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Two cases are reported in which pupillary pigment occlusion occurred after argon laser iridotomy, reducing visual acuity and preventing fundus visualization. Laser-induced inflammation and subsequent long-term miotic therapy are probably responsible for this complication. Periodic pupillary dilatation is recommended in eyes that require miotics to control their intraocular pressure after laser iridotomy.
Prolonged topical medication causes epidermalization of the conjunctiva in some patients. Loss of the normal conjunctival goblet cells, direct toxic effects on the corneal epithelium, and disturbance of lid function may combine to produce corneal changes which may be misinterpreted and treated with further potentially toxic compounds. Examples of conjunctival changes caused by miotic and non-miotic antiglaucoma therapy, mydriatics, preservatives, and antiviral compounds are presented.
The role displayed by urea (2-10%) solutions, on the miotic and mydriatic activities of pilocarpine hydrochloride and homatropine hydrobromide respectively, was investigated on the human eye. At different concentrations, urea exerts no effect on the miotic activity of pilocarpine, whereas in the case of homatropine a negative effect is experienced. For the parameters, area under pupil diameter--time curve (AUC) and maximum pupillary response (MPR), a linear relationship exists between response to homatropine and urea concentration. However, the dependency is more pronounced in conjunction with the MPR parameter.
A patient with unilateral angle-recession glaucoma had an ipsilateral increased intraocular pressure (IOP) with miotics despite open angles, and decreased IOP with cycloplegics. The following mechanism is proposed to explain these findings: Pilocarpine hydrochloride has been demonstrated experimentally to increase trabecular outflow and decrease uveoscleral outflow. In this eye with a severely compromised and unresponsive trabecular outflow, miotics served to impair uveoscleral outflow and cause a net rise in IOP. Similarly, an increase in uveoscleral outflow with cycloplegics served to decrease IOP. The use of atrophine sulfate in these rate cases may be of therapeutic value in lieu of systemic or surgical therapy.
Previous studies with use of animal models have shown that, for topically applied ophthalmic drugs, the fraction of dose absorbed into the eye is increased as the volume in which the drug is instilled is decreased. Such findings have not previously been confirmed in humans. In the present study, the miotic response to instilled doses of 20 and 50 microL of 0.5% pilocarpine hydrochloride was compared in ten adult human volunteers. Although the 20-microL drop represents a substantial dosage reduction, the miotic response was essentially equivalent to that obtained with the 50-microL drop. These findings imply that, due to the large drainage loss of topically applied ophthalmic drugs, volumes delivered by commerical ophthalmic droppers may in some cases be larger than required to achieve the desired response.
The maintenance of pupil dilation is necessary for the success of scleral buckling procedures and in prophylactic transconjuctival cryopexy. To assess the miotic effect that is induced by cryotherapy and the ability of diclofenac sodium 0.1% (a potent prostaglandin synthetase inhibitor) to overcome such an effect, we conducted a randomized, masked and controlled experiment on 18 rabbits. These were divided into three groups; each group had their eyes treated by cryotherapy in a controlled fashion. Two groups were treated preoperatively with dilating drops: a solution without diclofenac in one group and one with diclofenac drops in the second. Pupil diameters were measured with Castroviejo's calipers by an independent observer at regular intervals. A third group had no drops and were treated as a control. A highly statistical difference was observed in the reduction of the miotic effect of cryotherapy in those eyes treated by diclofenac.
Two men were accidentally exposed to vapors of sarin, a cholinesterase inhibitor and extremely toxic nerve gas. Diagnosis was confirmed by depressed cholinesterase activity, and fixed extremely miotic pupils. No other signs or symptoms developed and neither man required treatment. Recovery to normal cholinesterase activity was gradual over a 90-day period. Pupillary reflexes were not detectable until 11 days after exposure; the miotic pupils dilated slowly over a 30-45 day-period. Eye pain and blurred vision did not occur; visual acuity and amplitude of accommodation were improved for several weeks. Other functions not affected significantly were intraocular pressure, visual fields, color vision, heterophorias, and vergences.
