How the eye works

We need light to see what is around us and to see colour. Light

bounces off the objects we look at. These reflect different
amounts of light which we see as different colours.
Light rays enter the front of our eye through the clear cornea
and lens. It is very important that both the cornea and lens are
clear as this allows the light to pass directly through the front
of the eye to the retina. The cornea and lens bends light so that
it can focus on the retina at the back of our eye. This gives us a
clear, precise image. The cornea focuses the light towards our
retina. The lens fine tunes the focussing of this light
Our tears form a protective layer at the front of the eye and
also help to direct the light coming into our eye. The iris, the
coloured circle at the front of our eye, changes the size of the
pupil which allows different amounts of light into our eye. The
pupil is the dark hole in the middle of the coloured part of our
eye. The pupil gets smaller in bright conditions to let less light
in and gets bigger in dark conditions to let more light in.
The middle of our eye is filled with a jelly-like substance
called the vitreous. The vitreous is clear and allows light to
pass directly from the front to the back of our eye.
The retina at the back of the eye is a light-sensitive layer
which consists of rod and cone cells. These cells collect the
light signals directed onto them and send them as electrical
signals to the optic nerve at the back of our eye.
Rod cells are concentrated around the edge of the retina. They
help us to see things that aren't directly in front of us, giving us
a rough idea of what is around us. They help us with our
mobility and getting around by stopping us from bumping into
a things. They also enable us to see things in dim light and to
see movement.
Cone cells are concentrated in the centre of our retina where
the light is focused by the cornea and lens. This area is called
the macula. Cone cells give us our detailed vision which we
use when reading, watching TV, sewing and looking at
people's faces. They are also responsible for most of our colour
vision.
The optic nerve is made up of thousands of nerve fibres.
These fibres pass the electrical signals along to our brain where
they are processed into the image we are looking at.
Seeing can be likened to the process of taking pictures on a
film with a camera which you then get developed. The retina
is like a camera film which stores an image of what we are
looking at. The image directed onto the retina is then sent
along to the brain where it is processed, like developing a
camera film. Therefore we actually 'see' in our brain with the
light information sent to it from our eyes. This whole process
happens very quickly so that everything we see is in focus.
About thyroid eye disease
Thyroid eye disease (thyroid orbitopathy or TO) is actually a
condition of the soft tissues such as the fat and muscles
surrounding the eyes. The condition is characterised by a
period of inflammation and engorgement of these tissues,
followed by a healing response.
The condition most commonly occurs in association with an
overactive thyroid gland, but also occurs with an under active
thyroid gland; an identical picture sometimes occurs when the
thyroid gland is not itself affected.
Thyroid gland
The thyroid is one of the body's endocrine glands; these are
glands which produce hormones. Hormones are chemical
messengers in our blood streams, which co-ordinate long term
changes in function. The thyroid is located in the neck just
below the Adam's apple, and its hormones regulate our
metabolism.
Diseases of thyroid
The main problem affecting the thyroid is auto-immune
disease. Thyroid cancers also occur. The effect of thyroid
disease is felt as either an over-activity or under-activity of the
gland, and therefore either a speeding up or a slowing down of
metabolism.
Auto-immune disease and the thyroid
Auto-immune problems are caused by inappropriate behaviour
of the body's immune system. The immune system usually
fights off infection but in auto-immune disease it attacks the
body's own tissues with auto-antibodies. At the moment the
reason for this is not entirely clear.
Why thyroid problems affect the eyes
When an auto-immune attack starts on the thyroid, it responds
by producing more of its hormones. At the same time the auto-
antibodies attacking the thyroid gland also attack the tissues
around the eyes.
More information on thyroid problems is available from the
British Thyroid Association, details at the end of this page.
How thyroid disease affects the eyes
The commonest problem is dry eyes. This is because, in auto-
immune disease, more than one organ may be attacked, and
commonly the thyroid and all the orbital contents (the soft
tissues around the eye), including the lacrimal gland, are
attacked by the immune system. The lacrimal gland produces
the tears in our eyes, so when it is affected fewer tears are
produced. As a result, the eyes may feel dry and gritty. It is
worth noting that, although the eyes are described as 'dry', they
can water and produce more tears than normal.
As the orbital contents (the soft tissues around the eye) become
inflamed, all the tissues of the orbit become red and swollen.
 • The eyelids become puffy and red (lid swelling)
• The muscles of the eyelids contract, producing a staring
appearance (lid retraction)
• The muscles and fat surrounding the eye swells, pushing
the eyes forward so that they bulge out of the orbits
(exophthalmos)
• Lid retraction and exophthalmos make the dry eye
symptoms worse.
• The swelling of the muscles which move the eyes
produces unequal movements and double vision
(diplopia)
• The orbits may become painful, particularly on eye
movement.
How thyroid orbitopathy affects sight
If the muscles become swollen, then this can affect how well
the muscles are able to control the ability of the eyes to move
together. This can cause double vision. This is a symptom
which occurs when the eyes do not quite point in the same
direction and therefore each sends a slightly different message
to the brain. When this happens our brains 'see' two of
everything. This can make activities like reading very difficult,
