OPTIC NEURITIS AND ITS
MANAGEMENT
NEURO-OPTHALMOLOGY ESSAY
RESIDENT: ALIMUL HAQ
TUTOR: PROFESSOR DR SHEREEN FATHI
DEPARTMENT OF NEUROLOGY
KASR
AL AINY HOSPITAL
WORD
COUNT: 4625
INTRODUCTION
Optic neuritis is an inflammatory,
demyelinating condition that causes acute, usually monocular, visual loss. It
is highly associated with multiple sclerosis (MS). Optic neuritis is the
presenting feature of MS in 15 to 20 percent of patients and occurs in 50
percent at some time during the course of their illness [1].
The term 'optic neuritis' means
inflammatory optic neuropathy from any cause, but is sometimes used to refer to
acute demyelinating optic neuritis. In this article, 'optic neuritis' (ON)
refers to optic neuritis of any type, and 'acute demyelinating optic neuritis'
(ADON) will be used for that specific form. Other terms used in the literature
are papillitis (if the optic nerve head is affected) and retrobulbar neuritis
(if the nerve is affected more posteriorly).[2]
ADON is a common cause of ON in
parts of the world where multiple sclerosis (MS) is common. However, there are
many other possible causes which must not be overlooked, as they may require
different and urgent management. [2]
Neuromyelitis optica (NMO), also
known as Devic's disease or Devic's syndrome, is a rare condition in which
there are recurrent and simultaneous optic neuritis and myelitis of the spinal
cord. Lesions are different from those observed in MS, and the condition
requires a different course of treatment[2]
The term optic neuritis is sometimes
applied to other inflammatory and infectious conditions affecting the optic
nerve. These and other causes of optic neuropathy are discussed separately.[1]
The epidemiology, pathophysiology,
clinical features,types, Prognosis and diagnosis and treatment of optic
neuritis will be covered here.
EPIDEMIOLOGY —
Most cases of acute
demyelinating optic neuritis occur in women (two-thirds) and typically develop
in patients between the ages of 20 and 40 .
The incidence of optic neuritis is
highest in populations located at higher latitudes, in the northern United
States and western Europe, and is lowest in regions closer to the equator. In
the United States, studies have estimated the annual incidence of optic
neuritis to be as high as 6.4 per 100,000.In the United States, optic neuritis
occurs more frequently in whites than blacks ,In Asia, optic neuritis is
proportionately more common relative to the incidence of multiple sclerosis
than in the United States or western Europe [1].
PATHOPHYSIOLOGY —
The most common pathologic basis for
optic neuritis is inflammatory demyelination of the optic nerve. The pathology
is similar to that of acute multiple sclerosis (MS) plaques in the brain, with
perivascular cuffing, edema in the myelinated nerve sheaths, and myelin
breakdown. Inflammation of the retinal vascular endothelium can precede
demyelination and is sometimes visibly manifest as retinal vein sheathing.
Myelin loss exceeds axonal loss.
It is believed that the
demyelination in optic neuritis is immune-mediated, but the specific mechanism
and target antigen(s) are unknown. Systemic T cell activation is identified at
symptom onset and precedes changes in the cerebrospinal fluid. Systemic changes
also normalize earlier (within two to four weeks) than central changes. T cell
activation leads to the release of cytokines and other inflammatory agents. B
cell activation against myelin basic protein is not seen in peripheral blood
but can be demonstrated in the cerebrospinal fluid of patients with optic
neuritis [1].
As with MS, a genetic susceptibility
for optic neuritis is suspected. This is supported by an over-representation of
certain human leukocyte antigen (HLA) types among patients with optic neuritis
[1].
