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At least 613 records · Page 34Linked to original sources

Persistent symptoms after peripheral iridectomy for angle-closure glaucoma.

Symptoms that persist after operations for angle-closure glaucoma arise from different causes. In the presence of open peripheral iridectomies miotics may be beneficial or may close angles; wide pupil dilatation by phenylephrine used to diminish posterior synechiae may close angles; cycloplegic mydriatics will close some angles and open others. Unexpected bizarre reactions to eye drops may occur. Persistent chronic glaucoma will be more common after laser iridotomy than after correctly assessed filtering operations. The importance of gonioscopy in diagnosis and management is emphasised.

Acute Disease↗

Acute glaucoma--1941.

PURPOSE: To describe the treatment of acute glaucoma before the technological and pharmacological advances that followed World War 2. METHOD: A narrative of personal experience is presented. CONCLUSIONS: In 1941, acute congestive glaucoma received heroic treatment - strong miotics, blood-letting by leeches, purging with mercury. If satisfactory response did not occur within four hours, a broad iridectomy was performed on the hard, congested eye. Affected eyes commonly remained blind or with severely reduced vision.

Acute Disease↗

Malignant glaucoma following laser iridotomy.

BACKGROUND: A 69-year-old man presented with malignant glaucoma 10 days after an iridotomy for acute angle-closure glaucoma. METHODS: The case notes are reviewed, describing his presentation and treatment, including the technique of extracapsular cataract extraction with anterior vitrectomy. RESULTS: An excellent visual outcome was achieved with no recurrence of the malignant glaucoma. CONCLUSIONS: This case illustrates the recently established link between laser iridotomy and malignant glaucoma. Miotics and other possible causes are excluded, a surgical option is described and the importance of assessing central anterior chamber depth in cases of angle closure is emphasised.

Aged↗

Glaucoma prescribing trends in Australia and New Zealand.

PURPOSE: To summarize current practice styles and patterns associated with glaucoma management in ophthalmologists of Australia and New Zealand as derived from a survey. METHOD: A questionnaire was sent to all Australian and New Zealand ophthalmologists, which anonymously assessed demographic characteristics and prescribing patterns for each major class of glaucoma medication. RESULTS: A total of 761 questionnaires were sent with a response rate of 51%. Of respondents 14% were glaucoma subspecialists. In 69%, the first-line drug-class of choice was a prostaglandin analogue. New Zealand ophthalmologists favoured beta-blockers as their first-line agent because of cost, government restrictions and familiarity. Most respondents stated "hypotensive efficacy" as the most important factor in class choice. Alpha-2-agonists, carbonic anhydrase inhibitors and miotics were considered second-line agents, because of side-effects and lack of hypotensive potency. CONCLUSIONS: The choice of first-line agent for the treatment of glaucoma differed between Australian and New Zealand ophthalmologists, in part as the result of government restriction of prostaglandin-class drugs. Practice patterns seen in Australasia parallel the current evidence base reported in peer-reviewed literature.

Antihypertensive Agents↗

Correlations between acetylcholinesterase activity in guinea-pig iris and pupillary function: a biochemical and pupillographic study.

Acetylcholinesterase (AChE) in guinea pig iris was inhibited by methylisocyclopentylfluorophosphate (soman) administered topically or parenterally, and enzyme activity was correlated to pupillary diameter by infrared pupillography. After a single topical soman instillation into the conjunctival sac there was an almost linear relationship between the reduction in AChE activity and pupillary diameter. Topical administration of soman at 24-h intervals in doses capable of almost complete inhibition of AChE in iris was accompanied by a reduced miotic effect of this drug. This was indicated by a reduced rate of the soman-induced pupillary constriction, a less pronounced reduction in pupillary diameter, and a more rapid return of the pupillary diameter to normal size. The change in pupillary diameter occurred after three daily administrations and remained constant during 31 days of treatment. These observations were seen irrespective of inhibition of blood AChE. The decrease in response to repeated administration could not be explained by a reduced inhibitory effect of soman on AChE, by a more rapid de novo synthesis of AChE, or by a change in the number of the muscarinic receptors as determined by quinuclidinyl benzilate binding. When soman or DFP was administered subcutaneously in high doses a severe AChE inhibition was obtained in iris without any concomitant miosis.

