I found David Paterson, the first legally blind governor of New York, to have an interesting perspective. I can relate to him in living in a world that is between the sighted and non sighted worlds and how very difficult it is for people to grasp partial sightedness.
first legally blind governor in U.S. historyDavid Paterson to become new New York governorBy Reuters / March 12, 2008NEW YORK (Reuters) - New York Lieutenant Governor David Paterson was setto become the state's first black governor and the first legally blindgovernorin U.S. history, after the resignation of Gov. Eliot Spitzer Wednesday.Paterson, 53, became New York's first African-American lieutenantgovernor in November 2006. He has been legally blind since childhood,with only partialsight in his right eye.Spitzer resigned after media reports linked him to a prostitution ring.He said Paterson would take over Monday.The following are some facts about Paterson:Paterson was born in Brooklyn to Portia and Basil Paterson. His fatherwas the first non-white secretary of state of New York and the firstAfrican-Americanvice chair of the national Democratic Party.He earned his bachelor's degree in history from Columbia University,graduating in 1977, and completed his law degree at Hofstra Law Schoolin 1982.Paterson became a public servant in 1985 when he began representingHarlem in the New York State Senate, according to the New Yorkgovernor's Web site.In 2002, he became the body's minority leader, the first non-whitelegislative leader in New York state history.In 2004, he became the first legally blind person to address theDemocratic National Convention.In 2006, Paterson was elected New York's first African-Americanlieutenant governor.Paterson ran the New York City marathon in 1999.Paterson, an adjunct professor at Columbia's School for Internationaland Public Affairs, lives in Harlem with his wife, Michelle PaigePaterson, and theirtwo children.Additional information from a New York Times article FROM January, 08"As a disabled person, there's certain times that I don't want to appeartoneed that much help. When I was in college, when I was at Columbia, Ihad aprofessor - I actually Googled him, he passed away in 1986 and his namewasBasil Ruch, and he was a professor of history at Barnard College, and heshowedme a picture of Franklin Delano Roosevelt being carried into the 1932Democraticconvention. And he said that Roosevelt by 1932 was still able to walk acertaindistance, but not quickly, and he wanted to walk in, he wanted thecountry tosee him standing, and but what happened was, when he started to walk,and he gottoward the end, he was starting to be a little jittery, that a bunch ofsupporters, thinking they were helping him, grabbed him and picked himup andcarried him in. And you see in this picture - and I couldn't really seeit, buthe described it to me - he has this stern, angry look, because theymessed uphis moment. And I know what he was feeling. Because sometimes you wantto project a certainamount of strength. And you can project it if you're a woman, you canproject itif you're disabled, you can project it, but often the people who loveyou don'tsee the need for you to project it.I remember when I was in the D.A.'s office, and I conducted a hearingand it hadto do with a stalker who was bothering this woman. And I got to feelingwhen thewoman saw me holding the file up to my face and that kind of thing, andthestalker's looking at her, and she's kind of - I got that she didn'treally knowif I was able to handle this.And I went over to her and I said, "Listen, just in case we lose thishearing,don't worry, because when he goes outside, I'm going to kick his butt."I saidthat to her because I wanted her to know that I'm in charge of her case.Andthat's what I'm saying about projection."Q: Did you always think, with your disability, that you could followyour fatherinto politics, or was that something you came to over time?A: When I was 10 years old I watched Robert Kennedy speak at theDemocraticNational Convention and I wished I was him. And I think, again, therewas thatfamily connection - he was following in the footsteps of John, Hillaryfollowsin the footsteps of Bill, so I always relate to that, you know, kind offamilymember who has to deal with that shadow.When I was in college, though I had academic ability, I don't know thatI wasall that socially developed, or had a real difficult problem askingpeople forassistance, and had a lot of problems as a result of that. And I thinkas I hadmore problems, my ideas about being in politics, or following my fatherdwindled. I didn't see myself as - I think my self-esteem reallysuffered fromthat. ...Q: In terms of your vision, how much can you see?A: I am legally blind in my right eye, and totally blind in my left eye.I'mlooking at Armen [Meyer, a press aide who was in the room]. I know hehas awhite shirt on, I know he has a tie on, but from this distance I can'ttell youwhat color it is. I think it's a darker color. ...When I am in places where I am familiar, I will appear to see betterthan inplaces where I'm not. If I walked around my house, and you didn't know,you'dprobably think I have no vision problems.When I say I saw something, it's more like I sensed it. So when I saidthat wewere on a plane with the Clintons, and we're all eating pizza, I knewthat I waseating pizza and I knew they took pizza off the tray, so I assumethey're eatingit. I think people's perception of me sometimes is that I see more thanIactually do. But I play basketball, and I've done things that peoplewith my vision aren'tsupposed to do. I'm in this interesting sort of zone between the sightedand theunsighted, and have never really met anyone who I visually relate to,I've nevermet anyone who is kind of like me. ...My truest disability has been my ability to overcome my physicaldisability. Soin other words, as soon as people see that I can be independent, thenthey holdme to the standard that everyone else is. So I remember once I told theairlinesthat I had a sight problem, and they put me on this bus to go to a hotelbecausethere were no other flights out of the airport that night, and I gave upmy seatto everyone got on and they passed me, and then like this 90-year-oldwoman, whowas trying to get up the steps, and I couldn't take it anymore so Ihelped herup the steps, gave her my seat and took another seat. First stop, thebus drivertells me to get off. And I know that he's doing this now because hethinks Ihave no problem. He goes, "Go that way." And I almost fell in thewishing wellin front of this hotel. That's because he saw me able to fend formyself.And I think that's been my greatest disability, that as I've overcome myphysical disability, it just leads to other problems. So I think I havenowlearned - and I'm not doing this to be deceptive - but I don't act theway I didwhen I was 17, like I can do everything myself, because I realized theminute Ido that, no one helps me. So I learned to be a little more pragmaticabout life
Monday, March 31, 2008
Tuesday, March 25, 2008
Sunday, March 16, 2008
First Legally Blind Governor
Not only is David Paterson New York's first Black governor, he is NY's first legally blind governor. His blindness was caused by a childhood illness. He has some vision in one eye and no vision in the other. He went to law school AFTER being legally blind.
What is his message to me? Blindness is no excuse to not hold yourself to the highest standard of achievement. Many people, out of ignorance, will coddle us. The "tough love" mentality has to come from within. Hard? Absolutely! Worth it? Well, what is the alternative?
http://www.ny.gov/ltgov/
What is his message to me? Blindness is no excuse to not hold yourself to the highest standard of achievement. Many people, out of ignorance, will coddle us. The "tough love" mentality has to come from within. Hard? Absolutely! Worth it? Well, what is the alternative?
http://www.ny.gov/ltgov/
Tuesday, March 11, 2008
Rebuttal to my 2/15 Post
Facts quite often, I fear to confess, like lawyers, put me to sleep at noon. Not theories, however. Theories are invigorating and tonic. Give me an ounce of fact and I will produce you a ton of theory by tea this afternoon. That is, after all, my job. -Ray Bradbury, From the foreward to "Mars and the Mind of Man"
In my post from 2/15, I present two case studies and one larger scale study to make a theoretical case for the use of acetazolamide and RP, independent of CME. I am by no means in a position to advise anyone to take anything. I am simply presenting information I find interesting as well as connections that intrigue me.
An anonymous researcher replied to me via email. I am including his response below. It gives another perspective. He was kind enough to provide his input. If you have the time to read the full text of the University of London acetazolamide case study, you will find that the subject's visual field expanded substantially. The authors maintain this only happened after several months at a dose of 1000 mg. In the larger study the anonymous researcher comments on, the dosing was cut in half and the duration in a third, if memory serves. So, it was not really a valid replication of the case study.
