Category: The Science Stuff

Shimmering

Albert Einstein once said “the more I learn, the more I realize what I don’t know.” Apparently I am in good company, because I feel the same way.

With no immediate crises in my life and no immediate reason to freak out – and even with geographic atrophy and permanent retina damage, this state of affairs is possible! – I have been trying to get caught up with some research. I keep running into things I have no knowledge or understanding of.

Lin suggested that after over a year we should know SOMETHING about these things. We don’t. For example, I am still clueless about what I can expect concerning the progression of density of my ‘blind spots’.

And speaking of disease progression, (was that a smooth segue or was that a smooth segue??), I do have a couple of things to say about disease progression from that last article I read. Remember the one on GA?

The article opined all the new interest and hoopla about dry AMD came from the success with treating wet. However it wasn’t why I would think. You know, we have scaled that mountain and are looking for new summits sort of thing? Nope, the reason was they discovered that even after severely limiting the development of neovascularization in eyes, the eyes just kept right on progressing with dry AMD! Sorry, darlings.? It seems a former wet AMD eye becomes a dry AMD eye.

And dry AMD – to my great chagrin – progresses. How much? I assume it can take the entire macula but I have not seen that definitely stated anywhere. I have seen it stated that it generally stops with the macula. Maybe not such a ‘small’ favor. Could be a lot worse.

The last thing I learned from that article is how best to document disease progression. That is with something called cSLO FAF. Isn’t that informative? Exciting even!

OK, OK, just ‘funning’ with you. I looked it up. Fundus autofluorescence is diagnostic imagery. It detects fluorophores in the retina. Fluorophores being chemicals that re-emit lights shone at them. Research quoted by Wu in Use of Fundus Autofluorescence in AMD said risk of wet AMD can be predicted by a patchy reflection pattern and lots of ‘shimmer’ (my word) at the edge of a patch of geographic atrophy is predictive of cell death and growth of the GA. The more ‘shimmer’ the worse the trouble you are in. [Lin/Linda: We hadn’t had a music reference for some time.  When I hear the word ‘shimmer’, I think of John Lennon’s song “Julia” which uses the word ‘shimmering’, hence this page’s title. ::smile::]

So if anyone throws a bunch of letters ending with FAF at you and says you are going to have that, it may be they are checking for disease progression. I cannot remember ever having one, but it is noninvasive so no biggie. Should not hurt. Just more pretty pictures. Hopefully they will find something good.

Pretty much it for now. Will probably write some more nonsense between now and then, but Wednesday I am going to another support group meeting. They are demonstrating an electronic monocular called a Mojo and I want to see it. Will let you know!

Chat with you later!

 

written May 6th, 2o17 Continue reading “Shimmering”

Islands of Damage

I have got about 45 minutes before I need to get ready to walk and go to yoga. Had to go to my third job today, just for the half day. My husband took me up and did errands for the morning, then we went to lunch and picked up my framed photos for the contest in the fall. I am four months ahead of the game but I had to pay extra to get them done on time once before. Not doing that again.

Lin gave me an article entitled “The Journey of ‘Geographic Atrophy’ through Past, Present and Future”. Started reading it …finally… today. First thing I read is GA is ‘end stage’ dry AMD.

I knew it was advanced AMD but never gave a lot of thought to it being end stage. Does ‘end stage’ just mean the last stage or does it mean I have almost reached the end of the deterioration? Need to read on.

There is depigmentation of the cells This is a problem because it is the building up and depletion of pigment that allows us to see. In GA you can get to look in and see choroid blood vessels with no difficulty, as well.

I have seen images of my blood vessels in my choroid. Nothing between them and the camera. Essential, my choroid posed naked.?

The article said seeing the degree of degeneration even with the new technology is difficult. That is apparently why my retinologist saw no change in my scans even though I was perceiving an increase in density of my left scotoma.

The article also said there is high variability in the location, number and shape of individual lesions. The makes sense considering my blurry spot is up and right when looking at the Amsler Grid and my ‘sweet spot’ for eccentric viewing is lower and a little to the left. In other words if I center my poor, wrecked fovea at 1 or 2 on the clock face, I can see things between 9 and 3, courtesy of my ‘sweet spot’. Other people are different, of course. Putting each fovea on the center of the Amsler grid and seeing what blurs out can help you chart your scotomata. Then, learn to work around them.

I am not sure if this is good or bad. Exception in a limited number of cases, the fovea is spared until the end. Does that mean I am actually more abnormal than I have always believed or does it mean I am at the end of the process? Dunno.

See why I feel like a mushroom???? Jeez. Need information here!

Geographic? It appears early researchers (and by ‘early’ I am referring to the 1970s! Research and discoveries are traveling at light speed and there is no reason to lose hope something else helpful will be discovered soon) thought the sharp demarcation of lesions like ours looked liked borders of islands and continents as drawn on a map. That is where geographical came from. We have islands of damage in seas of healthy tissue.

Ok. Gotta run. There is lots more in the article though. Will let you know. Continue reading “Islands of Damage”

The Blind Spot – Part 2

Lin found about the best article on scotomata that I have seen thus far. It has some basic information. Stuff that I had inferred from other articles but had never been defined.

Scotomata are areas of vision loss surrounded by intact vision. Scotoma, as I said, is Greek for ‘darkness’. Again, not a happy thought.

A scotoma can be in one eye or two. It can be physiological. Everyone has a natural blind spot where your optic nerve is connected to the retina. We don’t realize it because our brain just fills in. No need to worry about physiological scotomata.

Scotomata can also be pathological. Because these are the result of a disease process, these are the ones we get to worry about.

Relative scotomata are the kind you can ‘see through’. You no longer have a full complement of cones but enough remain to sort of get the job done. I have relative scotomata in my eyes. Unfortunately, one of them probably just had a massive die off because it has gotten several shades darker.

When the scotomata go black you have something called absolute scotomata. Those are the areas in which the photoreceptors – in our case, cone cells – have pretty much all died.

A positive scotoma is one that is obvious to the owner of the eye. I KNOW – I am in fact positive! – I have blurry spots and I am aware one of them just darkened.

We had a comment from a reader who has a negative scotoma (maybe two). She wrote she quit driving when cars on the road would disappear and reappear. Her brain was ‘filling in’ the blank spot with a vision of an empty road.

Aren’t brains just amazing? Scary, but amazing. After all, that little trick could kill both the brain and its owner! (Or would that be its servant? Hmmmm….)

And that, my dears, is what I know about scotomata. Not much considering I am the ‘proud’ owner of two of them! Will they all progress to black? Dunno. I keep looking and asking and continuing to feel like a mushroom. You remember: keep me in the dark and feed me bullshit.

What I was told was it was not a conversion to wet. Reassuring but I never thought it was. I was told there was no obvious difference between my last OCT scan and this one. I guess that means the die off was not severely massive, only mildly massive (but I can still see the difference!!!).

I was also praised for being proactive with my vision care. Important for us all.