CLINICAL FEATURES
Acute features — Optic neuritis is
usually monocular in its clinical presentation. In about 10 percent of cases,
symptoms occur in both eyes, either simultaneously or in rapid succession . Bilateral
optic neuritis is more common in children younger than 12 to 15 years old and
also in Asian and black South African patients .Because bilateral symptoms are
relatively uncommon, they should suggest an alternative cause of optic
neuropathy. However, subclinical visual deficits in acuity, contrast
sensitivity, color vision, and visual field in the contralateral eye can often
be elicited by detailed visual testing in patients with clinically monocular
disease . Because these deficits usually resolve along with the clinical
deficits in the symptomatic eye, it is unlikely that these findings represent
prior episodes of optic neuritis. [1].
Other clinical features of optic
neuritis were systematically characterized in the Optic Neuritis Treatment
Trial (ONTT), which enrolled 457 patients, aged 18 to 46 years, with acute unilateral
optic neuritis. The two most common symptoms of optic neuritis are vision loss
and eye pain:
●Vision loss typically develops over
a period of hours to days, peaking within one to two weeks. Continued
deterioration after that time suggests an alternative diagnosis .Greater than
90 percent of patients in the ONTT had a significant decrease in central visual
acuity. In most, the visual acuities ranged from 20/25to 20/190 (median
visual acuity 20/60). However, some patients had 20/20 acuity
(11 percent), and, at the other extreme, a few had no light perception (3
percent).
●Eye pain occurred in 92 percent of
patients in the ONTT and often worsened with eye movement. The onset of pain
generally coincided with the visual acuity loss and improved along with it. [1]
Other common visual symptoms and
signs include:
●An afferent pupillary defect always
occurs in optic neuritis if the other eye is uninvolved and otherwise healthy.
This is demonstrated by shining a light alternately in one eye and then the
other and finding that the direct response to light is more sluggish in the
affected eye. The room should be dark, and the patient should fixate on a
distant target to prevent miosis due to accommodation. [1]
●The visual field defect in optic
neuritis is typically characterized as a central scotoma. However, in the ONTT,
almost all types of visual field defects were seen, including diffuse vision
loss and altitudinal, arcuate, hemianopic, and cecocentral defects.
Nonetheless, a defect that extends to the periphery should suggest a
compressive lesion, while an altitudinal defect, particularly an inferior
altitudinal defect, is more common in anterior ischemic optic neuropathy Visual
field defects usually resolve; in the ONTT, 56 percent had normalized at one
year and 73 percent had normalized at 10 years . [1]
●Papillitis with hyperemia and
swelling of the disk, blurring of disk margins, and distended veins is seen in
one-third of patients with optic neuritis. Two-thirds of these patients
have retrobulbar neuritis with a normal funduscopic examination .Papillitis is
more common in children less than 14 years old and in certain ethnic
populations, including black South Africans and Southeast Asians. Peripapillary
hemorrhages are rare in optic neuritis, but are a common accompaniment to
papillitis due to anterior ischemic optic neuropathy [1].
●Photopsias (flickering or flashes
of light) are often precipitated with eye movement and were reported by 30
percent of patients in the ONTT [1].
●Loss of color of vision out of
proportion to the loss of visual acuity is specific to optic nerve pathology.
Abnormal color vision by Ishihara plates was found in 88 percent of involved
eyes in the ONTT; this increased to 94 percent with the more sensitive
Farnsworth-Munsell 100 hue test [1].
●Other signs of ocular inflammation
may be observed by the ophthalmologist on funduscopic or slit lamp examination.
Perivenous sheathing or periphlebitis retinae can be seen in about 12 percent
of patients with optic neuritis and implies a high risk for multiple sclerosis
(MS) [1]. Uveitis, cells in the anterior chamber,and/or pars planitis are
uncommonly seen in optic neuritis and are more typical of infections and other
autoimmune diseases. [1]
Chronic features —
Even after clinical recovery,
signs of optic neuritis can persist. These signs in a patient without a history
of optic neuritis may suggest a previous, subclinical attack. When a patient
presents with a possible first attack of MS elsewhere in the central nervous
system, these signs are often sought because evidence of other demyelinating
episodes separated in "time and space" can affect prognosis and
treatment decisions.
Chronic signs of optic neuritis can include:
●Persistent visual loss. Most
patients with optic neuritis recover functional vision within one year.