The anticholinesterase agent echothiophate iodide (EI) and the cholinergic agent pilocarpine hydrochloride (pilocarpine), drugs commonly used in glaucoma therapy, cause miosis in rabbits as well as in man. In rabbits the miotic effect decreases after a few days of treatment, a phenomenon possibly due to a drug-induced decrease in the number of muscarinic receptors. However, the muscarinic pupillary contraction caused by stimulation of the retina with light is intact. In this investigation the miosis caused by the doses of EI was found to be very resistant to muscarinic or nerve blockade but inhibited by the substance P (SP) analog [D-Arg1,D-Pro2,D-Trp7,9, Leu11]SP, which seems to be a SP/SPLI blocker in the rabbit pupillary sphincter. Miosis caused by pilocarpine was partly inhibited by muscarinic blockade and partly by the SP blocker. In eyes treated with EI topically twice daily for three weeks, SP or the red pepper extract capsaicin, a releaser of SP-like immunoreactivity (SPLI), had less miotic effect than in control eyes. Capsaicin caused more pronounced miosis in eyes treated with topical pilocarpine for three weeks than in controls. The radioimmunoassay technique did not reveal a significant change in the amount of SPLI in the retinas or iris-ciliary bodies from EI-treated eyes as compared with the controls. It is concluded that, besides cholinergic miosis, EI causes non-muscarinic miosis, probably by release of SP or a related substance and that pilocarpine may have similar effects.
The effects of ruthenium red, an inorganic dye with known capsaicin antagonist properties, was investigated in the rabbit eye. At a dose of 0.24 nmol ruthenium red inhibited the inflammatory effects of capsaicin (1 or 8 nmol). Unexpectedly, when the dye was injected in doses ranging from 0.24 to 7.4 nmol, it caused an inflammatory response with constriction of the pupil (miosis) and a breakdown of the blood-aqueous barrier, leading to a rise intraocular pressure. Tetrodotoxin (30 nmol) inhibited the ruthenium red-induced rise in intraocular pressure but had less effect on the miotic response. The tachykinin antagonist spantide inhibited the miosis but had no effect on the rise in intraocular pressure. Ruthenium red induced an increase in substance P-like immunoreactivity and calcitonin gene-related peptide-like immunoreactivity in the aqueous humor. These levels were positively correlated with the rise in aqueous humor protein concentration. The ruthenium red-induced miosis and, to a less extent, the rise in intraocular pressure were inhibited by the Ca2+ channel-blocking agent omega-conotoxin GVIA (CTX), indicating a partial dependence on an influx of extracellular Ca2+. CTX also attenuated the miotic effect of capsaicin but had no effect on the capsaicin-induced rise in intraocular pressure. It is concluded that, in the rabbit eye, ruthenium red induces a neurogenic inflammatory response besides its capsaicin antagonist effects.
This lecture summarizes studies on the effects of some of the neuropeptides which seem to be present in somatosensory and autonomic nerves in the uvea. Release of these peptides is likely to explain nerve induced effects in the eye which are not due to classical transmitters. Trigeminal nerve fibres in the eye seem to contain substance P (SP), calcitonin gene-related peptide (CGRP), and cholecystokinin (CCK), parasympathetic nerve fibers from the facial nerve seem to contain vasoactive intestinal polypeptide (VIP), and peptide with histidine and isoleucine terminals (PHI), and sympathetic nerves seem to contain neuropeptide Y (NPY). Retrograde trigeminal nerve stimulation in rabbits causes hyperemia, miosis, a breakdown of the blood-aqueous barrier to plasma proteins and a rise in intraocular pressure (IOP). There is release of SP and CGRP or related peptides. The miosis seems to be due to SP and the other effects to CGRP and small amounts of arachidonic acid metabolites released by the peptides. SP has no miotic effect in monkeys and cats. However, CCK is a potent miotic in monkeys and causes contraction of the human pupillary sphincter muscle. It has no such effect in the lower species. The effect of CCK in primates seems to derive from the presence of CCK receptors of the A-type on the pupillary sphincter muscle, and can be blocked by lorglumide. Miosis can be produced in cats by the peptide endothelin; this effect is due to release of arachidonic acid metabolites. Facial nerve stimulation causes vasodilation in the uvea of rabbits, cats and monkeys. The effect cannot be abolished by muscarinic blocking agents.(ABSTRACT TRUNCATED AT 250 WORDS)
In previous studies we have shown that thyrotropin-releasing hormone (TRH) antagonizes many of the neural effects of neurotensin (NT). This study, evaluated the ability of TRH and two TRH analogs: 3 methyl-His-TRH and Phe2-TRH to affect NT-induced miosis in rabbits. In confirmation of previous findings, NT (30 micrograms) produced a significant miosis. The high (60 micrograms), but not the low (30 micrograms) dose of TRH significantly antagonized NT (30 micrograms)-induced miosis. Of interest was the observation that 3 methyl-His-TRH and Phe2-TRH were more effective than native TRH in blocking NT-induced miosis. The inhibitory effect of 3 methyl-His-TRH on the miotic response to NT exhibited long duration (approximately 60 min) when compared to native TRH and Phe2-TRH. TRH or the TRH congeners had no appreciable effects on pupillary diameter when administered alone. These findings indicate that TRH antagonizes the miotic response to NT, and suggest a hitherto undescribed peptide-peptide interaction involved in regulation of iris motility.