So, darkening of your scotomata apparently may occur. It probably means things are dying in there. That is my interpretation, though. I was told it was progression of the disease, but if you have a disease in which cells die, would not progressing be cells dying? Stands to reason; yes?

If you perceive a significant change in the density of your scotomata, call your doctor and go in for an OCT just to be on the safe side. Not much can be done for the progression of the dry, but on the off chance you are converting to wet, you need to catch it quickly.

Thus we end another ‘adventure’ in AMD. Anyone else having these problems? Sigh.

Continue reading “The Blind Spot – Part 2”

Always Learning More and More

Moving right along with the article I am reading (in Webvision’s Age-Related Macular Degeneration), I am finding a lot of new vocabulary and abbreviations. Have you heard of PEDs, for example? PEDs are not nylon footies. They are pigment epithelial detachments. They happen when a bunch of drusen join forces and push up the RPE layer of your eye. Since the RPEs are under the retina and need to be in contact with Bruch’s membrane in order to take care of the photoreceptors, having them jacked up is not a good thing.

There is more and more information suggesting Bruch’s membrane is not totally blameless in this whole debacle. I am not going to pretend to understand it but there is evidence structural and biochemical differences in Bruch’s membrane occur in those with AMD but not in people who do not have the disorder. It may not be all the fault of the RPEs.

Recently I have been seeing the terms classic, predominantly classic and occult to describe different forms of wet AMD. They are mentioned in the article I am reading but not well defined.

According to the American Macular Degeneration Foundation the terms classic, predominantly classic and occult describe the choroidal neovascularization (read “formation of new blood vessels in an inner layer of your eyeball”) that happens in wet AMD. Classic choroidal neovasculazation is characterized by well-defined boundaries. Average visual acuity is between 20/ 250 and 20/400.

Occult CNV sounds like it should be scary but it is actually the more benign. Occult lesions are not as well-defined as classic ones. They tend to leak less and average visual acuity is between 20/80 and 20/200. If given a choice, I would take this one!

Predominantly classic is, as it sounds, a mixed type. The other designation for this type is minimal classic.

According to Joachim Wachtin in Classical Choroid Neovascularization CNVs can also be classified by where they can be found in relation to the fovea. Some of them are directly under the fovea and are called subfoveal. Those that are extremely close to the fovea are called juxtafoveal and the ones that are farther away are called extrafoveal.

Like I said, lots of new vocabulary coming our way! But I do believe that, when in a strange land, you should always learn a few basic phrases. These are some basic phrases in the land of wet AMD.

My article takes a serious detour into science babble and I truly don’t understand much. Glaze over time! That means I am going to stop sharing info from it.

Hope these scraps of information fit into your ‘puzzle’ somehow. One of these days we will have gathered enough pieces of knowledge to actually figure out what the picture is!

In the meantime, keep on learning. In the famous words of Schoolhouse Rock, “….because knowledge is power!” Gather knowledge. Be powerful. Continue reading “Always Learning More and More”

The Blind Spot – Part 1

Tomorrow I go for another OCT scan. That is optical coherence tomography. It is the one you look at the cross and the machine goes click, click, click vertically and takes pretty pictures of your retina.

I think I told you I think the scotoma in my left eye is more opaque. I think it is called density but I cannot find any information on it.

I am not understanding why they don’t publish this stuff somewhere. How are you supposed to understand what is happening to you if there is no information?

I have been told AMD vision looks like gazing through glasses with Vaseline smeared on them. Nowhere have I heard things go black in the middle. However, my scotoma is darker and things are not ‘bleeding through’ as well. Is this natural progression of the disease?

I feel like a mushroom. Keep me in the dark and feed me bullshit.

Did a fair amount of research trying to find something on scotomata. That is the plural. Like stigma and stigmata; you know. Scotoma is Greek for darkness so that is not very encouraging.

There are several different types of scotomata. The one we with AMD have is a central scotoma but there are also ones that obliterate half the central visual field, hemianopic scotomata, and peripheral scotomata. Pareacentral scotomata are near the central vision. Bilateral scotomata occur as the result of a tumor impinging on the optic chiasm. This is all info from primehealthchannel.com.

medical-dictionary.thefreedictionary.com talks about absolute scotomata in which the light perception is totally lost. There are a number of articles online that come up when you google AMD and absolute scotomata. It is obviously possible, therefore, for an absolute scotoma to be the ‘end of the line’ for macular degeneration. How delightful.

On a positive note, many of the articles that mention absolute scotomata are about teaching people how to use eccentric viewing. They are generally pretty positive about their results. Once again there is hope for navigating around this mess.

If somebody actually TELLS me something about what is happening, I will let you know. I, for one, do not think you need to be treated like mushrooms. In return, if you know the answer, let me in on the secret!

And in other news, I am going to go to Mom Prom! The person who first offered to get me there apparently ‘thought better’ of it and never firmed up the arrangements, but I have another offer. Not really upset at the first person but I think people need to be honest with themselves before they open their mouths. If they are not going to follow through, don’t volunteer!

I also got the invitation to speak at the summer camp for blind and visually impaired high school kids. No clue what I am going to say. These kids have more experience with vision loss than I have. Any suggestions?

Getting late. Talk to you later.

  • About the title: There’s a GREAT YouTube channel called The Blind Spot that we highly recommend.  The title is not about that, it’s that scotomas are often called ‘blind spots’.

Continue reading “The Blind Spot – Part 1”

Always Learning More

Hey, there! I think I have found a good article on macular degeneration, our favorite but somewhat distasteful topic. The article is in Webvision and is entitled Age-Related Macular Degeneration. Another catchy title. The main author is Hageman.

Did you know the name up until around 1990 was ‘senile macular degeneration’? Makes it sound like our eyes have lost some of their mental faculties. Glad that was changed!

Also discovered the fovea is the center of the macula. It contains the highest concentration of cone photoreceptors and is the only region of the retina that can attain 20/20 vision.

I think when my optometrist said I had such an abrupt vision loss because the deterioration had reached the center of my macula she was talking about the loss of my fovea. That means 20/20 vision is no longer possible for me. Even if I use prisms or eventually get that eye max mono thingee, things will not be ‘perfect’. [Lin/Linda: she means the EyeMax Mono lens implant.]

This article says macular vision is 10% of vision! Estimates of degrees of arc of potential loss seem to be getting better, but don’t get too excited. Remember we are talking my interpretation of things I read. It is guess-work. I know nothing.

Although I used to think hard drusen sound more ominous than soft ones, it is actually the other way around. Hard drusen are smaller and soft ones are larger. If they are looking in your eyes and mention soft drusen, you have more of a problem than if they see hard drusen.

I thought that all dry AMD would progress to GA (geographic atrophy) if the person lived that long. This article says only 10 to 15% of dry AMD patients progress rapidly enough to ‘achieve’ GA. Interesting.

That means my visual state is something many of you will not have to experience. That is a good thing! And FYI? I am functional so you can remain functional as well.

