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PubMed1979

Mechanism of morphine-induced mydriasis in the cat.

Neurons that increased their firing rate in response to light stimulation were recorded from the pretectal region and the anterior oculomotor nucleus of sedated immobilized cats while morphine (2 mg/kg iv) was administered. The dose produced mydriasis and an increase in spontaneous firing rate of all light-sensitive neurons recorded from the anterior oculomotor nucleus. This suggested that morphine did not produce mydriasis through inhibition of the third nerve. Phenoxybenzamine, iv or topically, antagonized the mydriasis, indicating a peripheral source of sympathetic input as the basis for morphine-induced mydriasis. Morphine (2 mg/kg iv), administered 1 h after adrenalectomy, produced miosis and increased the spontaneous firing rate of light-sensitive neurons recorded from the oculomotor nucleus. These observations suggest that, in the cat, although morphine activates the oculomotor neurons to produce miosis, the effect is masked by the morphine-induced release of catecholamines, mainly from the adrenal glands, which produced mydriasis.

Action Potentials↗

PubMed1990

Comparison of prednisolone acetate and indomethacin for maintaining mydriasis during cataract surgery.

Preoperative topical nonsteroidal anti-inflammatory drugs such as flurbiprofen and indomethacin have been found to maintain mydriasis during cataract surgery. Steroidal anti-inflammatory drugs are commonly used to treat postoperative inflammation, but their effect on the maintenance of intraoperative mydriasis is unknown. Forty-six patients admitted for elective cataract surgery were randomly assigned to one of three treatment groups and received 1% prednisolone acetate, 1% indomethacin or artificial tears four times before surgery, in addition to standardized preoperative dilating drops and intraoperative epinephrine. Pupillary diameter was measured and the time interval noted five times during the surgery. During surgery the indomethacin group lost significantly less mydriasis than the control group. The mydriasis losses of the prednisolone acetate group were between those of the indomethacin and control groups, but these differences did not reach significance. We conclude that prednisolone acetate is less effective than indomethacin for maintaining mydriasis during cataract surgery.

Adult↗

PubMed1994

Unilateral mydriasis after induction of anaesthesia.

Unilateral mydriasis is a disturbing finding during anaesthesia and may indicate serious neurological injury. In addition, the assessment of abnormal neurological findings is limited during general anaesthesia, and therefore requires special consideration. I report finding a dilated right pupil (7 mm, nonreactive to light) after bronchoscopic tracheal intubation and induction of general anaesthesia in a frail, 74-yr-old woman with cervical subluxations and spinal cord impingement. The possible aetiology of the unilateral mydriasis includes the effects of anaesthetic agents, stellate ganglion block, impaired venous return from the head and neck, acute intracranial mass lesion or an haemorrhagic event, direct eye trauma, pre-existing medical or surgical conditions, and inadvertent direct deposition of alpha-adrenergic or anticholinergic agents in the eye. Consideration of these factors, the autonomic innervation of the eye, and an intraoperative "wake-up" test allowed satisfactory neurological assessment in this patient and surgery to proceed. Unilateral mydriasis, while unusual, may be seen during general anaesthesia and requires thorough knowledge of autonomic nerve pathways and pharmacology of the eye for correct diagnosis. In this case, mydriasis was considered to result from phenylephrine/lidocaine spray which was used to provide topical anaesthesia to the airway.

Aged↗

PubMed2003

[Mydriasis not reacting to light during an uneventful esophagectomy--drug-related side effect of Akrinor?].

We present a 72 year old patient who underwent an esophagectomy uneventfully. At the end of the procedure the anaesthetist diagnosed a mydriasis not reacting to light. The mydriasis lasted for 3 hours. 30 minutes after diagnosis a cranial computed tomography scan showed no abnormalities. The tracheal tube was removed after 16 h of artificial ventilation, the patient was awake and responded to questions. The neurological examination was normal, as well as the control CT scan. With regard to a mydriasis the following differential diagnosis have to be considered: cerebral ischemia, cerebral hematoma, metabolic encephalopathy, shock, and a drug side effect. We state that an alpha-mimetic effect of the drug mixture Akrinor, the patient had received shortly before diagnosis of the mydriasis, is the most likely explanation. One 2 mls syringe contents of 200 mg norephedrine-ethyl-theophylline and 10 mg noradrenaline-ethyl-theophylline.

Aged↗

PubMed1993

Amaurotic mydriasis.