Researchers do not find one case of an RPer making substantial gains in visual field of much interest. I, as a patient, do find it interesting. I also believe, when blindness is the alternative, RPers should have the option of trying experimental therapies with informed consent. RPers should not have to be in a clinical trial to have access to prescription drugs or other readily available therapies that could, possibly, help them. I do not believe we need to be babysat. RPers can understand risk/ benefit analysis and come to their own conclusions, with information on risks and management of those risks. Physicians need to be partners with patients, not gatekeepers.
For argument's sake, say I had some experimental therapies. Even with a positive change in my ERG, I am convinced I could walk in to the university near my house, get an ERG that shows normal vision from my flat line now and no one would raise an eyebrow. They would say, "Hmmm....that is unusual. She must not have had RP. It must have been something else." They would say this even if I presented in-depth information on the protocol I followed, backing it up with published research. My retinal specialist is a proactive guy, maybe he would write up a case study. When people read it they would say, "But she did so many things. How can we even attempt to make a causal connection?"
As RPers interested in actually trying to treat this thing, this is the mentality we face. Do not misunderstand, research is vitally important. But, do not count on these people to make any kind of common sense connections. Until something is effective in very large scale studies, no one cares.
Below is the research scientist's response. It was very kind of him to send this information. I appreciate his involvement and interest.
I read portions of the Friday, February 15 blog entry . In your point #2 you say, "There have been studies that have shown acetazolamide improves visual function in those who have RP but no CME." ... but the study that you cited does not say that at all. I think you have misunderstood the results. The authors, two of whom I know personally, merely reported the results that three patients showed improvement in their visual field -- an improvement that was not reproduced in the crossover study. In quantifying these visual field changes, they used the word "significant" which in conversational English almost always means "huge", but in research it means “unlikely to be explained by chance” (more on that later). But no matter how you define the term, these "significant improvements" in three patients would never cause a medical researcher to as much as raise an eyebrow or utter the sound “hmmmm” -- for a variety of reasons. Pilot studies by definition lack the statistical power of the gold standard placebo-controlled, double-blind large study, and therefore the goal of the pilot study can never be more ambitious than to suggest a interesting trend that might be worthy of further investigation (and the health risks and enormous expense of further investigation). It is a mistake of the highest order to suggest that the results of this pilot study demonstrate causation as your statement implies. Again, by definition, no one in the research community would ever interpret the results of any pilot study as causing anything. And especially since, as in this case, the numerically small positive observations were:
a) derived from subjective psychophysical rather than objective electrophysiologic measurements.
b) not reproduced in the crossover study Regarding A: An automated threshold-related 60° visual field is a brutally boring and stressful test (as I'm sure you probably know). Improvement or decline in performance after repeated trials can easily be attributed to "the learning effect" or fatigue respectively. In our glaucoma practice (where visual fields were, until recently, widely used), significance is usually reserved for changes observed in comparison to an average of three baseline measurements -- and even then, it is regarded with suspicion if the patient has false positive responses (suggesting anxiety or eagerness) and/or false negative responses (suggesting boredom, fatigue, Munchausen syndrome or malingering ). This "catch trial invalidation" can be factored out if the visual field is performed manually (Goldmann perimetry) by the same skilled perimetrist on each successive patient-visit. But these kind of visual fields are rarely done nowadays because it is slow, personnel-intensive and therefore quite expensive in terms of resources. For these reasons the visual field is seldom (or should I go out on a limb and say never) taken by itself to make patient management decisions. There are just too many opportunities to be wrong in any single interpretation. But fortunately, in glaucoma management at least, new, more sensitive and more objective technologies have emerged that will make the visual field a medical