Vision and EyeCare FAQ
Section 5: Disease of the Eye (Posterior Eye Disease)

5.1 Floaters and Spots in the Field of View

Floaters (muscae volitantes - "flying flies") are spots before the eyes of different shapes, sizes and number. They appear often when looking at a plain coloured field of view, eg blue sky, a wall. Typically when the patient tries to look at them they report that the spots "run- away". The spots are due to corpuscles circulating in the retinal vessels and specks within the vitreous. These opacities cause shadows to be cast onto the retinal sensory apparatus; the rods and cones; and thereby appear as dark spots in the field of vision. Slight cases or observations require no treatment.

There are other retinal and vitreous conditions that may cause increased presence of floaters indicative of more serious complications, for example, vitreous or retinal detachment. It is therefore advisable in the presence of an increased occurrence of floaters that you get a check-up by a eyecare professional.

5.2 Macular Degeneration

The macular is the innermost part of the central retina; an area where the retina has the highest concentration of cones (sensory apparatus of vision). The degeneration which occurs within this area of the retina can be due to a breakdown of the retinal receptor cells, leakage of exudate between the retinal layers and occasionally destructive bleeding.

As a result of the changes to the retina there is a decrease in central vision, often with little to no involvement in the peripheral retina. Hand magnifiers, spectacle magnifiers and low vision aids can be used by the patient to assist with reading.

More information can be obtained from the National Eye Institute located in Bethesda, MD on (301)496-4000.

Internet Resources include:
URL: (information on preventing macular degeneration with dietary carotenoids a medical sciences bulletin)
URL: (medical research and development with information on Ophthalmic research)

5.3 Retinal Detachments

The retina is one of the three layers of the human eye. The innermost layer is a complex and delicate layer (0.4mm in thickness) which lines the innerside of 2/3rds of eyeball. There are a number of sub-layers to this tissue which comprise the neural layers and photoreceptors necessary for vision.

Detachment of the retina is a separation of the neural retina from the pigment epithelium; a layer of pigment cells providing nutrients to the photreceptors and attaching the retina to the next outermost layer - the choroid. As a result of the separation there is a loss of function in the photoreceptors, vision is affected.

The accompanying symptoms of a retinal detachment include; blurring of vision, sensation of "flashing lights", loss of vision like a shade or curtain moving across the field of vision. The presence of a retinal detachment is a serious visual problem and should be thoroughly investigated by an eyecare professional.

Retinal detachment occurs in some hereditary conditions, e.g Stickler Syndrome. More information is available on the Web at
URL: Stickler Syndrome/Marshall Syndrome
URL: Stickler Syndrome - Who to Contact? Where to Go to Chat with Others?

5.4 Diabetes and The Retina

Diabetes causes a number of retinal changes which can include haemorrhages, micro-anueryisms of the capillaries, exudates, abnormalities of arteries and veins and retinal detachment. The combination of these changes can result in reduced vision to severe complications. The examination of the status of the diabetes and it's impact on the retina is assessed with a technique called fluorescein angiography.

Other information is available at
URL: (contains detailed information on diabetes and particular section on diabetic eye disease which includes questions and answers)

5.5 Retinitis Pigmentosa

Retinitis Pigmentosa is a degeneration of the retinal pigment epithelium. This is a single celled layer of pigment cells that is between the retina and the choroid, the second "coat" of the eye. In this condition pigment granules are lost from the epithelium layer and deposited in clumps in the retina.

See section [11.1] for details of a listserv group that discusses the condition RP.

This listserv ( contains the following information files:

GET RPLIST VITAMIN -> two letters regarding E. Berson's vitamin A study
GET RPLIST TRANSPL -> an article on retinal cell transplants
GET RPLIST REFSUM -> an article on Refsum's disease

5.6 Glaucoma

Glaucoma is a symptomatic condition and not a disease "sui generis". It is a collection of physicals signs: raised intra-ocular pressure, visual field loss, enlargement of the blind spot and changes in the appearance of the optic nerve head. There are a variety of clinical classifications of glaucoma.

