Little Rock Eye Clinic
Neuro-Ophthalmology Newsletter- November-2008 |
Neuro-Ophthalmology Newsletter
Andrew Lawton, M.D.
November 2008 - Volume V, Number 11
Convergence insufficiency can be a frustrating problem to approach particularly in children. The Convergence Insufficiency Treatment Trial Study Group specifically looked at children between 9 and 17 years of age (Arch Ophthalmol 2008; 126:1336-1349). They tested four different protocols: home-based computer and pencil push-up therapy, pencil push-ups alone at home, office based computer therapy with home reinforcement, and placebo office based computer therapy with home reinforcement. The children who underwent office based computer therapy far surpassed the other three groups in recovery of fusional vergence and proximity of near point of convergence. The authors recommended that children with convergence insufficiency follow a regimen of office-based therapy to assure compliance and performance.
Agazzi, et al (J Neurosurg 2008 e-published in October 2008) reported a patient who developed sudden blindness following a balloon procedure to relieve trigeminal neuralgia. After cadaver skull studies, the authors concluded that the needle used in the procedure penetrated the orbit through the inferior orbital fissure. When the balloon was inflated, it blocked venous outflow from the eye due to a sudden increase in intraocular and intraorbital pressure. This case report reinforces the importance of understanding the anatomy of the skull and orbit in invasive procedures to protect vital structures.
Fumihiko, et al (J Glaucoma 2008; 17:552-557), found evidence that the brain may be involved in glaucomatous optic nerve damage in a different way than we would normally consider. The authors evaluated 230 glaucoma patients and 230 age- and gender-matched controls using the Hope Anxiety and Depression Scale Questionnaire. The rate and severity of depression and anxiety were significantly higher in glaucoma patients than in non-glaucoma patients. The authors found no correlation between the use of beta-blocker agents for glaucoma and the incidence of depression. A mechanism for influence of psychological stress over optic nerve health was not hypothesized.
Bruce, et al (Neurology 2008; e-published in October 2008), looked at demographics and visual outcomes in 721 consecutive patients, 66 male and 655 female, with idiopathic intracranial hypertension to see if gender was an issue in severity of disease. Men were much likely to be older and to have obstructive sleep apnea. Men were less likely to express headache and more likely to comment on visual changes at evaluation. Men tended to have greater visual acuity loss and visual field changes than women. The authors concluded that men are twice as likely as women to end up with permanent visual loss from idiopathic intracranial hypertension than women and should be followed more closely.
Neuro-Ophthalmology Newsletter
Volume V, Number 11 - November 2008
Case Study
Patient V11 is a woman in her late 70s with a chief complaint of noting a sudden loss of vision in her right eye one week ago. The vision in her left eye did not change. She noted no pain in her right eye. Her vision may have improved a little in her right eye since then. She has been suffering from headaches for several months. The headaches tend to involve her temples but with additional diffuse aching. She has noted a tender spot anterior to her left ear. The headaches are constant. She has taken Neurontin and Naproxen with some decrease in her headaches but not relief. She has lost 20 pounds since the headaches began because of a loss of appetite and fatigue. She reported no jaw claudication, fever, or symptoms of polymyalgia rheumatica. She showed delayed filling of her retinal arteries on fluorescein angiography. A medical history was significant for osteoporosis and diverticulitis. A review of systems revealed no additional contributory factors in the dermatological, neurological, respiratory, cardiovascular, genitourinary, alimentary, and hematologic systems. The ocular history was significant for cataract surgery in both eyes. The family history indicated a retinal detachment, cancer, diabetes, hypertension, and lupus. The social history showed no tobacco or alcohol consumption. Current medications included Neurontin, Evista, and a pain pill. Allergies were reported to no medications.
