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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.
A mydriatic used for outpatient indirect ophthalmoscopy should produce prompt, maximal, transient mydrasis after a single instillation. Cycloplegia or systemic side effects should be minimal. A solution of tropicamide with phenylephrine hydrochloride seems to achieve this most effectively. In a general retina clinic population, the percentage of pupils dilated, the degree of dilation, and the resistence of the dilation to intense illumination were used to evaluate various concentrations of the drugs. Eight-tenths percent tropicamide with 5% phenylephrine adequately dilated 98.8% of the eyes, among which 25% had dark irides and 9% were receiving miotic therapy. Reduction of the concentration of either component produced less adequate mydriasis; an increase of the tropicamide concentration resulted in a saturated solution with drug precipitate forming on storage and a less adequate dilation. With the optimal combination, 1 drop adequately dilates the general population; 2 drops appear on more effective than 1.
A modified filtering operation for neovascular glaucoma provided control of intraocular pressure after 12 to 23 months in ten of 13 eyes. After long-term follow-up, 23 to 54 months, seven of ten eyes still had controlled IOP. Two eyes were receiving no medication, two required miotics, and three required maximal medical therapy, including carbonic anhydrase inhibitors. One eye had undergone cyclocryotherapy four years after trabeculectomy. Four of seven eyes with diabetic neovascular glaucoma retained ambulatory vision. The eye with neovascular glaucoma from central retinal vein occlusion lost useful vision. The underlying disease process is an important determinant of surviving visual function.
The efficacy of a new nonsteroidal anti-inflammatory agent, suprofen, for reducing pupillary constriction during cataract surgery was ascertained in a double-masked, multicenter, clinical study. Prior to surgery 1.0% suprofen or a placebo was instilled; the surgeon's normal regimen of mydriatics and cycloplegics was used. Suprofen (209 patients) was far more effective than the placebo (203 patients) in maintaining a dilated pupil prior to intraocular lens (IOL) implantation (or instillation of a miotic). The mean pupillary area prior to IOL implantation was 6.3 sq mm larger (20% larger) in patients treated with suprofen than in patients receiving the placebo. The investigators' subjective evaluations of the adequacy of pupil size for IOL implantation and of the difficulty of IOL implantation favored patients treated with suprofen over those receiving the placebo.
Acute elevation of intraocular pressure frequently follows pupillary dilation in patients with primary open angle glaucoma. A retrospective study of 60 patients (116 eyes) with primary open angle glaucoma was done to assess the frequency and severity of intraocular pressure elevation following dilation with 2.5% phenylephrine hydrochloride (Neo-Synephrine) and 1% tropicamide (Mydriacyl). Significant pressure elevation (greater than 5 mm Hg) occurred in 37 eyes (32%). Marked pressure elevation (greater than 10 mm Hg) occurred in 14 eyes (12%). The only significant risk factor found was treatment with miotics. The change of intraocular pressure one hour after dilation was compared with the one-hour postoperative change in intraocular pressure in those patients (12 patients, 18 eyes) who subsequently underwent argon laser trabeculoplasty. No statistically significant correlation was found. There is a potential hazard of routine dilation of eyes with open angle glaucoma.
We analyzed the determinants of serious falls among 489 ambulatory elders aged 65 years and older who received a comprehensive examination at a glaucoma consultation service. For the previous year, at least one fall requiring medical attention or restricted activity was reported by 9.6% (95% confidence interval [CI], 7.0% to 12.2%) of participants. Using logistic regression to adjust for potential confounding variables, the greatest single risk factor for falls was the use of nonmiotic topical eye medications (odds ratio [OR], 5.4; 95% Cl, 1.8 to 16.4). Additional risk factors for falls were female sex (OR, 2.3; 95% Cl, 1.1 to 4.7) and use of cardiac medications (OR, 2.5; 95% Cl, 1.1 to 5.6). Three other characteristics were also associated with the risk of falls: use of miotic eye medications (OR, 3.2; 95% Cl, 1.0 to 10.1); visual field impairment of 40% or greater (OR, 3.0; 95% Cl, 0.94 to 9.8); and use of sedatives (OR, 2.4; 95% Cl, 0.89 to 6.7). These findings suggest that ocular and systemic medications are the major predictors of falls even in this elderly population seeking ophthalmologic care for glaucoma. Medications appear to pose a greater risk for falls than even major visual impairment.
