The vitreous in idiopathic giant retinal breaks.
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BACKGROUND: Optic disc pits represent a rare congenital abnormality frequently associated with macular detachment. Several theories on the pathogenesis of the detachment have been proposed, but the issue still remains unclear. Treatment remains speculative as well; advocated treatments include eye-patching, bed rest, steroids, laser photocoagulation, pars plana vitrectomy with fluid-air exchange and optic nerve sheath decompression. METHODS: The Authors report on the case of an optic pit with associated macular detachment which developed an inner layer macular hole and, after an apparently insignificant skull trauma, a large macular break. The patient underwent a standard three-port pars plana vitrectomy, fluid gas-exchange, posterior scleral buckling and laser treatment. RESULTS: Twelve months after surgery the retina was flat, posterior buckling was evident and laser treatment pigmented. Visual acuity was 20/600. CONCLUSIONS: The presence of strands of condensed vitreous strands crossing the posterior lacuna and exerting traction over the macula and optic disc, support the theory of a possible tractional role of anomalous vitreous adhesion in the pathogenesis of the detachment and macular break. Anomalous vitreous adhesion over the posterior retina could be related to the malformative genesis of the syndrome, and the anomalous persistence of the Cloquet's canal or primary vitreous could be responsible for the traction.
Nine eyes of nine patients affected by retinal detachment with macular hole were treated with pneumoretinopexy and postoperative positioning. All the eyes were myopic (mean 13.3 d., sd 3.3), two were amblyopic and one was aphakic. The operative technique included eye softening and intravitreal SF6 gas injection only. Barrage laser photocoagulation was carried out after retinal reattachment. In seven eyes (77.8%) the retina reattached in a mean of three days and the visual acuity improved. No recurrences were observed after a mean of 11.6 months. No severe complications occurred. Vitreous flare was present in 44% and increase of floaters in 55% of the eyes. We believe that pneumoretinopexy can be employed as the first treatment in case of myopic retinal detachment with macular hole.
We performed a scanning electron microscopic observation of the posterior retinal surface of 59 autopsy eyes with spontaneous vitreous detachment. In 26 eyes (44%), there were remnants of the posterior vitreous membrane in the foveal area. These vitreous cortex remnants formed three basic patterns. They appeared either as disc-shaped collagenous membranes covering the fovea, as rings along the foveal margin, or forming a structure that resembles a cyst. Each of these patterns seemed to have a counterpart to various known clinical situations. These findings imply that remnants of the vitreous cortex membrane frequently remain attached to the fovea after apparent complete posterior vitreous detachment. The observed features would provide morphological basis for the interpretation of several clinical conditions that take place along the vitreoretinal interface at the fovea.
We unfolded and attached a giant retinal tear with an inverted edge using fluorosilicone oil while the patient was in the supine position. The advantages of high viscosity (10,000 centistokes) and specific gravity (1.31) fluorosilicone are discussed in this paper.
A 71-year-old man presented with a large disciform scar in the right eye and hard (nodular) as well as soft (granular) drusen scattered throughout the posterior pole of the left eye. A large serous pigment epithelial detachment was evident in the drusen area of the left fundus. Six months later a tear of the retinal pigment epithelium (RPE) occurred in the left eye. It was located exactly along the peripheral border of the drusen area instead of the border of the RPE detachment where it would have been expected. It is considered that reduced adhesion between the RPE and Bruch's membrane as well as the sharp change in tissue cohesiveness at the border of the drusen area and surrounding healthy tissue were relevant in the pathogenesis of this case.
Pattern reversal visual evoked potentials (VEPs) with checks of 50' and 12' were recorded in 15 patients with idiopathic unilateral macular hole. VEPs from the affected eyes were reduced in amplitude compared with those from the fellow eyes, especially with checks of 12' (percentage of the amplitude in the affected eye to that in the fellow eye was 86% +/- 19% with checks of 50' and 61% +/- 35% with checks of 12'). The latencies showed no statistically significant difference between the affected and the fellow eyes, although a marked interocular delay was found in a few patients. The degree of amplitude reduction and interocular delay had no relation to the size of the macular hole or visual acuity. The effects of experimental scotomata of various sizes on the VEPs, which were evaluated in nine normal subjects, were also variable among the subjects. We conclude that although the macula predominantly participates in the pattern VEP, an estimation of the extent of macular pathology from the VEP changes may be difficult because the VEP changes induced by a macular hole have wide individual variation and have no relation to the size of the hole.