At examination, visual acuity at distance without correction was 20/200 in the right eye and 20/30(-2) in the left eye. The right pupil measured 6 mm in the dark and 3 mm in the light. The left pupil measured 6 mm in the dark and 3 mm in the light. Both pupils constricted and dilated at symmetrical rates. A 3+ right relative afferent pupillary defect was noted. Both eyes moved fully in all directions. Pursuit and saccades were intact. Both eyes were properly aligned. An external examination revealed a normal appearance of the eyelids, orbits, lacrimal glands, lacrimal drainage system and regional lymph nodes. The pulse in her left temporal artery was diminished compared to her right. She reported tenderness to palpation just anterior to the left superficial temporal artery. Humphrey 24-2 threshold visual fields showed a diffuse, patchy central defect in her right eye and a full field in her left eye; the test was unreliable in her right eye and reliable in her left eye. A slit lamp examination demonstrated a normal appearance of the eyelids. The conjunctiva was quiet in both eyes. The corneal epithelium, endothelium, tear film, and stroma had a normal appearance. The anterior chambers were deep and quiet. The irises appeared normal. Both eyes contained posterior chamber intraocular lenses. Intraocular pressures by applanation were 12 mm Hg on the right and 13 mm Hg on the left at 9:40 AM. Following dilation, examination of the posterior segments revealed pink, flat optic discs with cup-to-disc ratios of 0.3 on the right and 0.3 on the left. The nerve fiber layers, maculae, retinal blood vessels, vitreous, and peripheral retinas were intact in both eyes. The patient was oriented to person, place, affect, and date.
Discussion of Case V10 from October 2008 Newsletter
The list of possibilities for producing a junctional scotoma in a young child is relatively limited. Pituitary adenoma is unlikely but two neoplasms must be considered: a glioma arising in the optic nerve or hypothalamus and a craniopharyngioma. Infectious processes such as tuberculosis and fungal disease are considerations. Sarcoidosis and vasculitis would be low on the list. As it turns out, an MRI demonstrated a large suprasellar mass consistent with a craniopharyngioma.
Craniopharyngiomas arise from remnants of tissue migrating from Rathke’s pouch to the adenohypophysis during embryologic development. If the tissue settles in an inappropriate location, it may proliferate into a mass. Often the mass becomes cystic because of hemorrhage or compromise of its vascular supply. These tumors tend to crop up in two age groups: individuals under the age of 20 years and those between 50 and 70 years old. About 50% of patients will have visual compromise at diagnosis. Children in particular tend to come in with severe visual loss since they are unlikely to report this issue to their parents. Patients may develop papilledema and hydrocephalus due to invasion of the third ventricle.
The management of craniopharyngioma can be very complex. Surgical excision may be able to remove most of the lesion but there is a tendency for these tumors to recur within two years of removal. In fact, autopsy studies have revealed residual tumor in 75% of patients managed surgically since the tumors tend to invade surrounding tissues. Tumor cells released into the CSF during surgery may seed other areas of the brain. Aggressive surgical management may yield a significant mortality rate because of compromise of important blood vessels although children tend to do much better after surgery than adults. Radiation therapy may be a useful adjunct to surgical management although there are obvious risks to radiating the skull in young children. Treatment often leaves patients with pituitary insufficiency and diabetes insipidus. .
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Neuro-Ophthalmology Newsletter-October 2008 |
Neuro-Ophthalmology Newsletter
Andrew Lawton, M.D.
October 2008 - Volume V, Number 10
Zoumalan, et al (Arch Ophthalmol 2008; 126:1257-1260), investigated the effectiveness of standard surgical procedures in decompressing cadaver orbits following the injection of blood into the retrobulbar space. The authors used ten human cadaver orbits and injected 22 ml of blood 1 ml at a time. After each 1 ml injection, they measured orbital pressure, intraocular pressure, and proptosis. Once the full 22 ml were injected, the authors performed a lateral canthotomy, cantholysis, and septolysis. Finally, they injected an additional 10 ml of blood. Prior to decompression, the mean orbital pressure was 68.4 and intraocular pressure 71.5 mm Hg. Following decompression, the mean orbital pressure dropped by 48 mm Hg and the mean intraocular pressure dropped by 50 mm Hg. Injecting the remaining 10 ml of blood resulted in additional significant rises in orbital and intraocular pressure despite the decompression. The authors concluded that surgical release of the orbit may be an effective means of decompression. The surgery may be inadequate, however, if further bleeding is not prevented.
Parbhu, et al (Ophthalmology 2008; 115:1620-1625), retrospectively compared the presentation and outcome of corrective surgery in 24 pediatric patients versus 31 adult patients suffering orbital floor fractures. Children required earlier intervention than adults because they more often suffered true trap-door fractures with entrapment of orbital contents. CT scan, an excellent diagnostic modality of entrapment in adults, frequently missed incarceration of tissue in children. The authors concluded that surgeons must be especially cautious in evaluating children with orbital trauma to allow for appropriate management.
