secondary glaucoma due to trauma

Ophthalmology & Optometry

Quote From Web
Sep 25, 2002 ... Dr. Elliot Werner: Secondary glaucoma is a glaucoma due to some other identifiable eye or systemic disease, such as uveitis, trauma, ...

Question
Hello Dr. Alpar,

One year ago I was punched twice in the eye and I didn't seek medical attention. The injury caused a chronic dull pain in that eye and a sharp pain whenever I looked up, down, to the side, or blew my nose. The eyball was red. All these symptoms lasted about two weeks. Since then, from time to time, I get a dull ache in that eye and my vision in that eye is now 20/30 when it has always been 20/20. My question is: should I worry about getting secondary glaucoma in the near future? I know that there is an increased risk for the disease after trauma but I don't know if the disease would materialize soon after the injury or decades later. Also, if the diminished visual acuity was caused by the injury, would it ever return to 20/20 on its own? Thank you

Quote From Web
Jul 26, 2009 ... Neovascular glaucoma is a severe type of secondary glaucoma that can .... When the lens capsule is ruptured due to trauma or surgery the ...

Answer
Kevin,

Three things can happen if you get punched in the eye.



1) You can get a traumatic iritis or inflammation in the eye. This can cause the iris, the colored part of the eye, to become stuck to the lens inside the eye. This in turn can cause an angle closure glaucoma. Inflammatory cells and/or red blood cells can also block the meshwork where the fluid leaves the eye, causing an inflammatory glaucoma. The pain is severe and does not go away without treatment.



2) The meshwork and the base of the iris can become dammaged. This is called "angle recession". People with traumatically recess angles can develope glaucoma decades after the injury.



3) The eyeball itself can be force back into the eye socket (orbit) and cause the thin bones that surround the eyes and sinuses to break. This is called a blowout fracture. The muscles that move the eye can be trapped in the fracture and cause double vision is certain postions of gaze. A thin section CT scan would pick up the blowout fractures. If you still have pain when you blow your nose, get a CT scan of your orbits.



I don't know why your vision is 20/30. If you damaged the retina, it probably will not return to 20/20. If the blow was severe enough, it could have caused a traumatic cataract. Some people become a little near sighted after injury and glasses will return the vision to 20/20.



See an eye doctor and get a comprehensive, dilated eye exam.



IMHO



Andrew J. Alpar, OD, FAAO

blindness from catarac surgery

2009-9-16 18:54:23
Laser Eye Surgery

Quote From Web
Oct 1, 2007 ... Overall, less than 5% of people develop a serious complication after cataract surgery. The risk of blindness after surgery is very low. ...

Question
My dad had catarac surgery on Feb. 4th. The patch was taken off on Friday and he is completely blind. No shawdows, just blackness. The doctor thinks its swelling. Is this something that sometimes happens? How long does it last. I know that they gave him some drops.

Can you answer my question?



Thank you!!



COlette Judy

Quote From Web
Dec 16, 2008 ... Blindness affects about 45 million people worldwide, and more than ... blindness · cataract surgery · london school of hygiene and tropical ...

Answer
Dear Colete Judy

normally immediately aftercataract surgery patients can see well within 48-72 hours but if there is some swelling due to surgery it takes time for vision to recover maybe taking 2-3 weeks for swelling to settle but it depends on what type of swelling in cornea or retina so kindly ask your ophthlamlologist what type of swelling and then reveret back to me

thanking you

personal regards

dr.manu C.Rajnani

HORMONES AND THE OPTIC NERVE

Hormonal imbalances or deficiencies are not traditionally thought of
as causes of optic nerve damage. Glaucoma can certainly contribute,
however, with its increasing intraocular pressure and resultant
pressure on the optic nerve.

Damage to the optic nerve can occur when a swollen eye compresses it.
One common reason is Grave?s disease, caused by an excess of thyroid
hormones. ?When swelling occurs within the orbit, the optic nerve can
become crushed, resulting in loss of vision.?


Other disorders of the optic nerve include optic neuritis
(inflammation of the nerve), optic neuropathy (damage to the nerve),
and papilledema (pressure in or around the brain causing compression
to the nerve where it enters the eye). Neuritis can be caused by
?viral infection (especially in children), vaccination, meningitis,
syphilis, certain autoimmune diseases such as multiple sclerosis, and
intraocular [within the eye] inflammation.? Neuropathy occurs as a
result of diminished blood supply (as in atherosclerosis or
vasculitis), certain toxins (such as lead, methanol, ethylene
glycol?antifreeze, among others), and nutritional deficiencies,
especially vitamin B12.

Intraocular Pressure in Steroid Injections

C. Stephen Foster, M.D.

Periocular steroid injection is an effective mode of treating uveitis, mostly without inducing steroid systemic side effects. Concern about globe perforation and about efficacy have prompted some to recommend a technique first popularized by Schlagel, injecting with a long 25 gauge needle along the surface of the eyeball, superotemporal, subTenon's, after the application of a pledget of topical anesthetic, and making a "sweeping" motion with the needle after penetration into Tenon's space in order to demonstrate that the globe had not been impaled on the tip of the needle.

