[Unilateral mydriasis associated with several areflexias; possible relation to Weill-Reys syndrome; mydriasis, accompanied by various areflexias].
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Humans↗
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Hydroxyamphetamine mydriasis in normal subjects and hydroxyamphetamine mydriasis in Horner's syndrome.
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Horner Syndrome↗
Pharmacological mydriasis and optic disc examination.
AIM: To determine whether pharmacological mydriasis leads to a significant difference in interobserver agreement of optic disc measurement compared with examination without mydriasis. METHOD: A cross sectional study was performed with a pair of observers examining the optic disc of two randomised groups of patients, one group before diagnostic mydriasis, and the other afterwards. Horizontal and vertical disc diameters and cup/disc ratios were measured with a 78 dioptre lens. The study was repeated with another observer pair and two further groups of patients. RESULTS: In study A 86 subjects were examined in total (52 without and 34 with mydriasis). In study B 87 subjects were examined (45 without and 42 with mydriasis). The 95% limits of agreement of the cup/disc ratio measurement differences were significantly larger without mydriasis (p<0.001 for all studies (F test)). For both studies examination after mydriasis gave significantly greater agreement for vertical and horizontal cup/disc ratios. The cases with good agreement (0.1 difference or better) for vertical cup/disc ratios were 37/52 (72%) and 34 /45 (76%) without mydriasis and 33/34 (97%) and 40/42 (95%) respectively with mydriasis. Similar differences were recorded for horizontal cup/disc ratios. Disc diameter measurement results showed similar differences in study A but were not affected by mydriasis in study B. CONCLUSIONS: Examination of the optic disc without pharmacological mydriasis gives significantly poorer interobserver agreement. In this study, the mean 95% limits of agreement values for all cup/disc ratio values were 0.27 for examination without mydriasis and 0.13 for examination with mydriasis. A measure outside these limits would suggest a real difference. This study indicates that mydriasis is important for reproducible clinical examination in glaucoma.
Cross-Sectional Studies↗
Changes in the shape of the anterior and posterior corneal surfaces caused by mydriasis and miosis: detailed analysis.
PURPOSE: To evaluate changes in the anterior and posterior corneal shape, corneal thickness, and anterior chamber depth (ACD) caused by mydriasis or miosis using scanning-slit corneal topography. SETTING: Department of Ophthalmology, Iwate Medical University School of Medicine, Iwate, Morioka, Japan. METHODS: Twenty-eight eyes of 28 healthy volunteers with refractive errors of -6.00 to +0.25 diopters were studied. One eye of each subject had instillation of tropicamide-phenylephrine hydrochloride (Mydrin P) to obtain mydriasis and of pilocarpine hydrochloride 2% (Sanpilo) to obtain miosis. To assess the corneal shape, the best-fit sphere (BFS), axial power, and tangential power were measured for the anterior and posterior corneal surfaces before and after mydriasis and before and after miosis using scanning-slit corneal topography (Orbscan version 3.0, Orbtek, Inc.). The pupil size, corneal thickness, and ACD were also examined before and after mydriasis and before and after miosis. RESULTS: The mean age of the patients was 31.1 years +/- 5.6 (SD) (range 20 to 46 years). The anterior BFS changed from a mean of 8.04 +/- 0.3 mm at the time of mydriasis to a mean of 8.00 +/- 0.3 mm at the time of miosis. The posterior BFS changed from 6.53 +/- 0.3 mm to 6.46 +/- 0.3 mm, respectively. Thus, the anterior and posterior cornea became significantly steeper after miosis (P<.01). The ACD was significantly more shallow after miosis than after mydriasis. However, there was no significant difference in corneal thickness after mydriasis or miosis. CONCLUSIONS: The anterior and posterior corneal shapes changed as a result of mydriasis and miosis, and the refractive power of the cornea significantly increased after miosis. To date, changes in refractive power from changes in pupil size have been attributed to a change in the refractive power of the crystalline lens; however, it is now thought that changes in corneal refractive power also occur.
Adult↗
[The Mydriasert insert: an alternative to eye drops for preangiographic mydriasis].