Dimitrova, et al (Graefes Arch Clin Exp Ophthalmol 2008; published online September 2008), looked at flow characteristics in the retrobulbar central retinal artery and vein in patients with diabetes. The divided patients into four groups: no diabetic retinopathy and no hypertension, no diabetic retinopathy but with hypertension, background diabetic retinopathy without hypertension, and background diabetic retinopathy with hypertension. Patients with diabetic retinopathy demonstrated a significantly lower peak systolic blood flow and end diastolic blood flow than those without diabetic retinopathy. The peak systolic blood flow was adversely affected by hypertension as well. The authors concluded that the study emphasized the importance of control of hypertension in patients with diabetes to preserve ocular function.
Donnelly and Subramanian (Am J Ophthalmol 2008, published online September 2008) randomly selected 47 patients from a general ophthalmology clinic to determine the effect of intraocular pulse pressure on spontaneous venous pulsations. Patients with glaucoma or elevated intracranial pressure were excluded. Intraocular pressure was measured by applanation an intraocular pulse pressure by Pascal Dynamic Contour Tonometer. Observers documented the presence or absence of spontaneous venous pulsations using direct ophthalmoscopy if the patients were not dilated and indirect ophthalmoscopy if the patients were dilated. The authors determined that the presence of spontaneous venous pulsations decreased in frequency as patients aged. Spontaneous venous pulsations were more readily identified if patients were dilated. All patients had spontaneous venous pulsations in at least one eye if they had an intraocular pulse pressure of 1.2 mm Hg or more. The authors concluded that, under normal circumstances, the absence of spontaneous venous pulsations may be a better predictive modality of elevated intracranial pressure then previously suspected.
Neuro-Ophthalmology Newsletter
Volume V, Number 9 - September 2008
Case Study
Patient V10 is a girl less than ten years of age with a chief complaint of developing headaches about a year ago. Her mother noted that she often squinted her right eye. She had an eye exam in August 2008 with an optometrist. The optometrist found mild hyperopia with best corrected visual acuities of 20/30 on her right and 20/20 on her left. She showed poor stereopsis at that time. Confrontation testing was full and pupillary responses were reportedly normal. She failed a school eye test this month and returned to the optometrist two days earlier than my exam. The vision in her right eye was now 20/200 best corrected. Her left eye was 20/25. She had a mild exotropia of the right eye. A review of systems revealed no additional contributory factors in the dermatological, neurological, respiratory, cardiovascular, genitourinary, alimentary, and hematologic systems. The ocular history was significant for the problems listed above. The family history indicated glaucoma. The social history showed she is a full-time student. Current medications included Sulfatrim and Tylenol. Allergies were reported to no medications.
At examination, visual acuity at distance with correction was counting fingers at four to six feet in the right eye and 20/25(-3) in the left eye. The right pupil measured 6 mm in the dark and 4 mm in the light. The left pupil measured 6 mm in the dark and 4 mm in the light. Both pupils constricted and dilated at symmetrical rates. A 1-2+ right relative afferent pupillary defect was noted. Both eyes moved fully in all directions. Pursuit and saccades were intact. She showed a 10 diopter right exotropia. An external examination revealed a normal appearance of the eyelids, orbits, lacrimal glands, lacrimal drainage system and regional lymph nodes. Confrontation and Humphrey 24-2 threshold visual fields showed an almost complete bitemporal hemianopia; the tests were unreliable. A slit lamp examination demonstrated a normal appearance of the eyelids. The conjunctiva was quiet in both eyes. The corneal epithelium, endothelium, tear film, and stroma had a normal appearance. The anterior chambers were deep and quiet. The irises appeared normal. Both lenses demonstrated clear anterior and posterior capsules, nuclei, and stroma. Both eyes were soft. Following dilation, examination of the posterior segments revealed moderate temporal pallor of her right optic disc and mild temporal pallor of her left optic disc with cup-to-disc ratios of 0.1 on the right and 0.1 on the left. The maculae, retinal blood vessels, vitreous, and peripheral retinas were intact in both eyes. The patient was oriented to person, place, affect, and date.
How does the differential diagnosis of this process in a child compare to that in an adult?
