Biomedical subjects

M O Gordon

Publications and source records attributed to M O Gordon.

28 records · Page 2Linked to original sources

PubMed1990

The dyschromatopsia of optic neuritis is determined in part by the foveal/perifoveal distribution of visual field damage.

Most hypotheses of acquired dyschromatopsia invoke the mechanism of selective damage to specific components of the afferent visual system to explain the predominance of red-green and blue-yellow hue-discrimination defects found in neural and retinal disorders, respectively. However, this pattern of hue-discrimination disturbance in ocular disease may vary. There are frequent exceptions which are inadequately explained by existing hypotheses. In an effort to explain the pattern and pathogenesis of acquired dyschromatopsias better, the authors examined patients with nonproliferative diabetic retinopathy (DR) and late-stage retrobulbar neuritis (RBN) using age-corrected Farnsworth-Munsell 100-hue testing and threshold static perimetry. As expected, most DR eyes showed some degree of relative blue-yellow dyschromatopsia (89%) with few showing a greater weighting towards red-green dyschromatopsia (11%). However, an approximately equal number of RBN eyes had a relative blue-yellow (48%) versus red-green dyschromatopsia (52%). For RBN, the authors found a strong association between the spatial distribution of field defect and the type of relative hue-discrimination disturbance. Eyes with greater field depression at the fovea relative to the perifovea showed a relative preponderance of red-green dyschromatopsia (68%) as opposed to blue-yellow dyschromatopsia (32%), whereas eyes with greater relative perifoveal impairment showed a relative preponderance of blue-yellow dyschromatopsia (100%). This relationship between the relative spatial distribution of visual field damage and the relative hue-discrimination deficit in RBN was statistically significant (P = 0.002). Such an association was not found for DR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Glaucomatous visual field damage. Luminance and color-contrast sensitivities.

Using a modified Humphrey perimeter, we evaluated 16 eyes with primary open-angle glaucoma and visual field loss (defects 0.5-3.0 log units in depth), and 14 normal eyes. Each eye was tested twice in random order with conventional luminance-increment static perimetry and with the perimeter modified to produce a high-luminance yellow adapting background and a blue test stimulus. The background was a broad-spectrum light of 500 nm and above (yellow), while the stimulus was a broad-spectrum light of 500 nm and below (blue). Paired comparisons were made between conventional and blue/yellow sensitivities for every point examined (1184 points in 16 diseased eyes and 1036 points in 14 normal eyes). Defect depths were determined by using the age-corrected norms distributed in the Humphrey Statpac software. In glaucomatous eyes, blue/yellow sensitivity showed greater impairment than did conventional perimetric sensitivity, in which defect depths were less than 1.0 log unit. However, for defects greater than 1.0 log unit in depth, conventional perimetric sensitivity and blue/yellow sensitivity showed equivalent degrees of damage. Receiver operating characteristic (ROC) analysis was used to compare the ability of blue/yellow and of conventional perimetry in distinguishing between glaucomatous and normal eyes. Results indicated that although blue/yellow color-contrast perimetry may be more sensitive for the detection of incipient glaucomatous damage, in the manifest stages of visual field damage blue/yellow color-contrast perimetry is no more sensitive than is conventional (luminance-increment) perimetry for defining the extent of glaucomatous visual field defects.

Adult↗

PubMed1989

Topical timolol administration reduces the incidence of glaucomatous damage in ocular hypertensive individuals. A randomized, double-masked, long-term clinical trial.

We conducted a randomized, double-masked, long-term clinical trial to determine whether topical timolol therapy was effective in delaying or preventing the onset of glaucomatous damage in moderate-risk ocular hypertensive subjects. In 62 patients, one eye was chosen randomly to receive timolol therapy twice daily while the fellow eye received placebo. During the course of the study, the mean +/- SD difference in intraocular pressure between the timolol-treated and the placebo-treated eyes was 2.3 +/- 2.6 mm Hg. Reproducible visual field loss developed in 4 timolol-treated eyes and 10 placebo-treated eyes. Progressive optic disc cupping was noted in 4 timolol-treated and 8 placebo-treated eyes. Using a computerized image analysis system, the mean +/- SD increase in optic disc pallor during the course of the study was 0.86% +/- 2.4% in the timolol-treated eyes as opposed to 1.80% +/- 3.6% in the placebo-treated eyes. This study provides evidence that lowering intraocular pressure by medical treatment reduces the incidence of glaucomatous damage in ocular-hypertensive individuals.

