Why Your Eyes Should Start Being Screened at Age 40

The American Academy of Ophthalmologists urges adults to start eye screening at age 40. That’s the age at which early symptoms of eye disease and vision changes typically start showing up. From the initial screening, your ophthalmologist can chart a course for follow-up exams.

Dr. Dan Hennessey sat down with Ashley Blackstone from THV Channel 11 to discuss what you can do to maintain good visual health. You can view the interview now and also read Dr. Hennessey’s tips for keeping your vision healthy below the video.

 

 

Dr. Hennessey’s Tips

1) Keep regular maintenance

The Academy’s recommendation of a baseline exam at age 40 doesn’t replace regular treatment of existing disease or injuries. Likewise, it doesn’t take the place of vision exams for corrective lenses or adjustments. If you are already seeing your eye doctor for an existing condition, it is vital to continue those visits and keep up with scheduled exams no matter what your age.

2) Establish a baseline

If you are fortunate enough not to need glasses or treatment for eye disease before the age of 40, then adults with or without symptoms or risk factors for eye disease need to see their optometrist or ophthalmologist to get a baseline eye screening when they turn 40. That’s about the time when eyes begin to show signs of aging and changes in vision. The eye doctor can map out a plan for follow-up exams based on the screening outcome.

And regardless of age, if you are at risk for eye disease — such as diabetes or hypertension or a family history of eye disease like glaucoma, macular degeneration or retinal detachment — you should see your optometrist or ophthalmologist if you haven’t already done so to determine an appropriate eye exam schedule.

3) Early diagnosis means early treatment

Your baseline evaluation may detect eye diseases that are common in people over 40, and that gives you and your eye doctor a better chance to preserve your vision with early treatment of any issues related to common vision abnormalities. Besides the eye problems already mentioned, there are conditions such as tear deficiency or ocular surface disease and computer vision syndrome that are more common past the age of 40. The evaluation can also reveal less common problems, like ocular tumors and narrow angle glaucoma, in a timely manner. Again, the sooner these issues are diagnosed, the better the chances are for successful treatment.

4) Thwart the stealthy sight thieves!

Common eye diseases in people 40 and older can exist for years or decades before becoming noticeable. For example, the most common form of glaucoma, open-angle glaucoma, has often been called the “sneak thief of sight.”  According to the American Optometric Association, half of all patients with glaucoma do not know they have it and will likely suffer extensive vision loss if left untreated.

If you’re age 40 or older, make a baseline eye exam your top priority.

Neuro-Ophthalmology Newsletter March 2013 – Volume X, Number 3

Neuro-Ophthalmology Newsletter

Andrew Lawton, M.D.

March 2013 – Volume X, Number 3

 

Upper eyelid retraction in patients with thyroid –related eye disease is potentially dangerous due to corneal exposure. Patients are distressed as well by the abnormal appearance. Surgical repair is effective but not practical until the inflammatory process stabilizes. Lee, et al (Graefes Arch Clin Exp Ophthalmol 2013; epuplished Sep 2012), set out to see if subconjunctival corticosteroid injections would be effective in management of lid retraction. The authors identified 95 patients with thyroid-related eye disease and a less than six month history of eyelid retraction and/or swelling. 55 patients for a total of 75 eyes received one to three injections of 20 mg triamcinolone acetate into the subconjunctival  space superficial to Mueller’s muscle at three week intervals. The remaining 40 patients representing 59 eyes received no treatment. 67% of patients treated with corticosteroids started out with severe swelling compared to 34% in the control group. 9 and 24 weeks after initiating the protocol, there was no differences in severity between the two groups. Significantly more patients receiving injections achieved clinical success at 24 weeks than in controls. The authors concluded that subconjunctival triamcinolone was effective in resolving eyelid swelling and retraction if initiate within the first six months of onset.

 

Another potential risk in thyroid-related orbital disease is optic nerve compression by enlarged extraocular muscles. One difficulty in management, however, is to determine the point at which surgery should be attempted to decompress the orbit. Weis, et al (Ophthalmology 2012; 119:2174-2178), reviewed CTs of 198 orbits in 99 patients with the condition and performed volumetric analysis to correlate with physical examinations. The best predictor of compressive optic neuropathy was the volume of the medial rectus muscle followed in order of significance by lateral rectus volume, superior muscle group volume, and total rectus muscle volume. Multivariate analysis indicated that medial rectus volume was the only independent predictor of compressive optic neuropathy. The authors found that simple maximum medial rectus diameter measurements could be used equally well as the full calculation of medial rectus volume. Orbital volume and distortion of the medial orbital wall did not predict optic nerve compression.