But patient acceptance of this style of periocular steroid injection, in our experience, is considerably less than for the technique of periocular injection with a short, 30 gauge needle through the preorbital septum just superior to the inferior orbital rim. Performed properly, elevating the globe slightly with a the nondominant index finger and also making a small sweeping motion after penetration of the septum, again to ensure that the sclera or globe has not been impaled on the tip of the 30 gauge needle, this method can be effectively employed for repeated injections, even for care of children as young as six years old.

The technique has been hypothesized by some to be less effective therapeutically and more given to steroid-induced pressures. We evaluated the intraocular pressure responses to transceptal periocular steroid injections as well as efficacy in a well-characterized, carefully followed group of patients with pars planitis. We identified 20 patients with no previous history of glaucoma, with minimal anterior chamber inflammation, and hence no need for use of topical or systemic steroids at the time of periocular injection for the active pars planitis. The patients were followed for a prolonged time, and their response to therapy (Snellan acuity, inflammation at the pars plana, and cystoid macular edema) as well as sequential intraocular pressure profiles were determined. The injections were given employing 40 milligrams of triamcinolone acetonide mixed with 0.5 of 2% lidocine without epinephrine. The injections were administered in the manner described above.

The average age of the patients was 31.7 years (range 11.68). Twelve patients received a single injection and 8 received a second injection over the three month period following the first injection. Three of the patients had received a prior injection of steroid before being included in this trial.

The mean increase in intraocular pressure at two weeks following injection was 1.1 mm Hg at six weeks post injection the mean IOP increase was 1.3 mm Hg. At three months post injection there was an average reduction in IOP of 0.3 mm Hg.

The Snellen acuity improved an average of 2.1 lines at the six week and three month visits. Seventy-nine percent of the patients had achieved visual acuity of 20/40 or better, and this maintained at the three month follow-up visit as well; the improved acuity was secondary to reduction in cystoid macular edema.

We conclude that the anterior transceptal route of administering periocular steroid in patients with intermediate uveitis showing no propensity for IOP elevations from past steroid use is both safe and effective, without evidence of a significant risk of provoking elevations in intraocular pressure, unlike several reports of this complication following the posterior subTenon's route of administration.

Ahmed Valve Implantation in the Management of Uveitic Glaucoma

C. Stephen Foster, M.D.

We evaluated the safety and efficacy of Ahmed valve implantation for the management of glaucoma associated with chronic uveitis in a retrospective cohort outcome study. Nineteen patients (21 eyes) with chronic uveitis underwent Ahmed valve implantation for uncontrolled glaucoma between 1995 and 1998. All patients had their uveitis controlled pre-operatively via immunomodulatory therapy. Ahmed valve implantation was performed, and immunosuppressive chemotherapy was continued in the early postoperative period for strict control of inflammation.

Our main outcome measures were control of intraocular pressure, with a secondary outcome measure being the number of anti-glaucoma medications required to achieve the desired intraocular pressure. Visual acuity and complications associated with the surgery were monitored.

The postoperative follow-up averaged 24.5 months. At the most recent visit all 21 eyes had intraocular pressures between 5 and 18 mm Hg. The average pressure reduction after Ahmed valve implantation was 23.7 mm Hg. The average number of anti-glaucoma medications required to achieve the desired intraocular pressure was reduced from 3.5 preoperatively to 0.6 postoperatively. No eye lost even a single line of Snellen acuity at the most recent postoperative visit. Two eyes developed hypotony in the course of follow-up, one resolved without specific intervention, and the other required autologous blood injections and tube ligature to correct the hypotony. One eye underwent Ahmed valve replacement for abrupt valve failure. Two eyes underwent penetrating keratoplasty for reasons believed to be unrelated to the glaucoma surgery.

CONCLUSIONS: Ahmed valve implantation can be an effective modality in the management of uveitic glaucoma. We attribute much of the success rate to our intolerance for inflammation, and aggressive perioperative immunosuppression.

Secondary Glaucoma

C. Stephen Foster, M.D.

Secondary glaucoma (SG) associated with uveitis is a challenging condition to manage, often with a frustrating outcome.¹ This problem has not been extensively addressed in the literature, and it seemed to us that it might be an under-appreciated yet important cause of vision loss in the population of patients with uveitis.

Our study of 1,254 patients with uveitis disclosed that nearly 10% had glaucoma as an additional vision-robbing feature of their disease, adding yet another dimension to the difficulties already posed by the inflammatory insult to the macula. Our data were similar to prior reports of the prevalence of glaucoma associated with selected specific uveitic entities.^2-12 The prevalence has been especially alarming in juvenile rheumatoid arthritis-associated uveitis. The prevalence in our JRA patients was not as high as that published in some prior studies, perhaps because of our philosophy of intolerance to chronic, even "low grade" inflammation and to chronic steroid use.