PURPOSE: Mydriasert is an insoluble ophthalmic insert, gradually releasing two well-known active ingredients: phenylephrine and tropicamide. It is indicated in presurgical mydriasis. The purpose was to evaluate its efficacy in obtaining mydriasis required for fluorescein angiography. MATERIAL AND METHODS: The ability of Mydriasert to provide mydriasis (defined by a pupillary diameter of at least 7 mm) compatible with a bilateral angiographic examination in optimal conditions was evaluated by a comparative, randomised versus active treatment (eye drops) open trial in 72 patients. RESULTS: All the patients obtained a stable mydriasis allowing angiography. In the Mydriasert group, mydriasis preparation required a mean of 10 min more (Student t test: p<0.001); however, near eyesight recovery was 15 min shorter on average (log-rank test<0.01%) and amounts of active ingredients administered to provide mydriasis were 5-10 times higher in the eye drops reference group. Cardiovascular parameters remained in the normal range in both groups. Three patients of the Mydriasert group presented one ocular symptom of local intolerance, which disappeared in 15 min (exact Fisher test not significant between the treatment groups, p=0.2394). No superficial punctate keratitis was detected during the trial. CONCLUSION: The treatment by Mydriasert can prepare preangiographic mydriasis as well as the reference treatment. The time required for mydriasis is slightly longer. Near eyesight recovery, faster with Mydriasert, could provide an improvement in patient safety and comfort at the end of the ophthalmologic visit.
Angiography↗
Comparison of the effects of clonidine on tyramine- and methoxamine-evoked mydriasis in man.
1. It has been reported previously that clonidine can potentiate tyramine-evoked mydriasis on the pain-free side of cluster headache patients. We examined whether a single oral dose of clonidine (200 micrograms) can also potentiate tyramine-evoked mydriasis in healthy subjects, using mydriasis to methoxamine, a directly acting sympathomimetic amine, as a control. 2. Eight healthy male volunteers participated in four weekly sessions. In the first two sessions (Experiment 1) the effect of clonidine or placebo on the mydriasis to tyramine hydrochloride eyedrops (75 mM; 2 x 10 microliters), and in the last two sessions (Experiment 2) the effect of clonidine or placebo on the mydriasis to methoxamine hydrochloride eyedrops (20 mM; 2 x 10 microliters) was examined. In both experiments subjects were allocated to drugs and sessions according to a double-blind balanced design. In both experiments, pupil diameter of both the treated and the untreated eyes was recorded in standard ambient light and in the dark, before, and 2 h after clonidine/placebo, via binocular infrared television pupillometry. Salivation (dental roll technique), systolic and diastolic blood pressure (sitting), heart rate, and self-ratings of mood and feelings (visual analogue scales), were also measured before, and 2 h after the ingestion of clonidine or placebo. 3. Both tyramine and methoxamine produced a significant mydriasis, which was more prominent in the light condition (change in resting pupil size; mm +/- s.e.mean: tyramine/light 1.05 +/- 0.28; tyramine/dark: 0.73 +/- 0.15; methoxamine/light: 1.65 +/- 0.28; methoxamine/dark: 0.85 +/- 0.15). Clonidine produced a significant miosis in the untreated eye which was more prominent in the light condition (change in resting pupil size; mm +/- s.e.mean: Experiment 1, light: -1.34 +/- 0.19; Experiment 1, dark: -0.46 +/- 0.1; Experiment 2, light -0.97 +/- 0.18; Experiment 2, dark: -0.29 +/- 0.17). Clonidine had no significant effect on either tyramine- or methoxamine-evoked mydriasis. 4. In agreement with previous reports, clonidine significantly reduced salivation (g, mean +/- s.e.mean; Experiment 1: -0.84 +/- 0.22; Experiment 2: -0.55 +/- 0.11), systolic blood pressure (mm Hg; Experiment 1: -17.5 +/- 3.76; Experiment 2: -23.38 +/- 4.67), diastolic blood pressure (mm Hg; Experiment 2: -12.38 +/- 2.05), alertness (mm; Experiment 2: -24.19 +/- 5.40), and anxiety (mm; Experiment 1: -13.82 +/- 4.60), indicating the presence of pharmacodynamically effective tissue levels of the drug. 5. These results show that a single oral dose (200 micrograms) of clonidine causes significant miosis in human subjects, and fails to potentiate tyramine-evoked mydriasis. This indicates that the pupil on the asymptomatic side of cluster headache patients is affected differently from the pupils of healthy volunteers by tyramine and/or clonidine.