Tilidine is an opioid analgesic that has been abused predominantly by the oral route. Studies of parenterally administered tilidine in animals did not clearly indicate a dependence potential of the morphine type. In this study we examined the abuse potential of orally and parenterally administered tilidine in humans. Both orally and intramuscularly given tilidine produced miosis and morphine-like subjective effects in non-dependent subjects. Oral tilidine was 1/8-1/10 as potent and intramuscular tilidine was 1/22 as potent as parenteral morphine in producing morphine-like subjective and miotic effects. Intramuscular tilidine suppressed and did not precipitate signs of abstinence in morphine-dependent subjects. However, intramuscularly given tilidine produced toxic effects not seen with morphine. Meperidine, codeine and d-propoxyphene produced morphine-like subjective and miotic effects, but also produced toxic effects at the highest doses tested. The results suggest that tilidine has a potential to be abused, that this potential is less than that of parenteral morphine and that tilidine is more likely to be abused orally than by the intramuscular route.
INTRODUCTION: News organizations and governmental agencies have reported substantial increases in the number of opioid-related overdose cases in recent years. OBJECTIVE: To describe the utilization of emergency medical services (EMS) for suspected opioid-related overdose cases in a rural state during the period 1997 through 2002. METHODS: Statewide EMS records were reviewed for 1997 through 2002. Data reviewed included prehospital diagnosis and medications given to all patients by prehospital providers. For cases with a prehospital diagnosis of poisoning or overdose, data reviewed included medications given to patients by prehospital providers, pupil size, and respiratory rate. All records were reviewed in a defined sequence. RESULTS: The study period encompassed 1,175,781 patient encounters. Poisoning or overdose patients accounted for 19,808 (1.7%) encounters. Naloxone was administered by the EMS provider to 2,668 (0.2%) patients. For all poisoning or overdose patients, 1,308 (6.6%) had miotic pupils, 450 (2.2%) had a respiratory rate of <12 breaths/min, and 1,569 (7.9%) received naloxone. During the investigation period, total EMS patient encounters increased 25%, while patients with a complaint of poisoning or overdose increased 47%. The incidences of EMS overdose patients with miotic pupils, respiratory rate <10 breaths/min, and naloxone administration increased 167%, 295%, and 154%, respectively. CONCLUSION: In this rural state, prehospital patients with findings suspicious for opioid overdose disproportionately outpaced the growth of all EMS encounters as well as general overdose encounters during the defined investigation period.
PURPOSE: To quantitatively assess pupillary functions after small pupil cataract surgery using the flexible iris retractor. METHODS: Subjects were 11 patients (12 eyes) with small pupils who underwent phacoemulsification and intraocular lens implantation. Pupils were enlarged using the flexible iris retractor intraoperatively, and postoperative iriscorder data were compared with the data of 20 normal controls who underwent standard phacoemulsification and intraocular lens implantation. RESULTS: Although pupillary area before light stimulus did not differ between the groups, contraction rate after light stimulus was significantly lower in the small pupil group than in the normal controls. The velocity of contraction and dilation was also significantly slower in the small pupil group. Wider pupillary stretching during surgery resulted in deteriorated pupillary functions after surgery. Eyes of patients on long-term miotic therapy with pilocarpine showed poorer pupillary reaction postoperatively. CONCLUSION: Inappropriate use of the flexible iris retractor causes an atonic, chronically enlarged postoperative pupil. To avoid postoperative pupillary complications, miotic pupils should not be stretched to larger than a 5.0 x 5.0 mm square.