For you ‘wet’ folks, the article once again cautions you to stay on top of things and get your shots. Left to its own devices wet AMD progresses to a cicatrical stage. Cicatrix is a fancy word related to scars and scarring. Disciform scars occur when fibrous tissues develop in Bruch’s membrane between the RPEs and the retina. Scarring is, needless to say, not good and can result in severe vision loss. Bottom line for this paragraph is: do not allow bleeds to happen to you!

Closing in on my 500 words and I still have pages to read in this article. I think I will close this page, read some more and start another.

And FYI, I emailed by doctor. And – while he also believes the increased density/opacity of my blind spot is related to expected disease progression – I am going in for a vision screen in two days. Perceivable changes in your vision? I expect you to call, too. Check it out.

written April 25th, 2017

Continue reading “Always Learning More”

Playing Clue

I really need to learn to keep my mouth shut. Yesterday I said all was quiet. Today I noticed the scotoma aka blind spot in my left eye was much more opaque than I remembered. De-freakin’-lightful. What exactly does THAT mean?

Since it is Sunday evening and not exactly an emergency, I don’t have a way to get an immediate answer. I shot off an email to my local retinologist. Should I panic or is this normal progression of the disease? Everything I have read says scotomas can be light gray, dark gray or black but nothing ever said if there is a progression and/or what that progression might be.

I looked online and it appears this opacity is called density. Maybe. That is what I supposed from reading a whole slew of article titles and descriptions trying to find something that describes what happens to scotomas as the disease progresses. You know full well I did not find such an article.

Really! These are not state secrets! Why can’t someone give us some basic information? They write books on what to expect when you are expecting and what to expect from your two-year old. Why not something on what to expect when you are losing your sight?!?!?

End of current rant. If you have any idea, let us know, ‘k? Sometimes I feel like I am playing a massively involved game of Clue or something. Was it Colonel Mustard in the garden with a pitch fork? Inquiring minds sincerely want to know.

The sad part is the availability of good knowledge in AMD has been a problem for years. I started listening to The First Year: Age-related Macular Degeneration. The book was written in 2006. Guess what HIS first rant was? Doctors who told him nothing. The author, Dan Roberts, did exactly what we did. He went online and found knowledge and comrades for his fight.  Reading his 10 questions that should get answers from the time of the diagnosis, I was happy to see we here are traveling a similar path as Roberts had. Roberts believes people with AMD should be told what to expect and how to find resources and live successfully. Now there is a novel idea! ?

He also has several other topics listed as chapter headings. We have covered a large number of them. Everything from ADA to stem cells and beyond. [Lin/Linda: click here Click here to preview the book.]

I will continue to listen to the book. It is already 11 years old but you never know what I might uncover between its imaginary covers (it is an audio book through BARD, ya know). Probably time for a rewrite….or we could write one ourselves. How do you like that for a scary idea?

So question: what would you want to see in a book on AMD, the life and times of men and women who have it, etc, etc? Might be a project here.

written April 24th, 2017

Continue reading “Playing Clue”

Electrician’s Nightmare

Rods and cones. I learned those words back in the sixties in science class. We were studying the eye.

Rod cells are concentrated in the peripheral sections of the retina. They work well in dim light. They play a key role in night vision. While we need rod cells for good, overall vision, they have their limits. Rod cells are lacking in sharp vision and color perception.

That brings us to the discussion of cones. Cones are located most densely in the center of the eye. Their jobs are to see sharply in bright light and to easily perceive color.

Considering many of us have trouble with sharp, central vision and ‘wash-out’ in bright light, as well as have trouble with color perception, it comes as no surprise that we, those with AMD, are a little short on cone cells. If you have seen images of the ‘divot’ in your macula, that cone-shaped hole should be full of cone cells. Mine is not.

Because we are a bit short on cone cells, cone cells were what researchers were trying to grow for us. After a number of years the breakthrough came at the University of Montreal and was published in 2015. The head researcher was Gilbert Bernier. Merci, Gilbert!

Dr. Bernier came to the idea there must be something that helps to grow all those cone cells in the macula. After all, the embryonic cells are pluripotent. That means they are capable of becoming any one of several different cells. What makes it so these particular cells became cone cells?

Bernier discovered a protein that limited the stem cells to becoming pretty much only cone cells. He actually achieved about 80% purity, a pretty much unheard of accomplishment before this.

Even more exciting, Bernier’s cells organized themselves into nice, pretty sheets of retinal tissue. Not a disorganized mess.

And if that were not enough, when his cells were injected into the eyes of healthy mice, they migrated to exactly where they were supposed to be!!!! Stem cells with the homing instinct! Pretty cool. They were doing the happy dance in Montreal.

This is a huge step but not yet the answer to replacing cone cells, the photoreceptors we lack, and ultimately our vision. As I have said before, the cone cells grown in the lab are like cell phones without a tower. They do what they should do but have no way to send the signal to the brain.

According to the Discovery Eye article on the optic nerve and how it links to the brain, there are approximately 125 million photoreceptors, rods and cones, in the human eye. These connect to two, different intermediate neuron types and 23 different kinds of other retinal ganglion cells. Some of the retinal ganglion cells communicate with as few as five photoreceptors.

In short, the eye would be an electrician’s nightmare! It is no wonder no one has been able to figure it out yet.

There is, however, a way for it to be done. The knowledge of the body – remember these cells both organize themselves and migrate accurately – is miraculous. The next step is finding out how to give the connect order. I suspect the Montreal crew is working on it even now.

Bonne chance, Gilbert, bonne chance. [“Good luck, Gilbert, good luck” for those of us who don’t know French.]

written April 14th, 2017

Continue reading “Electrician’s Nightmare”

Love Wikipedia

Just came back from walking the Beastie Baby. I use my monocular a fair amount on walks. There were several, large, black birds in the trees in a little woods. I used my monocular to see hooked beaks. That meant they were most likely turkey buzzards, carrion eaters. Hypothesis confirmed when the sweet, fetid stench reached me. There was a dead deer over the bank in the stream.

Turkey buzzards are amazing. Ugly as sin, but amazing. What I was able to smell at 15 feet, they have been known to smell from a mile away. Our friends with the Audubon Society tell us the turkey buzzards (aka turkey vultures) have the largest olfactory system of any of the birds.

Which has exactly nothing, nothing to do with AMD, but is an example of one of the distraction skills, thoughts. One cannot live (well) thinking of nothing but AMD and our collective predicament. Besides I think Fun Facts are fun!

But enough of the sideshow and back to the main event. I might – and that is a big might – have found an answer to my question about how many degrees of arc make up central vision. I found what I think is the answer in Wikipedia. And here I was looking in all those hoity toity profession journals expecting some help. Silly me!

Actually I got two answers. Neither is God-awful if you consider where I thought this condition was taking me, but one of the answers is significantly better than the other. The first, better, answer is central vision is 18 degrees of arc (refer to the image to the left; click here for a larger version). If you consider the outer rim of the macula to be the boundary between central and peripheral vision, 18 degrees of arc is central vision and what we might be expected to lose. That is 18 degrees out of a visual field of what I have read different places is pretty close to 180 degrees horizontally. That’s 1/10! A heck of a lot better than the total blindness I thought I was going to have.