Adolescent↗
Mediation of mydriasis in conscious rats by central postsynaptic alpha 2-adrenoceptors.
The alpha 2-adrenoceptor agonist, clonidine (0.001-1 mg/kg, IP), dose-dependently induced mydriasis in conscious rats (ED50 0.088 mg/kg). This response was maximal when measured 10 min after clonidine injection and was of about 30-min duration. The noradrenaline releasing agent, methamphetamine (0.75 mg/kg, IP), also increased pupil diameter. Clonidine (0.03 mg/kg, IP)-induced mydriasis was inhibited in a dose-related fashion by the alpha 2-adrenoceptor antagonists, idazoxan (0.03-3 mg/kg, IP) and yohimbine (0.03-3 mg/kg, IP), but was unaltered by the alpha 1- or beta-adrenergic antagonists, prazosin (1 and 3 mg/kg, IP) or pindolol (1 and 3 mg/kg, IP). Methamphetamine (0.75 mg/kg, IP)-induced mydriasis was similarly inhibited by idazoxan (1 mg/kg, IP) and yohimbine (1 mg/kg, IP). These data argued strongly that central alpha 2-adrenoceptors are involved in the mediation of mydriasis. The synaptic location of these receptors was determined using DSP-4 (50 mg/kg x 2, IP) to lesion noradrenergic neurones: this produced a 64% depletion of noradrenaline in the midbrain (containing the Edinger-Westphal nucleus responsible for mydriasis) and reduced the mydriatic effect of methamphetamine (0.75 mg/kg, IP) to a similar extent (72%), whereas clonidine mydriasis remained unaltered. Therefore, these results show that the mydriasis responses induced by either clonidine or methamphetamine are mediated by central postsynaptic alpha 2-adrenoceptors.
Adrenergic Agents↗
Alpha2-adrenoceptors do not mediate reflex mydriasis in rabbits.
The aim of this study was to identify receptors that mediate reflex mydriasis in pentobarbital-anesthetized rabbits, in which the cervical sympathetic nerve was sectioned unilaterally. Voltage-response curves of pupillary dilation were generated bilaterally by stimulation of the sciatic nerve. Evoked mydriatic responses were mediated mainly by efferent parasympathetic innervation, and, to a lesser extent, by sympathetic innervation. The alpha-adrenergic antagonist, phenoxybenzamine (0.3 mg/kg, intravenously (i.v.)), antagonized mydriasis of the neurally intact eye, but not that on the sympathectomized side. The alpha2-adrenergic antagonist, RS 79948 (0.3 mg/kg, i.v.), potentiated mydriasis of the normal eye, but was without either a potentiating or inhibitory effect on the mydriasis of the sympathectomized eye. In addition, the dopamine-receptor antagonist, haloperidol (1 mg/kg, i.v.), inhibited evoked mydriasis of the sympathectomized eye. These results suggest that, unlike some other species (cats and rats), alpha2-adrenoceptors do not mediate reflex mydriasis elicited by sciatic-nerve stimulation in the rabbit, and support the previous finding in humans that dopamine receptors may mediate this response.
Adrenergic alpha-2 Receptor Antagonists↗
Clonidine-induced hypoactivity and mydriasis in mice are respectively mediated via pre- and postsynaptic alpha 2-adrenoceptors in the brain.