Management of recurring hyphemas associated with posterior chamber intraocular lenses may include a combination of medical, laser, and surgical modalities. Miotic and laser therapies have often failed, and surgical treatment has primarily relied on removal of the offending lens. We describe herein a method for rotation of the intraocular lens that provides an effective means of preventing one form of recurrent intraocular hemorrhage.
OBJECTIVE: To investigate if a pronounced ciliary muscle contraction, induced by physostigmine salicylate, can abolish the ocular hypotensive effect of latanoprost, a prostaglandin analogue, via inhibition of the uveoscleral outflow. DESIGN: A randomized, crossover study that was double-masked for latanoprost. Physostigmine was the second factor in a 2(2) factorial experiment. PARTICIPANTS: A total of 20 male and female healthy volunteers (median age, 25 years; age range, 17-30 years). INTERVENTIONS: Between 7 AM and 7 PM, 1 drop of physostigmine salicylate (8 mg/mL) was instilled in 1 eye every other hour. At 8 AM, 1 drop of either latanoprost (50 mg/L) or placebo was instilled in both eyes. This protocol was repeated a second time with latanoprost administered to previously placebo-treated eyes and vice versa. MAIN OUTCOME MEASURES: Intraocular pressure differences were measured with Goldmann applanation tonometry hourly for 13 hours. RESULTS: Latanoprost reduced the intraocular pressure significantly at 3 to 12 hours after application with a maximal effect at 8 hours after the administration of the dose. The reduction that was obtained with physostigmine administered every other hour was more pronounced, was observed at 1 hour after the administration of the first dose, and increased throughout the day. A significant interaction was seen between 3 and 6 PM (i.e., at 7-10 hours after application of latanoprost). CONCLUSIONS: Latanoprost and physostigmine have a mainly additive ocular hypotensive effect. Thus, high doses of physostigmine did not abolish the eye pressure-lowering effect of latanoprost, but some interaction was seen at low intraocular pressures. It was concluded that any mechanical effect on the uveoscleral flow achieved with physostigmine is short-lasting compared with the effect obtained with latanoprost, and that latanoprost and miotics can be combined.
In nine cases of phencyclidine hydrochloride poisoning, early signs of overdose included drowsiness, nystagmus, miotic pupils, blood pressure elevation, increased deep tendon reflexes, ataxia, anxiety, and agitation. In more severe cases, seizures, spasticity, and opisthotonos were seen in addition to deep coma and respiratory depression. Treatment included removal by emetics or lavage, hydration, and a quiet, reassuring environment. Spasticity, agitation, and ocular manifestions responded to diazepam. Psychiatric intervention was instituted after the patients were stable and no longer agitated.
Specific and sensitive reverse-phase HPLC assays of buprenorphine and its metabolite in biological fluids were developed with sensitivities of 2-6 ng ml-1 using fluorimetric detection. Pharmacokinetics were monitored on acute bolus administration of buprenorphine in 6 dogs within the 0.7-2.6 mg kg-1 dose range. Toxicity was circumvented when terminal plasma concentrations were increased by infusing 3.7-4.8 mg kg-1 doses of buprenorphine over 3 h in six studies in 6 dogs. The terminal rate constants of the IV infusion studies from the triexponential fits of plasma concentration-time data averaged 41.6 +/- 7.5 h with an averaged total body clearance of 191 +/- 19 ml min-1. This terminal rate constant was in contrast to the less than 100 min half-life of the second exponential fitting of the less lipophilic morphine, naloxone, and naltrexone. The apparent volumes of distribution of buprenorphine, referenced to the total plasma concentration, were 33 +/- 61 (Vc, central compartment volume) and 663 +/- 891 (Vd, total body volume), indicative of a highly bound, sequestered or lipophilic drug. Unchanged buprenorphine was insignificantly renally (less than 0.2 per cent of the dose) and biliary (less than 0.6 per cent) excreted. The major route of buprenorphine disposition was by hepatic conjugation to glucuronide which was eliminated into the bile (about 92 per cent) with only small amounts appearing in urine (less than 1 per cent as metabolite). Minor metabolites excreted in the bile accounted for about 3 per cent of the administered dose. Direct IV administration of the metabolite, buprenorphine glucuronide, gave a terminal half-life of 6 h and more than 90 per cent of the systemically circulating metabolite was excreted in bile; only 10 per cent in urine. The oral bioavailability, estimated from the areas under the buprenorphine plasma concentration-time curve following IV and oral administration of buprenorphine in the dogs, was 3-6 per cent. There were no apparent correlations of the buprenorphine time course with cardiovascular parameters such as heart rate, ECG, and blood pressure. Miotic effect was significant. Respiratory depression was observed during the first 4 h after IV bolus injection, but not during the infusion studies.