Acetylcholinesterase↗

Ophthalmic contact lens with internal fixation light for examination of the optic nerve head.

Stereoscopic slitlamp examination of the optic nerve head in one-eyed patients is difficult because there is currently no way to provide the patient with a fixation target. This situation is often aggravated in glaucoma patients by a miotic and fixed pupil. We have developed a funduscopic contact lens which incorporates a fixation target, allowing the patient to view the target with the eye being examined. The device has been successfully tested on normal volunteers.

Contact Lenses↗

Substance P, neurokinin A and neurokinin B in the ocular response to injury in the rabbit.

1. Substance P (SP) and neurokinin A- (NKA)/neurokinin B (NKB)-like immunoreactivity (LI) were measured by radioimmunoassay in extracts of the rabbit uvea. The iris-ciliary body complex contained 3-4 times more NKA/NKB-LI than SP-LI. Tachykinins are thought to mediate many of the responses to ocular injury in the rabbit. Their possible role in the miosis and breakdown of the blood-aqueous barrier (BAB) was studied in vitro and in vivo. 2. In vitro, NKA had a more short-lasting contractile effect on the sphincter pupillae muscle than either SP or NKB, but SP was more potent than the other two. The tachykinin antagonist, spantide, dose-dependently suppressed the response to electrical stimulation (by 90% at 10(-4) M) and to the three tachykinins. An antiserum against SP (no cross-reaction with NKA or NKB) greatly suppressed the response to SP (by 90%) as well as to electrical field stimulation (by 40%). The responses to NKA and NKB were unaffected. 3. In vivo studies revealed that SP was more potent than NKA and NKB as a miotic. SP evoked a moderate breakdown of the BAB at high doses while NKA and NKB were virtually inactive. 4. We conclude that besides SP other tachykinins might play a role in the mediation of miosis in the rabbit eye but, of the three peptides investigated, only SP can be of importance for the breakdown of the BAB.

Animals↗

Peripheral contrast sensitivity for dynamic sinusoidal gratings in early glaucoma.

Automated contrast thresholds were established for dynamic, 2 reversals per sec phase-shifted, sinusoidal gratings in a 5 degrees circular test field centred 7.5 degrees from the fixation point in six positions in the visual field in 16 patients (age 56-76 years) with clinically established (optic disc or nerve fibre layer damage) early glaucoma, without visual field defects. For reference, contrast thresholds were also obtained in 16 sex-matched and age-matched controls. For all three spatial frequencies, thresholds were raised in the glaucoma group (0.5 c/deg: p = 0.0034-0.041, 2 positions n.s.; 1.0 c/deg: p = 0.0093-0.049, 1 position n.s.; 2.0 c/deg: p = 0.0011-0.041, 1 position n.s.). Deficiencies did not correlate to glaucoma type (simplex vs capsular), intraocular pressure level at examination, visual acuity, or local therapy (beta-blockers vs miotics). In the glaucoma group, there was a general loss of contrast sensitivity in all six positions tested in the visual field, reflected in roughly similar threshold elevations. Losses appeared slightly greater in the lower hemi-field. Definite contrast threshold elevations from the early glaucomatous process were established in this group of glaucoma patients without visual field defects. However, the method was considered to be of less value in glaucoma detection for individual subjects, due to the large overlap in threshold values between glaucoma patients and controls.

Aged↗

Quality of life among patients with glaucoma in Sweden.