 

Congenital optic nerve anomalies may indicate the potential for other ocular abnormalities. Shapiro et al (Ophthalmology 2012; epublished November 2012), retrospectively identified 15 patients with congenital optic nerve anomalies. They identified 15 patients of whom 9 patients had optic nerve hypoplasia. Other diagnoses included optic nerve coloboma, morning glory syndrome, and staphyloma. All patients received examination under anesthesia with wide angle retinal photography and fluorescein angiography. The authors assessed the severity of nonperfusion of the retina with concentration on the degree of fibrovascular proliferation, vitreous hemorrhage, and tractional retinal detachment. In patients with optic nerve hypoplasia, 75% of affected eyes showed severe peripheral retinal nonperfusion. 75% had fibrovascular proliferation, 19% had vitreous hemorrhage, and 63% had tractional retinal detachment. Six eyes with severe nonperfusion required laser treatments to nonperfused retina. Of other anomalies, 88% had mild to moderated nonperfusion, 25% had fibrovascular proliferation, 12 % had vitreous hemorrhage, and 25% had tractional retinal detachment. 67% of patients with optic nerve hypoplasia and 17% with other anomalies had congenital brain abnormalities as well. The authors concluded that physicians must screen for other ocular and brain abnormalities in these patients and that laser photocoagulation may be of benefit in preventing tractional retinal detachment.

 

Case Study

 

 

Patient X3 is a man in his 50s who has noted progressive double vision over the past six months. He described the diplopia as vertical and binocular. He reported a worsening of his symptoms if he looks down. He has no pain or discomfort although his eyes feel dry. He has lost over 100 pounds over several months; he attributed this to a painful shoulder injury that made him lose his appetite. He was referred with a presumed diagnosis of a fourth cranial nerve palsy. An MRI was read as normal; the patient brought the disc with him for my review. His medical history was otherwise unrevealing. He was taking medication for hypertension.

 

At exam, his visual acuity was 20/20 in each eye. He had no relative afferent pupillary defect. Confrontation testing was intact in both eyes. He demonstrated a significant decrease in depression of his right eye. He showed a 20 diopter right hypertropia in neutral position that decreased to 6 diopters in up gaze and increased to 45 diopters in down gaze. He had 1 mm of superior scleral show on his right. Hertel exophthalmometry revealed 3 mm of right proptosis. His intraocular pressure was within the normal range but 5 mmHg higher in his right eye than his left. His anterior segments appeared normal. His optic discs were pink and flat. His retinas were flat.

 

What are you suspecting? He had two abnormalities noted on systemic evaluation that indicated a specific diagnosis; what could they be? What would you do for your next steps?

Discussion of Case X1 from January 2013 Newsletter

 

Our patient has trochleitis. This has features consistent with an autoimmune process that roughly falls into the waste basket of idiopathic inflammatory orbital pseudotumor. Generally the cartilage of one trochlea becomes inflamed. The tendon of the superior oblique muscle may become inflamed as well.

 

Patients uniformly present with complaints of aching aggravated by moving the eye on the involved side. They may experience sudden sharp, stabbing pain as well. They will report significant tenderness on palpation of the region of the trochlea. Imaging studies and B-scan ultrasound may be of value and indicate swelling of the trochlea or the superior oblique tendon. Trochleitis is an unusual instigating factor for migraine headaches and treating the condition may result in improvement in the migraine pattern in a small number of patients.

 

Once the diagnosis is established mainline treatment involves non-steroidal anti-inflammatory agents such as Indomethacin and Naproxen. Patients may recover more quickly if the receive oral corticosteroids of a Kenalog injection to the region of the trochlea. The likelihood of relapse within one year is 25%. Trochleitis has been documented to be related to rheumatoid arthritis, systemic lupus erythematosus, scleritis, Brown’s syndrome and orbital myositis. A work up for these conditions may be of value in recurrent disease.

Neuro-Ophthalmology Newsletter February 2013 – Volume X, Number 2

Neuro-Ophthalmology Newsletter

Andrew Lawton, M.D.

February 2013 – Volume X, Number 2

 

It is well known that some patients on renal dialysis may develop elevated intracranial pressure in a pattern similar to benign intracranial hypertension. In most cases, this phenomenon is due to severe electrolyte imbalances. Elkabbai, et al (J Fr Ophthalmol 2012; 35:822), reported a patient on hemodialysis who developed elevated intracranial pressure with a normal composition without neurological complaints. Treatment with both Acetazolamide and corticosteroids did not improve the intracranial pressure. A radiographic study of the patient’s upper extremity arteriovenous fistula revealed inappropriately high flow. Correction of the arteriovenous fistula resulted in a restitution of normal intracranial pressure. The authors suggest that overperfusion of the arteriovenous fistula in some renal dialysis patients may be the culprit in elevating intracranial pressure.