and driving very dangerous. If someone develops double vision
then they must stop driving, it is illegal to drive with double
vision which isn't controlled.
If you do develop double vision then you have to inform the
Driver and Vehicle Licensing Authority (DVLA) and, usually,
they will contact your ophthalmologist for a medical report. If
your double vision then becomes controlled with glasses at a
later date the DVLA will declare you fit to drive. Not
informing the DVLA of double vision could have serious
consequences for your insurance status and you would be also
be driving illegally.
In severe Thyroid Orbitopathy, especially in younger patients
whose firm tissues do not allow the eyes to bulge forwards, the
pressure inside the orbits increases, compressing the optic
nerve and causing sight problems. The optic nerve carries the
messages from the eye to the brain and can be damaged by
pressure.
If the pressure starts to compress the optic nerve sight may
become dim, colours begin to look washed out, and the visual
field may constrict. If this starts to happen, then medical
attention needs to be sought as soon as possible, to reduce the
pressure on the optic nerve before permanent damage occurs.
The treatment options for optic nerve compression are steroids,
immunosuppressant drugs, orbital radiotherapy and emergency
orbital decompression surgery. These all aim to lower the
pressure on the optic nerve and hopefully avoid permanent
damage.
Treatment for thyroid disease
The first priority is to deal with the primary thyroid problem.
This is firstly with anti-thyroid drugs, and then with either
surgery or radiotherapy. The treatment of an overactive thyroid
often produces an under active thyroid, which then requires
treatment with thyroid replacement therapy. It is very
important to be aware that the treatment of the underlying
thyroid condition often makes the associated eye condition
worse, and to be ready for this.
Thyroid orbitopathy treatment
When the eyes are dry and gritty then the best treatment is to
use lubricating eye drops - artificial tears.
These can help to make the eyes feel more comfortable and
help to prevent the eye being damaged by being so dry.
Treatment for double vision
A variety of treatments are available depending on whether the
double vision is temporary or permanent. An orthoptist (an eye
professional who specialises in double vision) should be
involved in such treatments.
Occlusion
In this treatment, one eye is simply covered up so that the brain
receives only one image.
Prisms
Prisms work by bending light in a direction which
compensates for the angle between the eyes. They can be
tailored to the angle between the eyes and affixed to spectacles.
Stick-on prisms, often called Fresnel prisms, are used until it is
established that the angle is constant, at which point prisms,
can be incorporated into the spectacle lens by an optometrist.
In temporary double vision during the active stage of TO,
prisms may be the only treatment necessary. As TO burns out,
however, it often leaves some residual double vision requiring
surgical treatment.
Long term effect of thyroid orbitopathy
In the majority of cases, the active inflamed stage of TO burns
itself out in about two years, leaving a variable amount of
scarring, with lid retraction, exophthalmos or double vision.
A decision can then be made by the patient as to whether the
problems that are left are acceptable, or whether they are
severe enough to justify the risks of surgery.
If, after the thyroid orbitopathy has burned itself out, there are
still problems with the eyes (including exophthalmos, lid
retraction and double vision), then it becomes necessary to
decide whether or not to have further surgery to help improve
these things. Sometimes the problems that are left may only be
minor and someone may feel it isn't necessary to have more
treatment, or that the risks of the surgery outweigh the
problems that they have. However, there may be cases where
surgery is a more obvious choice.
If surgery is needed then it is carried out in the sequence of
orbital decompression, surgery to the muscles of the eye for
double vision, and surgery to correct the lid position.
Orbital decompression is carried out to place the eyes further
back in the orbits where they belong. This is normally
accomplished by removing a small amount of bone from inside
the orbit of the eye so that the eye can sit further back in its
socket. Occasionally fat may also be removed from the inside
of the orbit. One of the major risks of this surgery is the
development or worsening of double vision, so it should be
expected that after this surgery someone may need muscle
surgery as well. There is also a small risk of serious sight
problems with this surgery.
If someone is left with stable permanent double vision, surgery
is the treatment of choice to correct this. This surgery
lengthens the muscles of the eye so that the eyes are brought
back into alignment. This is usually done with an adjustable
suture technique. Muscle surgery may alter the position of the
eyelids and so it should be expected that at some point after
muscle surgery, lid surgery may be necessary.
Lid surgery aims to correct the position of the upper and lower
eyelids over the eyes, allowing proper closure.
To perform any of this surgery it is necessary for the thyroid
disease itself to be stable and for the active phase of the orbital
disease to have burnt out. Because of this some
ophthalmologists believe that early low dose radiotherapy
given early in the active phase of the TO can help improve the
outcome after the TO has burnt out.
All this means that if someone is left with problems once the
TO has burnt itself out then they could face a program of
operations to improve vision. Usually the operations are
performed in the following order: orbital decompression,
surgery to the muscles for double vision and surgery to correct
the lid position. Typically these operations are carried out over
about 18 months to 2 years.
With modern surgical techniques, very few people are left to
cope with the difficult after-effects of TO. The modern surgical
techniques now aim to restore the position, function and
appearance of the eyes to as near to normal as possible.