PURPOSE: To assess the health-related quality of life (HRQOL) in an unselected sample of patients with glaucoma. METHODS: The HRQOL was studied in a cross-sectional survey in 270 patients from two departments of ophthalmology in different parts of Sweden by using the Swedish Health-Related Quality of Life Survey, a generic HRQOL-instrument adapted from the Medical Outcomes Study. RESULTS: Compared to a random Standard Population Sample, the glaucoma patients showed lower mean score only in the scale of 'Pain' (p < 0.05, effect size 0.17), but higher mean score in 'Sexual functioning' (p < 0.01, effect size 0.35). Significant factors correlated to a lower score on HRQOL-scales were decreased visual acuity and visual field, and comorbidity of cardiovascular and non-vascular systemic diseases. Regarding the topical medications, beta-blockers with or without miotic agents had no negative impact on the HRQOL. CONCLUSION: Our findings indicate that health-related quality of life in glaucoma patients in general is good, especially when vision is intact, and that topical beta-blockers do not have any negative influence.

Aged↗

Ultrabiomicroscopic study of the effects of brimonidine, apraclonidine, latanoprost and ibopamine on the chamber angle and ciliary body.

The authors used the Zeiss Humphrey (Mod840, 50 MHz) ultrabiomicroscope to evaluate the changes that Brimonidine, Apraclonidine, Latanoprost and Ibopamine cause in the anterior chamber and on the ciliary body of healthy subjects. The eyes of 60 volunteers, separated into 4 groups according to drug instilled, were studied and the parameters analyzed were: anterior chamber depth (ACD), pupillary diameter (PD), angle opening at 500 microns from the scleral spur (AOD500), trabecular iris angle (TIA) and iris thicknesses (ID1 and ID3). The study showed the miotic effect of Brimonidine (S) that was accompanied by an angle opening (S). Apraclonidine and Latanoprost caused no statistically significant changes in the angle or in the ciliary body. Ibopamine caused mydriasis (S). The UBM, therefore, showed itself to be useful also in the study of the mechanism of action of drugs on the angular structures and on the ciliary body.

Adrenergic alpha-Agonists↗

In the eye (D-Pro2, D-Trp7,9)-SP is a substance P agonist, which modifies the responses to substance P, prostaglandin E1 and antidromic trigeminal nerve stimulation.

A substance P analogue, (D-Pro2, D-Trp7,9)-SP, has been described to have SP antagonistic and SP agonistic effects in different tissues. We have investigated the effects of (D-Pro2, D-Trp7,9)-SP on the sphincter pupillae muscle, the blood aqueous barrier (BAB) and the intraocular pressure (IOP) in the albino rabbit eye. We also investigated the modifying effects of (D-Pro2, D-Trp7,9)-SP on miosis, BAB damage and IOP rise caused by SP, prostaglandin E1 (PGE1), capsaicin and on the miosis caused by electrical intracranial antidromic trigeminal nerve stimulation (NV stim). Endogenous PG synthesis was inhibited by systemic indomethacin i.v., cholinergic influence on the pupil size was inhibited with biperiden, i.v., adrenergic nerve influence by cervical sympathectomy just prior to the expts. Tubocurarine chloride was used to cause relaxation of striated muscles in the expts with NV stim. We found 100 micrograms (D-Pro2, D-Trp7,9)-SP to cause miosis, breakdown of the BAB with heavy leakage of Evans blue into the ciliary processes and aqueous humor, and a rise in IOP. At 10 micrograms (D-Pro2, D-Trp7,9)-SP caused slight miosis and did not inhibit the miosis caused by SP or capsaicin, but caused a significant reduction of the miotic response caused by PGE1 and NV stim. The rise in protein concentration in the aqueous humor caused by SP or PGE1 was slightly but significantly lower after pretreatment with (D-Pro2, D-Trp7,9)-SP. Thus (D-Pro2, D-Trp7,9)-SP was found to act as a SP agonist on the sphincter pupillae muscle, on the BAB and IOP. However, (D-Pro2, D-Trp7,9)-SP seemed to have some SP antagonistic effects on mechanisms that require sensory nerve conduction e.g. miosis caused by PGE1 and NV stim. The antagonistic mechanism is not clear. The SP analogue may have an unspecific membrane stabilizing effect or a toxic effect or block SP receptors on the sensory nerve fibers. Such effects of (D-Pro2, D-Trp7,9)-SP may explain also why the rise in protein concentration in the aqueous humor caused by SP and PGE1 was lower in eyes pretreated with (D-Pro2, D-Trp7,9)-SP.