The other one is 30 degrees radius, which is unfortunately – check my math – 60 degrees of arc (refer to the image to the left; click here for a version).  A point 30 degrees from the center was chosen because after the first 30 degrees acuity declines sharply. There appears to be some sort of dividing line there.  Color vision also significantly decreased around the same place on the retina. The article also suggests 30 degrees radius is where good night vision ends.

So, the jury is still out on this one but we are getting closer to a verdict. The amount of loss that can be expected from geographic atrophy appears to be – and remember this is total speculation on my part; I know nothing! – somewhere between 18 degrees of arc and 60 degrees of arc. Those number are either a tenth of a third of our visual fields. Again, not great but better than what I thought was going to be true blindness. A small reason for optimism perhaps.

Right answer? Danged if I know. If you are going to see your doctor any time soon, do me a favor and ask. I really am curious. Continue reading “Love Wikipedia”

Clinical Trial Design: Part 2

Page 2, almost done. Promise.

Types of Variables

Good experiments have independent and dependent variables. The independent variable is the treatment. The dependent variable is the result or what they are measuring.

Again, the idea is to keep as much as possible the same between our two or more groups. The groups are generally treatment(s) and control. Control groups get the sham ‘treatment’. The only things that ideally should be different among the groups are the independent variables, treatments.

In reading a study you can tell what your chances are of getting a treatment by checking how many different treatments they are looking at. For example, if there are three, different quantities of stem cells they are inserting and only one control group, you have a 75% chance of getting a treatment.

The Statistics

After the experiment is done, the researchers do statistical magic and find out if there was a real effect of the treatment. They want to see if what happened could have happened by chance. If there is little chance that it did happen by chance, they are that much closer to finding an effective treatment. At least in the studies I am interested in, people in the control group are offered the effective treatments when the experiments are done. They are not out of luck.

Remember, the medical research we may volunteer for has been done many times on laboratory animals. Unless you are very brave and sign up for a phase 1 clinical trial, other people have had the procedure before you. Real research is published in reputable journals. Ask where their initial findings were published. If you don’t get a decent answer, be very cautious. If you do get a journal reference and cannot interpret it, send it along. I don’t guarantee we will get it right, but we will give it the old, college try.

Size of the study

Also, in research there is such a thing as a cohort. A cohort is a group of subjects going through the same treatment pretty much at the same time. Phase 1 cohorts are small, maybe 7 or 8 people, but phase 2 cohorts may be a couple of dozen people. There are more people in the higher phases. If you are told you are the only one or one of just a few, be suspicious.

Those are some of the things that legitimate research have as well as a couple of extra tips on making sure you are looking at a legitimate study. The information is pretty dry but having access to it is better than falling for a bogus offer and being rendered blind. That is, after all, what we are all trying to avoid!

Just remember, caveat emptor. Check things out very well first. Continue reading “Clinical Trial Design: Part 2”

Clinical Trial Design: Part 1

The Hypothesis

All good experiments start with a hypothesis. A hypothesis is an educated guess about what should happen under a certain set of conditions. For example, “stem cells can grow in the eye and replace worn out RPEs”.

The way I was taught, this statement is then ‘turned around’ to be the negative. “Stem cells cannot grow and replace worn out RPEs”. This ‘turned around’ statement is called the null hypothesis. This is what will or will not be disproven with our experiment. The idea is to see if we can generate a result that will be significantly different from the starting point. The null hypothesis predicts no change. We want to see if we can affect a change that is big enough to matter. Good so far?

The Plan

After deciding what we want to figure out, we need a plan. Our plan is our experimental design. We want to design our experiment so we are reasonably sure there are no stray influences that may have caused the results.

 

The groups

If we are comparing treatments or treatment versus no treatment, we need to make sure our groups are as similar as possible. If we want to see if our new exercise program is better than another training program we really would (ethically) not want 20 year olds in one group and 80 year olds in another.

This is part of the reason good experiments on clinicaltrials.gov list exclusions which means reasons why a person couldn’t be in the trial. They are looking for similar subjects. Another reason for exclusions may be related to the treatments they are using and people’s sensitivities to them. You don’t want a subject who has an allergic reaction to your treatment!

The Sample

Once we have our sample (all possible examples or cases of something is called the population), we should be reasonably sure we have controlled for most of the important variables. Variables are factors that can affect the outcome of our study. However, there are other variables we have to control for in our experimental design.

The Treatments

One of these is the Hawthorne Effect. Anyone who has ever taken intro to psych or industrial/organizational should remember the Hawthorne Effect. In a plant they were trying to increase productivity. The problem became, no matter what they did, production improved! These people could have been working in the dark with the heat turned up to 90F but they were going great guns.

The researchers discovered just the fact that they were noticing the workers and trying to do something for them was enough to increase productivity. It did not matter that working conditions worsened. The workers felt noticed. They wanted to please the researchers.

Placebo effect happens when subjects believe the ‘treatment’ is effective even though it is not. They may show improvement as a result of their belief.

You will see attempted control for the Hawthorne and Placebo Effects in studies that list themselves as ‘double blind’ or ‘double mask’. They will perform fake (sham) procedures on people in the control so they feel noticed and loved, too.

Double blind? The double is because doctors and nurses treat people getting the actual treatment differently. They may not realize it but they may be more encouraging to those actually getting the treatment than they are towards the people who are the controls. When a study is double blind neither the patients nor the people caring for them actually know.

That is my 500+ words for this one. One or two more pages and I should be done. Hang in there!

For more information, click here for Designing Experiments Using the Scientific Method from dummies.com.

Continue reading “Clinical Trial Design: Part 1”

Biochemistry Redux

Doxycycline and I have a ‘history’. Not totally a good one. Doxy is the medication given prophylactically when you are bit by a tick. Some doctors recognize waiting for the red ‘bull’s eye’ of Lyme disease before treatment may not be a good idea; others don’t.

The second time I was tick bit I had a doctor that gave me the doxy as a precaution. The first time I was bit I had a doctor who withheld it.

Having some clue of what can happen to a body that has contracted Lyme’s, I was livid. Fortunately – or unfortunately – I had access to about half a vial of veterinary doxy. See it coming?

Do not try this at home! I took the doggie doxy and apparently took a little too much. Doxycycline produces photosensitivity. I won’t bore you with the chemistry (I researched it at the time), but suffice it to say, the molecular structure of doxy is such that it will store light energy and release it over time. You ‘sunburn’ from the inside out! Don’t need a reference for this. This is personal experience talking. I had second degree sunburn in about a half an hour.

The moral of that story is avoid doggy doxy. Once more I am the star of a cautionary tale. Oy vey!

But the reason I even mention doxy and our conflicted relationship is this: Oracea is doxycycline and it is being researched as treatment for geographic atrophy. There may be hope for my relationship with doxy yet!

According to the good people at Medscape (3/12/17) doxy is being researched as a method of treating low-grade inflammation resulting from alternative complementary pathway activity in geographic atrophy.

