Medical Forum / Diseases and Disorders / Glaucoma / December 2004
Restoring Lost Sight
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Halterb - 20 Dec 2004 13:03 GMT Below is the link to an article titled "Restoring Lost Sight," from Emory University in Atlanta. In brief, a patient stares at a screen and waits for a dot to appear for one minute, daily. This is said to train the brain to activate neurons which respond to light in the area in which the dot appears. Evidently the device used is to be purchased by the patient, at a cost of $6000, which is not covered by insurance. If this approach is effective, it would seem there would be ways a person could simulate the system without going to this expense.
http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=10174
Ann B. - 21 Dec 2004 01:24 GMT >Below is the link to an article titled "Restoring Lost Sight," from Emory >University in Atlanta. In brief, a patient stares at a screen and waits for a [quoted text clipped - 6 lines] > >http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=10174 The article says the device is used for stroke or brain-injured patients. I assume their optic nerves are still OK, but parts of the brain were damaged. Perhaps, as with other functions, other parts ofthe brain can be trained to take over. I doubt this could help restore vision lost to Glaucoma, since the optic nerve cells are gone. Would be nice if something so simple as this could help us!
Cheers, Ann
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Halterb - 21 Dec 2004 01:44 GMT Ann responded to the Restoring Lost Sight article by saying:
>The article says the device is used for stroke or brain-injured >patients. I assume their optic nerves are still OK, but parts of the >brain were damaged. Perhaps, as with other functions, other parts >ofthe brain can be trained to take over. I doubt this could help >restore vision lost to Glaucoma, since the optic nerve cells are gone. >Would be nice if something so simple as this could help us!< This starts to get into the physiology of vision. It's my understanding that the label "optic nerve" isn't accurate--it's sometimes referred to as the "optic stalk," an extension of the brain, not really a "nerve" in the usual sense, and particularly subject to injury by lack of blood circulation (with the resulting lack of exygen). Evidently even low blood pressure can cause this sort of injury, as well as constriction of blood vessels. I suspect that is at least part of the reason for good results in some cases with this approach.
Mark Schmidt - 21 Dec 2004 02:56 GMT Sorry Halterb, Anne is more correct. The visual pathway from the eye to the back of the head (occipital cortex) contains many different components. Damage to any of these will have some form of effect on vision. In stroke victims the damage occurs in the brain, in glaucoma patients the damage occurs at the eye/optic nerve. Because of the nature of brains there is more scope for alternative treatment of the stroke patients. The glaucoma patients don't have that option. It is important to understand that once a nerve is dead, its dead, and there's no regrowth of nerves in humans, so death of nerves at the eye/optic nerve end is permanent and "training"such as is proposed in this study is impossible. In a brain, where some nerves may die but not all, there may be scope for usage of these other nerves.
Its also important to know that "staring at a dot" uses central vision which is the area least affected by glaucoma, and you could not adapt the training to nerves far off in the periphery of the retina.
I hope this clarifies a few points.
Best regards
Mark Optometrist Sydney, Australia
> Ann responded to the Restoring Lost Sight article by saying: > [quoted text clipped - 12 lines] > sort of injury, as well as constriction of blood vessels. I suspect that is at > least part of the reason for good results in some cases with this approach. Halterb - 21 Dec 2004 10:32 GMT Mark writes from Australia
>Sorry Halterb, Anne is more correct. The visual pathway from the eye to the >back of the head (occipital cortex) contains many different components. [quoted text clipped - 13 lines] > >I hope this clarifies a few points.< Goodai Mark!
"Oh ye of little faith." The post may have clarified the basis of skepticism, but it opens up the need for a bit wider view. As some visitors to this newsgroup may recall, I have never bought the "once a nerve is dead it's dead" position. My favorite reference is the Sakai, Murata, Amemiya five year study reported in the journal, Glaucoma, 1992:14:pages 167-170, reporting improvement in fields through the use of the methylcobalamin form of vitamin B-12. Among a number of other interesting studies is one found as long ago as 1980 in Clinical Ophthalmology, 74(3), page 289, on "The Treatment of Neuro-ophthalmological Disorders, with Particular Referemce to Neuropathy." More recently, Eisai Medical Services has developed protocols for treating various forms of neuropathy. "Optic nerve" protection and regeneration has received a lot of attention in recent years with some of the top authorities quoted in the national press as anticipating significant improviements in visual fields in the future..
Note from the article to which the original post linked. "The idea is to try to rehabilitate and improve visual field defects in patients who have suffered brain injury of various types," (Note "injury of VARIOUS types.")
I have reason to take an open-minded view of the implications of the NovaVision approach discussed in the article.
Ann B. - 21 Dec 2004 21:18 GMT >Goodai Mark! > [quoted text clipped - 19 lines] >I have reason to take an open-minded view of the implications of the NovaVision >approach discussed in the article. My understanding of all this very complicated physiological stuff is that there's a difference betweeen a dead neuron (which can't be brought back, at least in today's world) and an unhealthy one in the process of dying. The hope is that certain substances can delay or stop the process in an unhealthy neuron; thus we have the push for neuroprotective substances, improving circulation to better feed the neurons, etc. I grant you that perhaps, perhaps a very small perhaps
:), staring at a dot can act as a neuro-protectorant and thus delay the process of deterioration of the optic nerve, but personnally, I rather doubt it.
That said, I do feel it's important to keep an open mind and positvie attitude; perhaps in our lifetime ....