Chronic granulomatous anterior uveitis was the most frequent uveitis classification associated with SG in our patients, and in previous reports.^13,14 But SG was common in posterior and panuveitis and also was found in patients with pars planitis.

The most common presentation of SG was open angle (80% of the eyes). As mechanical blockage of the trabecular meshwork is usually a transient condition that responds to anti-inflammatory therapy,¹ glaucoma could be caused by microscopic outflow dysfunction due to inflammatory proteins, debris and cells, or normal serum components that may clog the trabecular meshwork.^1,15 In some specific inflammatory diseases (typically Posner-Schlossman syndrome), active substances of inflammation like prostaglandins and substance P have been implicated as causes of secondary open angle glaucoma, with important consequences for therapy. ^1,4 Uveitic SG may also could be related to trabecular endothelial cell loss secondary to aggressive phagocytic activity and autolysis.^16-18 Since trabecular meshwork is a part of the uveal tract, it may become directly involved in the inflammatory process (trabeculitis),¹⁹ a putative common mechanism for glaucoma in herpetic uveitis. Peripheral anterior synechiae were found in 14% of the SG affected eyes. Ultrasound biomicroscopy of the anterior segment may be used to detect alterations of angle and ciliary body structures in patients with uveitis and hazy media and may help in elucidating mechanisms of glaucoma in these patients.

Although most of SG cases were secondary to idiopathic uveitis, sarcoid and JRA-associated uveitis, a study of the relative frequency of SG per disease showed that herpes virus (simplex and zoster) associated uveitis was most likely to cause SG (23%). Previous reports showed similar rates (13-33%), addressing the importance of glaucoma for the visual outcome in these patients.⁴ Since chronic oral acyclovir therapy reduces the recurrence rate of uveitis in patients with HSV uveitis,²⁰ we believe that the increasing frequency of this therapeutic strategy will lower the relative frequency of SG in herpes virus-associated uveitis populations in coming years.

SG was present in 16% of our JRA-associated uveitis patients; other authors report¹⁴ to 27%.^3,8,21 (of JRA-associated iridocyclitis patients developing glaucoma.) This Is particularly troubling since this disease occurs in children and chronic inflammation that has so often been present before and after involvement of an ophthalmologist.²² Such chronic or recurrent inflammation may explain why 7 of 11 JRA-associated uveitis patients with glaucoma had uncontrolled glaucoma at the time of the data analysis.

Four patients (5 eyes) had had argon laser trabeculoplasty performed as part of their treatment. Four of the 5 eyes (80%) were therapeutic failures and trabeculectomy was then performed. In three of the 5 eyes which had ALT, ,an acute flare-up of uveitis occurred following the procedure despite pre-treatment with topical steroids. We do not advocate ALT as part of our treatment regimen in patients with uveitis related glaucoma.

This report examined patients with uveitis related secondary glaucoma seen at a tertiary referral center during a ten year period. Our surgical procedure of choice in patients with uncontrolled uveitis related glaucoma was conventional trabeculectomy until 1990. Our current procedure of choice is a mitomycin-C trabeculectomy or insertion of a drainage implant in those patients who fail medical therapy. Siegner et al recently reported on their experience with the Baerveldt glaucoma drainage implant. ²³ Successful outcome was achieved in 10 of the 11 patients with uveitic glaucoma following insertion of the drainage implant. Our experience has been similar (manuscript in preparation) and we believe that these newer surgical treatment modalities will be of great benefit to our uveitic glaucoma patients. But real progress in this area of uveitis-associated glaucoma will only come with the increasing recognition by ophthalmologists that total, earlier control of intraocular inflammation, employing a stepladder approach to achieve that goal is more in the overall interests of the patient than is "acceptance" of low grade chronic inflammation.

REFERENCES:

1. Yaldo M K, Lieberman M F (1993): The Management of secondary glaucoma in uveitis patients. Ophthalmol Clin N Am 6:147-57.

2. Jabs D A. Johns C J (1986): Ocular involvement in chronic sarcoidosis. Am J Ophthalmol 102:297-301.

3. Key S N III, Kimura S J (1975): Iridocyclitis associated with juvenile rheumatoid arthritis. Am J Ophthalmol 80:425-29.

4. Krupin T, Feiti M E (1989): Glaucoma associated with uveitis. In Ritch R, Shields M B, Krupin T (eds.) The Glaucomas. St Louis: Mosby 1205-21.

5. Falcom MG, Williams HP. Herpes simplex kerato-uveitis and glaucoma. Trans Ophthalmol Soc UK. 1978;98:101-4.

6. Ohno S, Char D, Kimura S et al (1977): Vogt-Koyanagi-Harada syndrome. Am J Ophthalmol 83:735-40.

7. Lubin J, Albert D, Weinstein M (1980): Sixty five years of sympathetic ophthalmia. Ophthalmology 87:109-21.

8. Wolf M D, Lichter P R, Ragsdale C G (1987): Prognostic factors in the uveitis of juvenile rheumatoid arthritis. Ophthalmology 94:1242-6.