 

One of the more cosmetically disfiguring complications of facial surgery or repair of facial injuries may be hypertrophic and hyperpigmented scars. The etiology of this process is tension on wound edges yielding widening of the scar. Procedures that reduce tension on the wound can improve wound healing. Ziade, et al (J Plast Reconstr Aesthet Surg 2013; 66:209-214), enrolled 30 patients in a study to see if early injections of Botulinum toxin would weaken muscles sufficiently to lessen wound tension and improve healing. Patients were randomized into two groups of either Botulinum injections within 72 hours of surgery or no injections. The investigators followed patients for a year using an independent observer to assess the degree of scarring and by six medical specialists using standardized photographs. 24 patients completed the year of follow up. The review by the six specialists indicated improved wound appearance in treated patients versus untreated patients. The authors concluded that Botulinum injections can be of benefit to healing in patients with facial wounds, particularly younger patients with wounds perpendicular to the reduced tension lines of facial skin.

 

Sarcoidosis may present with a broad spectrum of neurological findings depending upon the sites of involvement. Langrand, et al (QJM 2012; 105:981-995), retrospectively identified 24 patients (10 women and 14 m3n) who developed involvement of the region of the pituitary and hypothalamus. Mean age was 31.5 years but the age range was broad between 8 and 69 years. 11 patients had been previously diagnosed with sarcoidosis. 22 patients had anterior pituitary dysfunction with diabetes insipidus in 12 patients. Patients tended to have degreased gonadotropin, TSH, and prolactin levels. MIR showed evidence of involvement of the infundibulum, the pituitary stalk, and the pituitary gland itself. 22 patients received Prednisone therapy with poor return of function of the adenohypophysis. 12 treated patients had improfvement of their changes on MRI. Oddly, there was no correlation between improvement on MRI and improvement in hormone production. Involvement of the hypothalamus and pituitary gland tended to be associated with a higher risk of sinus involvement and more diffuse neurosarcoidosis. The authors advised physicians to always consider the possibility of the hypothalamus and pituitary gland being the initial site of presentation for sarcoidosis and that these patients are at higher risk for more severe process.

 

Case Study

 

Patient X2 is a woman in her late 30s who reported having a headache behind her right eye for the past three weeks. Initially, the pain came and went but for the past three days it has been constant. She has noted a haze in her vision in the right eye. Her pain is increased by eye movement. The day before this exam her right upper eyelid was mildly swollen and her right upper eyelid mildly droopy. Her medical history was non-contributory. Her ocular history indicated a diagnosis of retrobulbar optic neuritis of her right eye five to six years earlier.

 

At exam, her visual acuity was 20/15 in her right eye and 20/20 in her left eye. She had no relative afferent pupillary defect. Humphrey perimetry was full in both eyes. She had no proptosis. Both eyes moved fully in all directions. Her eyes were aligned. She reported tenderness in her superior sulcus. Her optic discs were crowded but symmetrical in appearance.

 

The provisional diagnosis of idiopathic inflammatory orbital pseudotumor was made. She received a prescription for Prednisone 40 mg daily and an appointment for CT of her orbits.

 

She returned in one week. Her pain enhanced by eye movement had persisted despite the Prednisone. The CT was reported as negative for extraocular muscle enlargement or a mass. She now reported distinct tenderness just underneath the superior orbital rim nasally.

 

 

What is the diagnosis? Are you surprised that oral Prednisone was ineffective? What mode of therapy would you try now?

Discussion of Case X1 from January 2013 Newsletter

 

Many medications have unintended side effects that can be disabling. It is inherent in our care for our patients that we understand the complications of the medications we prescribe. The above patient is reporting side effects of Topiramate

 

Interestingly, the most common visual complaints with Topiramate are abnormal eye movements and diplopia. The more serious complications occur, however, because of medication effects on the ciliary body. Topiramate can cause ciliary body swelling and effusion. This results in a shift in the position of the lens and induced myopia. Should the enlargement of the ciliary body enlarge sufficiently, the iris root rotates forward and blocks the trabecular meshwork. The development of angle closure glaucoma may be difficult to make on basic eye exam because affected patients usually are atypical for this process: they have deep anterior chambers centrally and they are myopic. Gonioscopy should be performed in all cases when this complication is suspected. Anterior segment OCT and ultrasound may be of diagnostic value as well. Angle closure glaucoma may occur within days of the start of treatment but generally does not develop if the patient makes it several months out without developing glaucoma.