Since brain alpha 2-adrenoceptors occur both pre- and postsynaptically, experiments were carried out to determine the synaptic locations of those receptors mediating clonidine-induced hypoactivity and mydriasis. Intraperitoneal (i.p.) injection of clonidine (1-3000 micrograms/kg) to mice dose dependently induced these two responses and also decreased brain concentrations of 3-methoxy-4-hydroxyphenylglycol (MHPG). The ED50 values were: 120 micrograms/kg for hypoactivity (95% confidence limits 103-140 micrograms/kg), 54 micrograms/kg for mydriasis (95% confidence limits 40-74 micrograms/kg) and 18 micrograms/kg for MHPG reduction (95% confidence limits 8-36 micrograms/kg) suggesting that these responses could all be presynaptically mediated. However, methamphetamine which increases noradrenaline turnover was found to dose dependently produce mydriasis, but not hypoactivity, after peripheral (0.1-5 mg/kg i.p.) or central (0.5-10 micrograms i.c.v.) injection. The mydriasis produced by methamphetamine (0.5 mg/kg i.p.) was abolished by i.c.v. injection of 1 micrograms idazoxan or yohimbine, but not 2.5 micrograms prazosin or pindolol, showing this effect was mediated by central alpha 2-adrenoceptors. Methamphetamine (1-10 micrograms i.c.v.) potentiated the mydriasis induced by clonidine (50 micrograms/kg i.p.) suggesting this was a postsynaptic alpha 2-adrenoceptor response. By contrast, methamphetamine (1-10 micrograms i.c.v.) dose dependently reversed clonidine (100 micrograms/kg i.p.) hypoactivity indicating this response was mediated by presynaptic alpha 2-adrenoceptors. These hypotheses were confirmed by destruction of noradrenergic neurones using DSP-4 (100 mg/kg i.p. x 2). This treatment prevented the mydriasis response to methamphetamine (0.5 mg/kg i.p.), but not clonidine (100 micrograms/kg i.p.) and markedly attenuated clonidine (100 micrograms/kg i.p.) hypoactivity.
Animals↗
Effect of mydriasis on visual field area in retinitis pigmentosa.
PURPOSE: The effect of mydriasis on Goldmann visual field area in patients with retinitis pigmentosa has not been suitably defined. The aim of this study is to determine whether visual field area in these patients varies with pharmacologic mydriasis. METHODS: Fifteen adult patients with retinitis pigmentosa were studied prospectively. Goldmann visual fields with II4e and V4e isopters were obtained in both eyes before and after full pharmacologic mydriasis of the right eye. The isopter areas were quantified and analyzed to determine the effect of mydriasis on visual field area. RESULTS: The difference in the right eye isopter areas was compared with the difference in the left eye isopter areas using paired t tests, where the differences were computed from areas obtained before and after dilation of the right eye. Mydriasis had no significant effect on the visual field in terms of isopter area difference (II4e, P = 0.87; V4e, P = 0.45) and percent change in isopter area (II4e, P = 0.81; V4e, P = 0.24). CONCLUSION: Pharmacologic mydriasis had no appreciable effect on the Goldmann visual field area in a selected group of patients with retinitis pigmentosa. These findings suggest that visual fields of such patients obtained in the dilated or undilated state can be meaningfully compared.
Adult↗
[Efficacy and efficiency of preoperative mydriasis: drops versus ocular insert].
OBJECTIVE: The primary objective of this study was to compare eye drops and inserts in terms of the quality of preoperative mydriasis. The secondary objective was to evaluate the safety and ease of use of each modality. PATIENTS AND METHODS: Prospective randomized and simple blinded study. Patients were randomized into two groups: the insert protocol (atropine 1%, diclofenac 0.1% collyrium and Mydriasert) or the eye drop protocol (atropine 1%, diclofenac 0.1%, tropicamide 0.5%, and phenylephrine 10% collyrium). Fifty-one patients were included: 25 in the insert protocol and 26 in the drop protocol. Mydriasis quality was evaluated by nurses and surgeons. The ease of use was estimated by the number of gestures required to obtain mydriasis and the difficulties encountered. Safety was evaluated at the patient's bedside. RESULTS: Mydriasis of at least 6 mm was obtained in 92% of the patients in the insert protocol (23/25) and 85% of the patients in the drop protocol (22/26) (NS). Four patients lost their insert during the study. Of the patients in the insert group, 16% (4/25) experienced stinging in their eyes, as did 23% (6/26) of patients in the group using drops (NS). To reach effective mydriasis, the insert protocol required fewer nurse gestures per patient than the drop protocol (3.0 versus 8.3; p<0.001). CONCLUSION: With the protocol using an insert, preoperative mydriasis is not inferior to that obtained with drops only and is more efficient in terms of nurse time and number of gestures. Nurses should be trained in appropriate handling of the insert and avoiding the loss of the device.
