplitude
increase in latency increase in latency
Specific Syphilis, cat- Multiple sclerosis - hypertension, Giant cell arteritis,
associations scratch disease, diabetes, hypertension,
Lyme’s disease glaucoma diabetes
Prognosis Good Good Good with relief Depends on initial Poor
of raised ICT visual acuity

disc swelling that may on occasion be associated with conditions. Spontaneous resolution of the disc edema
the development of a macular star figure. These and recovery of visual acuity serve as distinguishing
mimicking conditions include papilledema, anterior features of neuroretinitis from papilledema and
ischemic optic neuropathy, and infiltration of the optic ischemic optic neuropathy.
disc by tumor.14 Systemic hypertension may also produce
both optic disc swelling and a macular star figure. The Investigations: (Table 3)
disk edema and retinopathy resolves after the
hypertension is controlled.29 Optic disc swelling in Investigation into the etiology of neuroretinitis should
patients with systemic vascular disease like diabetes begin with a careful history including questioning
and hypertension can be differentiated form regarding sexually transmitted diseases, cat-scratches,
neuroretinitis by the absence of abrupt visual loss, skin rashes, tick bites, lymphadenopathy, fever, and
background retinopathy and a medical history of such flu-like illnesses. Complete physical and ocular
12 Kerala Journal of Ophthalmology Vol. XVIII, No. 1

Table 3. Investigations into the etiology of Neuroretinitis

Ocular
Color vision, contrast sensitivity, Central fields, Fluorescein angiography, VEP
Systemic
Blood culture-cat scratch disease
VDRL and FTA-ABS- Syphilis
Viral serology
Mantoux , chest X ray
ESR
Lumbar Puncture- opening pressure, cells, proteins, glucose,
CSF culture for bacteria especially leptospirosis and fungi
Immunofluorescent antibody test- cat scratch disease
ELISA- Toxoplasmosis, Toxocariasis
Polymerase chain reaction- cat scratch disease
Neuroimaging

examinations are essential. Screening with serological that requires therapy. No treatment is required in the
testing for treatable diseases such as cat-scratch disease, idiopathic group as the disease is self-limiting.
syphilis, and Lyme disease, analysis of CSF, Cat-scratch disease is usually described as a benign,
neuroimaging may be desirable in the appropriate self-limited illness. 30 Patients with neuroretinitis
setting. In the absence of a proven etiology a diagnosis associated with cat scratch disease have been treated
of Leber’s idiopathic stellate neuroretinitis may be with prednisolone, dexamethasone, clindamycin,
entertained. ciprofloxacin, trimethoprim-sulfa, or tetracycline and
all had improved vision.31,32 Doxycycline and rifampicin
VEP is useful in the setting of multiple sclerosis where
appear to shorten the course of disease and hasten
there is a latency of the P100 wave and a decrease in
visual recovery. Long-term prognosis is good, but some
amplitude. It may be abnormal in neuroretinitis. ERG
individuals may acquire a mild postinfectious optic
assesses the functional integrity of the retinal layers
neuropathy.
and hence normal in disorders involving ganglion cells
and optic nerve as in optic neuritis and neuroretinitis. Patients with neuroretinitis and secondary or late
syphilis should be treated with intravenous penicillin,
and patients with Lyme disease should also be treated
Treatment
with an appropriate antibiotic such as ceftriaxone,
Treatment of neuroretinitis depends on whether there amoxycillin, or tetracycline. Though systemic steroids
is an underlying infectious or inflammatory condition have been tried, there is no definite evidence that such

Fig 1. Neuroretinitis with vasculitis involving the Fig 2. Grade IV hypertensive retinopathy mimicking as
superotemporal vessel. Neuroretinitis.
March 2006 Renuka Srinivasan - Neuroretinitis 13

treatment alters either the speed of recovery or the 14. Duke-Elder S, Dobree JH:Diseases of the retina.
In Duke-Elder (ed); System of Ophthalmology, vol.10
ultimate outcome.19 The prognosis in most cases of
London, Henry Kimpton, 1967, pp. 126-127.
idiopathic neuroretinitis is excellent as it is self limiting. 15. Bird AC, Smith JL, Curtin VT. Nematode optic neuritis.
Am J Ophthalmol 1983; 95:480-486.
Conclusion 16. Forooghian F, Lam WC, Hopkins J, Dhanda D. Bilateral
Neuroretinitis with Peripapillary Serous Retinal
Thus in most cases, neuroretinitis represents a self- Detachments in a patient with HIV and HBV.
Arch Ophthalmol 2005; 123: 1447-1449.
limiting, benign, systemic inflammatory process with
17. Labalette P, Bermond D, Dedes V, Savage C. Cat-scratch
rarely a specific etiology being identified. The extent disease neuroretinitis diagnosed by a polymerase
of diagnostic examination should be predicted based chain reaction approach. Am J Ophthalmol 2001; 132:
on the presence or absence of associated constitutional 575-576
symptoms. Vision should be expected to recover within 18. Lesser RL, Kornmehl EW, Pachner NR, et al. Neuro-
ophthalmologic manifestations of Lyme disease.
weeks to months. Nevertheless, the ophthalmologist
Ophthalmology. 1990; 97:699-706.
should use caution in predicting ultimate visual
19. Dreyer RF, Hopen G, Gass JDM, Smith JL: Leber’s
prognosis. idiopathic stellate neuroretinitis. Arch Ophthalmol
1984;102: 1140-45.
20. Kennedy C, Carter S. Relation of optic neuritis to multiple
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