Alprostadil↗

Miosis and plasma prostaglandin E metabolites during endotoxin fever.

The time course and intensity of miosis accompanying endotoxin (ET) fever was studied in goats concomitant with radio-immunoassay of plasma PGE metabolites. The i.v. injection of ET (E. coli lipopolysaccharide; 0.25 micrograms kg-1) induced a biphasic miosis correlated in time with the biphasic febrile response. Plasma PGE metabolites rose from an undetectable level to a mean of 2 nmol l-1 during the early fever phase, but fell to an undetectable level during the second fever phase in spite of persisting pronounced miosis. Like light-induced pupillary constriction, the ET miosis was antagonized by corneal application of atropine. A corresponding miotic response to ET was obtained also in the sheep. It is concluded that ET-induced miosis requires cholinergic nerve conduction, and that its direct cause is not systemic liberation of PGE. It is suggested that rather some nervous or humoral stimulus developing in conjunction with ET fever acts upon the same brain stem locus as that mediating the pupillary light reflex.

Animals↗

Endotoxin-induced prostaglandin (PGF2 alpha) biosynthesis, fever and miosis in dexamethasone-treated goats.

Prostaglandin-releasing, adrenocortical, febrile and miotic responses to endotoxin (ET) (E. coli lipopolysaccharide; 0.25 microgram kg-1) were studied in goats with and without prolonged dexamethasone influence. The i.v. injection of ET induced a three-fold peak elevation in plasma 15-ketodihydro-PGF2 alpha at 1.5 h post-injection, that is, between the first and second phase of the temperature elevation. During the latter phase, the plasma concentration of this primary PGF 2 alpha metabolite gradually returned to basal level, which implies that the second phase of ET fever is not PG dependent. The PG response exhibited a similar pattern, but was less pronounced in the dexamethasone-ET experiments, where the duration of maximum temperature elevation and of the miosis became shortened by about 20 min, and the typical biphasic pattern of ET fever was no longer seen. The ET-induced rise in plasma aldosterone concentration was completely blocked by dexamethasone. The corresponding rise in plasma cortisol concentration was prevented for 2 h, but was later only partially inhibited in spite of the repeated dexamethasone treatment.

Aldosterone↗

Responses to antidromic trigeminal nerve stimulation, substance P, NKA, CGRP and capsaicin in the rat eye.

In the rat eye, intracameral injections of substance P in doses of 10-30 pmol caused a maximal long-lasting miosis and a leakage of plasma proteins into the aqueous humor, indicating a breakdown of the blood-aqueous barrier. Neurokinin A seemed equipotent to SP, but calcitonin-gene-related peptide (CGRP) (17 pmol) caused neither miosis nor protein leakage into the aqueous humor. The same result was obtained when CGRP was administered intravenously. Intracameral injection of capsaicin caused only a transient miosis which could not be repeated with further injections, even though the pupillary sphincter was still able to react to exogenous SP. Antidromic electrical stimulation of the trigeminal nerve caused plasma extravasation in the skin and a breakdown of the blood-aqueous barrier with an increased protein content in the aqueous humor. The stimulation did not affect the pupil size. The results indicate that in rat eyes SP and NKA are miotics, but the amounts that can be released from sensory nerve endings are too small to cause persistent miosis. These peptides are more likely to play a role in the neurogenic breakdown of the blood-aqueous barrier. CGRP at the same dose affects neither the pupillary sphincter muscle nor the barrier.

Animals↗

Accommodation as the primary cause of low-luminance myopia. Experimental evidence.

