Myocardial ischemia with fluorouracil and floxuridine therapy.
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Biomedical subjects
Publications and source records attributed to C D Phelps.
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A topical carbonic anhydrase inhibitor, 6-amino-2-benzothiazolesulfonamide (aminozolamide), which is an analogue of ethoxzolamide, was studied in 18 patients with ocular hypertension. Significant lowering of intraocular pressure was achieved with a single 50-microL gel application compared with the untreated control eye. The onset of action occurred within two hours and lasted at least eight hours. No systemic side effects were elicited. Topical carbonic anhydrase inhibitors may be an important alternative in the medical management of glaucoma.
To provide a bank of normal perimetric data, we tested the central and peripheral visual fields of 102 novice normal subjects using the Humphrey automated perimeter. All eyes used for visual field testing were first carefully examined to be sure that they were, indeed, normal. We calculated population means and standard deviations of each test location and for each decade for age. Average differential light sensitivity decreased with advancing age: -0.5 dB/decade at fixation, -0.6 dB/decade in the central (30-2) field, and -06. dB/decade in the peripheral (30/60-2) field. However, neither the slope nor the shape of the hill of vision changed with aging. Short-term fluctuation was not constant throughout the visual field, but instead was greater in the periphery than the center.
One way of judging if a visual field is abnormal, particularly when a patient has unilateral or asymmetric disease, is to compare the suspicious visual field to that of the normal eye. This assumes that in normal individuals the two visual fields are symmetrical. To determine the extent of normal symmetry, the authors examined the central visual fields of both eyes of 20 normal subjects with program 30-2 of the Humphrey perimeter. The inter-ocular sensitivity difference at single pairs of locations ranged from 0 to 9 decibels with large differences occurring most frequently in the upper field. Confidence intervals constructed from this set of normal data predict that asymmetry exceeding 6 decibels should occur in fewer than 1% of test locations and that asymmetry of overall mean sensitivity exceeding 1.4 decibels should occur in fewer than 1% of normal subjects.
In four patients with open-angle glaucoma, blood was present in the region of Schlemm's canal. The blood had four characteristics that distinguished it from other more common causes of blood in Schlemm's canal: it was observed with a Zeiss goniolens, a lens that has no flange, and thus was not an artifact of the examination technique; the blood could not be expelled from Schlemm's canal by raising IOP with para-limbal suction unless the pressure in the eye exceeded the diastolic ophthalmic artery pressure level; as IOP approached this high level, the amount of blood in Schlemm's canal progressively decreased, eventually diminishing to a single point of reflux that was always in the same location; and at this point the blood pulsed in and out of Schlemm's canal with each beat of the heart. These findings suggest a pathological anastomosis between a deep limbal artery and Schlemm's canal. The high arterial pressure transmitted into Schlemm's canal could, in turn, lead to an elevation of IOP.
One hypothesized cause of low-tension glaucoma is chronic or intermittent ischemia of the optic nerve. Since the optic nerve and brain are both parts of the central nervous system and share a common blood supply, the authors wondered if patients with low-tension glaucoma might also have clinical or radiographic evidence of cerebral atrophy. In this study, 27 patients with low-tension glaucoma were examined using neurobehavioral testing, electroencephalography, computerized tomographic scan, neurological history, and physical examination. In only a small number of patients were these tests abnormal. However, 12 of the 27 patients gave a history of common or classic migraine. This unexpected finding raises the possibility that migraine-related ischemia might be the pathogenic mechanism in some cases of low-tension glaucoma.
The authors administered a standardized headache questionnaire to 54 patients with low-tension glaucoma, 182 patients with primary open-angle glaucoma, 126 patients with ocular hypertension, and 493 normal subjects. Patients with low-tension glaucoma had headaches with or without features of migraine (unilateral headache, nausea or vomiting, or visual prodromata) more frequently than did any of the other groups. The higher prevalence of headache in low-tension glaucoma patients, who were usually elderly, was especially striking when their age was considered, since headaches are less common in elderly normal subjects than in young normal subjects. Headaches were present in 86% of elderly low-tension glaucoma patients (70 yr of age or older) but in only 64% of elderly normal subjects (P = 0.04) and only 59% of elderly ocular hypertensive patients (P = 0.02). Because migraine is an ischemic disorder, its possible association with low-tension glaucoma has etiologic and therapeutic implications.