However, on testing, deficits in color vision, contrast sensitivity, stereo
acuity, and light brightness are detectable in most patients at up to two years
●A relative afferent pupillary
defect remains in approximately one-fourth of patients two years after
presentation .
●Color desaturation refers to a
qualitative inter-eye difference in color perception that can be tested by
comparing vision of a red object with each eye. A patient with monocular
"red desaturation" may report that the red color appears "washed
out," pink, or orange when viewed with the affected eye.
●Temporary exacerbations of visual
problems in patients can occur with increased body temperature (Uhthoff's
phenomenon). Hot showers and exercise are classic precipitants.
●Optic atrophy to at least some degree
almost always follows an attack of optic neuritis, despite the return of visual
acuity .Normal, 20/20 visual acuity requires less than one-half of
normal foveal axons .The disc appears shrunken and pale, particularly in its
temporal half (temporal pallor).[1]
The disk pallor extends beyond the
margins of the disk into the peripapillary retinal nerve fiber layer.
●The pattern-shift visual evoked
response remains delayed in most patients, even with visual recovery. Although
latencies continue to shorten (improve) up to two years after presentation,
abnormalities are seen in most (80 percent) at two years [1].
Causes of optic neuritis (ON)[3][4]
|
|
|
Type
|
Conditions/notes
|
|
Acute
demyelinating ON
|
The most
common cause of ON in regions where MS is relatively common (Caucasian
populations and high latitudes).
|
|
Ischaemic
optic neuropathies
|
Giant cell
arteritis (cranial arteritis), anterior and posterior optic neuropathy,
diabetic papillopathy.
|
|
Corticosteroid-responsive
ON
|
|
|
Other
inflammatory causes
|
Post-infection,
post-vaccination, neuroretinitis, acute disseminated encephalomyelitis.
|
|
Infections
|
Tuberculosis,
syphilis,[8] mycoplasma and other respiratory tract infections, Lyme
disease,[9] toxocariasis,[10] helminthiasis, cryptococcosis, viral ON (a rare complication
of chickenpox),[11] Q fever,[12] periorbital infections (orbital cellulitis, severe suppurative
sinusitis). Other viral infections which have been known to cause ON include
measles, mumps, rubella, herpes zoster, infectious mononucleosis.
|
|
Nutritional
|
Vitamin B12
deficiency.
|
|
Drugs and
toxins
|
|
|
Inherited
|
Leber's
hereditary ON.
|
|
Optic
neuritis in children
|
Viral
infection is a common cause.
|
[2]
Typical
Features of Acute demyelinating optic neuritis :
Adult patient age
<45.
Symptoms:
Unilateral reduction in
vision.
Time course: Acute or
subacute onset of visual loss, which progresses for ≤2 weeks.
Spontaneously improves
within 3 weeks in nearly all patients.
Pain - periocular,
onset preceding or with visual loss, worse on eye movement, does not disturb
sleep. [2]
Patients with multiple
sclerosis (MS) may have recurrent attacks of ON, which means that a history of
previous episodes of decreased vision in the same or fellow eye may be
elicited.
Signs:
Visual loss varies from
mild to no perception of light.
Ipsilateral relative
afferent pupillary defect (RAPD).
Loss of contrast and
colour vision out of proportion to loss of acuity.
Normal or swollen optic
disc; disc pallor occurs later (4-6 weeks after onset).
Visual field defect -
any type.
Normal macula and
peripheral retina. [2]
Warning'
or atypical features suggesting another cause
Patient
aged <12 or >50, black or Asian race.
Symptoms: Bilateral
reduction in vision.
Time course:
Vision loss continuing
to progress >2 weeks after onset.
No recovery by 5 weeks
after onset.
Pain - absent, or
severe enough to disturb sleep/restrict eye movements, or pain persisting >2
weeks after onset, or pain following onset of vision loss.
History suggesting
another cause - eg, autoimmune or inflammatory conditions, infection,
malignancy, immunosuppression, systemic symptoms.