Humans↗
Pilocarpine mydriasis in mice.
In several rodent species pilocarpine and oxotremorine produce mydriasis, rather than the miosis which is characteristic of most other species. We have established that pilocarpine is a mydriatic drug in mice, a species in which the action has previously not been described, and that this effect occurs after local ocular, intraperitoneal (IP) or intracerebroventricular (ICV) application. Arecoline produces miosis or mydriasis (depending on dose) following direct ocular application but mild mydriasis after IP or ICV injection. Atropine also produces mydriasis in mice, and the effect of pilocarpine is additive with that produced by atropine and is not antagonized by antihistamines. Direct ICV pilocarpine injection produces mydriasis at doses equivalent to those used systemically. Pilocarpine mydriasis probably results from inhibition of parasympathetic activity.
Animals↗
Rat clonidine mydriasis model: imidazoline receptors are not involved.
The clonidine mydriasis model in rats has been widely applied in preclinical research to characterize alpha(2)-adrenoceptor antagonistic properties of drugs. The present study was undertaken to pharmacologically determine if imidazoline I(1) receptors are also involved in this model system. Sigmoid dose-response curves for pupillary dilation were produced in pentobarbital anesthetized rats by intravenous administration of increasing doses of agonists (guanabenz for alpha(2)-adrenoceptors, clonidine for both alpha(2)-adrenoceptors and imidazoline I(1) receptors, and rilmenidine for imidazoline I(1) receptors). Two antagonists (RS 79948 for alpha(2)-adrenoceptors and efaroxan for imidazoline I(1) receptors) were used to antagonize the mydriasis elicited by those three agonists, with antagonistic potencies calculated. In additional experiments, we examined the effect of the selective imidazoline I(1) receptor antagonist, AGN 192403, on clonidine-induced mydriasis. The results showed that pupillary response curves elicited by guanabenz, clonidine and rilmenidine were competitively antagonized by both RS 79948 (0.03-1 mg/kg) and efaroxan (0.03-1 mg/kg) in a dose-related fashion. The potencies of either antagonist against the three agonists were not significantly different. AGN 192403 (5 mg/kg) did not significantly shift the clonidine mydriasis curve. These results suggest that imidazoline I(1) receptors are not functionally involved in the rat clonidine mydriasis model and support this in vivo system as a useful model for studies of alpha(2)-adrenoceptors.
Adrenergic alpha-Agonists↗
Histamine H3 receptor-mediated inhibition of sympathetically evoked mydriasis in rats.
This study was designed to determine if the histamine H3 receptor agonist R-alpha-methylhistamine would play a role in modulation of sympathetically evoked mydriasis in anesthetized rats, and if so, to ascertain the specific receptor subtype(s) involved. Reproducible frequency-response curves of pupillary dilation were generated by stimulation of the cervical preganglionic sympathetic nerve (1-32 Hz). Systemic administration of R-alpha-methylhistamine (0.3-3.0 mg kg(-1)) produced a dose-related inhibition of the evoked mydriasis. The greatest inhibition was seen at lower frequency levels, with about 43% depression observed at 2 Hz. The specific histamine H3 receptor antagonist, clobenpropit (3.0 mg kg(-1), i.v.), blocked the inhibitory effect of R-alpha-methylhistamine, whereas neither the histamine H2 receptor antagonist, cimetidine (5.0 mg kg(-1), i.v.), nor the histamine H1 receptor antagonist, chlorpheniramine (0.5 mg kg(-1), i.v.), was effective. The histamine H2 receptor agonist, dimaprit (10 mg kg(-1), i.v.), was also without effect on the evoked mydriasis. R-alpha-methylhistamine (3.0 mg kg(-1)) did not inhibit phenylephrine-induced mydriasis. These results support the conclusion that R-alpha-methylhistamine produces inhibition of sympathetically evoked mydriasis via histamine H3 receptor stimulation, presumably by an action on presynaptic histamine H3 receptors.