anachronism in the next few years. However, patients will still get serial visual fields as long as the test is still being paid for by the insurance companies, in spite of the fact that glaucoma docs rely upon them less and less.Regarding B:I just flipped a coin 13 times and got ThhTThhhThhhT = 8 Heads + 5 Tails. There are also two runs of three heads in a row. What should I make of this apparent bias towards heads? If I didn't tell you that I was flipping a coin, but instead I just simply showed you some results where there were 8 positive outcomes and 5 ambiguous or negative outcomes, you might be justified in thinking that "something is going on here" that is worthy of further investigation.After 13 more flips I get: TTThhhhThhhhT = a repeat of 8 positive outcomes + 5 negative or ambiguous outcomes! Even more exciting is the fact that in this series there are two runs of four heads in a row! We could be seduced into thinking that we are definitely on to something in our little "pilot study."Now I'm going to put my 13 pennies in a shot glass, shake it up and then dump it on the table. I get: 5 positive outcomes + 8 negative or ambiguous outcomes. Repeating the shot last method yields: 6 positive outcomes + 7 negative or ambiguous outcomes. If I repeat these trials enough times, regardless of the method, I will eventually, according to statistical theory, achieve the results predicted by the known mathematical probability, which is of course 0.5 -- or 6.5 Heads + 6.5 Tails. But if we do not know the probability of any event occurring, which of course is the case in every study (otherwise it would not be a study), then much larger numbers are needed to detect a "significant" event and then to announce that such an event was statistically unlikely to have occurred as a result of chance alone.So in summary, the three solitary "positive" findings would be more interesting if they were objective measurements (i.e. electrophysiologic) and if they were reproducible. With more concrete objective data, the authors might get funding and FDA approval for an even larger (but still pilot) study -- say, with 20 or 30 people. But because no reproducible, unarguably positive result was found, this paper serves as a warning to other researchers who discover it during their literature review "don't travel down this particular rabbit-hole." The NIH is never going to fund a full blown study using such weak data, and the FDA would object to a large study for similar reasons -- authorizing the "off label" use of a drug that can produce significant side effects on the basis of a one-time observation of 3 visual field improvements -- which could not be reproduced even within the same pilot study. The in-vitro studies that you cited offer a biochemical mechanism of action which no doubt fueled, and might continue to fuel, occasional research interest. But the lack of hard evidence means that medical research is a long long long long way away from suggesting any of the carbonic anhydrase inhibitors as a treatment for RP, and any physician who prescribes it to a patient who does not have a proven case of glaucoma is taking a huge medical-legal risk. The statement at the bottom of one of the papers you cited "These experiments suggest a promising approach to treatment of RP17 that might delay the onset or possibly prevent this autosomal dominant form of RP"... is pretty standard "research speak" for .... "I want my paper to be cited in more treatment-related journals." It is the, "how is this research relevant" statement that nearly every research paper optimistically and triumphantly makes in closing, and it should not be taken as if a new cure has been discovered. However, the presumed strategy of getting it cited in journals other than biochemical abstracts didn't work, as to date it has been cited only by four other papers -- all of them biochemical works, and none of those were follow-up studies pertaining to RP.You probably regard the response you're getting from U.S. doctors as somewhat gutless, uncaring and maybe even inhumane. But demonstrating a promising in-vitro mechanism is light years away from prescribing it as a therapy -- at least in the United States. A colleague sent me an e-mail suggesting that I watch 60 minutes tonight for a segment on FDA surveillance gone wrong. I got busy and missed it. Did you watch it? I'll try to find the video or transcript online later but the very existence of such a story supports the "damned if you do and damned if you don't" criticism that no doubt influences the FDA's usual abundance of caution when it comes to authorizing new treatments.
In my post from 2/15, I present two case studies and one larger scale study to make a theoretical case for the use of acetazolamide and RP, independent of CME. I am by no means in a position to advise anyone to take anything. I am simply presenting information I find interesting as well as connections that intrigue me.