Deterioration after
withdrawal of corticosteroids (if given).
Signs:
Severe visual loss - no
perception of light.
Lack of RAPD. [2]
Temporal field defect
in contralateral eye.
Unusual ocular findings
- eg, marked ocular inflammation, markedly swollen optic disc, marked disc
haemorrhages, macular star.[2]
NATURAL HISTORY
Natural
history of acute ON is to worsen over several days
to 2 weeks end then to improve. Improvement intially is rapid and starts
approximately 3 weeks after
onset.
Recovery of vision is nearly complete by 5 weeks after onset. Improvement
continues up to 1 year. Lana--Peixoto and Andrade reported (2001) that the
clinical features of childhood ON differ from those observed in adults. In
children is a better visual outcome and a lower conversion rate to multiple
sclerosis than in adults. [5]
DIFFERENTIAL DIAGNOSIS —
In a young child, infectious and
postinfectious causes of optic nerve impairment should be considered as
alternatives to optic neuritis, while in an older patient (>50 years),
ischemic optic neuropathy (due, for example, to diabetes mellitus or giant cell
arteritis) is a more likely diagnosis than optic neuritis.
Alternative diagnoses should also be
considered in patients with a bilateral presentation or those with other
neurologic or systemic symptoms.
In cases of recurrent optic neuritis
that are not due to neuromyelitis optica or MS, other causes of recurrent optic
neuritis should be thoroughly investigated (such as sarcoidosis, lupus, chronic
relapsing inflammatory optic neuropathy (CRION), or paraneoplastic optic
neuropathy (serum CRMP-5/CV2 antibody)). [1].
EVALUATION AND DIAGNOSIS
Diagnosis —
. In general, optic neuritis is
a clinical diagnosis based upon the history and examination findings. Because
important findings on funduscopic examination help differentiate typical from
atypical cases of optic neuritis, an ophthalmologic examination should be
considered an essential feature of the clinical evaluation. Magnetic resonance
imaging study of the brain and orbits with gadolinium contrast provides
confirmation of the diagnosis in most cases and also provides and assessment of
the risk of subsequent multiple sclerosis.
Further diagnostic testing is
directed toward excluding other causes of visual loss in atypical cases [1]
Magnetic resonance imaging —
A magnetic resonance imaging
study (MRI) of the brain and orbits with gadolinium contrast provides
confirmation of the diagnosis of acute demyelinating optic neuritis and
important prognostic information regarding the risk of developing MS. [1]
Innovations in MRI technology (eg,
short tau inversion recovery [STIR], fast spin echo [FSE], and fluid-attenuated
inversion recovery with fat suppression techniques [FLAIR], diffusion tensor
imaging [DTI]) have improved imaging of the optic nerve .Optic nerve
inflammation can be demonstrated in about 95 percent of patients with optic
neuritis with gadolinium contrast-enhanced MRI of the brain and orbits . The
longitudinal extent of nerve involvement as seen on MRI correlates with visual
impairment at presentation and with visual prognosis [1]. Gadolinium
enhancement persists for a mean of 30 days since onset [1]. The signal abnormality in the nerve can
still be seen after recovery of vision, and is also present in as many as 60
percent of patients with MS who do not have a clinical history of optic
neuritis [1].
The brain MRI often shows white
matter abnormalities characteristic of MS . Typical lesions are ovoid,
periventricular, and larger than 3 mm.
The reported prevalence of white matter
abnormalities varies substantially among patients with optic neuritis (23 to 75
percent) .In the ONTT, almost 40 percent of patients had MRI lesions, but this
trial represents a selected patient group [7]. Small case series of unselected
patients have noted a higher coincidence of MRI brain lesions [1]. Individuals with white matter
abnormalities are at a higher risk of developing MS.
The yield of spinal cord imaging is
low in unselected patients. Among 115 patients presenting with optic neuritis,
MRI abnormalities in the spinal cord were seen in only four patients with a
normal brain MRI [1].