The alternative complementary immune system in me is ‘the gang that couldn’t shoot straight’. My good cells are being taken out by ‘friendly fire’. Reducing the effects of the alternative complementary immune system in me would be a good thing. [Lin/Linda: Sue’s referring to what she found out from a genetic test she had. Click here to read more about this.]

The Medscape article veers into uncharted waters for me but I will attempt to translate. It appears doxy can interfere with some of the molecular pathways – read series of actions that are supposed to produce something – that end up creating the conditions that lead to geographic atrophy. It lists oxygen species, matrix metalloproteinase, caspase activation, cytokine production and complement activation. Oh, good grief! Social scientist here! Never took biochemistry.

According to Wikipedia, reactive oxygen species are a normal byproduct of the metabolism of oxygen. In times of environmental stress on the cells, levels can build. It ties in with oxidative stress.

Matrix metalloproteinase are enzymes that break down matrix proteins (don’t ask because I don’t know!). Caspases are enzymes having to do with programmed cell death and cytokines are used by cells to send messages to other cells.

Did I mention I am not a biochemist? Don’t understand it except to say it all – magically! – has something to do with causing divots in maculas. Doxy is supposed to, maybe, could be, slow it down.

Clinical trials of doxycycline – under the brand name of Oracea – are underway. Check clinicaltrials.gov for locations near you. I doubt they would give you too much, but just the same, try to stay out of the sun! Continue reading “Biochemistry Redux”

The Truth Is Out There

Another Saturday afternoon that I don’t feel like doing a cursed thing. In DBT this week we talked about not discounting positives in life. To practice what I preach I would have to say I exercised, fed and walked the dog, cleaned up and fed myself. I have tried to do dishes in the dishwasher but the top rack stuff did not get clean. Last time this happened, I poured a whole bottle of vinegar in the bottom of the machine and let it sit over night. The acid ate whatever was gunking up the works.

Hey, housekeeping tip!  We aim to cover all possible topics. Even those I know little about!

I continue to look for an answer to how many degrees of arc make up a central vision loss. Dr. William Goldberg in A Guide to Understanding Your Peripheral Vision says a normal visual field is 170 degrees. That is almost half a circle. Of that, 100 degrees are peripheral vision. 70 degrees are central vision. If you think of a protractor, that would take a pretty good chunk out of the middle, but you would still have 50 degrees of arc on either side of that wedge. Not as bad as some representations I have seen.

No clue if I am figuring this out correctly, but it’s a place to start. I asked the representative from the International Macular and Retinal Association the answer and she did not know either. She is going  to ask around.

Peripheral vision is broken up in three sections: far, middle and near. When we pick a preferred focal point for eccentric viewing, we naturally try to pick a place in the near peripheral. Color vision and discrimination are worse on the edges.

I have a couple of more in-depth articles to read on that. To be continued.

Still interested in the Nat Geo article on ending blindness. I learned all sorts of stuff about the eye. Did you know the eye is the only place you can look right at the brain without drilling a hole?  Eyes are a part of the brain!  During fetal development the eyes grow away from the brain, sort of like on stalks; maybe? The stalks analogy was mine.

Eyes, like the brain, are immune privileged. That means it does not have a strong immune response to ‘invaders’. You want to try a new treatment and don’t want the immune system to go crazy? Try it in the eye. Having the ‘perfect’ place means all sorts of studies can be done in the eye. More experiments mean more chances of finding cures. Stem cells and gene therapies all have a better chance of working in the eye so why not start with trying to cure an eye disease? Great idea!

One more time, if we have to be losing our sight, this is the best time in the history of man to be doing it. Keep the faith. To quote Mulder and Scully, “the truth is out there”. We are hot on its trail! Continue reading “The Truth Is Out There”

Good Thought, Bad Thought

Back again in the same day. You do know I am ridiculously hard to get rid of; don’t you??

This is the page I was going to write before my ZoomText, inelegantly put, took a dump. Now I will write it.

I went to see my local retinologist Monday. Great guy. He is good. His kids are good. I feel I see him enough I get to inquire about the boys.

I also feel like I am becoming ‘friends’ with my tomography tech. We chat. I asked about the enhanced depth tomography. He had the capability with his machine and since it would not cost any extra, he ran it on me. The pictures were pretty. I saw my optic nerve and my ‘divot’, geographic atrophy, but did not have the training to see much else.

The tomography tech pointed out two veins in my choroid. They were old veins, not new ones. It is sort of bizarre to realize how relatively deep the hole is in my macula, but that is a part of the definition of geographic atrophy; the damage is choroid deep.

Neither my local retinologist nor I believe I will convert to wet AMD. He has put me back to twice yearly for my check-ups. It was my understanding, and my retinologist confirmed, that wet developed as an adaptation (sort of) to the dry form of AMD.

The way I understand it, when the RPEs and the photoreceptors are not getting enough oxygen and nutrients they send out the SOS . They need supplies! They are starving! The body responds by establishing new supply lines in the form of new blood vessels. The only problem is these vessels are inferior. They break and the bleed. Problem not solved. The fix does not work so well.

I got the impression I am back to twice yearly visits – and he does not think I am a candidate for wet AMD – because I don’t have a lot of macula left. Now he did not say that. It was an impression but I am usually pretty good at those. I don’t think there is much for my body to try to save anymore.

Good thought and bad thought. Or actually bad thought and good thought. Bad thought that I may have reached this level so quickly. Good thought: could the slide be over? Will I soon stop losing vision?

Now, cheating my sweet little patootie off and using eccentric viewing and guess work to the max, my vision tests as 20/50. Am I really 20/50? No, but I cheat well. And they know I cheat, by the way. I tell them every time.

If I can cheat and test at 20/50, that means I have decent functional vision. I can do a lot with that. Not so bad.

So why all the horror pictures of visual fields that are 90% bleach white with decent vision around the edge? If this is a ‘central vision loss’ problem, what is the definition of central vision?

No clue, but Lin and I are on the hunt. Let ya know. Continue reading “Good Thought, Bad Thought”

Highlight: Here’s a GREAT website especially for those with wet AMD

Lin/Linda here: Every once in a while I find a website and/or Facebook page that stands out.  Here’s one of those.

The website and Facebook page are called The Science of AMD: Our vision is to save your vision.  It is presented by the Amgiogenesis Foundation. Their headquarters are in Cambridge, Massachusetts.

Click here to go to the website. From there, you can connect to Facebook, Twitter or YouTube using icons in the upper right corner.

What is angiogenesis? From the website: “Angiogenesis is the process used by the body to grow blood vessels. In healthy adults, normal angiogenesis occurs in healing wounds and reproduction, but in all other situations, it is abnormal.”

It’s what causes wet AMD: “Wet AMD is caused by abnormal angiogenesis, when new vessels grow under the macula, disrupting the central region of the retina. These new blood vessels bleed and leak fluid, causing the macula to bulge or lift up from its normally flat position, impairing central vision. If left untreated, scar tissue can form, and central vision is irreversibly lost.” 