Treatment details
- eyedrops to reduce aqueous fluid production, increase fluid drainage.
- laser trabeculotomy to increase outflow of the aqueous humor.

Glaucoma may be defined as "those situations were IOP is too high for normal functioning of the optic nerve head (Shields, 1992.) IOP is closely linked to aqeous humor (clear, watery, fluid in the eye) dynamics. IOP is a function of aqeous humor outflow (AHO) and production (AHP) (IOP = AHO - AHP). Therefore pharmaocological treatment is aimed at either increasing outflow or decreasing production of aqeous humor. IOP is measured by many different types of machines by your health care proffesionals. These exams are important because as with hypertension, when symptoms are noticed by the patient the damage has already been done.

For patients who are refractory to medical treatment a surgical operation is performed. This operation makes an external drainage system for the AH and thus increased outflow. This proceedure called a trabeculectomy, is done in the operating room with local anesthesia. Sucess rates for normal risk patients is very high.

Other information located on the Web includes:
URL: (What is Glaucoma?)
URL: (extensinve information on glaucoma including definition, treatment, research and drug information)

5.7 Cataracts

Cataracts are opacifications of the crystalline lens of the eye, causing a loss of transparency. The crystalline lens is the "focussing" mechanism of the human eye. The change in light transmission is due to accumulation of water and/or denaturation of the lens protein. A variety of factors cause cataracts, eg diabetes, eye trauma, age related changes. The predominant symptoms of cataract are an increasing loss in vision. There can be associated fluctuations in the vision depending on water changes in the lens. The rate at which the cataract changes varies depending on physiological factors.

The surgical procedure is described below (contribued by Dr W.Wan M.D):

There are two standard techniques for modern cataract surgery: phacoemulsification (PE) and nucleus expression or planned extracapsular cataract extraction (ECCE). There are numerous variants on these, especially PE, which may get advertised as no-stitch, one-stitch, clear cornea, topical, etc. In general: 1) PE is technically more difficult to learn, however, once you learn it, most surgeons feel it is a better technique in their hands; 2) the incidence of complications is dependent on the surgeon and the patient population, not the particular technique used (PE was previously thought to have a greater incidence of complications, but this was primarly due to a learning curve; for a given surgeon, the complication rate will be lowest with the technique that he is best with); and 3) PE is generally quicker than ECCE, but again this is very surgeon-dependent.

My personal preference is for PE 95% of the time; ECCE is reserved for cases where it may be better than PE based on the type of cataract, the patient, the surgical goals, and occasionally the type of equipment available. (If you want to know how I decide which are in that 5%, you need to go to ophthalmology residency!) PE generally offers quicker visual recovery, and arguably quicker healing and overall rehabilitation, better wound stability, and less risk of disastrous complications such as an expulsive hemorrhage during surgery. However, the bottom line is, good surgeons get good results with either technique, pick a surgeon who gets good results and let him decide what technique is best for you in his hands. (Even then, of course, keep in mind that although it is 95% successful, cataract surgery IS surgery, and complications can occur.)

The indication for removing the cataract in a second eye is the same as the first: If the decreased vision in that eye is bothering the patient. (Unless there is some other eye disease, e.g. glaucoma or inflammation being caused by the cataract, or it is preventing management and treatment of some other eye problem in the interior of the eye, which would be unlikely if it is mild.)

Other internet resources that provide information on cataracts
(Eye Radiation and Environmental Research Laboratory)

(EyeCare Connection homepage with information on cataracts)

(Lens and Cataract Researcher Internet Directory)

( American Society of Cataract & Refractive Surgery - patient FAQ on cataract)

5.8 Uveitis:

Internet resources:
(The Wilmer Eye Institute - has a page on ocular immunology )

(SUNY at Buffalo Ophthalmology Dept - Case presentation on ocular pathology and uveitis)

5.9 Ocular Migraines:

5.9.1 Introduction:

The following is an attempt to give an_introduction_only to this vast subject with protean manifestations.

Migraine affects about 10% of the population. It affects all ages from babies to adults although age does seem to have a protective quality.

