The optic nerve is the nerve of vision. It carries images of what we
see coded as electrical impulses, from our eye to our brain. The
optic nerve is like a cable of electrical wires, and consists of
about 1,200,000 separate tiny wires, or nerve fibers. Each of these
carries a part of the information. If some or all of the nerve fibers
do not do their job, our vision becomes blurred.

Optic neuritis is the medical term used to describe an inflammation
of the optic nerve. The nerve tissue becomes swollen and red, and the
nerve fibers do not work properly. If many of the nerve fibers are
involved, the vision may be very poor, but if the optic neuritis is
mild, vision is nearly normal. Many diseases and conditions may cause
optic neuritis, which may affect the optic nerve of one or both eyes.

Some people, especially children, develop optic neuritis following a
virus illness such as mumps, measles, or a cold. In others, optic
neuritis may occur as a sign of a neurologic disease affecting nerves
in various parts of the body. In a rare condition called Leber's
optic neuropathy, which often runs in families, a special kind of
optic neuritis may appear in both eyes within a short span of time.
Most of the time, however, we cannot discover a cause for optic
neuritis. In those cases, we call the neuritis idiopathic, meaning
that no particular cause can be found.

Optic neuritis usually comes on suddenly, and the patient notices
vision is blurred in one or both eyes. The vision is also dim, like
somebody turned down the lights, and colors may appear to be washed
out. There may be pain in the area of the eye socket, especially when
moving the eyes. The vision may continue to get worse over a week or
two, and may seem worse after exercising or a hot bath.

A careful description of these symptoms is important to your doctor
in the diagnosis of optic neuritis. Since the optic nerve enters the
back of the eye where it appears as a small disc, your eye doctor can
examine it by looking in your eye with a special instrument called an
ophthalmoscope. Swelling of the optic nerve may or may not be visible
depending on whether the optic neuritis is affecting the optic nerve
near the eyeball.


OPTIC NEURITIS

Since optic neuritis can be confused with many other causes of poor
vision, an accurate medical diagnosis is important. If a cause can be
found and treated, further damage may be prevented. Ultrasound, CT
scans or visual brain wave recordings might be ordered. Other tests
which may be performed include color vision, side vision, and pupil
reactions to light.

Unfortunately, there is no good treatment for optic neuritis.
Cortisone-like medications (steroids) can be prescribed, but in most
cases they are not effective. Fortunately, most patients with optic
neuritis improve without treatment. In some cases, the vision may
return to normal. In other cases, good but incomplete improvement
occurs. A few patients fail to recover normal vision, especially
those with special conditions.


http://www.grolaser.com/laservisioncorrection/patienteducation/opticne
uritis.html


http://www.djo.harvard.edu/OA/ON/ON.html

---------------------------------------------------------------------
-----------
A Review of Optic Neuritis

Ken Graham M.D.
Department of Ophthalmology, Massachusetts Eye and Ear Infirmary,
Harvard Medical School, Boston, MA .
Joseph Rizzo M.D.
Department of Ophthalmology, Massachusetts Eye and Ear Infirmary,
Harvard Medical School, Boston, MA

Address correspondence to:
Ken Graham M.D.
Massachusetts Eye and Ear Infirmary, Harvard Medical School
243 Charles Street
Boston, MA 02114



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PURPOSE



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Optic neuritis is inflammation of the optic nerve. The cause of the
inflammation and the most appropriate treatment is a subject of
debate. This article will review a typical case of optic neuritis,
the clinicalmanifestations of optic neuritis, and the findings of the
Optic Neuritis Treatment Trial.

INTRODUCTION



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Optic neuritis is a serious condition which typically involves
theyoung adult population. Years ago it was thought that one third
ofoptic neuritis patients would go on to have neurological symptoms
frommultiple sclerosis (MS). More recent long term studies indicate
that over decades the risk of developing MS is much higher.(1)
Ophthalmologists must be alert to the symptoms of optic neuritis
andthey must be aware of the more serious complications to which
these symptoms are linked

CASE PRESENTATION



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A 30 year old caucasian man presented with 2 weeks of gradually
worsening vision in his left eye.