What’s so special about the website?
  • From a design standpoint, you can change the size of the font and the color of the font & background, you can choose a version of the site in any of 7 languages as depicted by flags, it’s easy to navigate.
  • Format of content includes printed text, videos, audio, graphics, PDF files and more.
  • This is not just for the US, there are resources available for other countries as well.
What information can I find there?

There’s a menu with Learn, Treat, Resources, Connect, About, Donate.  I suggest you start at Learn!   The emphasis is on how angiogenesis causes wet AMD and what can be done to treat it.

OK, now go and explore! Let me know what you think!

Electron Rustlers

Let me preface this page by explaining how I passed chemistry: I did not understand a word the teacher said. He was so far out in left field I was never going to find him. I say it was bad teaching but maybe I was not being very bright.

Two of my friends sat behind me designing race cars. Never listened to a word of the lecture. After being confused for 45 minutes, I would turn around to the guys and they would clear everything up in 45 seconds.

I was terrified to try physics. That was the end of me and the hard sciences.

Moral of the story? You probably should not listen to me try to explain oxidative stress.  You have been warned so I am forging ahead.

I keep running into titles like The Role of Oxidative Stress in AMD. Great. It is important. What the hey is it?

Revisiting my horrible experience in chemistry my junior year, I vaguely remember learning atoms have electrons that spin around the nucleus in shells. Shells are orbits and for simplicity sake we will say they go out from the nucleus in concentric circles. (They really don’t but cut me a break. Two kids drawing race cars saved my chem grade.)

Each of the shells has an ideal number of electrons that orbit there. Although a shell is generally OK without the ideal number, it still tries to have that number. Sometimes it loses some electrons. Sometimes it steals some electrons and sometimes it shares some electrons with another atom that is also longing for its ideal number.

This desire to be ‘whole’ and to fill its outer shell with the ideal number of electrons is what is called being reactive. Often being reactive is a great thing for an atom. It gets to hook up with other atoms and make all sorts of crazy new molecules.

However there are times reactivity is not a good thing. Sometimes an atom may do some ‘electron rustling’ and steal from a neighbor. That atom is now out of kilter and it does some electron rustling of its own. Before you know it, there is a full-blown range war going on in your atoms. There is no peace in the valley!  This is oxidative stress.

Oxidative stress, just like a range war, can leave a lot of destruction in its wake. With all that electron rustling happening, things get damaged and broken. This is some of what is happening in our eyes.

You cannot totally eliminate oxidative stress but there are ways to restore the peace. Enter antioxidants.

Antioxidants have electrons to give to that first electron rustler. They allow that atom to be ‘complete’ by donating some electrons to fill its outer shell. If that atom has its needs satisfied early, it won’t feel the need to go rustle. Range war – errrrrrr, oxidative stress – averted.

Vitamins C and E are antioxidants. Also vitamin A. [Lin/Linda here: if you have Stargardt’s Disease, you do NOT want any extra vitamin A. Click here to read more about why that is.] Eating red, orange and yellow fruits and veggies can be very good for you. You can also get antioxidants in supplements. However, like all good things, they should be indulged in with moderation.

So that is my take on oxidative stress. I hope the guys would be proud of me.

Click here for another explanation of oxidative stress by Dr. Andrew Weil.

Continue reading “Electron Rustlers”

The Waiting Game

Yesterday was my third appointment with Regillo. Quite frankly I was hoping for great things. Hoping I would get a definitive answer and it would be positive! No such luck. My ‘answer’ was another “maybe”.

What criteria are they using? No clue. I was told my eye condition certainly qualifies me. Beyond that, I got no inkling of what I need to do to move up the list.

After a year and a half, I am getting more and more frustrated and antsy. If there is a way to become a prime candidate, I don’t know what it is.

Anatomy of the eye-click on the image for more information

I did learn a few things. Contrary to what I read, the good doctor says everyone has a suprachoroidal space (SCS). [Lin/Linda here: the SCS is the space between the sclera (outer part of eye) and choroid (space below RPEs).  It’s important in both clinical studies Sue is referred to because both insert the stem cells into this space; more about the clinical trials below). Not sure why the difference between what I read and what he said. I know I read something about ‘forcing’ (my term) an SCS in guinea pig eyes. They did it by injecting saline solution between the appropriate layers. Maybe the difference is between having a space and having a medically useful space? I might be wrong but I got the impression the delivery system works better when there is fluid in the SCS. Maybe not. Anyway, everyone has one. I am just not sure if you need the fluid to accommodate the delivery system. If you really want to know, check with your eye doctor. I am still trying to piece this all together.

The next thing I found out was the Ocata/Astellas study may resurrect sooner than I was originally told. I had heard two years or more and now I am being told 2017. Sweet.

I was asked which one I preferred. The one I would prefer is the first one to come to fruition! I will be dancing in the streets to be asked to participate in either one of them.

So that is where I stand now. I have been given two strong maybes. Is that a guarantee I will get something or do two nothings equal nothing? It is driving me crazy!

So back to practicing my distress tolerance skills. I have to ACCEPTS my situation. Engage in activities and contribute to others. I have to compare my situation to those of others and be grateful; things could be worse. Doing things to laugh will help me to have opposite emotions and I can push away problems I cannot solve at present. I can also have pleasant thoughts and intense sensations that distract me from my frustrations. It can be done. I have done it for a year and a half. I can keep on.

written 12/16/2016

Continue reading “The Waiting Game”

Highlight: What is Myopic Macular Degeneration?

There are quite a few eye diseases that cause degeneration of the macula. The most common forms of macular degeneration are defined by age, at least in part:  1) Age-Related MD (AMD or ARMD) and 2) Juvenile MD (JMD) – several inherited and rare diseases that affect children and young adults including Stargardt’s Disease, Best Disease, and juvenile retinoschisis.

There is another form of macular degeneration called Myopic Macular Degeneration or Myopic Maculopathy.

What is myopia?

If you have trouble seeing things far away like road signs, your eye doctor may have said that means you are nearsighted because you can see things near better than far.   Some people call it being shortsighted.  The medical/optical term is myopia.

Top of diagram shows normal eye & vision. Below, myopic eye and vision.

Myopia occurs when the eyeball is too long relative to the focusing power of the cornea and lens of the eye (see diagram above). This causes light rays to focus at a point in front of the retina, rather than directly on its surface.   It can also be caused by the cornea and/or lens being too curved for the length of the eyeball. In some cases, myopia is due to a combination of these factors. Click here for more information.

There are different degrees of myopia: mild, moderate and high (also called pathological myopia).   The higher the degree, the higher chance of the degeneration of the macula.  Click here for some other risks for high myopia including retinal detachment, macular detachment, glaucoma and macular holes.