The levels of acetylmethadol and its active biotransformation products were quantitated in the plasma and urine of subjects on acetylmethadol maintenance by the use of solvent extraction and gas-liquid chromatography. The time-course of plasma acetylmethadol, noracetylmethadol, and dinoracetylmethadol over 48 hr was determined concurrently with the time-action of pupillary constriction in 8 subjects receiving an average oral maintenance dose of 50 mg. The plasma level of acetylmethadol reached a peak at 4 hr and had nearly disappeared by 24 hr. The mean apparent half-life was 7 hr. The plasma level of noracetylmethadol peaked at 4 to 8 hr and slowly declined over the next 40 hr. The mean apparent half-life of noracetylmethadol was 48 hr. Dinoracetylmethadol plasma levels remained relatively constant throughout the dosing interval. The miotic effect reached a peak at 8 hr and decayed at a rate slower than that of plasma elimination of acetylmethadol but more rapidly than that of noracetylmethadol and dinoracetylmethadol. Substantial variation in the plasma levels of the compounds was observed in subjects after the same doses. The study indicated that the relatively long duration of opiate effects of acetylmethadol results from biotransformation to active and persistent metabolites.
The most conspicuous short-term effects of exposure to organophosphates are miotic pupils and a reduced visual field. Two men accidentally exposed to vapors of sarin, a cholinesterase inhibitor and extremely toxic nerve gas, showed these effects but no adverse effects on near- or far-visual acuities, oculomotor functions, intraocular pressure or color vision. However, reports of other accidental exposures to organophosphorus compounds suggest that there are visual and ocular changes, including myopia and decreased visual acuity.
The relationship between morphine plasma concentration and pupil diameter was evaluated 2-10 h following intravenous administration of morphine sulfate (10 mg). Seven healthy male volunteers received 10 mg of morphine intravenously following pretreatment for 4 d with either cimetidine (300 mg po four times a day) or placebo in a single blind, balanced crossover study. Pupil diameters were measured directly from contact prints using calipers and a photographed millimeter scale. Cimetidine pretreatment had no significant effect on pupil size either before or after morphine administration or on morphine pharmacokinetics. The relationship between morphine plasma concentration (2-10 h postdose) and pupil diameter was evaluated from the pooled data from both morphine treatment periods by perpendicular least-square regression. In each individual, a strong relationship existed between morphine plasma concentrations and pupil diameter (r = -0.76 to -0.91; p less than 0.05). Weaker correlations for both pupil diameter (r = -0.65; p less than 0.0001) and the absolute change in pupil diameter from baseline (r = 0.72; p less than 0.0001) for the grouped data probably reflect intersubject variation in morphine sensitivity. Thus, the miotic response to an intravenous dose of morphine varies in proportion to morphine plasma concentration.
Aceclidine can dissociate accommodative and outflow facility responses in monkeys and humans. We sought to determine if different muscarinic receptor subtypes control outflow facility, accommodative and pupillary responses to aceclidine in the living rhesus monkey eye, as a possible basis for this separation. Each eye was cannulated with one branched and one unbranched needle. Baseline measurements (of outflow facility by two-level constant pressure perfusion; refraction by Hartinger coincidence refractometry and pupil diameter by vernier calipers) were recorded after anterior chamber exchange with (one eye) or without (opposite eye), muscarinic receptor subtype antagonist (pirenzepine, AF-DX 116 or 4-DAMP). The eyes were then exchanged a second time with these solutions plus added aceclidine. The response to aceclidine (the differences from baseline) in the presence or absence of antagonist were compared. The M3 muscarinic receptor subtype antagonist 4-DAMP was the most potent inhibitor of all three responses to aceclidine. The dissociation of accommodative, outflow facility and miotic responses to aceclidine in rhesus monkeys does not appear to be due to differences in the muscarinic receptor subtypes that can currently be distinguished pharmacologically.