History of present illness:

The patient had been seen once by a neurologist 2 years previously
for flashes. At that time a head CT was normal. The patient was lost
to follow up with the neurologist, but the flashes had continued for
the 2 year period. The patient has a history of color blindness. The
patient also reported posterior pressure and tightness with left eye
movement for the past week. The patient reported his vision in the
left eye worsened when showering. The patient did not experience
visual changes with activity or movement. Patient denied a history of
trauma, redness, discharge or headache.

Past medical history: negative

Social history: negative

Medications: none

No known drug allergies

Examination:

The exam revealed a vision of 20/20 OD and 20/30 OS. The patient was
only able to get the control plate correct on the color plates in
both eyes consistent with his history of color blindness. The
external exam revealed no ptosis, and no resistance to retropulsion.
His pupils were reactive to light, changing from 4 to 2mm
symmetrically. There was a left afferent pupillary defect. Hertel
measurement with a base of 102 was 19 OD and 18 OS. Extraocular
movements were full OU, though the patient reported a "tight" feeling
on OS abduction. Tension was 15 OU. Slit lamp exam was normal OU.
Dilated exam was normal OU with no disc edema. Humphrey visual fields
showed an inferior altitudinal defect OS ( Fig 1and 2).



Figure 1. Humphrey visual field OD.

Figure 2. Humphrey visual field OS.

One week follow up:

The patient reported continued decreasing vision OS. The exam
revealed visual acuity of 20/20 OD and 20/400 OS. The OS afferent
pupillary defect remained. The rest of the exam was the same.
Goldmann visual fields were done and showed a central scotoma OS
(slide 3).



Figure 3.Goldmann Visual Field OS.

A MRI was done at this time and showed inflammation of the left optic
nerve (slide 4), and white matter hyperintensity of the left
occipital (slide 5) and right frontal(slide 6) lobes. Possible
treatment with corticosteroids was discussed with the patient. He
chose to be observed with no corticosteroid treatment.



Figure 4. MRI demonstrating optic nerve white matter hyperintensity.

Figure 5. MRI demonstrating left occipital lobe hyperintensity.



Figure 6. MRI demonstrating right frontal lobe hyperintensity.

One month follow up:

The patient reported marked recovery of vision OS, but had some
blurring in bright sunlight. The patient was on no medications. His
vision was 20/20 OU. There was no afferent pupillary defect and
no "tightness" on eye movement. The rest of the exam was unchanged. A
Humphrey visual field showed improvement in the central scotoma .

CLINICAL MANIFESTATION



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Optic neuritis typically presents with a triad of symptoms: loss of
vision, dyschromatopsia and eye pain. The initial attack is
unilateral in 70% of adult patients and bilateral in 30%. The mean
age of onset of optic neuritis is in the third decade of life, but
can occur from the first to the seventh decades. The annual incidence
of optic neuritis ranges from 1.4 to 6.4 new cases per 100,000
population. (2,3) Associated visual symptoms are reduced perception
of light intensity and Uhthoff's symptom (visual deficit induced by
exercise or increased body temperature).(4)

The visual loss may be subtle or profound. Complete loss of vision
may be caused by a single plaque. In some cases the vision may be
20/20 with the only symptoms being blurred vision on exertion or
other isolated symptoms.(5) The rate of visual decline varies. Visual
loss may occur over hours (rarely) to days (most commonly). The nadir
is usually about 1 week after the onset.(6)

The prognosis for visual recovery is usually good. The majority of
patients (65-80%) recover visual acuity of 20/30 or better.(7,8) Most
cases will recover visual acuity in a few months, although the
patients will often report some residual visual defect. There have
been reported residual abnormalities in contrast sensitivity, color
vision, visual field loss, and light brightness.(9-12)

In a patient with optic neuritis, the vision may improve, but the
risk for development of multiple sclerosis is high. This risk does
not decrease over time.(1) In the past a number of patients have been
treated with oral or intravenous corticosteroids in the hope of
improving visual recovery and decreasing the incidence of multiple
sclerosis. To help resolve the controversy of corticosteroids, the
Optic Neuritis Treatment Trial was formed.