Myopic Macular Degeneration

People with high myopia/pathological myopia are at risk for damage to the macula from the stretching of it as the eyeball grows throughout life.  Here’s a good description of what happens: “As the eyeball grows and stretches, it may also cause an area of atrophy and/or cracks in the layers under the retina. These cracks can serve as conduits for abnormal blood vessels to grow under the retina. These vessels can hemorrhage and scar which is similar to what happens in wet macular degeneration. The onset of the nets of abnormal blood vessels, called Fuch’s spots, often occur in the 4th to 6th decades of life. Approximately 5% of pathological myopia patients develop Fuch’s spots, which lead to damage in the macular region of the eye and a subsequent loss of central vision.” From http://www.lowvision.org/Pathological%20Myopia.htm

Not all people who are myopic get Myopic Macular Degeneration.

Click here for an explanation of how the atrophy can occur as well as how the blood vessels grow into the macula.

The symptoms are similar to AMD & JMD as well.  Click here to learn more about them.  This article will take you to stories of people who have Myopic MD.

Click here for a first-hand account of the disease from a person with it.

Other links:

Myopic Macular Degeneration

American Academy of Ophthalmology Diagnosis and Treatment of CNV in Myopic Macular Degeneration

Degenerative Myopia

Treatment Patterns for Myopic Choroidal Neovascularization in the United States, article published July 2017 edition of AAO Journal (AAO is American Academy of Ophthalmologists).

 

 

I Am Not a Doctor

Commentary: Lin just sent me a post from someone in the Facebook group. She asked for my reactions. The person is claiming he completely reversed neovascular (wet) AMD with nutritional treatments. Here goes.

First the disclaimer. I am not a doctor. I am not a nutritionist. I am a woman with dry AMD who has tried to educate herself about her disorder. Therefore I do not, by any stretch of the imagination, have all of the answers. End of disclaimer.

That said, let me congratulate him on his greatly improved vision! I am glad he are doing well.

I know some of what he says is true. In general the diets of those in the developed world are atrocious. We should be eating many more fruits and vegetables, especially our leafy greens, than we do. The reason taking the AREDS/AREDS2 supplement works to slow the progression of the disease is probably our poor diets. If we ate well, the supplements would not be so needed. [Lin/Linda: I have to mention that there is some risk taking the AREDS or AREDS2 with 80mg zinc.  It can cause problems in the genitourinary tract but there is evidence that for people with certain genes, that high dose of zinc can cause their AMD to progress faster. Since not everyone has easy access to the genetic tests, there are supplements with no zinc or less zinc.  Check out this post for more information.]

Angiogenesis is the growth of new blood vessels. This is a hallmark of wet AMD. There is some evidence angiogenesis is part of the healing process and may be triggered by inflammation (Reiner O. Schlingemann in Role of Growth Factors and the Wound Healing Response in Age-Related Macular Degeneration). There is also evidence that retinal hypoxia (in English? Your retina is gasping for oxygen) is a trigger for angiogenesis and neovascular (wet) AMD. (Citation same guy. It is so nice not to have to follow APA format? [Lin/Linda: APA is the American Psychological Association and when you write something for them, you need to follow a very strict format for references to articles.]

That said, theoretically it is possible he hit upon a combination of nutrients that would reduce inflammation and increase oxygenation to his retina, thus somehow stopping the angiogenesis. Did this happen? No clue. I am just sort of a slightly-too-smart-for-my-own-good, visually impaired lady. (Gets me in a lot of trouble.) Is it possible? Sure. “There are more things in heaven and earth, Horatio, than are dreamt of in your philosophies.” (That is the bard, of course).

Now, it would be my supposition – again totally unfounded – he was not in advanced AMD and had not experienced much if any photoreceptor death i.e. geographic atrophy. Unfortunately from what I have been told dead is dead with those. They would not have come back.

That is pretty much my take on it. Again when it comes down to it, I know nothing but I have a helluva lot of opinions. Don’t believe me. Offer your opinions. What do you folks think? Continue reading “I Am Not a Doctor”

Illegal, Immoral or Fattening

Everything I like is either illegal, immoral or fattening.

Hold that thought. I will get back to it.

One of the problems with living in a social world and having a progressive disease is we worry people. We worry people a lot. My friend with whom I walk and kayak was very distressed when I told her my eyes were deteriorating. Yes, I know it is going faster than anticipated. Sorry. Sorry. Mea culpa. This is not exactly my idea of a good time either.

Everyone wants to help and everyone has a theory as to what to do. I try to take it in the spirit it was intended. Being nagged is a sign of love and worry and generally happens (at least in my unsubstantiated opinion) when there is little else they can do.

After all, it is not like they can circulate a petition and get me cured!

Anyway, this friend’s answer to my problem is statins. Leave it to the exercise fiend to want to attack the fat! She has seen the latest study covered in magazines and newspapers and she has decided I need to sign up for a clinical trial with statins. Oh, my…

I promised I would contact them. And I will, I really will, but first I got the journal article on their phase 1 trial. That was interesting reading.

Regression of Some High-risk Features of Age-related Macular Degeneration (AMD) in Patients Receiving Intensive Statin Treatment made me wonder several things. First of all, why are these titles all so long? Second thing: are there really over 100 genes that contribute to the development of AMD? Third thing: are there really several different ‘types’ of AMD? If there are – and they say there are – it makes sense there has been no quick, one-size-fits-all answer.

The reason they stressed all the different ways you can develop AMD as well as the different varieties of AMD was to highlight the fact statins may not work as well with all forms of AMD. Their study focused on people with multiple, large, soft drusen. Remember the drusen are the piles of fatty ‘eye poop’ that are not getting cleaned up and therefore interfere with the care and feeding of the photoreceptors. The thought was if statins can clean the fat out of your arteries, they can clean it out of your eyes. At least some eyes.

The reason the researchers thought statins might be able to help was based at least in part on mouse research. Mice fed a high fat diet showed changes similar to human aging and development of AMD. Given statins, they improved.

Which brings me back to my original point. Everything I like is either illegal, immoral or fattening. Now I have to add it is bad for my eyes! Fat – what is life without butter? Or bacon? Or a nicely marbled cut of meat? What is this world coming to if butter can make you blind? ??

Fortunately that last, little part has not been proven. I also think I would persist in my bad habits (Gives brand new meaning to “Can I do it until I need glasses?”; doesn’t it?).

So, quick recap: there is some evidence statins can remove large, soft drusen. The article sounded as if their procedure would be most promising for people in the early stages of the disease as well. If this describes you, you might want to check it out. Continue reading “Illegal, Immoral or Fattening”

I Have Macular Degeneration…Now What?

June 2023 There’s an announcement that since Sue has not written any new journal pages for some time, the site has been archived until we can decide if the work necessary to make sure all information is accurate and up-to-date can be made. In the meantime, you’ll get some pages ‘not found’ or ‘private’ until that decision has been made. The emphasis for several years has been on the Facebook group.

Where can I quickly find information about AMD?

One of the best resources available is from the Prevent Blindness organization’s website called Guide Me.  You answer a few questions and you will get a personalized guide with important aspects of AMD based on your answers:

Click here to go to Guide Me.

Click here to watch a 4-minute video that explains what AMD is, what causes it, and what can be done about it.

Click here for a good list of Frequently Asked Questions.