Animals↗
Clonidine produces mydriasis in conscious mice by activating central alpha 2-adrenoceptors.
Intraperitoneal (i.p.) injection of the alpha 2-adrenoceptor agonist clonidine (1-3000 micrograms/kg) produced dose-dependent pupil dilatation in conscious C57/Bl/6 mice with an ED50 of 54 micrograms/kg (95% confidence limits 40-74 micrograms/kg). This response was rapid in onset and of approximately 30 min duration. The alpha 2-adrenoceptor antagonists idazoxan (1 or 3 mg/kg i.p.) and yohimbine (1 or 3 mg/kg i.p.) both produced dose-related miosis, but the alpha 1- and beta-adrenoceptor antagonists prazosin (1 or 3 mg/kg i.p.) and pindolol (1 or 3 mg/kg i.p.) were without effect. These doses of idazoxan and yohimbine potently reversed the mydriasis induced by clonidine (100 micrograms/kg i.p.), while prazosin and pindolol were again ineffective. Clonidine-induced mydriasis was also unaltered by the 5-HT antagonists, methysergide (2.5 mg/kg i.p.) and ketanserin (0.1 mg/kg i.p.) or 0.1 mg/kg i.p. of the dopamine antagonists, haloperidol, SCH 23390 and BRL 34778. A dose of 0.25 microgram clonidine, which was ineffective when administered i.p., produced marked mydriasis after intracerebroventricular (i.c.v.) injection. In addition, the mydriasis produced by i.p. injection of clonidine (100 micrograms/kg) was abolished by i.c.v. dosing of 2.5 micrograms idazoxan or yohimbine, but again not by prazosin or pindolol. Together, these data provide strong evidence to indicate that clonidine-induced mydriasis is exclusively mediated via central alpha 2-adrenoceptors and that this response provides a useful model for studying the function of these receptors.
Adrenergic alpha-Agonists↗
The effect of mydriasis from phenylephrine on corneal shape.
PURPOSE: A previous study reported that pharmacologically-dilated pupils changed the corneal shape. Researchers used mydriatic agents with significant cycloplegic effect. The current study investigates the effect of mydriasis on corneal shape using phenylephrine alone, where phenylephrine has minimal effect on the accommodative system and whether corneal topography can be done after pupil dilation. METHODS: Forty-four young healthy subjects with one eye randomly selected for mydriasis were used in this study. Twenty-two received one drop of 2.5% phenylephrine (group 1); the other 22 subjects had one drop of 0.4% benoxinate instilled prior to the application of 2.5% phenylephrine (group 2). They were matched for age and refractive error. Anterior chamber depth, pupil size and corneal parameters were compared before and after mydriasis. The corneal parameters included best-fit sphere (BFS), surface asymmetry index (SAI), surface regularity index (SRI) and the axial and tangential powers in the form of flattest and steepest powers, and in the form of M, J(0), and J(45) vector presentation. RESULTS: Group 1 and group 2 subjects had similar pre-mydriatic baseline ocular parameters. The mean (+/- SD) pupil dilation was 1.24 +/- 0.59 mm for group 1 and 1.80 +/- 0.95 mm for group 2. The dilation was significantly larger in group 2 (unpaired t-tests: t = 2.36, p = 0.02). There were no significant changes in corneal parameters from mydriasis in either group. CONCLUSIONS: Previous investigations used mydriatic agents, which affected not only the pupil size but also accommodation. The current study found that mydriasis from phenylephrine, with minimal effect on accommodation, did not result in significant corneal alteration, and corneal topography can be measured after pupil dilation with phenylephrine.