Cheers, Ann
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Mark Schmidt - 24 Dec 2004 01:16 GMT Hello again
I agree with you in principle, but at present we are comparing apples with oranges. The Optic "Nerve" is a huge collection of neurons. An individual nerve is a neuron. In terms of a single nerve/neuron that is dead, it is dead. But in the context of the collective term "The Optic Nerve", there will be hundreds of thousands of healthy neurons, unhealthy neurons, dying neurons and dead neurons. Chemical treatments may protect healthy and unhealthy neurons, and relieve or slow the death of dying neurons (to which you correctly refered) but none of them can redeem a dead neuron. If you would like a challenge, you may like to do a neurology literature survey seeking any reference to reviving a completely dead mammalian neuron and report your findings back to this newsgroup. If you do find one, I can promise you that you will provide extraordinary hope to glaucoma patients everywhere.
Best wishes to yourself and all readers of this NG for Christmas
Mark in Sydney
> Mark writes from Australia > [quoted text clipped - 39 lines] > I have reason to take an open-minded view of the implications of the NovaVision > approach discussed in the article. Halterb - 24 Dec 2004 04:41 GMT Hello again, Mark, in the land down under, who replied:
>I agree with you in principle, but at present we are comparing apples with >oranges. The Optic "Nerve" is a huge collection of neurons. An individual [quoted text clipped - 9 lines] >promise you that you will provide extraordinary hope to glaucoma patients >everywhere.< I confess--my hope IS to "provide extraordinary hope to glaucoma patients"! It took exactly .08 second to find this quotation: "...extensive advances in neuroscience have made optic nerve (and spinal cord) regeneration a reality in laboratory mammals..." (British Journal of Ophthalmology, May 1998, page 577). There's also good information at the Spinal Cord Injury Network. Of course, we're not only comparing apples and oranges, but kumquats, cranberries and, at this time of year, partridges in pear trees. What is one talking about when discussing restoring lost sight/vision"--nerves, neurons, cells, axons, myelination, physics, metaphysics or what?
Taking Thoreau's advice to "Simplify," let's say we have an area of an optic "nerve" which is not transmitting visual information, assumed by a hole in a field test. How do we really know what's wrong? There are several things that could be wrong. So let's work on those we can work on and reconnect some axons that were breaking the circuit; and let's get some insulation around bare spots that are in effect short circuiting stuff; and let's get blood circulating better; and let's pep up lazy cells that haven't been doing their jobs--and see what happens. If vision starts being transmitted again, in effect the "nerve" has been "regenerated"--we don't really care to know how each proton or electron gets around. It may be that a new pathway has formed, or an old one has started functioning again, but the end result is improved vision. And that may be just what was happening in the Sakai, and other studies--where they found vision that wasn't there, now is.
Regards.
Halterb - 21 Dec 2004 01:48 GMT Ann responded to the Restoring Lost Sight article by saying:
>The article says the device is used for stroke or brain-injured >patients. I assume their optic nerves are still OK, but parts of the >brain were damaged. Perhaps, as with other functions, other parts >ofthe brain can be trained to take over. I doubt this could help >restore vision lost to Glaucoma, since the optic nerve cells are gone. >Would be nice if something so simple as this could help us!< This starts to get into the physiology of vision. It's my understanding that the label "optic nerve" isn't accurate--it's sometimes referred to as the "optic stalk," an extension of the brain, not really a "nerve" in the usual sense, and particularly subject to injury by lack of blood circulation (with the resulting lack of oxygen). Evidently even low blood pressure can cause this sort of injury, as well as constriction of blood vessels. I suspect that is at least part of the reason for good results in some cases with this approach.
Halterb - 24 Dec 2004 13:32 GMT Hello again, Mark, in the land down under, who replied:
>I agree with you in principle, but at present we are comparing apples with >oranges. The Optic "Nerve" is a huge collection of neurons. An individual [quoted text clipped - 9 lines] >promise you that you will provide extraordinary hope to glaucoma patients >everywhere.< I confess--my hope IS to "provide extraordinary hope to glaucoma patients"! It took exactly .08 second to find this quotation: "...extensive advances in neuroscience have made optic nerve (and spinal cord) regeneration a reality in laboratory mammals..." (British Journal of Ophthalmology, May 1998, page 577). There's also good information at the Spinal Cord Injury Network. Of course, we're not only comparing apples and oranges, but, this time of year, turtle-doves, golden hens and partridges in pear trees. What is one talking about when discussing restoring lost sight/vision"--nerves, neurons, cells, axons, myelination, physics, metaphysics or what? And when we say "nerve regeneration" the very meaning of the word regeneration suggests creating, or regenerating, a new "nerve" (or neuron/cell) not necessarily reviving an old, worn out one--so I suppose I would agree with you that one little neuron could be kapoot. Countless cells die every day, but thanks to the telomeres and other stuff along our DNA strings, they get replaced with nice new ones.
Taking Thoreau's advice to "Simplify," let's say we have an area of an optic "nerve" which is not transmitting visual information, assumed by a hole in a field test. How do we really know what's wrong? There are several things that could be wrong. So let's work on those we can work on and reconnect some axons that were breaking the circuit; and let's get some insulation around bare spots that are in effect short circuiting stuff; and let's get blood circulating better; and let's pep up lazy cells that haven't been doing their jobs--and see what happens. If vision starts being transmitted again, in effect the "nerve" has been "regenerated"--we don't really care to know how each individual proton or electron gets around. It may be that a new pathway has formed, or an old one has started functioning again, but the end result is improved vision. And that may be just what was happening in the Sakai, and other studies--where they found vision that wasn't there, now is.
Regards.
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