Amaurotic mydriasis is characterized by larger than normal pupils in patients with visual loss. In sought to establish whether amaurotic mydriasis can reliably identify different kinds of visual loss and whether this static measurement might prove useful in discerning "balanced" bilateral optic neuropathies where no relative afferent pupillary defect (RAPD) is detected. Patients with binocular pregeniculate visual loss, patients with balanced binocular pregeniculate loss without RAPD, and patients with monocular pregeniculate visual loss had significantly larger pupils than age-matched controls. Although pupils of patients with binocular pregeniculate visual loss (20/50 or better in one or both eyes) were significantly smaller than pupils of age-matched patients with binocular pregeniculate deficits of worse than 20/50 in one or both eyes, no such correlation between Snellen visual acuity and amaurotic mydriasis was found in patients with monocular pregeniculate visual loss. Amaurotic mydriasis is a clinically useful phenomenon that may identify pregeniculate disease in the absence of a RAPD or distinguish pregeniculate from postgeniculate visual loss.

Blindness↗

PubMed1999

[Clinical use of mydriasis with 10% phenylephrine and its antagonism by 0.5% dapiprazole].

BACKGROUND: Dapiprazole hydrochloride is an alpha-1-adrenergic inhibitor that anticipates the mydriatic effect of phenylephrine in dilator muscle receptors in a competitive way. The aim of this study was to determine for which indications for mydriasis pupil dilation by phenylephrine alone is sufficient and if the reversal by dapiprazole is convenient and the practical. MATERIAL AND METHOD: In 286 eyes of 147 outpatients, the pupil was dilated for fluorescein angiography-FLA (100 eyes of 50 patients), examination of the fundus-Fd (99 eyes of 52 patients), central argon laser coagulation-cALC) (64 eyes of 32 patients), peripheral argon laser coagulation-pALC (16 eyes of 9 patients) and Nd:YAG capsulotomy (7 eyes of 4 patients) with phenylephrine 10% eyes drops, followed by reversal by dapiprazole 0.5%. The width and mobility of the pupil were tested at intervals of 10 min. When mydriasis by phenylephrine was insufficient, tropicamide was applied additionally. RESULTS: In 98% of FLA with scanning laser ophthalmoscope, 75% of cALC, 76% of Fd, 62% FLA with fundus camera and 38% of pALC, mydriasis could be reached that was sufficient for the indication. Diabetics showed significantly more sluggish pupil mobility (t1/2: P < 0.05 mydriasis, P < 0.005 reversal). The mean duration after using dapiprazole until reaching the starting value (+/- 1 mm) of the pupil was 44.3 +/- 26.3 min. In 86% of the examined eyes, the pupil reached its starting value within 1 h. The subjective degree of satisfaction with the application of dapiprazole was "satisfied" to "very satisfied" (5.4 +/- 1.4 points on a scale from 1 to 7 points). DISCUSSION AND CONCLUSION: In fundus examination, fluorescein angiography by a laser scanner, diagnostic retinal examination and central laser coagulation, the combination phenylephrine/dapiprazole was most suitable. In our opinion, the combination is less suitable for peripheral argon laser coagulation and fluorescein angiography using a fundus camera.

Adolescent↗

PubMed1979

Clonidine mydriasis in the rat.

Pupillary responses to clonidine (3--100 micrograms/kg, i.v.) and epinephrine (1--30 micrograms/kg, i.v.) were observed in anesthetized rats. Clonidine caused a dose-dependent mydriasis which was effectively antagonized by pretreatment with yohimbine (1.5 mg/kg, i.v.). Pretreatment with phentolamine (5 mg/kg, i.v.) was less effective in antagonizing this clonidine-induced mydriasis. Phenoxybenzamine (2 mg/kg, i.v.) was almost without effect. In contrast, both phentolamine and phenoxybenzamine blocked the pupillary dilation produced by epinephrine while yohimbine pretreatment resulted in no antagonism of epinephrine-induced mydriasis. These results suggest that clonidine-induced mydriasis in the rat is mediated by a central adrenergic inhibitory mechanism.

Adrenergic alpha-Antagonists↗

PubMed1982

Central and peripheral components of morphine mydriasis in mice.

Mice treated with morphine (intracerebroventricularly, retrobulbarly or intraperitoneally) demonstrated dose related bilateral mydriasis. Intracerebroventricular (ICV) injection was much more potent than either retrobulbar (RB) or intraperitoneal (IP) injections. Morphine applied topically onto one eye resulted in bilateral mydriasis which was more marked in the treated eye. The mydriatic effect was antagonized by naloxone administered either IP or ICV or given on one eye. Here again, ICV naloxone was most effective. Naloxone eye drops diminished the mydriasis produced by systemic morphine bilaterally but more in the treated eye. These results suggest that in mice the mydriasis produced by morphine is mainly of central origin, but a local ocular effect also occurs.