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Thirty-two eyes with idiopathic macular holes and one eye with a traumatic macular hole were assessed by pattern-reversal electroretinography, ganzfeld electroretinography and pattern-reversal visual evoked potentials. Results were inspected for qualitative abnormalities and then measured in comparison with fellow eyes and 41 control eyes of similar age. Qualitative abnormalities occurred in some eyes with macular holes, most commonly a reduction in pattern-reversal electroretinogram or pattern-reversal visual evoked potential amplitude; 15' check amplitudes were significantly lower in eyes with macular holes than in control eyes, but no significant difference in latency was found. Control pattern-reversal electroretinogram and pattern-reversal visual evoked potential amplitudes were noted to decline with age, and paired t-tests on an age-matched subgroup of eyes with macular holes and control eyes showed appreciable differences only in the pattern-reversal electroretinogram q-r (N95) amplitude.
We report two female patients, a mother and daughter, with bilateral foveal changes that resembled those of X-linked recessive juvenile retinoschisis. The 23-year-old daughter had flat retinoschisis at the temporal periphery with multiple small inner-layer breaks in both eyes. There was foveal retinoschisis with fine radial folds. The optic disc was dragged to the nasal side. The 49-year-old mother also had foveal retinoschisis in each eye but there was no peripheral retinoschisis. In the left eye several retinal breaks with minimal retinal detachment were found. Electrophysiological findings in both cases were similar. Single-flash electroretinogram (ERG) showed normal a-wave and decreased b-wave, presenting a negative shape. Averaged scotopic and photopic ERGs showed slightly reduced b-waves, but they were within normal ranges. Visually evoked potentials were subnormal. Ophthalmoscopic and electrophysiologic findings were compatible with X-linked recessive juvenile retinoschisis, but an autosomal dominant inheritance was most likely. Our cases do not follow previously reported characteristics and may represent a new clinical entity.
Proliferative vitreoretinopathy (PVR) is a reactive process of the ocular tissue after perforating trauma, retinal detachment, and surgical manipulations. Although several studies, most of them experimental, have focused on the detection of specific etiologic factors in the development of PVR, there is compelling evidence that PVR is nothing more than a physiologic tissue repair process with undesirable consequences for the retina. Important features of PVR involving the role of platelets, mononuclear phagocytes, and fibroblasts parallel the chain of events observed in tissue repair elsewhere in the body. Numerous experimental models for PVR, originally designed to find specific stimuli for the generation of intraocular traction membrane formation, have shown that the process of PVR is the common pathway of the eye's reaction to vitreoretinal trauma of any kind. Accordingly, vitreoretinal surgeons could learn a lot from the work of other disciplines, e.g. surgery and dermatology, on wound healing, and the factors known to modify wound healing elsewhere in the body should be taken into consideration. The well-established impairment of tissue repair processes caused by medical treatment with corticosteroids and cytotoxic agents suggests a combined medical approach to PVR as an adjunct to surgical treatment, using refined methods of application and dosage. Steroids and cytotoxic drugs will influence the course of PVR by suppressing macrophage recruitment and the initial inflammatory reaction as well as the proliferative phase of wound healing with traction retinal detachment, respectively.
A new case of pigmented paravenous retinochoroidal atrophy is described. Besides the characteristic fundus picture, this 21-year-old male showed a remarkable difference in retinal function between the two eyes, the function of the left eye being much more impaired. This might suggest a progressive condition, in which the right eye lags behind. In addition this patient had a vitreoretinal degeneration resulting in five peripheral retinal tears in the right eye.
Pars plana vitrectomy was performed on a six-year-old boy with complete retinal detachment associated with a morning glory disc of his left eye. Perfluorodecalin was injected to unfold the retina. During surgery, perfluorodecalin leaked repeatedly under the retina. This case demonstrates that a retinal hole in tissues lying within the optic disc anomaly provides a communication for fluid and perfluorodecalin between the subretinal space and vitreous cavity resulting in a rhegmatogenous retinal detachment in the morning glory syndrome.