9. Obenauf C D, Shaw HE, Sydnor C F, Klintworth G K. Sarcoidosis and its ophthalmic manifestations. Am J Ophthalmol 86:648-53.

10. Liesegang T J (1982): Clinical features and prognosis of Fuchsä uveitis syndrome. Arch Ophthalmol 100:1622-6.

11. Jones N P (1991): Glaucoma in Fuchs' heterochromic uveitis: aetiology, management and outcome. Eye 5:662-7.

12. Hey E, de Vries J, Langerhorst C T, Baarsma G S, Kijlstra A. (1993): Treatment and prognosis of secondary glaucoma in Fuchsä heterochromic iridocyclitis. Am J Ophthalmol 116:327-40.

13. Shields M B (1982): Glaucomas associated with ocular inflammation. In: A study guide for glaucoma. 295-310. Williams & Wilkins, Baltimore

14. Shields M B (1989): Glaucomas associated with ocular inflammation. In: Text book of glaucoma. Williams and Wilkins, Baltimore. 110.

15. Epstein D L, Hasimoto J M, Grant W M (1978): Serum obstruction of aqueous outflow in enucleated eyes. Am J Ophthalmol 86:101-5.

16. Richardson T, Hutchinson B, Grant W M (1977): The outflow tract in pigmentary glaucoma: A light and electron microscopic study. Arch Ophthalmol 95:1015-20.

17. Rohen J, van der Zypen E (1968): The phagocytic activity of the trabecular meshwork endothelium: An electron microscopic study of the vervet (ceropithecus aethiops). Von Graefes Arch Klin Exp Ophthalmol 175:143-7.

18. Sherwood M, Richardson T (1980): Evidence for in vivo phagocytosis by trabecular endothelial cells. Invest Ophthalmol 16(suppl):66.

19. Rot M, Simmoms R (1979): Glaucoma associated with precipitates in the trabecular meshwork. Ophthalmology 86:1613-7.

20. Rodriguez A, Power W J, Neves R A, Foster C S (1995): Recurrence rate of herpetic keratouveitis in patients on long term oral acyclovir. Doc Ophthalmol 90:331-40.

21. Kanski J J, Shun-Shin G A (1984): Systemic uveitis syndromes in childhood: An analysis of 340 cases. Ophthalmology 91:1246-50.

22. Tugal-Tutkun I, Havrlikova K, Power W J, Foster C S (1996): Changing patterns of childhood uveitis. Ophthalmology 103:375-83.

23. Siegner S W, Netland P A, Urban R C Jr. et al (1995): Clinical experience with the Baerveldt glaucoma drainage implant. Ophthalmology102:1298-1307.

glucosamine and glaucoma?

Question:

Hi, My pressure went down from 27 to 18 since I have been using Glucosamine.
I take it for joint pain but noticed it influences my eye pressure too!

Anyone else had this experience? A search on internet told me there is a correlation.

Answer:

Glucosamine is very interesting because, theoretically, it could worsen the glaucoma because it is found in high concentration in the eye drain in abnormal eyes with glaucoma.

Yet, it might lower eye pressure for reasons that are not well known.

No good proof, just yet!

Remember, correlation does not mean one thing causes another, only that the two are linked somehow.

Check out the research on circumen, from the tumeric root, and glaucoma.

That product does show potential.

Natural Holistic Healing Ways for Glaucoma

Question:

Does anyone know of effective natural ways to heal glaucoma? Acupuncture, herbs, homeopathy, specific mega doses of vitamins or...?

Answer:

how about eating lots of steamed spinach and cooked carrots spinach for lutein, fermented cod liver oil, Co Q 100 Soft Gels, bilberry herb/eyebright?vitamins A, B1 (thiamine) and C. Increase intake of healing foods that are high in vitamins A, B, C and E, beta-carotene and anti-oxidants

fish bilberry and sweet potatoes and lots of grassfed butter

from now on wear 100% UVA UVB blocking sunglasses that fit snugly to head minimizing light that enters through the sides of sunglasses-see article on sunglasses
http://www.glaucoma.org/living/a_guide_to_sung.php


i found these expensive eye drops awhile back they might help Dr Z sells them:Pleo (TM) Muc 5X Eye drops

http://www.drz.org/asp/store/DetailP...?ProductID=495

Pleo Muc Eye Drops 5X, known in Germany under the name Mucokehl Eye Drops 5X. Homeopathic Opthalmic Demulcent Medicine by Sanum/PleoSanum.

European practitioners report that this remedy may be useful as supportive therapy for

* glaucoma
* cataracts
* conjunctivitis
* macular degeneration

and help support normal eye function by improving micro-circulation inside the eye.

dont give up nothing is impossible

Comparison of laser vs non-laser glaucoma treatment?