Anterior surgical approaches to cataracts in juvenile rheumatoid arthritis (JRA) patients are compromised by chronic anterior and posterior uveitis, miotic pupils, and posterior synechiae. The authors retrospectively reviewed the results of pars plana lensectomy and vitrectomy in ten eyes from seven JRA patients with cataracts associated with chronic iridocyclitis and vitritis. Visual acuities improved from 20/100 or worse preoperatively to 20/60 or better postoperatively. Transient postoperative hypotony lasting 1 week to 4 months occurred in four of the ten eyes. Patients with glaucoma continued to require antiglaucoma therapy after surgery. Pars plana lensectomy and vitrectomy provides a theoretically preferrable approach to complicated cataracts and vitritis in JRA patients because it allows removal of peripheral lens material in the presence of a miotic pupil, eliminates the potential for synechiae to the posterior capsule and/or anterior hyaloid, and clears the visual axis of inflammatory debris.
Unlike acquired oculomotor nerve palsy in childhood, the congenital form is usually considered to be an isolated disorder, not associated with other neurologic or systemic disease. In a series of 14 patients with this diagnosis, 10 had associated neurologic disorders. Clinical-neuroradiologic correlation identified the brainstem as the site of the lesion in some patients. The ipsilateral pupil was involved in 12 patients and was miotic with a trace or no reaction to light on the side of the palsy in 8 of the 12 patients. In two of these eight patients, the pupil was documented to be dilated and fixed in early infancy and subsequently became miotic at several months of age, concurrent with emergence of other signs of aberrant reinnervation. Pupillary miosis as a result of aberrant reinnervation appears to be much more frequent after congenital than acquired pupillary-involving oculomotor palsy. Four patients showed better visual acuity in the paretic eye, an unexpected finding. The paretic eye appeared to have a fixational advantage if the patient had nystagmus, presumably due to asymmetric dampening of the nystagmus. Significant anisometropia and astigmatic errors in the paretic eye were present in essentially all patients.
BACKGROUND: This study determines how pupil size, anisocoria, and ambient light influence miotic responses to dilute pilocarpine. The aim is to establish whether mechanical properties of the iris affect miotic behavior using a cholinergic agonist and, if so, to define a more specific clinical definition of supersensitivity testing for suspected tonic pupil disorders. METHODS: The right pupil of 42 normal subjects was first dilated with phenylephrine to create an experimental anisocoria. Then, pilocarpine 0.1% was placed in both eyes. Net constriction of the larger right pupil was determined by subtracting the amount of pilocarpine-induced constriction of the control left pupil from the amount of pilocarpine-induced constriction of the experimental right pupil. Pupil diameters were measured in room light and darkness. RESULTS: In only a few subjects, the larger right pupil became smaller than the left pupil after pilocarpine administration. Net constriction of the right pupil was greater when determined in room light than in darkness. The amount of net constriction of the right pupil showed good correlation with the degree of baseline anisocoria when evaluated in room light, but not so in darkness. CONCLUSION: Pupil size, degree of anisocoria, and light conditions influence the amount of pilocarpine-induced change in anisocoria. If a patient's larger pupil becomes the smaller pupil in darkness after dilute pilocarpine is applied to both eyes, then it is likely that such a response occurred independent of mechanical properties of the iris, and likely represents a supersensitive response. Ophthalmology.
PURPOSE: To examine the positional relations of the iris, lens, ciliary processes, and zonules in eyes with the pigment dispersion syndrome (PDS). METHODS: High-resolution, anterior segment ultrasound biomicroscopy was performed on 16 untreated eyes of 11 patients with PDS. Scanning was repeated on four eyes after miotic treatment and four eyes after laser iridotomy. RESULTS: Mid-peripheral iris concavity could be demonstrated in 56%, irido-zonular contact in 25%, and irido-ciliary process contact in 75% of untreated eyes with PDS. Repeat scanning after laser iridotomy or pilocarpine therapy showed resolution of the iris concavity and irido-zonular contact in all eyes receiving these therapies. Irido-ciliary process contact persisted in some eyes. CONCLUSION: The authors' findings demonstrate the structural relations among the iris, lens, zonules, and ciliary processes in vivo that characterize the PDS. Miotic therapy and laser iridotomy eliminate the iris concavity in all patients with this finding, supporting the hypothesis of reverse pupillary block. Irido-ciliary process contact may be another mechanism causing release of pigment. This issue merits further clinical and histologic study.