Administration, Topical↗

PubMed1988

Intraocular pressure response to topical dexamethasone as a predictor for the development of primary open-angle glaucoma.

In a retrospective study we reviewed the records of 788 subjects who had been corticosteroid tested with 0.1% dexamethasone four times daily to one eye for six weeks. All subjects had normal kinetic visual fields and optic nerve heads in both eyes at the time of testing and were followed up for a minimum of five years. Some subjects had normal baseline intraocular pressures whereas others were considered to have ocular hypertension. Of 276 individuals who were high corticosteroid responders (intraocular pressure greater than 31 mm Hg during dexamethasone administration), 36 (13.0%) developed glaucomatous visual field loss during the follow-up period. Only nine of 261 individuals (3.4%) who were intermediate responders (intraocular pressure 20 to 31 mm Hg during dexamethasone administration) and none of 251 individuals who were low responders (intraocular pressure less than 20 mm Hg during dexamethasone administration) developed glaucomatous visual field loss. However, the ability of the intraocular pressure response to dexamethasone to predict the development of glaucomatous visual field loss was not as good as the predictive power of a multivariate model that included patient age, race, baseline intraocular pressure, baseline outflow facility, baseline cup/disk ratio, and systemic hypertension.

Adult↗

PubMed1988

Retinocortical conduction time in diabetics with abnormal pattern reversal electroretinograms and visual evoked potentials.

Clinically evident retinal vascular disease in patients with diabetes mellitus may be preceded by an increase in visual evoked potential latency in electrophysiologic testing. This increase may indicate either retinal or optic nerve dysfunction. To determine the origin of the latency increase we initiated a cross-sectional study of simultaneous pattern-reversal electroretinograms and visual evoked potentials. We recorded transient (3.8 reversals/second) pattern electroretinograms and visual evoked potentials using both 15' and 60' high-contrast black-white checks. Fifty-five diabetic patients (34 with no retinopathy and 21 with background retinopathy) and 34 age-matched visual normals (controls) were tested. Group data in diabetics showed significant latency increases in both tests, but not significant differences in retinocortical conduction time were noted. These results suggest that the increases in visual evoked potential latency exhibited by diabetic patients with little or no retinopathy usually reflect altered retinal function rather than optic neuropathy. Two patients with background retinopathy exhibited retinocortical conduction times that exceeded the normal mean by more than two standard deviations, suggesting that optic neuropathy may occasionally occur in diabetic patients with background retinopathy.

Adult↗

PubMed1988

The relationship between hue discrimination and contrast sensitivity deficits in patients with diabetes mellitus.

In an attempt to elucidate more fully the pathophysiologic basis of early visual dysfunction in patients with diabetes mellitus, color vision (hue discrimination) and spatial resolution (contrast sensitivity) were tested in diabetic patients with little or no retinopathy (n = 57) and age-matched visual normals (n = 35). Some evidence of visual dysfunction was observed in 37.8% of the diabetics with no retinopathy and 60.0% of the diabetics with background retinopathy. Although significant hue discrimination and contrast sensitivity deficits were observed in both groups of diabetic patients, contrast sensitivity was abnormal more frequently than hue discrimination. However, only 5.4% of the diabetics with no retinopathy and 10.0% of the diabetics with background retinopathy exhibited both abnormal hue discrimination and abnormal contrast sensitivity. Contrary to previous reports, blue-yellow (B-Y) and red-green (R-G) hue discrimination deficits were observed with approximately equal frequency. In the diabetic group, contrast sensitivity was reduced at all spatial frequencies tested, but for individual diabetic patients, significant deficits were only evident for the mid-range spatial frequencies. Among diabetic patients, the hue discrimination deficits, but not the contrast sensitivity abnormalities, were correlated with the patients' hemoglobin A1 level. A negative correlation between contrast sensitivity at 6.0 cpd and the duration of diabetes also was observed.

Adult↗

PubMed1984

Color perimetry of glaucomatous visual field defects.

A color video tangent screen has been devised, using microcomputer control of a video display to produce colored perimetric test objects matched in luminance to a white surround at 10-foot lamberts . Perimetric isopters for varying degrees of color saturation were determined by kinetic perimetry. This form of color perimetry was used to examine one eye of each of 40 patients with open-angle glaucoma as well as 20 glaucoma-suspect patients. For the first 23 eyes with manifest glaucomatous visual field defects, a masked comparison was made between the results of color perimetry and conventional perimetry with a Goldmann perimeter. For these 23 eyes, color perimetry did as well as luminance perimetry in 14, was less sensitive in 2, and was more sensitive in 7. All defects that were detectable by conventional perimetry were successfully demonstrated by the color method. Such defects often appeared to be greater in extent when mapped by the color method as compared to conventional luminance perimetry.