OPTIC NEURITIS TREATMENT TRIAL



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The Optic Neuritis Treatment Trial (ONTT) was a multicenter study in
which 389 patients with acute optic neuritis were randomly assigned
to one of three treatment groups. The first group was given oral
prednisone (1 mg/kg daily) for 14 days. The second group was given
intravenous methylprednisolone, 250 mg four times daily for three
days, followed by oral prednisone for 14 days. The third group was
given an oral placebo for 14 days.

The eligibility criteria for the ONTT selected for patients with
typical clinical features of optic neuritis. These criteria were: age
range of 18 to 46 years; acute unilateral optic neuritis with visual
symptoms of 8 days or less; a relative afferent pupillary defect and
a visual field defect in the affected eye; no previous episodes of
optic neuritis in the affected eye; no previous corticosteroid
treatment for optic neuritis or multiple sclerosis; and no systemic
disease other than multiple sclerosis that might be associated with
optic neuritis.(13)

All patients in the ONTT had blood testing to exclude collagen
vascular disease (antinuclear antibody), syphilis (FTA-ABS), and a
chest x-ray to detect sarcoidosis. A lumbar puncture was optional and
was performed in 141 patients. Antinuclear antibody was positive in a
titer 1:320 or greater in 3% of patients. Of these patients, only one
developed a connective tissue disease in the first two years of
follow up. FTA-ABS was positive in 1.3% of the patients, and none
were judged to have syphilis. A chest x-ray did not show evidence of
sarcoidosis in any patients. CSF analysis never yielded unsuspected
information. Based on these results, chest x-ray, blood tests, and
lumbar puncture are deemed not to be necessary in evaluating patients
with typical clinical features of optic neuritis.

The efficacy of corticosteroid therapy in optic neuritis has been
controversial. The ONTT showed that intravenous methylprednisolone
followed by oral prednisone speeds the recovery of visual loss, but
there were no significant differences in visual acuity comparing the
three groups at 6 months. Unexpectedly, oral prednisone was found to
increase the risk of recurrent optic neuritis. Thus, treatment with
oral prednisone in standard doses is no longer advised.

The ONTT also evaluated the relationship between optic neuritis and
multiple sclerosis. A standardized detailed neurologic examination
was performed at study entry, at 6 months, at 1 year and then yearly.
Clinically definite multiple sclerosis was diagnosed when new
neurologic symptoms developed that were attributable to demyelination
in one or more regions of the central nervous system. Treatment with
the intravenous followed by oral corticosteroid regimen reduced the
rate of development of MS during the first 2 years. This was
particularly evident in patients with three or more brain MRI signal
abnormalities consistent with demyelination in locations
characteristic of MS. By 3 years, this treatment effect had subsided.

The ONTT therefore recommends obtaining a brain MRI to assess the
risk of developing MS. The MRI is used to assist in the decision of
whether to use IV steroids. It is unknown if repeat IV steroids at 2
years would continue to affect the rate of development of MS. Other
prospective studies using beta interferon are currently in progress.
(14)

REFERENCES



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----------


1. Rizzo JF, Lessell S: Risk of developing multiple sclerosis after
uncomplicated optic neuritis: A long term prospective study.
Neurology 38:185-190, 1988.

2. Brewis M, Poskanzer DC, Rolland C, et al: Neurological disease in
an English city. Acta Neurol Scand 42 (Suppl 24):1, 1965.

3. Wray SH: Optic Neuritis. Principles and Practice of Ophthalmology.
Volume 4, 2539-2568.

4. Percy AK, Nobrega FT, Kurland LT: Optic neuritis and multiple
sclerosis. Arch Ophthalmol 87:135,1972.

5. Nikoskelainen E: Symptoms, signs and early course of optic
neuritis. Acta Ophthalmol 53:254, 1975.

6. Lillie WI: The clinical significance of retrobulbar and optic
neuritis. Am J Ophtahlmol 17:110, 1934.

7. Perkin GD, Rose CF: Optic Neuritis and its Differential Diagnosis.
Oxford, Oxford University Press, 1979, p 206.

8. Celesia GG, Kaufman DI, Brigell M, et al: Optic neuritis: A
prospective study. Neurology 40:919, 1990.

9. Sanders EACM, Volkers ACW, van der Poel JC, et al: Estimation of
visual function after optic neuritis: A comparison of clinical tests.
Br J Ophthalmol 70:918, 1986.