Question:

I am having unstable IOP. In addition,the preservative BAK in my eye

drops appear to be giving me trouble. I finally decided that

surgery,trabeculectomy is the way to go. My left eye suffers severe

reduction of central vision because of a central retinal vein occlusion.

The trabeculectomy is to be done on my "good" rightey to preserve its

central vision. Needless to say, this makes me nervous.

I was surprised to find out that the surgery is planned to be true

cutting rather than laser based. I was under the impression--perhaps

incorrectly--that laser treatment avoided much of the risk associated

with actual cutting. Where can I get a good comparison of the pros and

cons of laser surgery as opposed to scalpel surgery? I want to be armed

with knowledge when I ask more questions.

===============

Answer:

I have a non-surgery bias. Just how unstable is the IOP? And could
other eye drops not using BAK be tried? I am a Xalatan user and "side
effects" don't seem to be a problem. Uses BAK as I understand. What
effects are you having?

Glaucoma drop comparison?

Question:

The newest eyedrops used for reducing intra-ocular pressure (IOP) seem
ridiculously expensive. In particular, I have been looking at Xalatan or
Travatan. Where can I find a comparison of the relative benefits of these
new drugs compared to old generics. For example, I am already using generic
brimonidine thre times a day. Many years ago, timolol, then available only
as Timoptic worked very well indeed.

And there is always pot. I never used any before but I expect I would have
not trouble growing it. I would prefer not to smoke it. How does it get used
for glaucoma? Would it make sense to try making eye drops from it?

Answer:

>The newest eyedrops used for reducing intra-ocular pressure (IOP) seem
>ridiculously expensive.

They are (relatively) expensive.

>In particular, I have been looking at Xalatan or Travatan. Where can I
>find a comparison of the relative benefits of these new drugs compared
>to old generics.

Your eye doctor should be the best source.

>For example, I am already using generic brimonidine thre times a day.
>Many years ago, timolol, then available only as Timoptic worked very
>well indeed.

If your IOP is consistently at its "target" level, your quality of
life is acceptable and the side effects are acceptable, then there is
probably little reason to change from what you are taking.

Personally, I almost never use anything but a prostaglanding analog --
one of those "ridiculously expensive" drops -- as a "first line drug"
on my glaucoma patients. In layman's terms, "they rule" and are a
Godsend for my patients -- much like timolol was when all we basically
had was pilo and epinephrine.

>And there is always pot.

Forget pot. Its use in the management of glaucoma is nil.

ADHD + stimulants + glaucoma = ?

Question:


After a year and a half of university hell, I finally saw a psychiatrist and started treatment for ADHD—and, like many of you have probably experienced, it was like a giant lightbulb went on over my life.

For the first time I could listen to entire lectures, take reading notes, manage my finances, avoid constant guilt/anxiety over being chronically scattered, remember appointments, keep my apartment organized...etc.

World-changing. Then, yesterday, my pharmacist noticed that Adderall is contraindicated in patients with glaucoma, which I have.

Long story short, he called my doctor, and my doctor called me and told me to stop taking the meds—without offering any alternatives. So now I am in the MADDENING position of knowing how beautiful it is to be able to function like a normal human being...and having that all fall apart.

Now I am looking forward to...I'm not even sure.

I don't think I could stand to go back to the way I was, knowing what it feels like to be medicated.

I spent today trying to study, failing, crying out of frustration, trying again, etc.

Not pretty. So, I guess my plea for help is: if you know of any fast-acting non-stimulant treatments for ADHD, please share!

(Strattera etc. may be options but I would really like something I can start using in the next few days...graaah midterm season!) Alternatively, if anyone else out there has glaucoma and ADHD and has figured out a way to counteract the IOP-increasing effect of the stimulant meds, or found other successful treatments...please let me know!


Answer:
Talk to your eye doctor and see if he is treating patients on ADHD meds.

ADHD meds can make a hypertensives BP skyrocket (or anyones) but BP meds can be adjusted for that.

Seems the same logic may apply to glaucoma.

Your eye doctor would be able to say for sure.

He could then contact your ADHD doctor if its possible for you.

If your eye doctor has no experience in the matter seek another eye doctors advice.

Answer:

I would first consult a Ophthalmologist and see what possible problems you could have in the future.

Low dose beta-blocker is your best bet for cutting the peripheral stim effects of the adderall....keep dialogue open between you and doctor.

He should be the one looking for a solution not you. Keep us posted


Answer
Thanks for the replies, both of you!

I'm currently waiting to see a new psychiatrist (the medication incident coincided with me deciding to switch doctors, so there's about a week of downtime) so I can get a referral for an ophthalmologist and also look at other treatment options.

Not much of an update, I'm afraid.

(:

Answer:

Sansserifs, That is really rum luck about the medication.

One thing that can still be very helpful is aerobic exercise multiple times a day.