 

If Topiramate ocular complications are suspected, patients should discontinue the medication immediately. Medical therapy for glaucoma parallels that usually used for patients with narrow angle glaucoma. Unfortunately, since the mechanism for development of glaucoma with Topiramate is independent of pupillary block, laser peripheral iridotomy tends to be ineffective and should not be attempted.

 

For basic care purposes, other potential systemic complications of Topiramate may be induced by or affect decision making in eye care provider management of these patients. Treatment with other medications of the carbonic anhydrase inhibiting class including Acetazolamide, Methazolamide, and Dorzolamide in conjunction with Topiramate can increase the risk for metabolic acidosis and kidney stone formation. Patients should know that many Gingko formulations contain a contaminant 4′-O-methylpyridoxine which may cause nerve toxicity in conjunction with Topiramate. Please warn patients not to take Ginkgo with Topiramate.

Neuro-Ophthalmology Newsletter December 2012 – Volume IX, Number 12

Neuro-Ophthalmology Newsletter

Andrew Lawton, M.D.

December 2012 – Volume IX, Number 12

Physicians generally agree on how to initiate corticosteroid therapy in the management of giant cell arteritis. The trickier part of the process is to decide how quickly to taper the medication and get patients off the drug. Espigol-Frigole, et al (Ann Rheum Dis 2012; epublished September 2012), chose to assess the expression of interleukin 17A, a protein known to stimulate inflammation in autoimmune diseases, in the walls of temporal artery biopsy specimens from patients with giant cell arteritis. In all, 57 patients with giant cell arteritis were selected prospectively and followed for a mean of 4.5 years. Key data collected included relapses, the time necessary to achieve a maintenance Prednisone dose of less than 10 mg daily, and the time necessary to wean patients off Prednisone completely. The authors measured interleukin mRNA in temporal artery biopsy specimens from all 57 patients plus 19 controls without giant cell arteritis. The authors found increased interleukin 17A activity to be significantly increased in active patients compared to controls. Patients with higher interleukin levels tended to have fewer relapses and took less time (25 weeks vs 44 weeks) to achieve a maintenance dose of less than 10 mg Prednisone daily. The authors concluded the interleukin 17A activity in temporal artery biopsies can be used to predict the response to Prednisone therapy.

 

Because of the risk for permanent visual loss, a number of new treatment modalities are under investigation for central retinal vein occlusion. Aggemann, et al (Graefes Arch Clin Esp Ophthalmol 2012; epublished September 2012), compared radial optic neurotomy vs intravitreal triamcinolone as therapies. The study prospectively studied 87 patients who were randomly assigned to one of three groups: neurotomy, a single intravitreal injection of 4 mg Triamcinolone Acetonide, or placebo. 47% of patients treated with neurotomy demonstrated an improvement in visual acuity compared to 10% of placebo-treated individuals and 20% of patients treated with Triamcinolone. These numbers were statistically significant. 35% of patients receiving placebo lost more than three lines in visual acuity compared to 8% in the neurotomy group. The authors concluded that radial optic neurotomy may prove to be a more effective treatment for central retinal vein occlusion than single dose intravitreal Triamcinolone injection.

 

Establishing the diagnosis of giant cell arteritis may be a tricky business even with multiple blood parameters measured and temporal arteries biopsied. Murchison, et al (Am J Ophthalmol 2012; 154:722-729) sought to evaluate the usefulness of criteria generated by the American College of Rheumatology for the diagnosis of giant cell arteritis in patients with both positive and negative temporal artery biopsies. The authors retrospectively reviewed all 112 patients presenting to their service between October 2001 and May 2006 who had temporal artery biopsies. Key data collected included blood test results, biopsy results, and the progression of visual loss after diagnosis. 9 of the 35 patients with positive temporal artery biopsies wound not have been diagnosed with giant cell arteritis alone using the ACR criteria alone. 16 additional patients met only two criteria and required positive biopsies to establish a diagnosis. 11 of 39 patients with negative biopsies met ACR criteria and would have been diagnosed with giant cell arteritis without a biopsy. Diagnostic agreement between the ACR criteria without biopsy and biopsy alone was only 51.4%. With biopsy added to criteria, the correlation increased to 73%. The authors concluded that ACR criteria are insufficient to diagnose giant cell arteritis and that all patients suspected of having the disease should have temporal artery biopsy performed.