An anonymous researcher replied to me via email. I am including his response below. It gives another perspective. He was kind enough to provide his input. If you have the time to read the full text of the University of London acetazolamide case study, you will find that the subject's visual field expanded substantially. The authors maintain this only happened after several months at a dose of 1000 mg. In the larger study the anonymous researcher comments on, the dosing was cut in half and the duration in a third, if memory serves. So, it was not really a valid replication of the case study.
Researchers do not find one case of an RPer making substantial gains in visual field of much interest. I, as a patient, do find it interesting. I also believe, when blindness is the alternative, RPers should have the option of trying experimental therapies with informed consent. RPers should not have to be in a clinical trial to have access to prescription drugs or other readily available therapies that could, possibly, help them. I do not believe we need to be babysat. RPers can understand risk/ benefit analysis and come to their own conclusions, with information on risks and management of those risks. Physicians need to be partners with patients, not gatekeepers.
For argument's sake, say I had some experimental therapies. Even with a positive change in my ERG, I am convinced I could walk in to the university near my house, get an ERG that shows normal vision from my flat line now and no one would raise an eyebrow. They would say, "Hmmm....that is unusual. She must not have had RP. It must have been something else." They would say this even if I presented in-depth information on the protocol I followed, backing it up with published research. My retinal specialist is a proactive guy, maybe he would write up a case study. When people read it they would say, "But she did so many things. How can we even attempt to make a causal connection?"
As RPers interested in actually trying to treat this thing, this is the mentality we face. Do not misunderstand, research is vitally important. But, do not count on these people to make any kind of common sense connections. Until something is effective in very large scale studies, no one cares.
Below is the research scientist's response. It was very kind of him to send this information. I appreciate his involvement and interest.
I read portions of the Friday, February 15 blog entry . In your point #2 you say, "There have been studies that have shown acetazolamide improves visual function in those who have RP but no CME." ... but the study that you cited does not say that at all. I think you have misunderstood the results. The authors, two of whom I know personally, merely reported the results that three patients showed improvement in their visual field -- an improvement that was not reproduced in the crossover study. In quantifying these visual field changes, they used the word "significant" which in conversational English almost always means "huge", but in research it means “unlikely to be explained by chance” (more on that later). But no matter how you define the term, these "significant improvements" in three patients would never cause a medical researcher to as much as raise an eyebrow or utter the sound “hmmmm” -- for a variety of reasons. Pilot studies by definition lack the statistical power of the gold standard placebo-controlled, double-blind large study, and therefore the goal of the pilot study can never be more ambitious than to suggest a interesting trend that might be worthy of further investigation (and the health risks and enormous expense of further investigation). It is a mistake of the highest order to suggest that the results of this pilot study demonstrate causation as your statement implies. Again, by definition, no one in the research community would ever interpret the results of any pilot study as causing anything. And especially since, as in this case, the numerically small positive observations were:
a) derived from subjective psychophysical rather than objective electrophysiologic measurements.