Animals↗

PubMed1976

Effective degree of mydriasis with phenylephrine and tropicamide.

The mydriatic effects of several concentrations of phenylephrine and of tropicamide were studied in 84 young adults for 90 min following topical instillation. Pupillary diameter was estimated (a) under ambient photopic illumination and (b) when illumination was increased to that associated with direct ophthalmoscopy. Evaluation was made of the "degree of mydriasis," i.e., the difference in pupillary diameter between the eye receiving the mydriatic agent and the contralateral control eye when the pupillary light reflex was stimulated. In subjects with light or hazel irides, phenylephrine caused maximal dilatation in 60 to 75 min, mean values being 5.6 mm with 1 drop of 2%, 6.0 mm with 2 drops of 2.5%, and 7.1 mm with 1 drop of 10%. Maxiumum degrees of mydriasis were 3.0 mm with 2 drops of 2.5% and 3.1 mm with 1 drop of 10%. With 0.5% tropicamide, maximum diameter was 8.0 mm in 30 min in subjects with light, hazel, or brown irides, and the maximum degree of mydriasis was 5.0 mm. It is concluded that when a mydriatic agent is used to facilitate intraocular visualization, neither specification in terms of (a) maximum diameter under ambient illumination nor (b) degree of mydriasis provides optimal characterization. It is suggested that the "clinically effective diameter," i.e., pupillary diameter under illumination corresponding to that to be used during examination, would be the most useful specification.

Adaptation, Ocular↗

PubMed1981

Xylazine-induced mydriasis in rats and its antagonism by alpha-adrenergic blocking agents.

Pupillary response to xylazine (10-300 micrograms/kg, i.v.) norepinephrine (1-30 micrograms/kg. i.v.) and atropine (3-100 micrograms/kg, i.v.) were observed in rats anaesthetized with pentobarbital. Xylazine caused a dose-dependent mydriasis which was antagonized by a selective alpha 2-adrenergic blocking agent, yohimbine (2.5 mg/kg, i.v.). was less effective in antagonizing this effect of xylazine. A selective alpha 1-adrenergic blocking agent, prazosin (2.5 mg/kg, i.v.) was ineffective in reducing the xylazine-induced mydriasis. In contrast, both phentolamine and prazosin blocked the pupillary dilation produced by norepinephrine, while yohimbine was much less effective in antagonizing norepinephrine-induced mydriasis. Atropine also induced a dose-dependent mydriasis which was not affected by yohimbine pretreatment. The present study suggests that the mydriatic effect of xylazine in the rat is mediated by an adrenergic mechanism, possibly by stimulating the alpha 2-adrenergic receptors in the iris and CNS.

Adrenergic alpha-Antagonists↗

PubMed1981

Xylazine-induced mydriasis: possible involvement of a central postsynaptic regulation of parasympathetic tone.

Intravenous injection of xylazine (0.01-1 mg/kg) produced a dose-dependent mydriasis associated with a depression of tonic ciliary nerve activity in anesthetized cats. Xylazine-induced mydriasis was apparent in the sympathectomized iris but was absent in the parasympathectomized, physostigmine-treated iris. Epinephrine (30 micrograms/kg, i.v.) produced a slightly greater mydriasis in the sympathectomized iris than in the parasympathectomized, physostigmine-treated iris. The alpha 2-adrenergic blocking agent, yohimbine (0.5 mg/kg, i.v.) antagonized the pupillary dilation and reversed the depression of ciliary nerve activity induced by xylazine administration. In rats pretreated with reserpine (7.5 mg/kg, s.c., 20 h) and alpha-methyl-p-tyrosine (250 mg/kg, i.p., 5 h), intravenous injection of xylazine (0.01-1 mg/kg) resulted in mydriasis of similar magnitude as control animals. However, xylazine induced bradycardia in the control group but not in the pretreated animals. The results suggest that pupillary dilation produced by i.v. xylazine is primarily the result of a central inhibition of parasympathetic tone to the iris. It also appears that xylazine produces this effect via postsynaptic alpha 2-adrenergic mechanisms, while it produces bradycardia through a presynaptic alpha 2-adrenergic mechanism.

Animals↗

PubMed1981

Role of sympathetic system in morphine-induced mydriasis in rat.