Steady-state macular (9 degrees x 9 degrees) electroretinograms in response to either sinusoidal flicker (focal electroretinogram) or counterphased sinusoidal gratings (pattern electroretinogram) were recorded in 14 patients with inner lamellar macular holes, in 4 patients with full-thickness macular holes and in 14 age-matched controls. Fourier analysis of focal and pattern electroretinograms yielded three main components: a first and a second harmonic to flicker, and a second harmonic to pattern. Recent evidence indicates that the first harmonic to flicker is of receptoral origin, whereas the flicker and pattern second harmonics represent, at least in part, the activity of different generators in the inner retina. When compared to controls, patients with inner lamellar holes showed significant amplitude reduction and phase delay for both flicker and pattern second harmonics, but not for the flicker first harmonic. Patients with full-thickness holes showed significant amplitude reduction also for the flicker first harmonic. These results indicate a prevalent functional involvement of the inner retina in lamellar macular holes, which can be clinically detected by evaluating focal and pattern electroretinogram second harmonics.
Electroretinograms (ERG) and electro-oculograms (EOG) were studied in 88 eyes of 44 male patients with X-linked recessive retinoschisis. Differences of fundus appearance, ERG, and EOG between the eyes of each patient were analyzed. Fundus abnormalities were symmetrical in 77.3% of the cases. The amplitude of the ERG a-wave was normal in 26.1% and was abnormally low in 73.9%. The amplitude of the b-wave was below normal in all eyes; thus a small b-wave/a-wave ratio, which is characteristic of X-linked recessive retinoschisis, was observed in every case. The light peak to dark trough (LP/DT) ratio of the EOG was normal in 90.8% of the cases. The relative electrophysiological differences between the two eyes were calculated and showed that a-wave amplitude was not different between eyes in 75.0% of the cases; b-wave amplitude was not different in 77.3% of the cases; b-wave/a-wave ratio was symmetrical in 93.2% of the cases; and the LP/DT ratio was consistent between eyes in 86.8% of the cases. These results suggest that in most cases of X-linked recessive retinoschisis the fundus appearance, ERG, and EOG are similarly affected in both eyes of the patient.
Spatial contrast sensitivity functions were evaluated in 30 patients with macular disorders and 16 age-matched control subjects. Eighteen of the affected eyes had macular holes and the rest had isolated macular problems. A loss in spatial contrast sensitivity in the central visual field indicated a relative scotoma resulting from macular dysfunctions. The nature and size of a localized scotoma such as the type caused by a macular lesion was estimated by measuring spatial contrast sensitivity as a function of retinal area centered on the fovea. Such spatial-contrast-threshold perimetry was found to be helpful in differential classification of macular holes. Spatial contrast sensitivity and visual resolution improved with increasing retinal area even in the eyes with macular holes, but never reached normal sensitivity for spatial frequencies above 5 cycles per degree (cpd) within our experimental conditions. The loss in sensitivity to low spatial frequencies (less than or equal to 5 cpd) was found to be apparent and a function of the retinal area stimulated. The summation curves (contrast sensitivity vs. stimulus size) were abnormal for all spatial frequencies. The 'critical' sizes (i.e. the stimulus size above which no increase in sensitivity occurred) were always larger in the affected eyes than those in the normal. Thus 'critical' areas of complete summation in the parafovea may be a better measure of functional integrity of central retina in the presence of a foveal lesion than the visual resolution that varies with the retinal area and location activated. Evaluation of contrast sensitivity of the parafoveal regions with nonfunctional fovea also indicated existence of similar mechanism of spatial vision in the fovea and the parafovea.
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The effects of cryotherapy, transcleral massage, or directed irrigation on exposed retinal pigment epithelial (RPE) cells at the base of an experimental retinal hole were studied in living rabbit eyes. Cryotherapy or massage with or without vitrectomy failed to release RPE cells or result in preretinal membrane formation. Directed irrigation dispersed viable RPE cells into the vitreous and produced cellular precipitates with membranes on the inferior retina, although the membranes tended to regress within 6 weeks after surgery. These results suggest that healthy RPE cells at the base of retinal tears are not easily released into the vitreous and may not contribute to the formation of preretinal membranes found in proliferative vitreoretinopathy.