b) not reproduced in the crossover study Regarding A: An automated threshold-related 60° visual field is a brutally boring and stressful test (as I'm sure you probably know). Improvement or decline in performance after repeated trials can easily be attributed to "the learning effect" or fatigue respectively. In our glaucoma practice (where visual fields were, until recently, widely used), significance is usually reserved for changes observed in comparison to an average of three baseline measurements -- and even then, it is regarded with suspicion if the patient has false positive responses (suggesting anxiety or eagerness) and/or false negative responses (suggesting boredom, fatigue, Munchausen syndrome or malingering ). This "catch trial invalidation" can be factored out if the visual field is performed manually (Goldmann perimetry) by the same skilled perimetrist on each successive patient-visit. But these kind of visual fields are rarely done nowadays because it is slow, personnel-intensive and therefore quite expensive in terms of resources. For these reasons the visual field is seldom (or should I go out on a limb and say never) taken by itself to make patient management decisions. There are just too many opportunities to be wrong in any single interpretation. But fortunately, in glaucoma management at least, new, more sensitive and more objective technologies have emerged that will make the visual field a medical anachronism in the next few years. However, patients will still get serial visual fields as long as the test is still being paid for by the insurance companies, in spite of the fact that glaucoma docs rely upon them less and less.Regarding B:I just flipped a coin 13 times and got ThhTThhhThhhT = 8 Heads + 5 Tails. There are also two runs of three heads in a row. What should I make of this apparent bias towards heads? If I didn't tell you that I was flipping a coin, but instead I just simply showed you some results where there were 8 positive outcomes and 5 ambiguous or negative outcomes, you might be justified in thinking that "something is going on here" that is worthy of further investigation.After 13 more flips I get: TTThhhhThhhhT = a repeat of 8 positive outcomes + 5 negative or ambiguous outcomes! Even more exciting is the fact that in this series there are two runs of four heads in a row! We could be seduced into thinking that we are definitely on to something in our little "pilot study."Now I'm going to put my 13 pennies in a shot glass, shake it up and then dump it on the table. I get: 5 positive outcomes + 8 negative or ambiguous outcomes. Repeating the shot last method yields: 6 positive outcomes + 7 negative or ambiguous outcomes. If I repeat these trials enough times, regardless of the method, I will eventually, according to statistical theory, achieve the results predicted by the known mathematical probability, which is of course 0.5 -- or 6.5 Heads + 6.5 Tails. But if we do not know the probability of any event occurring, which of course is the case in every study (otherwise it would not be a study), then much larger numbers are needed to detect a "significant" event and then to announce that such an event was statistically unlikely to have occurred as a result of chance alone.So in summary, the three solitary "positive" findings would be more interesting if they were objective measurements (i.e. electrophysiologic) and if they were reproducible. With more concrete objective data, the authors might get funding and FDA approval for an even larger (but still pilot) study -- say, with 20 or 30 people. But because no reproducible, unarguably positive result was found, this paper serves as a warning to other researchers who discover it during their literature review "don't travel down this particular rabbit-hole." The NIH is never going to fund a full blown study using such weak data, and the FDA would object to a large study for similar reasons -- authorizing the "off label" use of a drug that can produce significant side effects on the basis of a one-time observation of 3 visual field improvements -- which could not be reproduced even within the same pilot study. The in-vitro studies that you cited offer a biochemical mechanism of action which no doubt fueled, and might continue to fuel, occasional research interest. But the lack of hard evidence means that medical research is a long long long long way away from suggesting any of the carbonic anhydrase inhibitors as a treatment for RP, and any physician who prescribes it to a patient who does not have a proven case of glaucoma is taking a huge medical-legal risk. The statement at the bottom of one of the papers you cited "These experiments suggest a promising approach to treatment of RP17 that might delay the onset or possibly prevent this autosomal dominant form of RP"... is pretty standard "research speak" for .... "I want my paper to be cited in more treatment-related journals." It is the, "how is this research relevant" statement that nearly every research paper optimistically and triumphantly makes in closing, and it should not be taken as if a new cure has been discovered. However, the presumed strategy of getting it cited in journals other than biochemical abstracts didn't work, as to date it has been cited only by four other papers -- all of them biochemical works, and none of those were follow-up studies pertaining to RP.You probably regard the response you're getting from U.S. doctors as somewhat gutless, uncaring and maybe even inhumane. But demonstrating a promising in-vitro mechanism is light years away from prescribing it as a therapy -- at least in the United States. A colleague sent me an e-mail suggesting that I watch 60 minutes tonight for a segment on FDA surveillance gone wrong. I got busy and missed it. Did you watch it? I'll try to find the video or transcript online later but the very existence of such a story supports the "damned if you do and damned if you don't" criticism that no doubt influences the FDA's usual abundance of caution when it comes to authorizing new treatments.
Subscribe to:
Posts (Atom)