10. Griffin JF, Wray SH: Acquired color vision defects in retrobulbar
neuritis. Am J Ophthalmol 86:193, 1978.

11. Van Dalen JTW, Greve EL: Visual field defects in multiple
sclerosis. Neuro-ophthalmology 2:93, 1981.

12. Hess RF, Plant GT: The psychophysical loss in optic neuritis:
spatial and temporal aspects. In Optic Neuritis. Cambridge, Cambridge
University Press, 1986, p 109.

13. Beck RW, Cleary PA, et al: Optic Neuritis Treatment Trial. Arch
Ophthalmol 3:773-775, 1993.

14. Beck RW, Trobe JD: What we have learned from the Optic Neuritis
Treatment Trial. Ophthalmology 10:1504-1509, 1995.

NATURE CURE
Neuritis
Neuritis is one of the serious nervous disorders. It refers to an
inflammation of the nerves, involving a single nerve or a series of
nerves. At times, several different groups of nerves in various parts
of the body may be involved. This condition is known as polyneuritis.
It is also known as polyneuropathy, for strictly speaking, the
condition is not an inflammation, but a change in the state of the
nerves resulting in weakness, loss of the reflexes and changes of
sensation.
Symptoms
The main symptoms of neuritis are tingling, burning, and stabbing
pains in the affected nerves. IN severe cases, there may be numbness
and loss of sensation and paralysis of the nearby muscles. Thus a
temporary paralysis of the face may result from changes in the facial
nerves on the affected side. During the acute stage of this
condition, the patient may not be able to close the eyes due to loss
of normal tone and strength by the muscles on the affected side of
the face. Neuritis may also be caused by pernicious anaemia,
involving the nerves of the spine. The patient with this condition
may find it very difficult to walk in the dark.

Causes
The chief cause of neuritis is chronic acidosis, that is, excessive
acid condition of the blood and other body fluids. All the body
fluids should be alkaline in their reaction ,but when the acid waste
matter is continuously formed in the tissues over a long period due
to a faulty diet, it results in acidosis. Wrong habits of living ,
over work , etc., lower the tone of nervous system and contribute
towards neuritis. This disease can also result from a variety of
nutritional deficiencies and metabolic disturbances such as faulty
calcium metabolism, deficiencies of several B vitamins like B12, B6,
B1, pantothenic acid and B2 and general toxaemia.
Other causes of neuritis include a blow, a penetrating injury a bad
bruise or heavy pressure over a nerve trunk and dislocation and
fractures of the bones. Any violent muscular activity or over-
extension of the joint as in sprains may injure the nerves and cause
neuritis. The condition may also result from certain infections such
as tuberculosis, diptheria, tetanus, leprosy and diabetes mellitius,
poisoning with insecticides, mercury, lead, arsenic and alcohol.