The general mechanism seems to be a constriction of blood vessel(s) followed by a dilation the the vessel. The aura (when present) accompanies the vasoconstriction and the headache (when present), the vasodilation.

There are identifiable "trigger factors" notably:

1. certain foods. Caffiene (coffee, colas, chocolate), citrus fruits, alcohol, nitritate and nitrites, aged cheese, and others.
2. hormonal changes esp. puberty, pregnancy, menopause and "the pill".
3. fatigue/stress. This can be physical (heat/cold) or emotional
4. bright lights
5. loud noises
6. trauma
7. refractive error

As well, there are cerain associations with migraine. Cyclic vomiting as a child, car or motion sickness, a family history of migraine, drusen of the optic nerve.

5.9.2 Classification of migraine:

I. Common migraine. The comprises about 80% of those with migraines. It is the typical "sick headache" possibly with mood changes. The headache can be localized or generalized. It may last for hours to days.

II.Classical migraine. The triad of aura, headache, nausea+/-vomiting, and a feeling of "being out of sorts". It is typically of shorter duration than the common migraine. The aura may be any sort of neurologic deficit but of course the ones we see are usaully visual. The visual aura usually starts near fixation and expands to the periphery then dissappears to be followed by the headache. The aura may be jagged, coloured lines, "grey blotches" or "missing patches" or many other type of visual disturbance. Classical migraine account for about 10% of migraines.

III. Complicated migaine (expanded below)
3.Retinal (or ocular, see below)

IV. Cluster headaches SEVERE episodic unilateral head or facial pain, nasal stuffiness, +/-ipsilateral Horners, lacrimation.

Complicated migraine expanded:

1. Cerebral

This is a headache which may be severe and focal neurologic signs which last longer than the headache. This is the hallmark of the complicated migraine in which the neurologic deficit may even be permanent. For example, there can be permanent visual field defects.

2. Ophthalmoplegic migraine

The patient is usually young (less than 30, usually less than 20). There is a severe unilateral headache. As_the_headache_clears, one or more ocular muscles on the side of the headache become paretic and may take days or weeks to recover their function. As you can appreciate, the first time this happens, the patient is subjected to a lot of investigations including angiograms as this is mimicing such things as aneurysm, tumour and other very bad things. If the ophthalmoplegia recurs, the sequence of events and the previously negative tests are reassuring.

3. Retinal migraine (ocular migraine)

The patient is typically under 40 and suddenly loses a portion (retinal) or all (ocular) of the visual field in one eye. There is rarely headache. Never, according to some experts. The differentiation between retinal and ocular migraine is how much of the visual field is affected. In other words, what vessel has been affected. If it is distal to the bifurcation at the optic nerve head, it is retinal. If it involves the central retinal artery, all of the vision is lost and it can be called ocular migraine. Note too, that there are seldom if ever flashing lights with this form of migrain. Again, the vision recovers (ususally, sometimes permanent) in 20 to 45 minutes. With ocular migraine there can be retinal hemorrhages, vitreous hemorrhages. macular edema, ischemic swelling of the optic nerve.

4. Basilar migraine

Mimics vertebrobasilar attacks. Bilateral blurred vision, vertigo, ataxia, nausea, incoordination, loss of balance, speech difficulties.

5. Other

There is a host of symptom-complexes which fit the criteria for migraine. Sudden, episodic, self-limited, lasting 30-45 minutes. These can be chest pains, vomiting, neurologic symptoms and many others. These are sometimes called migraine equivalents.

The most common migraine type problem that I see in my practice is that of a person who may or may not have previously had migraine diagnosed who has a 15-30 minute episode of visual disturbance, often quite classically starting off small near fixation and expanding to fill a hemifield. When the probable diagnosis is explained to the patient, the response is almost invariably "Oh, but it can't be migraine, I don't have a headache!"

Remember, if it walks like a duck and quacks like a duck, it's probably migraine.

5.10 Chorioditis:

Choroiditis is an inflammation of the choroid, the second "coat" of the eye. This tissue layer is a vascular rich layer located between the sclera (outer white coat) and the retina (sensory layer).


© Grant Sayer , email:


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