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A 15-year follow-up examination of a boy with Rieger's syndrome showed that the anterior segment changes in this disease may be slowly progressive in the absence of glaucoma or miotic treatment. The patient also had two recently recognized systemic features of the syndrome, umbilicus cutis and hypospadias.
Relative hypotony in the affected eye was present in 40% of patients with uncomplicated unilateral retinal detachments. The average pressure asymmetry was only 1.3 mm Hg, but in one out of every four patients the difference was 3 mm Hg or more. In a control group, such a difference occured in only one out of every twenty patients. Relative hypotony persisted for longer than six months after scleral buckling operation, occuring even in patients that did not exhibit hypotony preoperatively.
In a study of 130 cases of unilateral retinal vein occlusion uncomplicated by rubeosis, we found that more than 80% of the patients had a lower intraocular pressure (IOP) in the eye with the occlusion than in the fellow normal eye. The reduction of IOP was greater with central than with branch vein occlusion, greater with hemorrhagic than with venous stasis retinopathy, and greater in patients who had high pressures in their fellow eyes. The pressure reductions persisted during follow-up periods of up to two years. How retinal vein occlusion lowers IOP is obscure and may involve more than one mechanism. Outflow facility was increased (compared to the fellow eye) in hemorrhagic retinopathy and in branch vein occlusion, both of which are association with retinal ischemia, but not in venous stasis retinopathy. Calculated rates of aqueous formation were low in central vein occlusion but not in branch vein occlusion.
Using materials available in any ophthalmology clinic, we constructed a useful and reliable instrument for measuring episcleral venous pressure. The instrument, a modification of the pressure chamber method of Seidel, utilizes a latex membrane and an air-filled chamber. These modifications facilitated ease of preparation for the measurement. Episcleral venous pressure in normal subjects was 9.0 +/- 1.6 mm Hg (mean +/- S.D.). Measurement of episcleral venous pressure facilitated diagnosis of diseases such as arteriovenous fistula and superior vena caval obstruction, which block drainage of venous blood from the orbit.
What is the cause of glaucoma in Sturge-Weber syndrome? Looking for the answer to this puzzling question, we examined 21 patients with the disease. Sixteen patients had gglaucoma: three bilateral and 13 unilateral. Episcleral hemangiomas were visible in all glaucomatous eyes. In general, the more extensive the hemangioma, the more severe was the glaucoma. During gonioscopy, blood could easily be made to reflux into Schlemm's canal of glaucomatous eyes. Often the canal separated into multiple fine channels. Episcleral venous pressure, which we measured in 11 patients, was high in all glaucomatous eyes. These observations suggest that glaucoma in Sturge-Weber syndrome is caused by elevated episcleral venous pressure. Most likely, veins draining aqueous from the canal of Schlemm are part of an intrascleral or episcleral hemangioma. The canal of Schlemm itself may be part of the hemangioma. Arteriovenous shunts in the hemangioma raise episcleral venous pressure, which in turn elevates intraocular pressure.
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In a survey of 817 patients undergoing primary operations for retinal detachment, glaucoma was present in 9.5%. Ocular hypertension (intraocular pressure [IOP] greater than 21 mm Hg) was present in an additional 6.5%. Primary open-angle glaucoma; the type of glaucoma most frequently encountered, occurred in 4% of the patients. Aphakic eyes and eyes with peripheral anterior synechiae had high prevalences of glaucoma. A high percentage of eyes with posttraumatic angle recessions had either glaucoma or elevated IOPs. Miotics used in the treatment of glaucoma could not be definitely implicated as a cause of retinal detachment. The rate of successful retinal reattachment was the same, whether or not glaucoma was present. However, a good visual result occurred less frequently in patients with glaucoma.
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