In the majority of cases of Hyperthyroidism, TSI autoantibodies are directly responsible

(>85%); this makes the detection of TSI a fundamental aspect of a correct diagnosis, and
monitoring their levels during treatment a diagnostic necessity. Another cause of
Hyperthyroidism is Thyroid nodules which are abnormal growths in the Thyroid which
over produce Thyroid hormones, causing the same type of symptoms as antibody driven
hormone over production. Patients can have single or multiple nodule growth and these
are usually benign. Thyroiditis or swelling of the Thyroid may also be caused by viral
infections.

Read more at Suite101: Causes of Hyperthyroidism: Is It Graves' Disease or Toxic

Multinodular Goiter or Thyroiditis?
http://autoimmunedisease.suite101.com/article.cfm/causesofhyperthyroidism#ixzz0cWV
XSYvU

Euthyroid Graves' disease is a condition characterized by the signs and symptoms of

thyroid eye disease in the absence of thyroid dysfunction.

Euthyroid Graves' disease is an autoimmune condition that causes the characteristic eye
symptoms of Graves' ophtalmopathy, which is more commonly known as thyroid eye
disease (TED), in the absence of thyroid dysfunction. Most patients with euthyroid
Graves' disease go on to develop thyroid disease within 12-18 months after eye
symptoms develop. Most of these patients develop Graves' disease, an autoimmune
thyroid disorder, although a smaller number of patients may develop autoimmune
hypothyroidism. About 15-20 percent of patients with euthyroid Graves' disease never
develop thyroid dysfunction. However, even though patients with euthyroid Graves'
disease are considered to have normal thyroid function based on blood tests for thyroid
function, they can have transient symptoms of both hypothyroidism and hyperthyroidism.
Patients with euthyroid Graves' disease typically have high levels of both stimulating and
blocking TSH receptor antibodies (TRAb). While stimulating TRAb, which are also
known as thyroid stimulating immunoglobulins or TSI, stimulate thyroid cells to produce
excess thyroid hormone in Graves' disease, the blocking TRAb in euthyroid Graves'
disease prevent TSI from causing hyperthyroidism. Each of these antibodies cancels out
the effects of the other on thyroid function. However, because they are both capable of
eliciting an immune response in eye muscle (orbital) tissue, they contribute to signs and
symptoms of TED.
The most significant changes in TED involve congestion and infiltration of orbital
muscle, causing the eyeball to appear swollen. The eye muscle in TED also has limited
motion caused by this congestion, causing limited upward or downward gaze. Muscle
restriction also contributes to double vision (diplopia). The muscle fibers in TED do not
change but deposits of white blood cells and immune system chemicals lodge between
the fibers causing orbital congestion. Typical symptoms in TED include eyelid retraction,
puffiness (orbital edema), proptosis or exophthalmos (bulging forward of the eyeball), lid
lag, photophobia (light sensitivity), conjunctival inflammation, double vision, redness,
optic nerve compression, and keratitis.
Patients with euthyroid Graves' disease may also develop pretibial myxedema, a skin
condition that is also caused by the combination of both blocking and stimulating TRAb.
In pretibial myxedema, the skin of the lower legs and shins is most likely to be affected.
Symptoms include puffy, mottled skins with waxy brown lesions. Occasionally, the skin
of the upper arms and back may also be affected.
Euthyroid Graves' disease is diagnosed in patients with symptoms of TED who have
normal thyroid function tests (FT4, FT3 and TSH) with elevated levels of TRAb. Patients
with euthyroid Graves' disease may also have high levels of thyroglobulin and/or TPO
antibodies. Imaging tests, especially MRI or CT scans, may also be used to assess orbital
congestion, and an exophthalmometer may be used to measure proptosis. An orbital
ultrasound may also used to measure enlargement of orbital muscles. Ultrasounds may be
followed over time to assess disease progression and treatment response.

