Biomedical subjects

W M Hart

Publications and source records attributed to W M Hart.

13 recordsLinked 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↗

PubMed1990

Motion perception is abnormal in primary open-angle glaucoma and ocular hypertension.

Several lines of evidence suggest that the large optic nerve fibers, which form the magnocellular retinocortical pathway, are preferentially susceptible to early glaucomatous damage. It is evident from studies of the functional architecture of the visual system that the magnocellular pathway underlies the global perception of motion. Therefore, we have developed a psychophysical technique for assessing motion detection thresholds in patients with ocular hypertension (OHT) and primary open-angle glaucoma (POAG). For this purpose we employed a dynamic random dot display that contained varying degrees of a coherent motion signal embedded within a background of random motion noise. We used this technique to measure motion thresholds in POAG patients (n = 37), OHT patients (n = 14), and age-matched controls (n = 39). Motion thresholds were elevated by 70% for the POAG group and 44% for the OHT group relative to controls. In the same patients, no significant deficit in form discrimination was found as measured by Pelli-Robson charts. Our results demonstrate that significant motion perception deficits are evident in POAG and OHT. These findings support the suggestion that significant and selective damage to the magnocellular pathway occurs in OHT and POAG and indicate that motion threshold testing may reveal preclinical optic nerve disease in early POAG.

Contrast Sensitivity↗

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

Modified grid laser photocoagulation for diabetic macular edema. The effect on the central visual field.

Modified grid laser photocoagulation has been shown to stabilize visual acuity in patients with diabetic macular edema, but the effect on extrafoveal visual function is uncertain. Automated static threshold perimetry was performed on 64 eyes of 36 patients before and after modified grid therapy with the argon green or krypton red laser. Twenty-eight eyes underwent two grid treatments for persistent macular edema. For all eyes tested, average threshold sensitivity in the central 5 degrees dropped 3.44 dB (standard deviation [SD], 3.79 dB) after the first treatment and 6.86 dB (SD, 5.02 dB) cumulatively after the second treatment. Qualitatively, the grayscale displays of the central visual field were darker after treatment, but the scotomata from laser photocoagulation could not be distinguished from those due to macular edema. The foveal threshold showed no significant change. In a subgroup of patients tested, color vision was not significantly improved and nearly all patients exhibited a tritan defect before and after treatment. No difference was detected between the argon and krypton groups. This suggests that with modified grid laser photocoagulation visual acuity and foveal threshold are preserved at the expense of generalized loss of threshold sensitivity across the central 10 degrees of the visual field.

Color Perception↗

PubMed1979

Multivariate analysis of the risk of glaucomatous visual field loss.

In a retrospective study, 92 patients with ocular hypertension, ie, intraocular pressure of 21 mm Hg or higher, and no evidence of glaucomatous visual field defects, were observed for five years. Visual field defects developed in one or both eyes of 33 patients during the five-year follow-up period, while none were detected in the remaining 59. Values for suspected risk factors, determined at the outset of the follow-up period, were subjected to a multivariate analysis with use of linear discriminant analysis and a multiple logistic function. Models of risk providing maximum separation of the two patient groups (visual field loss vs no visual field loss) found that the risk factors having the greatest significance for prediction of visual field loss included vertical estimates of cup/disc ratio, mean IOP during the period of observation, a positive family history of glaucoma, and age. Factors having the lowest predictive values included IOP response to topical dexamethasone, plasma cortisol suppression, and a history of systemic hypertension.

Glaucoma↗

PubMed1979

The metabolism of dihomo-gamma-linolenic acid in man.

Orally administered dihomo-gamma-linolenic acid (DHLA) is well absorbed in man; it appears in blood after ca. 4 hr first as triglyceride ester and later as phospholipid. After sustained-dosing, DHLA penetrated membrane pools and all phospholipid components but, depending on the dosage, reached a metabolic equilibrium in 4-16 days. Intact platelets do not accumulate arachidonate following DHLA administration, and species differences occur in the capacity of animals to metabolize DHLA to arachidonic acid (AA). The rat appears to be unusual in having a very active hepatic delta5-desaturase enzyme system. Potentially antithrombotic changes in platelet function which followed the administration of DHLA to man were accompanied by a significant increase in the capacity of platelets to synthesize PGE1. Concomitant increases in PGE2 synthesis do not apparently result from an increased production of AA and suggest that DHLA, or a DHLA metabolite, interferes with the metabolism of AA. Effects on thromboxane and prostacyclin synthesis are being studied.