 

Case Study

 

Patient X1 is a man in his mid-30s who developed the sudden onset of difficulty seeing objects past 8 feet from him. The next day anything more than a foot away was blurry. Eventually, anything past three inches was blurred. His vision began to clear two days before my exam.

 

His medical history was significant for ankle surgery, an appendectomy, pericarditis, a bipolar disorder, and depression. His ocular history was as above. His family history was significant for arthritis, cancer, diabetes, heart disease, kidney disease, hypertension, and systemic lupus. Current medications included Depakote, Wellbutrin, and Topamax. A social history indicated smoking 30 cigarettes daily and social alcohol consumption. He reported no allergies to medications.

 

At exam, his manifest refraction was -0.25+0.25×110 degrees on his right and -0.75+0.75×90 degrees on his left. Although he was only 20/30 at distance with the above refraction, he was J1+ at near without correction.

 

What is likely going on here?

Discussion of Case IX12 from December 2012 Newsletter

 

This patient has Wallenberg’s lateral medullary syndrome. This collection of findings is due to a lesion of the lateral medulla. Understanding the components of the syndrome requires knowledge of the regional anatomy. Key clinical components of this syndrome include ipsilateral decrease in pain and temperature sensation of the face, Horner’s syndrome, ataxia, difficulty speaking, and difficulty swallowing. Patients generally report decreased pain and temperature sensation on the opposite side of the body. Patients may report the sensation of being pulled toward the side of the lesion with associated “corrective” deviation of their eyes when closed. Saccades toward the side of the lesion may overshoot; those away from the lesion come up short. Pursuit may be affected as well. They may have vertigo and nystagmus, usually horizontal. The sense of taste may be altered on the ipsilateral side of the tongue. Hiccups frequently accompany the syndrome.

 

In older patients, the most likely etiology is occlusion of the ipsilateral vertebral or posterior inferior cerebellar artery. In younger patients, demyelinating disease is a significant possibility. Key anatomical structures involved include the medullary vestibular nuclei, nucleus and spinal tract of cranial nerve V, the ventral spinocerebellar tract, the lateral spinothalamic tract, the nucleus ambiguous, the nucleus of cranial nerve IX, and the sympathetic tract.

 

Fortunately, as with this patient, the probability of recovery is good. In this instance, MRI was negative indicating neither an infarct nor demyelination.

The Sneak Thief of Sight

Fifty percent of people with Glaucoma do not know they have Glaucoma. As a part of National Glaucoma Awareness Month in January, Dr. Lydia Lane sat down with Ashley Blackstone on Today’s THV to discuss what glaucoma is, why 50 percent do not know they have it and why it is called “The Sneak Thief of Sight.”

You can watch Dr. Lydia Lane’s interview below or read for a more in-depth conversation further down.

What is glaucoma?

Glaucoma damages the eye’s optic nerve. This vital nerve sends signals from your retina to your brain – allowing you to see images clearly.

In a healthy eye, a clear fluid circulates inside the front portion of your eye.  To maintain a constant healthy pressure, your eye continually produces a small amount of this fluid while an equal amount of this fluid flows out of your eye. If you have glaucoma, the fluid does not flow out of the eye properly.

Experts say that nearly 50 percent of people with glaucoma don’t even know they have it. How is that possible?

That’s why it’s called the Sneak Thief of Sight. It’s possible to lose up to 40 percent of your vision before you notice. That’s because there are no symptoms or obvious signs in the early stages of glaucoma. It often begins with blind spots in your peripheral vision – something you might not notice right away. That’s why it’s so important to set up a regular exam with your eye doctor. There are several tests we can do to check for the disease … and if caught early we can begin treatment.

Are there people more at risk for glaucoma than others?

Although people over 60 are at higher risk, glaucoma can affect someone of any age. Some risk factors include having diabetes or a family history of glaucoma and people who are severely nearsighted. Also at higher risk are people of African, Asian, and Hispanic descent. Even if you aren’t at risk, you should have a complete eye disease screening by age 40, and once you reach age 65 you should have an exam every year or as recommended by your doctor.

Glaucoma isn’t reversible but is it treatable?

Treatment depends on a couple of factors – the type of Glaucoma you have been diagnosed with and the stage at which you are diagnosed. Your doctor will come up with a treatment plan based on how you respond to his or her interventions. This could be medication in the form of eye drops that reduce pressure or surgery to address fluid in your eye.

There is no cure, BUT if found early, and treated you can slow or even prevent further vision loss.