Preventing Graves' Ophthalmopathy / Thyroid Eye Disease

Tuesday May 13, 2008
In a plenary lecture at the recent European Congress of Endocrinology, held in Berlin, Germany from May 3-7, 2008
case that while there are many open questions about Graves' opthalmopathy -- also known as thyroid eye disease
including a key factor in preventing the condition.

• In Graves' ophthalmopathy, the targets of the autoimmune attack are cells known as orbital fibroblasts
• Swelling of muscles and fat around the eye are responsible in part for the symptoms and signs of Graves

' ophthalmopathy,

•
• Better outcomes are seen for patients who are euthyroid (TSH is in the normal range)
• Immunosuppression treatment is recommended only in active Graves' ophthalmopathy, and the most
• effective immunosuppression treatment is corticosteroid treatment, specifically IV pulses of
• methylprednisolone
• At present, anticytokine treatment (Rituximab) is promising, but still being studied

"The discontinuation of smoking constitutes primary, secondary and tertiary prevention.

Thyroid Eye Disease and Graves Opthamolopathy

A Look at Thyroid-Related Eye Conditions

by Mary Shomon

There are many different names you might find for the autoimmune eye condition
that is often seen with thyroid disease, including:

• Thyroid Eye Disease, sometimes abbreviated as TED

• Graves' Opthamolopathy
• Thyroid-associated orbitopathy (TAO)
• Grave's orbitopathy

Thyroid Eye Disease is an autoimmune eye condition that, while separate from
thyroid disease, is often seen in conjunction with Graves' Disease. The condition,
however, is seen in people with no other evidence of thyroid dysfunction, and
occasionally in patients who have Hashimoto's Disease. Most thyroid patients,
however, will not develop thyroid eye disease, and if so, only mildly so.
Thyroid Eye Disease is known to go through varying degrees of severity, and can go into periods of
remission as well. When it has been inactive for a period of around a half a year, it's less likely to recur.
Smoking and Thyroid Eye Disease
It has been noted that the eye disease develops more frequently and is more severe
among women who smoke. See Smoking: The Little Known Links to Thyroid
Disease.
According to a Jan. 27, 1993 article in the Journal of the American Medical
Association, smokers are twice as likely as nonsmokers to develop Graves' disease.
According to that article, smoking also apparently worsens eye problems in people
with Graves' disease.
Researchers have also recently learned that smoking reduces the effectiveness of
treatments for thyroid eye disease. The researchers reviewed the outcomes of 300
Graves' disease patients with mild eye symptoms treated with radioiodine alone or
with steriods, and 150 with serious eye complications who received steroids and
radiation therapy for their thyroid eye disease.
Among Graves' disease patients who had milder eye symptoms, smokers were more
likely to progress to more serious thyroid eye disease than nonsmokers. Radioidone
and steroid treatment for thyroid eye disease was also four times more effective in
dealing with the eye symptoms for nonsmokers than smokers. This same relationship
also applied to patients with more serious thyroid eye disease. ("Smoking affects
Graves' disease treatment," Annals of Internal Medicine, 1998;129:632-635.)
Treatments
In milder cases of Thyroid Eye Disease, often all that is needed is lubricating eye
drops or ointments for moisture, wraparound sunglasses to avoid glare, bedroom
humidifiers to reduce dry eye problems. When double vision occurs, some patients
respond to the addition or prism lenses in their eyeglasses. For pain, swelling and
redness, short courses of the steroid prednisone are sometimes prescribed. Symptoms
often return after the course of prednisone therapy, however.
Some doctors recommend orbital radiation, which can be successful in some patients.

In rare cases, when medical treatment has not resolved the retracted and puffy
eyelids, or double vision, doctors will recommend corrective surgery. For some good
before and after pictures of Thyroid Eye Disease surgery results, see the Eyelid-
Doc.com website.
Eyelid surgery is primarily cosmetic in nature, and is designed to bring the eyelids
into a more normal position, to improve appearance.
Surgery for double vision works with the muscles that control eye movement.
In a very small percentage of patients, the swelling in the orbital area impairs vision
by pressing on the optic nerve. In these cases, a surgery called orbital decompression
is needed in order to prevent severe complications.
The Issue of Radioactive Iodine Treatment (RAI) for Graves' Disease
Radioactive Iodine (RAI) treatment is the preferred treatment in the U.S. for Graves'
Disease and its resulting hyperthyroidism. According to the New England Journal of
Medicine, however, radioiodine therapy for Graves' hyperthyroidism is more likely to
apparently cause or worsen Thyroid Eye Disease than is antithyroid drug therapy.
This worsening can be temporary however, and may in some cases be prevented by
use of the steroid prednisone.