Adult↗
alpha 2-Adrenoceptor agonists induced mydriasis in the rat by an action within the central nervous system.
1 The effects of intravenous administration of the selective alpha 2-adrenoceptor agonists clonidine, UK 14,304 and guanoxabenz on rat pupil diameter were investigated. 2 In rats anaesthetized with pentobarbitone, each agonist produced a marked dose-related increase in pupil diameter; the rank order of potency was: clonidine greater than UK 14,304 greater than guanoxabenz. 3 Pretreatment with the selective alpha 2-adrenoceptor antagonist, RX 781094 (0.5 mg/kg, i.v.), produced a parallel 30-40 fold shift to the right of the dose-pupil dilator response curves for the three agonists. Yohimbine (1.5 mg/kg, i.v.) produced about a 10 fold rightward shift of the dose-response curve for guanoxabenz. In contrast, the alpha 1-selective antagonist, prazosin (0.5 mg/kg, i.v.), failed to affect the dose-response relation for guanoxabenz. 4 Several antagonists of varying selectivities towards alpha 1- and alpha 2-adrenoceptors were tested for their ability to reverse the maximal mydriasis induced by guanoxabenz (0.3 mg/kg, i.v.). The rank order of potency of the antagonists producing a 50% reversal of this effect was: RX 781094 greater than yohimbine greater than piperoxan = rauwolscine greater than mianserin greater than RS 21361. Neither corynanthine nor prazosin reversed the guanoxabenz-induced mydriasis. 5 Topical application of RX 781094 (0.1 to 3% w/v solutions) onto one eye produced a slow reversal of guanoxabenz-induced mydriasis; the time course and degree of reversal were virtually the same in both eyes. 6 Intracerebroventricular administration of RX 781094 (1.25-15 micrograms total dose) caused a rapid dose-related reversal of the maximal mydriasis induced by guanoxabenz (0.3 mg/kg, i.v.). 7 Guanoxabenz (0.3 and 1.0 mg/kg, i.v.) did not produce any dilation of the physostigmine-constricted undamaged pupil of the pithed rat. Intravenous adrenaline was found to produce a small mydriatic effect, while atropine completely antagonized the effects of physostigmine in this preparation. 8 These results indicate that alpha 2-adrenoceptor agonists induce mydriasis in the rat through a central alpha 2-adrenoceptor mechanism. However, the site of action within the central nervous system remains to be determined.
Adrenergic alpha-Agonists↗
Effect of mydriasis and different field strategies on digital image screening of diabetic eye disease.
AIMS: To assess the effects of (1) mydriasis and (2) single versus three field photography on screening for diabetic eye disease using digital photography METHOD: Slit lamp examination findings were compared to digital fundal photographs for the detection of any retinopathy and for referable retinopathy in 398 patients (794 eyes). A Topcon TRC-NW6S digital non-mydriatic fundus camera was used. Three photographic strategies were used: undilated single field, dilated single field, and dilated multiple fields. The photographs were presented in random order to one of two retinal screeners. For the single field photographs the screeners were masked to the use of mydriatics. In 13% of fundal photographs, grading was performed by both, rather than just one grader. RESULTS: Mydriasis reduced the proportion of ungradable photographs from 26% to 5% (p<0.001). Neither mydriasis nor three field photography improved the sensitivity or specificity for the detection of any retinopathy or of referable retinopathy when compared with undilated single field photography. The sensitivity and specificity for detecting referable retinopathy using undilated single field photography was 77% (95% CI 71 to 84) and 95 % (95% CI 93 to 97) respectively. Using dilated single field photography the figures were 81% (95% CI 76 to 87) and 92% (95% CI 90 to 94) respectively. Using dilated three field photography the figures were 83% (95% CI 78 to 88) and 93% (95% CI 91 to 96) respectively. Intergrader reliability for the detection of referable retinopathy in gradable photographs was excellent (Kappa values 0.86-1.00). CONCLUSIONS: Mydriasis reduces the technical failure rate. Mydriasis and the three field photography as used in this study do not increase the sensitivity or specificity of detecting diabetic retinopathy.
Adolescent↗