The effects of three doses (5, 30, and 60 mg/kg) of morphine on pupillary diameter (PD) were studied in rats that were either normal, neurotransmitter antagonist pretreated, guanethidine pretreated, cervical sympathectomized, or adrenalectomized. Morphine produced a dose-dependent increase in PD and exophthalmos. In addition, the PD concurrently underwent fluctuations. alpha-Adrenergic antagonists blocked both mydriasis and exophthalmos, whereas a beta-adrenergic antagonist had no significant effect. This suggested a role for the sympathetic nervous system. However, cervical sympathectomy or guanethidine pretreatment only partially blocked the increase in PD or exophthalmos. Adrenalectomy also partially blocked the mydriasis and exophthalmos. Adrenalectomy combined with guanethidine pretreatment completely blocked morphine-induced mydriasis but no exophthalmos. Thus, the results suggest that both direct sympathetic innervation and hormonal action from the adrenals are involved in morphine-induced mydriasis in the rat.

Adrenalectomy↗

PubMed1989

[Aqueous flare and cells after mydriasis in normal human eyes].

The influence of mydriasis on aqueous flare intensity and cell number was investigated in normal human eyes. A mixture of 0.5% phenylephrine and 0.5% tropicamide (Mydrin P) was topically instilled in 173 eyes of normal subjects ranging from 20 to 79 years old, and measurements with a laser flare-cell meter were carried out before and 1 hour after the application. For statistical analysis, subjects were divided into groups based on ten-year age intervals ranging from 20-29 years to 70-79 years. Aqueous flare intensity was significantly decreased by mydriasis in all age groups. Prior to drug application, aqueous cells were observed in none of the cases, while after mydriasis, apparent aqueous floaters appeared in 9.2% of the cases, all of whom were over 40 years of age. Appearance of aqueous floaters following mydriasis was not accompanied by an increase in aqueous flare intensity. Time course of changes in aqueous flare intensity after topical instillation of 5% phenylephrine and 0.4% tropicamide were investigated separately. Tropicamide decreased aqueous flare intensity in normal young human subjects, and values at 1 and 1.5 hours post-application differed significantly from those of the contralateral control eyes. The instillation of phenylephrine in normal young subjects resulted in a significant decrease of aqueous flare at 3 hours post-application. Observed decreases in aqueous flare intensity by a commonly used mydriatic agent, a combined solution of phenylephrine and tropicamide, was considered to be the result of the pharmacological effects of tropicamide.

Adult↗

PubMed1997

Risk of acute angle-closure glaucoma after diagnostic mydriasis in nonselected subjects: the Rotterdam Study.

PURPOSE: To report the prevalence of narrow anterior chamber angles on slit-lamp examination and the incidence of acute angle-closure glaucoma (AACG) after diagnostic mydriasis in nonselected white subjects aged 55 years and over. METHODS: Of all subjects in the population-based Rotterdam Study (n = 7983), 6760 participated in the ophthalmologic examination and received both tropicamide 0.5% and phenylephrine 5% eye drops for diagnostic mydriasis. No exclusion criteria (e.g., level of intraocular pressure, presence of narrow anterior chamber angles, history of or treatment for glaucoma) were used. After the ophthalmologic examination, all participants received thymoxamine 0.5% drops in both eyes and were warned about the symptoms of AACG. RESULTS: The prevalence of narrow angles was 2.2% and was twice as high in women. In two subjects (0.03%), an attack of AACG developed in one eye after diagnostic mydriasis. After medical therapy, peripheral iridotomies were made with a Nd:YAG laser, and both eyes healed without loss of visual acuity or visual field. CONCLUSIONS: In nonselected white subjects of 55 years of age or older, the 2% prevalence of narrow anterior chamber angles is similar to that in a mixed black and white population in the United States. According to our protocol, 3 in 10,000 subjects are likely to develop AACG after diagnostic mydriasis followed by miotic drops.

Acute Disease↗

PubMed1993

Reversible mydriasis during strabismus surgery in children.

A study was made of changes in pupil diameter during strabismus surgery performed on 84 children aged from 1 to 12 years. Several factors influencing the appearance of reversible changes in pupil diameter during surgery were examined. The pupil diameters of both eyes were inspected during the course of the operation, and the reactions of manipulated eyes were compared to those of the non-manipulated eyes. Two types of general anesthesia were used, inhalation anesthesia and combined intravenous-inhalation anesthesia, depending upon the patient's body weight. Patient's age and sex, type of anesthesia, surgical procedure and the manipulated eye muscles were documented. The study demonstrated that mydriasis did not occur in patients operated under combined intravenous-inhalation anesthesia, while 74% of those operated solely under inhalation anesthesia developed mydriasis. This mydriasis only occurred during surgical manipulation of the eye muscles. The amount of traction on the other muscles, and the depth of anesthesia were not related to pupil diameter.