Dr. John Ratey in his book Spark and Delivered from Distraction discusses how exercise can act like a dose of Adderall and Prozac combined in increasing the levels of dopamine and serotonin.

Guys should aim for 75% or their maximum heart rate and gals for 65% for optimum focus.

Think of it a bit like short acting Ritalin -- the first hour is the golden one and the effects of improved focus can last from 2 - 4 hours depending on the person.

Even just a 10 minute burst of exercise can help the brain get back down to business.

That's definately how I got through college (back in the dark ages without medication) -- lots of running, climbing stairs, and pacing the halls.

It's especially helpful if you're getting enough Omega III fatty acids to build the neurotransmitters the exercise stimulates. Other wholistic helpers include reducing the amount of refined food which immediately turns to sugar in your system causing your insulin to spike and then drop quickly leaving your brain with less glucose (the ADD brain already battles that issue in the frontal lobes) and music can also help stimulate the brain. I hope you can find a medication that is helpful without worsening your glaucoma, but in the mean time -- go for a jog or brisk walk before those mid-terms or while studying for them -- it'll help!

Answer:

Wellbutrin might be worth a try?

It takes 3 weeks to start working, but I found it quite helpful.

Answer

First, let me start off by saying that have not tried ADHD drug bifemelane .

However, I have seen some good things about its potential use for ADHD, Parkinson's, autism, dementia, memory loss, and even some mood disorders.

It's definitely a versatile drug!

However, I also read that bifemelane has actually been suggested as a possible treatment for glaucoma . I don't know a whole lot more about this drug bifemelane at the moment, but if you are concerned about glaucoma, this sounds like something you might want to check into.

Good luck! Quote: : Alternatively, if anyone else out there has glaucoma and ADHD and has figured out a way to counteract the IOP-increasing effect of the stimulant meds, or found other successful treatments...please let me know!

Answer:

Quote: : Talk to your eye doctor and see if he is treating patients on ADHD meds.

ADHD meds can make a hypertensives BP skyrocket (or anyones) but BP meds can be adjusted for that.

Seems the same logic may apply to glaucoma.

Your eye doctor would be able to say for sure.

He could then contact your ADHD doctor if its possible for you.

If your eye doctor has no experience in the matter seek another eye doctors advice.

I just discovered how bad Adderall is for people with Glaucoma.

To be honest, I won't be going back to my doctor.

The only time her name will be coming out of my mouth is when I have the opportunity to make sure she has a bad name.

Right now I don't think I want my Glaucoma specialists talking to my doctor, shes ignorant and hes not much of a people person so that could be bad for everyone involved. Quote: : So now I am in the MADDENING position of knowing how beautiful it is to be able to function like a normal human being...and having that all fall apart.

Now I am looking forward to...I'm not even sure.

I don't think I could stand to go back to the way I was, knowing what it feels like to be medicated.

I spent today trying to study, failing, crying out of frustration, trying again, etc.

Not pretty. What a tease huh?

I know how you feel, at least your doctor gave you a call and your pharmacist noticed it.

I found out after looking at Adderall on drugs.com, I was planning out a diet and thought I'd make check to see if it said to avoid or include anything specific.

I'll be calling my Eye Doctor tomorrow for some info, probably finding a new doctor as I would recommend you do as well, and letting my previous know what I think.

I really can't beleive that the pharmicist didn't catch this, my stuff is usually filled through the techs and the one time the actual pharmicists fills mine its complete fail. I don't know what your whole take is on the situation.

I feel pretty teased, really foolish and I've really been questioning my judgement.

I've gone to this doctor for some time, she seemed ok and all that trust for her and the profession is gone.

Above all else, I have this massive amount of anger, the last 40 hours or so the smallest little frustrations have been sending me through the roof.

I'm the type of person thats usually really calm, rarely ever gets mad..

But when I do.. no one wants to be around and I'm smart enough to seperate myself from the situation.

Kind of hard in this scenerio though. Let me know what you find out, I'll post my findings as well.


Answer:
I struggle with ADHD and depression, also have glaucoma.

Does Bifemelane have a brand name.

I'd appreciate further suggestions on meds that don't up IOP.

Blindness vs. brain dead, some choice.

Can sinusitis/inflamation cause high IOP?

no. not usually.

there are limited number of new questions on this website per day. if you have multiple questions pertaining to the same or similar complaints, please post them in the 1 thread you already started instead of starting a new thread. this will keep others from being denied asking their question b/c the daily quota had been filled...just for future reference :)

Glaucoma Alternative Medicine ? - discussion in the Drugs.com community

Question
Hello folks ... This is my first post ( new herein ) I suffered from glaucoma since 2003 January looking forward to hearing remedies of natural type ... not medicinal droplets ... Thanks and cheers ... [B)][:I][?] There are no strangers in this world, only friends waiting to be met and made

Reply:

Have you already looked at glaucoma from the psychosomatic point of view?


Reply:

Marijuana is just a dried plant from the ground.

No additives, no mechanical processing, just a little smelly plant.