Discussion of Case V9 from September 2008 Newsletter
The presence of ptosis raises a differential diagnosis of a levator dehiscence, third cranial nerve palsy, Horner’s syndrome, myasthenia gravis, and other local lid issues. The pupillary asymmetry with a smaller right pupil than left more pronounced in the dark supports the diagnosis of Horner’s syndrome.
As you can see above, I have moved to Neosynephrine testing to replace Cocaine and Hydroxyamphetamine. Cocaine and Neosynephrine are equally effective in diagnosing Horner’s syndrome. Neosynephrine, however, is not a controlled substance alleviating the headache of concerns about theft and the need for recording every drop dispensed. Hydroxyamphetamine is not commercially available any more (it’s a long story) except as a combined drop with Tropicamide as a routine dilating agent. Besides, dilation lag is as good as any of the three in confirming the diagnosis without any need for eye drops.
Possible locations for a precipitating factor would be first order neuron (from hypothalamus to intermediolateral cell columns in the upper thoracic spinal cord), second order neuron (from thoracic cord up over the apex of the lung and along the common carotid artery to the superior cervical ganglion), and third order neuron (intracranial). With an isolated Horner’s syndrome, the biggest concerns would be a mediastinal process (lung carcinoma, lymphoma, sarcoidosis, etc.) or dissection of the wall of the carotid artery.
The information I left out had to do with historical data that suggested a specific etiology for his Horner’s syndrome. He complained of night sweats. He was found to have a positive PPD ten years earlier but chose not to have antibiotic prophylaxis. He had not had a chest x-ray since the positive PPD. My immediate concern was tuberculosis.
Luckily for this patient, his chest CT was clean. After a negative MRI of the head, his neurologist and I concluded that his Horner’s syndrome combined with his headaches put him in the cluster headache category. Cluster is classically associated with signs of sympathetic dysfunction that may become permanent.
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MAY 2007- CONTACT LENS CARE GUIDELINES |
Guidelines for Contact Lens Care – from Little Rock Eye Clinic May 2007
The American Academy of Ophthalmology has issued updated guidelines on contact lens care due to a recent investigation into Acanthamoeba keratitis infections. The guidelines now advise that “in general….rubbing the lenses during cleaning is considered to be a superior method of cleaning”, beyond what is recommended for “no-rub” contact lens solutions.
In addition, the guidelines acknowledge the rise in incidence of Acanthamoeba and fungal keratitis since 2004. “The etiology of this rise is currently being
investigated, but may be associated with inadequate antimicrobial efficacy of multipurpose solutions.”
Peroxide-based lens care systems (e.g. Clear Care) may be more effective than multipurpose solutions.
Please consult with anyone in our Contact Lens Department regarding questions or concerns you may have regarding your lens care system.
LREC main # 501-224-5658
Contact Lens Dept. – 501-687-0182
LREC West CL Dept. 501-687-0800
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Vitamins and the Eye |
*Supplemental vitamins have only been shown (scientifically) to be beneficial to ocular health in the presence of vision loss related to Macular Degeneration.*
The result of the 'Age Related Eye Disease Study' (AREDS) was: in people with vision loss related to macular degeneration supplemental vitamins lowered the risk of disease progression by about 25-30%. The viatmin formulation studied and found beneficial in macular degeneration was:
Vitamin C 500mg
Vitamin E 400IU
Beta Caroteen (Vitamin A) 15mg (25,000IU)
Zinc 80mg
Copper 2mg
This formulation is marketed by Bausch and Lomb as 'Ocuvite PreserVision'.
What's Up With Eye Vitamins:
Recently you may have read a recommendation that persons under the age of 70 do not need supplemental vitamins. This recommendation may be related to recent reports that taking high levels of vitamin E (an antioxidant) is associated with increased mortality. "High Dosage" in this report was greater than or equal to 400IU.
The American Academy of Ophthalmology and National Eye Institute are recommending those persons taking "eye vitamins" for prevention of further worsening of macular degeneration to stay on the medicine. The level of vitamin E (400IU) taken in the AREDS was not associated with increased mortality in this study group of over 3500 patients. And in further analysis of 3 separate studies with patients (over 12,000) taking 400IU of vitamin E there was no increased mortality.
It is our recommendation that you consult your eye M.D. prior to stopping your "eye vitamin" if you are currently taking it for macular degeneration.
How do Vitamins/Minerals Effect Macular Degeneration?