Aged↗

PubMed1983

Calibration of the Dicon Auto Perimeter 2000 compared with that of the Goldmann perimeter.

We empirically evaluated the calibration of the Dicon Auto Perimeter 2000 by comparing the results of threshold static perimetry with those for the same group of normal subjects examined by conventional manual static perimetry with the Goldmann perimeter. At 10 to 20 degrees of eccentricity in the visual field (including the entire Bjerrum region), there was no significant difference between threshold levels expressed as Goldmann equivalent stimuli by the Dicon instrument and the results obtained by examination with the Goldmann perimeter. The slopes of the linear meridional profiles from the two instruments were significantly different, however. The slope of the profile measured with the Dicon perimeter was flatter than that produced by Goldmann perimetry, so that threshold values inside 10 degrees of eccentricity were higher, whereas threshold values outside of 20 degrees of eccentricity were lower. Though statistically significant, these differences were small (2 dB at most). The difference in slopes can be attributed to a difference in stimulus sizes, because the area of the Dicon stimulus is eight times that of the size I Goldmann test object and twice that of the size II test object.

Adult↗

PubMedDate not supplied

Perioperative control of blood glucose in diabetic patients: a two-step protocol.

Perioperative control of blood glucose in patients with diabetes has been difficult due to frequent occurrence of hypoglycemia or hyperglycemia. We developed a two-step protocol for management of insulin-treated patients during general anesthesia. Regular insulin was given intravenously before anesthetic induction according to the step I formula (initial): initial blood glucose - 150/10 = U. Regular insulin was then given during surgery according to the step II formula (hourly): blood glucose 150-250 mg/dl = 2 U; blood glucose greater than 250 mg/dl = 4 U. Fluid replacement of 5% dextrose with lactated Ringer's solution, 3 ml/kg estimated ideal body weight, was given hourly and additional lactated Ringer's solution was given as indicated. Thirty patients received preoperative (long- or intermediate-acting) insulin and were managed by the two-step protocol. Ten patients received preoperative (long- or intermediate-acting) insulin and were managed by a standard method used in the same institution. Thirty patients did not receive preoperative insulin and were managed by the two-step protocol. All patients underwent retinal surgery under general anesthesia. In comparing the two groups pretreated with insulin, patients treated by the standard method had significantly higher (mean) blood glucose levels (360.2 +/- 100.4 mg/dl) than those treated with the two-step protocol (181.2 +/- 50.8 mg/dl) (P = 0.0001) at the end of surgery. Of the two-step protocol patients, those pretreated with one-half the usual morning dose of long- or intermediate-acting insulin had lower (mean) blood glucose levels (225 +/- 87 mg/dl) than patients not pretreated (310 +/- 130.8 mg/dl) (P = 0.0069) the morning after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus↗

PubMedDate not supplied

Photodocumentation of corneal scarring. Collaborative Longitudinal Evaluation of Keratoconus Study Group.

PURPOSE: A standardized system for photodocumenting corneal scars and for evaluating these photographs does not exist and is essential for clinical research. To address this need, we developed a system for photographing and evaluating corneal scars. METHODS: In the "Development Phase," we tested several procedures in small samples totaling 40 eyes of 20 keratoconus patients. In the "Test Phase," we used an independent sample of 150 eyes of 82 keratoconus patients. Fifty-nine of these 150 eyes had corneal scars, and 91 of the eyes did not as determined by the clinician. RESULTS: The photography protocol requires four central parallelepiped and two whole cornea oblique photographs after pupil dilation. With the clinician as gold standard, this technique yielded sensitivity of 96% and specificity of 83%. Evaluation of the corneal photographs as to the presence or absence of corneal scarring was performed independently by two masked readers. Agreement between clinicians on the presence of corneal scarring was 0.99 (kappa); agreement between readers for the presence of scarring was 0.80 (kappa). CONCLUSIONS: The corneal photography protocol we describe is recommended for use in clinical investigations of cicatricizing corneal disease and appears robust enough to be used in multicenter studies.

Corneal Diseases↗