Age Factors↗

PubMed1996

8-OH-DPAT-induced mydriasis in mice: a pharmacological characterisation.

8-Hydroxy(di-n-propylamino)tetralin (8-OH-DPAT; 0.1-50 mg/kg i.p.) evoked a dose-dependent mydriatic response in conscious mice (ED50 = 5.8 mg/kg i.p.) which was maximal after 10 min. 8-OH-DPAT (2 mg/kg i.p.)-induced mydriasis was attenuated by the alpha 2-adrenoceptor antagonists, idazoxan (1 and 3 mg/kg i.p.) and yohimbine (1 and 3 mg/kg i.p.), by the 5-HT1 receptor antagonists, pindolol (10 mg/kg i.p.) and quipazine (2 mg/kg i.p.), and by the selective 5-HT1A receptor antagonist, (-)-N-tert-butyl-3-[4-(2-methoxyphenyl)piperazin-1-yl]-2-phenyl propionamide ((-)-WAY 100135; 1-10 mg/kg s.c.). These data argue that both central alpha 2-adrenoceptors and 5-HT1A receptors are involved in the mediation of mydriasis induced by 8-OH-DPAT. The synaptic location of these receptors was determined using either N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4; 100 mg/kg i.p.) or 5,7-dihydroxytryptamine (5,7-DHT; 75 micrograms i.c.v.)+p-chlorophenylalanine (PCPA; 200 mg/kg i.p.); these lesioning procedures respectively produced highly significant losses of whole brain noradrenaline (72% depletion) and 5-HT (78% depletion). The former abolished 8-OH-DPAT (5 mg/kg i.p. (ED50)) mydriasis, whereas the latter was without effect. 8-OH-DPAT (0.5-5 mg/kg i.p.) also dose-dependently increased the noradrenaline metabolite, 3-methoxy-4-hydroxy-phenylglycol (MHPG), in mouse whole brain minus cerebellum. Taken together these results show that 8-OH-DPAT initially stimulates 5-HT1A receptors, and it is likely that this is followed by release of noradrenaline onto postsynaptic alpha 2-adrenoceptors, the latter effect being responsible for the mydriatic response.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1995

Benign episodic unilateral mydriasis. Clinical characteristics.

PURPOSE: To describe the clinical features of the syndrome of neurologically isolated episodic unilateral mydriasis. METHODS: Information was obtained by reviewing the case records of 24 patients evaluated by the author and collected by polling other neuro-ophthalmologists. RESULTS: Nineteen patients were women. The median age was 31 years. Fourteen patients had migraines. The median interval between onset of events and evaluation was 6 months. The median duration and frequency of events were 12 hours and two to three per month, respectively. Most patients did not identify any factor that could precipitate an occurrence. The most common associated symptoms during an episode included visual blur in 15 patients, headache in 9, and orbital pain in 5. Eleven patients were examined during an attack. Three patients who were examined had impaired near vision, four had impaired accommodative function, and six had an anisocoria that increased with added ambient light. None of these patients had a tonic pupil or cholinergic agonist-induced pharmacologic mydriasis. Five other patients examined during an attack had normal vision and unimpaired direct light reactivity of their large pupil. No neurologic disorder was identified after neurodiagnostic testing, clinical evaluation, and natural history observation. CONCLUSIONS: The syndrome of idiopathic episodic unilateral mydriasis probably comprises a heterogeneous group of conditions that result in parasympathetic insufficiency of the iris sphincter in some patients, and sympathetic hyperactivity of the iris dilator in others. Patients with episodes similar in characteristics to the ones described in this survey appear to have a benign neurologic prognosis, and do not require further neurodiagnostic studies.

Adolescent↗

PubMed2000

Mydriasis and glaucoma: exploding the myth. A systematic review.

AIMS: To investigate the risk of inducing acute glaucoma following mydriasis. METHODS: Systematic review of published research 1933-1999. RESULTS: The risk of inducing acute glaucoma following mydriasis with tropicamide alone is close to zero, no case being identified. The risk with long-acting or combined agents is between 1 in 3,380 and 1 in 20,000. The presence of chronic glaucoma constitutes no additional risk. CONCLUSIONS: Mydriasis with tropicamide alone is safe even in people with chronic glaucoma. It should be advised in all patients when thorough retinal examination is indicated.

Glaucoma↗