8,11,14-Eicosatrienoic Acid↗

PubMed1979

Optic disk edema in sarcoidosis.

A 24-year-old woman had bilateral optic disk edema. A granulomatous uveitis and macular edema subsequently ensued. Histologic examination of a biopsy specimen taken from an area of marked hilar adenopathy revealed noncaseating epithelioid cell tubercles. No other associated systemic findings were noted, and after a course of topical and systemic corticosteroid therapy, the ocular manifestations disappeared.

Adult↗

PubMed1978

Quantitative visual field and optic disc correlates early in glaucoma.

A retrospective study was made of persons with ocular hypertension and normal initial visual fields. Seventy eyes were followed, and glaucomatous visual field defects developed in 25 of these eyes. In eyes with ocular hypertensio, the area enclosed by the central visual field isopter (I2e) was significantly smaller than that previously reported for an age-corrected group of eyes with normal intraocular pressure. In the absence of glaucomatous visual field defects, isopter areas were not releated to cup-disc ratios. Coincident with visual field loss, reductions in both peripheral (I4e) and central (I2e) isopter areas correlated linearly with increases in the cup-disc ratio. Prior to visual field loss, the I4e isopter area wassignificantly smaller among those eyes destined to lose visual field.

Adult↗

PubMed1978

Cytomegalovirus in juvenile iridocyclitis.

We cultured cytomegalovirus from lens material aspirated from the eye of a 4-year-old boy who had a severe bilateral iridocyclitis and secondary cataracts. There were neither systemic manifestations of congenital disease nor chorioretinitis.

Child, Preschool↗

PubMed1977

Visual field changes in ocular hypertension. A computer-based analysis.

A minicomputer system has been developed to digitize and store visual field data. In 110 cortiocosteroid-nonresponding subjects aged 10 to 75, the area of the i4e and i2e isopters and of the blind spot changed linearly as a function of age. Within this population the same visual field parameters were randomly distributed with respect to intraocular pressure. In 32 cortiocosteroid responders (increase in intraocular pressure to over 31 mm Hg after topical administration of corticosteroids) with normal visual fields, the central visual field area (i2e isopter) was reduced as a nonlinear function of IOP. Increases in IOP in excess of 8 mm Hg were required to produce significant mean reductions in central visual field area.

Adolescent↗

PubMed1977

Management of dysthyroid optic neuropathy.

The diagnosis of dysthyoid ophthalmopathy is based on clinical observation of characteristic ophthalmic abnormalities. Proper diagnosis and initiation of treatment should not be delayed because a patient is found to be euthyroid. Although visual problems in dysthyroid ophthalmopathy are uncommon this disorder can result in permanent severe visual loss if optic neuropathy is not detected early and managed properly. Oral corticosteroid therapy and surgical decompression both seem to have a place in the treatment of dysthyroid ophthalmopathy with optic neuropathy.

Adrenal Cortex Hormones↗

PubMedDate not supplied

Acquired dyschromatopsias.

Theories of color vision have been founded on behavioral observations of how the human eye distinguishes colors and mixtures of colors. Studies of congenital dyschromatopsias (inherited disorders of color vision) have been important to the development of these theories. Subsequent studies of acquired dyschromatopsias (disorders of color vision caused by disease) were understandably influenced by these concepts. Theories to explain the patterns of color vision impairment found in acquired diseases (for example, preferential hue discrimination defects) have stressed the likelihood of selective damage to specific components of the afferent visual system (photoreceptors, ganglion cells, synaptic elements, axons etc.). More recent evidence suggests, however, that impairment of color vision by diseases of the retina and optic nerve is commonly nonspecific, and not the result of selective impairment of individual neural mechanisms responsible for mediating color vision. Rather, the patterns of acquired dyschromatopsias often appear to be related to a physiologically heterogeneous distribution of color vision in the foveal and perifoveal visual field, coupled with a tendency for the visual field defects caused by acquired diseases to be unevenly distributed in these same areas.

Color Perception Tests↗