Lumbar puncture —
Lumbar puncture is not an essential
diagnostic test in optic neuritis, but should be considered in atypical cases
(eg, those with bilateral presentation, <15 years in age, or symptoms
suggesting infection)
Approximately 60 to 80 percent of patients
with acute optic neuritis have nonspecific abnormalities in the cerebrospinal
fluid (CSF), including lymphocytes (10 to 100) and elevated protein [1].
Other CSF findings in optic neuritis
can include :
●Myelin basic protein in about 20
percent
●IgG synthesis in 20 to 36 percent
●Oligoclonal bands (OCB) in 56 to 69
percent
The presence of OCB implies a higher
risk of developing MS. However, since OCB are also associated with white matter
lesions on brain MRI, their presence is not clearly of independent prognostic
importance [1]
Other testing —
When there are relevant clues to an
alternative diagnosis , measurement of the erythrocyte sedimentation rate,
antinuclear antibodies, and angiotensin converting enzyme levels and serologic
and CSF tests for Lyme disease and syphilis should be obtained [1]
Fluorescein angiography —
Fluorescein angiography is not routinely performed in the
evaluation of optic neuritis and is often normal. Up to 25 percent demonstrate either
dye leakage or perivenous sheathing . These findings may identify patients at
somewhat higher risk for developing MS. [1].
Visual evoked response —
A delay in the P100 of the visual
evoked response (VER) is the electrophysiologic manifestation of slowed
conduction in the optic nerve as a result of axonal demyelination. This test is
not usually helpful in the diagnosis of acute optic neuritis, unless there is a
suspicion that the visual loss is functional.
Abnormalities in the VER can persist
after recovery of full vision. At one year, 80 to 90 percent will be abnormal;
35 percent will return to normal at two years . The VER is often employed to
find evidence of previous, asymptomatic, episodes of optic neuritis, but the
sensitivity and specificity are imperfect [1].
The multifocal VER is a technical
advance that appears to be more sensitive and specific for identifying optic
neuritis, but this technology is not generally available [1].
VISUAL
FIELD TEST
Virtually any
type of optic nerve visual field loss can occur in optic neuritis, including
altitudinal, arcuate, central or cecocentral, diffuse,and even unilateral
hemianopic visual field defects or asymmetric upper nasal quadrantanopsia.22,23
Visual field defects are often found in the contralateral eye[5]
Contrast
sensitivity impairment is found in virtually all patients with optic
neuritis,
usually parallels the severity of visual loss.
OPTHALMOSCOPY
The optic disc
appears normal (retrobulbar ON) in about two-thirds of patients. Optic disc
swelling will be present in 20 to 40% of cases or, if the patient has
experienced a previous clinical or subclinical attack of optic neuritis, pale.
Both the swelling and the pallor are nonspecific findings in ON, and neither is
useful in distinguishing demyelinating ON from the ON that may accompany other
inflammatory or infectious diseases. The degree of swelling does not correlate
with the severity of optic nerve disfunction. Optic disc or peripapillary
hemorrhages are uncommon[5]
Optical coherence tomography —
Optical coherence tomography
(OCT) measures the thickness in the retinal nerve fiber layer and detects
thinning in most (85 percent) of patients with optic neuritis . These
abnormalities are also common in patients with MS who do not have a clinical
history of optic neuritis . While lower values correlate with impaired visual
outcome, the utility of OCT as a prognostic tool is limited in that abnormal
values do not show up until early swelling disappears. In one study, OCT was
less sensitive than VER in detecting subclinical optic neuritis
A number of studies have found that
a greater severity of optic nerve injury seen on OCT suggests neuromyelitis
optica rather than optic neuritis associated with multiple sclerosis [1].