Treatment
Treatment of neuritis by painkilling drugs may give temporary relief
but it does not remove the trouble effectively. The pain is relieved
for the time being at the cost of the health of other parts of the
body, especially the heart and the kidneys, and the neuritis remains.
The best treatment for neuritis is to ensure that the patient gets
optimum nutrition, well assimilated with all the vitamins and other
nutrients. The emphasis should be on whole grains, particularly whole
wheat,brown rice, raw and sprouted seeds, raw milk, especially in
soured form, and home-made cottage cheese.
In this regimen, the breakfast may consist of fresh fruits, a handful
of raw nuts or a couple of tablespoons of sunflower and pumpkin
seeds. Steamed vegetables, whole wheat, chappatis and a glass of
butter-milk may be taken for lunch. The dinner may comprise a large
bowl of fresh, green, vegetable salad, fresh home made cottage
cheese, fresh butter and a glass of butter milk.
In severe cases, the patient should be put on a short juice fast for
four or five days before being given the optimum diet. Carrot, beet,
citrus fruits, apple and pineapple may be used for juices.
All vitamins of the B group have proved highly beneficial in the
prevention and treatment of neuritis. The disorder has been helped
when vitamins B1, B2, B6, B12, and pantothenic acid have been given
together, and extreme pain,weakness and numbness in some cases have
been relieved within an hour.
The patient should avoid white bread, white sugar,refined cereals,
meat, fish, tinned foods, tea, coffee, and condiments which are at
the root of the trouble, by continuously flooding the tissues with
acid impurities.
Certain remedies have been found highly beneficial in the treatment
of neuritis. One such remedy is soyabean milk. A cupful of soyabean
milk mixed with a teaspoonful of honey should be taken every night in
this condition. It tones up the nervous system due to its rich
concentration of lecithin, vitamin B1 and glutanic acid. Soyabean
milk is prepared by soaking the beans in water for about 12 hours.
The skin of the beans is then removed and after a thorough wash, they
are turned into a fine paste in a grinding machine. The paste is
mixed with water, three times its quantity. The milk should then be
boiled on a slow fire, stirring it frequently. After it becomes
little cooler, it should be strained through a cheese cloth and sugar
added.
barley brew is another effective remedy for neuritis. It is prepared
by boiling one-quarter cup of all natural pearled barley in two
quarters of water. When the water has boiled down to about one
quarter, it should be strained carefully. For better results, it
should be mixed with butter-milk and lime juice.
Raw carrot and spinach have proved valuable in neuritis as both these
vegetables are rich in elements, the deficiency of which has led to
this disease. The quickest and most effective way in which the body
can obtain and assimilate these elements is by drinking daily at
least half a litre of the combined raw juices of carrot and spinach.
The patient should be given two or three hot Epsom-salt baths weekly.
He should remain in the bath for 25 to 30 minutes. The affected parts
should also be bathed several times daily in the hot water containing
Epsom salt - a table- spoon of salt to a cupful of hot water. The
patient should undertake walking and other moderate exercises.

http://www.healthlibrary.com/reading/ncure/chap65.htm

http://www.nationalmssociety.org/%5CSourcebook-Optic%20Neuritis.asp

http://www.dog.org/1999/e-abstract99/597.html




_______
Behavioral, Structural, Functional Abnormalities
associated with various Heavy Metal Toxins

Published in the August issue of Alternative & Complementary
Therapies
(a magazine for doctors) and Published in the April issue of Townsend
Letter for Doctor's & Patients.



http://www.extremehealthus.com/behavior.html

Neuritis
Neuritis is one of the most serious nervous disorders. It refers to
an inflammation of the nerves, involving a single nerve or a series
of nerves. At times, several different groups of nerves in various
parts of the body may be involved. This condition is known as
polyneuritis. It is also known as polyneuropathy, for strictly
speaking, the condition is not an inflammation, but a change in the
state of the nerves resulting in weakness of the reflexes and changes
of sensation.
Symptoms
The main symptoms of neuritis are tingling and burning and stabbing
pains in the affected nerves. IN severe cases there may be numbness
and loss of sensation and paralysis of the nearby muscles. Thus,
temporary paralysis of the face may result from changes in the facial
nerves on the affected side. During the acute stage of this
condition, the patient may not be able to close the eyes due to loss
of normal tone and strength in the muscles on the affected side of
the face. Neuritis may also be caused by pernicious anaemia,
involving the nerves of the spine. The patient with this condition
may find it very difficult to walk in the darkness.

Causes
The chief cause of neuritis is chronic acidosis, that is, an
excessive acidic condition of the blood and other body fluids. All
the body fluids should be alkaline in their reaction, but when the
acid waste matter is continuously formed in the tissues over a long
period due to a faulty diet, it results in acidosis. Wrong habits of
living, over- work , etc., lower the tone of the nervous system and
contribute towards neuritis. The disease can also result form a
variety of nutritional deficiencies and metabolic disturbances such
as faulty calcium metabolism, deficiencies of several B vitamins like
B12, B6, B1, pantothenic acid and B2 and general toxaemia. Other
causes of neuritis include a blow, a penetrating injury, a bad bruise
or heavy pressure over a nerve trunk and dislocation or fracture of
the bones. Any violent muscular activity or over extension of the
joint as in sprains may injure the nerves and cause neuritis. The
condition may also result from certain infections such as
tuberculosis, diptheria, tetanus, leprosy and diabetes mellitus,
poisoning with insecticides, mercury, lead, arsenic and alcohol.


http://www.healthlibrary.com/reading/diet/neuritis.htm