Click here to go to a great site maculardegeneration.net where you will find articles written by people with macular degeneration and caregivers. They also have a Facebook page.

What other websites are helpful?

Here are some of our favorites:

Click here to find out should I take the AREDS or AREDS2 supplements?

Click here for a video that covers important information about AMD

Click here for a description of dry vs. wet AMD (we are not recommending any products in this article, but be aware that the site may profit from some products they advertise.)

Click here for an explanation of the stages of AMD (we are not recommending any products in this article, but be aware that the site may profit from some products they advertise.)

Click here to read about what happens if you have AMD in only one eye

Click here for some answers to common questions about depression after diagnosis

Click here for an article about how vision rehabilitation helps prevent long-term depression

Click here for a very comprehensive page about wet AMD

Click here for a very comprehensive page about dry AMD

Click here for an article about how fast AMD progresses

Click here for 10 questions to ask your doctor

Click here to find a support group (I’ve been told that this site may not be up-to-date. Ask your eye specialist for a referral.)

Click here for eye-healthy foods including a Healthy Vision Grocery List (2/14/2022 site wasn’t formatting properly.) Click here to read the answer to the question ‘What should I be eating or not eating to hopefully slow the progression of my AMD?’

Click here to find out what vision changes/symptoms to look for (we are not recommending any products in this article, but be aware that the site may profit from some products they advertise.)

Click here to find out about the people who can help you (what are the differences between the types of eye doctors, do I need to see a specialist, etc)

Click here for tips on how to make the most of the vision you have (section toward the bottom of the page; lots of other good information on the whole page)

Click here for a FAQ (Frequently Asked Questions) from the Macular Disease Foundation Australia.

Click here for a FAQ (Frequently Asked Questions) from our Facebook group.

Where can I do more research?

You can do searches on the Internet – there is a LOT of information there.  We have done a lot of research and here’s how you can find it.

Click here to go to How to Navigate and Search Our Website.

Join our very active Facebook group Our Macular Degeneration Journey. There’s lots more information there as well as support whenever you need it.

How do I move around on the website?

Click here to go to How to Navigate and Search Our Website.

To find about more about me, about Sue, about our project, go to the menu at the top of the page.

Reviewed 02/14/2022

 

 

 

 

Smile for your Picture!

My OCT scan showed no extra veins. That is a good thing but what is an OCT scan?

You have had them. It is that machine with the vertical row of little crosses. You are supposed to stare at the brightly lit one while the horizontal line clicks up and down.

The proper name for an OCT scan is Optical Coherence Tomography. Wikipedia has an article on it and I would refer you who enjoy physics to that article. Social scientist here. I got just about nothing out of it.

However, the article does have a section for the layman and it’s called ‘Layperson’s Explanation’! Even that section requires a bit more than a rudimentary understanding of the physical sciences. In bigger words it says OCT uses light to look into things that you cannot see into (opaque). It takes images by paying attention to the light reflected off of what it wants to see and ignoring the light reflected off of other things. Or maybe knowing those images are in the background. I think. Social scientist here; remember?

Click the photo for more information about the results of an OCT
Click the photo for more information about the results of an OCT
OCTMacular Normal vs Wet_021
Click the photo for information about the OCT test results.

The images that are made are three-dimensional. That means if there are veins where they are not supposed to be, the doctor can see them as ‘bumpy’ spots on the image. Conversely, if you have geographic atrophy and a ‘divot’ the three-dimensional image will show that there is a concave spot.

Get it? I think I do. Maybe.

OCT is great for vision stuff like AMD. It does not penetrate through tissue like sound, but with eyes, it doesn’t have to. You can go through that handy little peep-hole called the pupil. OCT images are of high quality. They are immediate. I got my results the next day. It would have been the same day but the doc was at his other location and I was the last appointment of the day.

And finally, you as the patient don’t require a lot of preparation. They normally dilate your eyes but this week I discovered even that is not required. My experience technician just “shot” through my pupil and the images apparently came out fine. My technician has done this for a while and has become a real “straight shooter”!?

And that is what I think I know about optical coherence tomography. Social scientist here.

Continue reading “Smile for your Picture!”

News: Summary of AMD Research & Developments for past 12 months – June 2016

Here’s an excellent summary of the research and developments in the field of AMD.  It’s done by Dan Roberts of mdsupport.org which is a site I highly recommend for both information and support.

Click here for the audio with slides presentation. You don’t have to be able to see the slides, the audio is very clear.

Click here for a transcript of the presentation.

 

Wrinkles

As I said before, now that I am officially one of the visually impaired, I seem to have acquired ‘clearing house’ status. I hear about people with all sorts of vision related stuff. Sometimes I pass it along. Recently I heard of a new -to me – wrinkle in macular problems. And I literally mean a new wrinkle!

A friend of a friend is upset because his vision is all wavy. He thought he was developing Macular Degeneration. He is of “of a certain age” and the symptoms are similar.

Turns out he has something called macular pucker. I had never heard of it so I looked it up.

Disclaimer one more time: I am not a doctor. Reading two web articles and watching a nine-minute YouTube video does not equal a medical education.

Consult your eye health professional for information and treatment if you believe there is anything – ANYTHING – funky about your vision.

Here goes. My two article and one video info:

The goop that is in your eye and keeps you eye plump and round is called the vitreous. As it gets older the vitreous liquefies and clumps. I think of it as what happens to a bowl of chocolate (I love chocolate!) pudding that was forgotten and overstayed its welcome in the back of the fridge. You know how parts of it get watery and parts get hard and it separates from the bowl? That is apparently what happens in your eye.

The clumpy parts can become floater. Mine looks like a mosquito larva. (And who said you would never use the stuff you learned in tenth grade biology?) Anyway, if I turn my head just right my ‘larva’ swims across my field of vision. Cheap entertainment.

Back on track. As the vitreous separates from the retina (think pudding receding from the side of the bowl) it sometimes sticks. If the vitreous sticks and pulls on the macula, scar tissue forms. The scar tissue may warp and contract. This can cause the macula to distort and you get the aforementioned wrinkle in your vision.

Macular pucker is not Macular Degeneration.

My sources said it is often in one eye only and generally the condition of the eye does not degenerate. If the damage is too great and interferes with daily functioning, a vitrectomy will often be helpful.

I did describe a vitrectomy before. Basically they suck all of the goop out of your eye and replace it with gases or oil or salt water. Getting the vitreous out of your eye stops it from pulling on the retina. That should stop the wrinkle from getting worse and it might even bounce back a bit.

Macular pucker. Hope that was educational.

Continue reading “Wrinkles”

Highlight: What is Advanced Macular Degeneration?

About 10 years ago, my elderly father was diagnosed with dry AMD and then later we were told it was ‘advanced’ and that he had ‘geographic atrophy’.  At the time, I didn’t understand what that was.

Here’s an excellent article about what those terms really mean.  It’s on the great website WebRN: Macular Degeneration.  If you haven’t looked at it, I recommend that you do after you read this article.

Advanced AMD & Geographic Atrophy

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