Aquaporin-4-specific serum
autoantibody —
Patients with recurrent optic
neuritis may be particularly at risk neuromyelitis optica (NMO) or Devic's
disease. This is particularly true for patients with a normal brain MRI and
those with optic neuritis events in rapid succession or with a presentation of
severe vision loss . In one series of 51 patients with either severe or
recurrent optic neuritis, six patients were seropositive for the
aquaporin-4-specific serum autoantibody, a sensitive biomarker for NMO while 10
patients were seropositive for antibodies to myelin-oligodendrocyte
glycoprotein (MOG), which has also been associated with NMO . In other studies,
seropositivity for the aquaporin-4-specific serum autoantibody was predictive
of subsequent NMO among patients with recurrent optic neuritis. The serum NMO
antibody test is suggested for individuals with recurrent ON, particularly if
the MRI brain is negative for any abnormal T2/FLAIR lesions outside
of the affected optic nerve(s). The role for testing MOG antibodies is
investigational. [1].
Management
Consider corticosteroids during the
acute phase:
Treatment with methylprednisolone
speeds up visual recovery in the acute phase, but has no effect on final visual
acuity. Side-effects of corticosteroids can be serious. Therefore, they are
usually reserved for patients who need to hasten visual recovery, such as those
with poor vision in the fellow eye or bilateral visual loss, or for
occupational reasons.
Recommended treatment is
methylprednisolone 1 g daily for three days. [2]
Oral prednisolone is not recommended
because of (uncertain) evidence that it may increase the recurrence rate.
There is no treatment that can reverse
poor visual outcome in the long term.
Information for patients is
important (see 'Prognosis', below).
Consider brain MRI, to give
information about the risk of developing MS.
Consider referring to a neurologist
for assessment of the patient's risk of developing MS, and the value of
disease-modifying drugs in this context (see 'Role of disease-modifying drugs',
below).
For Pulfrich's phenomenon (disturbed
perception of movement), symptoms may be helped by using spectacles with a
tinted lens over the unaffected eye, to balance the delay in conduction from
the other side.[2]
For Uhthoff's phenomenon symptoms
(worsening vision with raised body temperature), avoid hot environments and
take cool drinks; reassure patients that this symptom is reversible and does
not further damage vision. [2]
Intravenous immunoglobulin has
generally been found to be of no benefit. One trial (small and non-randomised,
using a different regimen) reported improved vision with immunoglobulin
treatment. [2]
Prognosis
Visual prognosis
·
The Optic Neuritis Treatment
Trial (ONTT), was a large study of ADON with 15-year follow-up, and found that:
·
93% of patients showed
improvement within five weeks of onset of ADON; vision continued to improve for
up to one year. One year after onset, 93% had visual acuity better than 6/12 in
the affected eye. At 15-year follow-up, 92% had acuity better than 6/12 in the
affected eye, and only 1% had vision worse than 6/60 in both eyes.
·
The severity of initial visual
loss seems to be related to the final visual outcome; however, even with
initial visual acuity of ≤6/60, 85% recover vision to 6/12 or better.
·
Although visual outcome is good
in objective tests, many patients experience subjective reductions in vision,
colour vision, contrast sensitivity or depth/movement perception after recovery
from ADON. [2]
Risk of
recurrence
·
ADON can recur in either eye.
·
The risk of recurrence was 35%
over 10 years in the ONTT. [2]
Risk of
developing MS
·
ADON is associated with MS.
·
In the ONTT, for adults with a
single episode of unilateral ADON, the risk of MS was 38% at 10 years after
onset, and 50% at 15 years.[16] Another study found the MS risk was 54% after 30 years. The risk
of developing MS is lower for children and for men. [2]
·
MRI of the brain gives
information about the risk of developing MS. The presence of white matter
abnormalities increases the MS risk and their absence reduces it. In the ONTT,
the risk of developing MS at 15-year follow-up was 25% for patients with no
lesions on MRI, and 75% for those with white matter lesion(s).[2]
Role of disease-modifying
drugs
·
Interferon beta increases the
time interval to relapse in MS. Trials suggest that, in a scenario such as a
patient with ADON and white matter lesions on brain MRI, where the risk of
developing MS is relatively high, interferon beta may similarly delay the onset
of MS symptoms.
·
However, bear in mind that:
·
Many patients with a first
episode of ADON and an abnormal MRI scan will not develop MS.