A long term study was undertaken to evaluate the efficacy of combined guanethidine (1%) and adrenaline (0.05-0.5%) therapy in controlling intra-ocular pressure in 89 patients with chronic open angle glaucoma, in whom ocular tensions proved difficult to control on miotics and/or carbonic anhydrase inhibitors. Visual acuity, fields of vision, applanation tension, size of the pupil, anterior chamber depth and gonioscopic examination of the angle were recorded before and during treatment. The follow-up extended over a period of 12 to 42 months, the mean being 28 months. The combined therapy was found to lower the intra-ocular pressure significantly in a large number of patients and the most potent combination was guanethidine 1% and adrenaline 1/4% and the average fall of intraocular pressure with the combined therapy was around 8 mm Hg. Intolerance to the combined preparation was noticed in three patients during a period of 12-18 months with the symptoms of sore eyes, conjunctival hyperaemia and lid irritation of such severity that the treatment had to be withdrawn. Resistant to treatment developed in four patients during a period of 12-36 months and treatment had to be changed. Addition to guanethidine (1%) and adrenaline up to 1/4% to pilocarpine therapy (2-4%) in eyes with narrow angles did not result in any appreciable change of the width of the angle, the size of the pupil and the depth of the anterior chamber.
Following the first recording of electroretinographic responses in man to a barred pattern by Riggs and associates (1964) in normal and by Lawwill (1973, 1974) in clinical cases, the first striking observation of a complete loss of pattern electroretinogram (PERG) after injurious section of the optic nerve by Groneberg & Teping (1980) has led to the conclusion that the PERG originates from proximal retinal structures different from those responsible for the luminance electroretinogram (LERG). Typical changes of the PERG are seen during branch occlusion of the central retinal artery and vein. In ocular hypertension without visual field loss and glaucoma-related papillary changes the PERG is decreased at intraocular pressures above 26 mm Hg. In cases of primary glaucoma with regulated intraocular tension and without using miotics the amplitude of the PERG reflects the damage to the inner retinal layers. This favorably compares with the P100 latencies of the visual evoked cortical potential (VECP) which in primary glaucoma were partly within, partly outside the normal range. Other retinal diseases showing amplitude changes in the PERG are primary macular dystrophy, diabetic retinopathy, and the acute stage of optic neuritis. In all these cases the Ganzfeld LERG may be normal or nearly normal, whereas the PERG undergoes typical changes. On the contrary a highly preserved PERG can be recorded in cases of retinitis pigmentosa where the electrooculogram light rise and the LERG are already missing. In light of these findings the recording of PERG constitutes a new promising method of clinical electroretinography reflecting the activity of the hitherto omitted innermost retinal layers. It thereby contributes essentially to the location of disturbances within the visual system.
Light does not cause a miotic response in mammals after a topical application of atropine. However, such common sense is based on the pupillary response to visible light. We found ultraviolet (UV) caused slight but evident miosis, even when the patient did not perceive visible light. In order to understand this mechanism further, we conducted in vitro experiments using hamsters. The in vitro hamster iris contracted even when the retina was withdrawn in an incubation solution. The contraction of the hamster pupil caused by visible light was inhibited by procaine, quinacrine, and by the withdrawal of divalent cations, but not by indomethacin, AA861, FPL55712 or autonomic blocking agents. UV-induced miosis was very delayed, continuing after cessation of UV stimuli. Nordihydroguaiaretic acid did not inhibit the miosis induced by UV and/or visible light. The UV-induced miosis was not significantly affected by allopurinol or verapamil, suggesting mechanisms other than neuronal mediation and oxidative stress. This study shows that the isolated hamster iris can react to UV and visible rays. UV-induced miosis is different from the miosis caused by light reflex. To our knowledge, UV-induced miosis has not yet been reported.
The decline in visual function observed in older adults has been attributed to a deterioration in optical quality, decreased neural function, or a combination of both of these factors. One way of separating their contribution is to design a simulation of the optics of the elderly eye and examine its effect on the visual performance of younger observers. The age-related reduction in pupil size was simulated by the administration of an ophthalmic miotic drug, whilst a neutral density filter was included to account for the increased absorption of the ocular media. An optical cell containing a critical concentration of 500 nm diameter polystyrene microspheres in suspension was used to simulate light scatter. The spatiotemporal contrast sensitivity of an older group of observers was then compared with that of a younger group with and without the optical simulation. The contrast sensitivity of the younger group was consistently better than that of the older, and the presence of the optical simulation produced no significant effect on performance. This suggests that, under normal viewing conditions, it is primarily neural factors which underlie the deterioration in visual quality experienced by older observers.