It is thought that production of highly reactive and damaging compounds called 'free radicals' may cause the changes in Macular Degeneration. However, this is not proven. Antioxidant vitamins (vitamins C and E and beta carotene) may work against these 'free radicals' to help slow the progression of the disease.
Zinc is a common mineral found in the body and has a high concentration in the macula.
Zinc is a necessary for many chemical reactions in the body to occur normally. Studies have shown low levels of zinc in older persons. Supplemental zinc may be important for eye health and slowing macular degeneration.
These vitamins and minerals may slow macular degeneration progression. They will not restore vision that has been lost to macular degeneration.
If you've looked for eye vitamins at your local pharmacy/store, you may have seen multiple different brands/formulations. We have listed below the formulations of a number of vitamins found on the shelf at one local pharmacy.
Ocuvite Preservision
Vitamin C 500mg
Vitamin E 400IU
Beta Carotene (vitamin A) 15mg (25,000IU)
Zinc 80mg
Copper 2mg
Ocuvite Preservision Lutein
Vitamin C 452mg
Vitamin E 400IU
Beta Carotene (vitamin A) none
Zinc 70mg
Copper 2mg
Lutein 10mg
Ocuvite
Vitamin C 200mg
Vitamin E 60IU
Beta Carotene (vitamin A) 1000IU
Zinc 40mg
Copper 2mg
Lutein 2mg
Ocuvite Extra
Vitamin C 300mg
Vitamin E 1000IU
Beta Carotene (vitamin E) 1000IU
Zinc 40mg
Copper 2mg
Lutein 2mg
Riboflavin, Manganese, Selenium, Niacinamide, L-glutathione
Ocuvite Lutein
Vitamin C 60mg
Vitamin E 30IU
Beta Carotene (vitamin E) none
Zinc 15mg
Copper 2mg
Lutein 6mg
ICaps with Lutein
Vitamin C 400mg
Vitamin E 150IU
Beta Carotene (vitamin A) 660IU
Zinc 60mg
Copper 4mg
Lutein 4mg
These vitamins have different formulations. One specific difference to be aware of is the vitamins without Beta Carotene. Beta Carotene SHOULD NOT be taken by current smokers or those who recently stopped smoking. Taking Beta Carotene by smokers increases the risks of cancer development. |
WHAT'S NEW? CORNEAL THICKNESS |
WHY THE SUDDEN INTEREST IN MEASURING THE THICKNESS OF THE CORNEA? I THOUGHT THE PROBLEM WAS THAT MY PRESSURE WAS ELEVATED.
As surprising as it seems, there is only one way to measure the exact pressure inside the eye. It is necessary to stick a needle into the eye and hook it up to a gauge to know exactly what the pressure is in the eye. As drastic as it sounds, that is also true for measuring blood pressure. If a surgeon or cardiologist needs to know exactly what your blood pressure is, then it is necessary to stick a needle into an artery so that a measurement can be made. You might say, “but I have my pressure measured all the time.†In actuality, your doctor or nurse “estimates†the pressure in your arteries by putting on a cuff which compresses the skin, fat, muscles and blood vessels. This is a reasonably accurate test, but it is not perfect.
The test we typically use in the office to “estimate†the pressures is applanation tonometry. In this test, a drop of anesthetic and dye is placed on the surface of the eye and a slight pressure is placed against the eye to flatten a portion of it. By measuring the amount of force it takes to flatten the eye, we can estimate what the pressure is inside the eye. When Hans Goldmann developed this technique in 1953, he felt that the thickness of the cornea would not influence the readings, and this was generally held to be true for over 40 years.
In the 1990’s, however, several people began measuring corneal thicknesses and found that patients with high pressures tended to have thick corneas. It was quickly recognized that some cases of ocular hypertension were simply patients who had thick corneas and more force was need to flatten the cornea. When the Ocular Hypertensive Study (OHTS) was published, further relation between pressure, corneal thickness and glaucoma damage was seen. It was clearly shown that patients with thinner corneas were more likely to sustain damage than patients with thick corneas. Although the Little Rock Eye Clinic has been measuring the corneal thickness of ocular hypertensives since 1996, these recent findings have convinced us of the importance of looking at the corneal thickness on all patients with glaucoma or suspicion of glaucoma, and pachymetry has become a routine part of testing.
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