·
Treatment is only partly
effective - eg, six years of interferon beta treatment prevents one relapse.
·
The visual prognosis is good
even if MS develops. [2]
MAJOR STUDY FINDINGS FOR TREATMENT
OF OPTIC NEURITIS BY AMERICAN ACADEMY OF OPTHALMOLOGY:
Combination drugs
speed recovery. ONTT helped define the role of corticosteroids in the
treatment of acute optic neuritis. When the study originated, many doctors were
treating the condition with oral corticosteroids. The study looked at oral
prednisone vs. high-dose intravenous methylprednisolone vs. placebo and found
that the IV methylprednisolone followed by a tapering course of oral prednisone
accelerated visual recovery by a few weeks. [4]
Recovery of vision
occurs with or without treatment. The investigators found that the choice of regimen has no
effect on final visual outcome. Most patients in the placebo group recovered
vision, on average, in six to eight weeks. Oral prednisone alone was no better
than placebo with respect to visual recovery and, in fact, was associated with
twice the risk of recurrent optic neuritis. It is no longer recommended for an
initial episode of typical, presumed demyelinative optic neuritis. The therapy
should include either high-dose methylprednisolone or nothing, Dr. Beck
explained [4].
White matter lesions
predict MS. The initial findings, published 16 years ago, in 1992,
still apply today, said Dr. Beck. But in addition to determining a therapeutic
regimen, the ONTT defined the risk factors for development of MS among patients
with optic neuritis. The presence of asymptomatic white matter lesions on the
MRI scan is the strongest predictor for MS. Few patients at the start of the
study had any history of MS, but over time the numbers grew. [4]
Outcome favorable and
stable. For
the majority of patients, even those with MS, the visual outcome is good. Those
who develop MS are more likely to exhibit abnormal visual function findings,
but their vision is normal about 60 percent of the time.
There was little or no
change in visual acuity in the affected eye between the 10- and 15-year
examinations, in most patients. After 15 years, 72 percent of patients with
optic neuritis had visual acuity of 20/20 or better; and 66 percent had acuity
of 20/20 or better in both eyes.[4]
Conclusion
Patients with MS
may develop disturbances of visual sensory function and disorders of ocular motor
system. These disturbances may precede, or occur coincidentally with neurologic
manifestations. Sometimes, disturbances
of the visual
sensory system are themselves asymptomatic but may be important findings that
establish the diagnosis of MS in a patient with a single symptomatic
neurologic
deficit. Visual impairment occurs in numerous patients with MS and may be the
presenting symptom. MRI scanning of the brain should be undertaken
in all cases of
acute ON for diagnostic and prognostic purposes. Disorders of ocular motor
system are frequently the initial sign of multiple sclerosis and occur
as its
presenting sign weeks, month, or years before other neurologic symptoms and
signs develop[5]
Finally The most common presentation is inflammatory, demyelinating,
idiopathic, or “typical” ON, which may be associated with multiple sclerosis.
This must be differentiated from “atypical” causes of ON, which differ in their
clinical presentation, natural history, management, and prognosis. Clinical
“red flags” for an atypical cause of ON include absent or persistent pain,
exudates and hemorrhages on fundoscopy, very severe, bilateral, or progressive
visual loss, and failure to recover. In typical ON, steroids shorten the
duration of the attack, but do not influence visual outcome. This is in
contrast to atypical ON associated with conditions such as sarcoidosis and
neuromyelitis optica, which require aggressive immunosuppression and sometimes
plasma exchange. The visual prognosis of typical ON is generally good. The
prognosis in atypical ON is more variable. Future therapeutic directions may include enhancing
repair processes, such as remyelination or adaptive neuroplasticity, or
alternative methods of immunomodulation. Pilot studies investigating the safety
and proof-of principle of stem cell treatment are currently underway. [3]
REFERENCE:
5)
Cerovski et al.: Multiple Sclerosis and
Neuro-Ophthalmologic Manifestations, Coll. Antropol. 29 (2005) Suppl. 1:
153–158