Low-luminance myopia of subjects with one normal eye and one aphakic eye was measured with a laser optometer. Low-luminance myopia was registered in the normal eyes, but no such myopia could be found in the aphakic eyes. The same subjects' aphakic eyes were further tested with miotic and dilated pupils. Miosis or mydriasis did not significantly alter the results as compared with measurements obtained with normal pupil size. These results would appear to be the first direct experimental evidence that accommodation is the primary cause of low-luminance myopia.

Accommodation, Ocular↗

The immediate IOP response of Nd-YAG-laser iridotomy and its prophylactic treatability.

The response of IOP in the normotensive human eye to Neodym-YAG-laser iridotomy was investigated in this study. In 2 series of 10 patients, each unilateral laser iridotomy was performed with a YAG-laser prior to cataract surgery. In one group laser iridotomy was done without pre-treatment, in the second group laser iridotomy was preceded by treatment with 1% pilocarpine. Close follow-up of IOP before and after surgery was carried out with the Non-Contact-Tonometer. Laser iridotomy caused average IOP rises of 10 mmHg, which could be identified as early as 20 min after surgery, with a maximum of response after 80 min, and a declining IOP from 100 min post-operatively onwards. Pre-treatment with pilocarpine eyedrops could be reduce the laser-mediated IOP rise to less than one fourth. These results recommend a mild miotic for routine pre-treatment for iris laser surgery in order to cope with acute pressure rise as one of the major problems in these procedures.

Cataract Extraction↗

Pseudoexfoliation syndrome as a risk factor for acute ciliary block angle closure glaucoma.

Two patients presented with unilateral ciliary block angle closure glaucoma and bilateral pseudoexfoliation (PSX) syndrome and were treated successfully with posterior sclerotomy (one case), extracapsular cataract extraction and posterior chamber lens implantation. None of the eyes had undergone previous ocular surgery except Nd: YAG-laser iridotomy. Axial lengths as measured with A-scan ultrasonography were 22.48 mm and 24.30 mm. During follow-up of 5 and 12 months, intraocular pressure was well controlled without antiglaucoma medication in both patients. We suspect that the well-known changes of the zonula origin at the ciliary epithelium in PSX syndrome lead to anterior subluxation of the lens with consecutive ciliary block angle closure glaucoma. Ciliary block angle closure glaucoma seems to be another serious complication in PSX syndrome. Therefore, miotics should probably be used with care in PSX eyes with signs of zonular alterations because they may trigger this mechanism.

Aged↗

Diffuse visual field loss and glaucoma.

It is often claimed that general reduction, or diffuse loss, of perimetric sensitivity is an early sign of glaucoma. Our clinical experience and the results of a few other studies led us to believe otherwise. To investigate factors associated with diffuse field loss we reviewed 4222 Humphrey 30-2 threshold tests from 1582 eyes of 862 patients followed at our department. Most of these patients had ocular hypertension or glaucoma. Each field test was evaluated with the Glaucoma Hemifield Test of the Statpac 2 program. The Glaucoma Hemifield Test classifies field test results as within or outside normal limits regarding localized field loss and general shifts in sensitivity. General reduction of sensitivity without concomitant localized loss was found in 117 tests from 81 eyes of 69 patients. Corresponding patient records were found for 60 eyes of 60 patients. Media opacities or miotic therapy were noted in 46 eyes (77%), 10 eyes (17%) had end-stage field loss, and in 2 eyes (3%) other non-glaucomatous ocular pathology explained the diffuse loss of sensitivity. Thus, general reduction of differential light sensitivity as an isolated finding was almost always associated with reasons other than early to moderate glaucoma in this material mainly consisting of patients with glaucoma or increased intraocular pressure. Since only 2 out of the 1582 eyes had general reduction of sensitivity that was not explained by non-glaucomatous reasons, we conclude that purely diffuse field loss was not a sign of glaucoma.

Aged↗