Eat it. Jesus Christ will help you through.

-Betsy

Diabetes and Glaucoma optometric pearls

Diabetes and Glaucoma optometric pearls | Optometry | Student Doctor Network
I made a blog entry about different pearls for the management of glaucoma and diabetic retinopathy patients, and I thought that it would be nice to share them.

Here they are: Diabetics: Ask what the patient's last blood glucose (particularly fasting) and HbA1c were.

Ask if it has been under good control.

These numbers are super helpful with predicting the likelihood of diabetic retinopathy, or how bad it is if they have it.

Ask how long the patient has had diabetes.

It is well recorded in the literature that the longer the patient has had diabetes, the higher the risk for retinopathy.

According to the American Diabetes Association, 10% of those who had been diagnosed for less than 5 years had retinopathy, 39% for those diagnosed 5-14 yrs, and a whopping 70% for those diagnosed for more than 15 years.

Record the pertinent negatives.

What does this mean?

Basically, record the main things that we check for in the eye for diabetics: check carefully for neovascularization of the iris, disc, and elsewhere (NVI, NVD, and NVE, respectively).

Also, check for clinically significant macular edema (CSME).

In other words, if you didn't see any of these signs, record "no NVI, NVD, NVE, CSME" Glaucoma: For glaucoma patients on medication, it's important to ask specific questions about compliance;

Don't simply ask "are you good with taking your drops?".

Ask them when they last took their medication.

Also ask them how often they forget their drops, if they do at all.

These questions are important for you to determine if the IOP that you're taking is falsely high or not, or if you're wondering why there are more defects in the threshold visual field test you just took.

It is not uncommon for glaucoma patients to be poor with compliance, especially if their vision is good and there is no immediate risk to vision loss.

Remember that suspicions for glaucoma are raised with race (especially African Americans) and a history of glaucoma in the family (in addition to your optic nerve head evaluation, threshold visual fields result, etc).

Make sure to take note of these facts in your assessment.

For every diagnosis of glaucoma, it is important to do gonioscopy.

In order to truly diagnose an open angle glaucoma, you must rule out other causes of glaucoma e.g.

Pigmentary dispersion, etc.

I'd love to hear of your own optometric pearls, and they don't have to be about glaucoma or DR.

If this post gets enough replies, I'd like to make a web page full of selected pearls, with your permission and due credit of course!

Thanks in advance, your contribution would benefit many!



Correct me if anyone disagrees, but this is what I've read and also have experienced regarding glaucoma therapy: 1.

Travatan and Xalatan fall under the same mechanism of action as prostaglandin analogues, versus Lumigan, which is a prostaglandin analogue that works slightly differently.

I forget the reason, someone here may know.

Therefore, if you are currently using Travatan but it is not working well, consider switching to Lumigan instead of Xalatan, since they work the same. 2.

Lumigan tends to lower IOP better than Travatan, which lowers IOP better than Xalatan. 3.

Lumigan is usually associated with the most conjunctival hyperemia, so I don't usually start Lumigan as first line therapy.

If a patient is using another prostaglandin analogue (Travatan or Xalatan), this tends to "prep" the eye and it will not be as hyperemic after switching to Lumigan later on. 4.

Azopt tends to be the best secondary agent when combined with a Prostaglandin analogue.

This is when compared to other drops like Alphagan or a beta blocker. 5.

Alphagan (and Combigan) can cause systemic sedation.

Patients may feel "tired or sleepy" when using these eye drops.

Make sure you instruct them to do punctal occlusion after drop instillation. 6.

Pseudoexfoliative glaucoma responds best to a beta blocker, followed by Prostaglandin 7.

I've heard that IOP is highest at 2am, is this true?!? I'll update this post if I think of anything else.



This attached lecture is an excellent evidence based review of treatment options. Also, in my experience Alphagan is my preference as a secondary/additive agent.



Quote: : Correct me if anyone disagrees, but this is what I've read and also have experienced regarding glaucoma therapy: 1.

Travatan and Xalatan fall under the same mechanism of action as prostaglandin analogues, versus Lumigan, which is a prostaglandin analogue that works slightly differently.

I forget the reason, someone here may know.

Therefore, if you are currently using Travatan but it is not working well, consider switching to Lumigan instead of Xalatan, since they work the same.

Lumigan (bimatoprost) is a prostamide, and the other prostaglandin analogues are not.

A good way to remember that: bimatoprost isn't as potent, so this is why Lumigan's drug concentration is 0.03%, where the others are 0.004% (Travatan) and 0.005% (Xalatan).



Quote: : 7. I've heard that IOP is highest at 2am, is this true?!? We've been taught it is highest right before waking up, around 5-6 am for normal schedule sleepers.

So 2,5,6 am, whatever, sometime early morning Oh, and if someone for example works the night shift, their IOP peak won't be the same time, it will change based on their sleep schedule.



Quote: : Correct me if anyone disagrees, but this is what I've read and also have experienced regarding glaucoma therapy: 1.

Travatan and Xalatan fall under the same mechanism of action as prostaglandin analogues, versus Lumigan, which is a prostaglandin analogue that works slightly differently.

I forget the reason, someone here may know.

Therefore, if you are currently using Travatan but it is not working well, consider switching to Lumigan instead of Xalatan, since they work the same. 2.

Lumigan tends to lower IOP better than Travatan, which lowers IOP better than Xalatan. 3.

Lumigan is usually associated with the most conjunctival hyperemia, so I don't usually start Lumigan as first line therapy.

If a patient is using another prostaglandin analogue (Travatan or Xalatan), this tends to "prep" the eye and it will not be as hyperemic after switching to Lumigan later on. 4.

Azopt tends to be the best secondary agent when combined with a Prostaglandin analogue.

This is when compared to other drops like Alphagan or a beta blocker. 5.

Alphagan (and Combigan) can cause systemic sedation.

Patients may feel "tired or sleepy" when using these eye drops.

Make sure you instruct them to do punctal occlusion after drop instillation. 6.

Pseudoexfoliative glaucoma responds best to a beta blocker, followed by Prostaglandin 7.

I've heard that IOP is highest at 2am, is this true?!? I'll update this post if I think of anything else.

A couple of thoughts: On the prostaglandins: don't go straight for the "if the Xalatan doesn't work well, go with Travatan" try to know the reasons.

Studies are showing that Travatan works better in black patients than Xalatan. Lumigan causes less of the hyperpigmentation problems with the other 2, less headaches (as symptoms ) but will give more conj hyperemia. Also, recent, recent studies and discussions in glaucoma are moving away from "whichever lowers IOP best" when you can have a low IOP but still have NFL loss.

Some studies are recommending for newly diagnosis, use a prostaglandin to get the IOP controlled, then transfer to a Alphagan- as it is a neuroprotectant.

I encourage everyone to read new literature on neuroprotectants. Jack Kanski (love him) has listed several items of interest to prescribe: Betaxolol, Alphagan, Vit E, and Ginko Biloba.

These items have nueroprotective qualities to them, with the drugs having proved VF saving results. This explains renewed interest in some poly glaucoma drugs as they are incorporating a proven IOP lowering substane with a paired nueroprotectant. Please research this! Good luck everybody!



Quote: : courage everyone to read new literature on neuroprotectants. Jack Kanski (love him) has listed several items of interest to prescribe: Betaxolol, Alphagan, Vit E, and Ginko Biloba.

These items have nueroprotective qualities to them, with the drugs having proved VF saving results. This explains renewed interest in some poly glaucoma drugs as they are incorporating a proven IOP lowering substane with a paired nueroprotectant.

Any relevant articles on this?

My understanding is that the whole "neuroprotection" thing is still very much just speculation without any solid research behind it...



Quote: : Any relevant articles on this?

My understanding is that the whole "neuroprotection" thing is still very much just speculation without any solid research behind it...

There are about 10 years of studies done on Timolol vs Brimonidine showing that Timolol does keep the IOP lower, but visual field continues to restrict over the years, while Brimonidine does not lower IOP as much, yet visual field is preserved.

Betaxolol is also showing this preservation of the VF. This is why I said Alphagan is quickly becoming a preferred polypharmacy with a Beta Blocker or Prostaglandin. Its not a bunch of hocus pocus--- unless someone claims to know HOW this works.

That is not yet certain. I'll repost tomorrow concerning the articles for those wanting to read this info for themselves.



Quote: : There are about 10 years of studies done on Timolol vs Brimonidine showing that Timolol does keep the IOP lower, but visual field continues to restrict over the years, while Brimonidine does not lower IOP as much, yet visual field is preserved.

Betaxolol is also showing this preservation of the VF. This is why I said Alphagan is quickly becoming a preferred polypharmacy with a Beta Blocker or Prostaglandin. Its not a bunch of hocus pocus--- unless someone claims to know HOW this works.

That is not yet certain. I'll repost tomorrow concerning the articles for those wanting to read this info for themselves.

I agree, brimonidine is my preferred agent for adjunctive therapy, but I think they're still plenty of work left to prove this neuroprotection thing.



Info can be found in: Glaucoma, by Jack Kanski: http://www.amazon.com/Glaucoma-Jack-...4873501&sr=8-1 articles: http://www.pubmedcentral.nih.gov/art...?artid=1936355 I have two more, but cannot find them for some reason. The research started about 1999, and is continuing.

Also, this nuero-protection stuff seems to be hocus-pocus when discussed regarding Parkingsons, but the glaucoma test-trails are promising. thanks for the interest.



Quote: : I agree, brimonidine is my preferred agent for adjunctive therapy, but I think they're still plenty of work left to prove this neuroprotection thing.

I just returned from vision expo and the consensus was that the whole "neuro protection" thing was such a titanic failure that Allergan shelved the entire thing after spending $65 million.