Efficacy of apraclonidine 0.5% in the diagnosis of Horner syndrome in pediatric patients under low or high illumination

PURPOSE: To evaluate the efficacy and safety of apraclonidine 0.5% in the diagnosis of Horner syndrome in pediatric patients. DESIGN: Prospective, interventional case series. METHODS: Ten pediatric patients with a diagnosis of Horner syndrome and 10 age-matched controls with physiologic anisocoria underwent pharmacological testing with apraclonidine. The difference between the pupil diameters of both eyes under low (room light off) and high (room light on) ambient illumination before and one hour after apraclonidine was instilled was recorded. Any adverse effects during the examination or reported by the patient's parents were recorded. RESULTS: The mean differences in pupil diameters before and after apraclonidine testing in the Horner syndrome group were -2.05 mm and 0.97 mm, respectively, under low illumination (P = .0049) and -1.48 mm and 1.1 mm, respectively, under high illumination (P = .0051). Three patients with Horner syndrome showed positive values (reversal of anisocoria) only under high ambient illumination, but not under low illumination. There was no statistical difference in the mean differences in pupil diameter before and after apraclonidine testing in the control group. Conjunctival hyperemia was noted in two patients with Horner syndrome and in three patients in the control group. No systemic adverse effects were noted during the examination or were reported by patients' parents. CONCLUSIONS: The application of apraclonidine in pediatric patients is safe and effective in the diagnosis of Horner syndrome. The reversal of anisocoria was more obvious under high (room light on) ambient illumination.     

False negative apraclonidine test in two patients with Horner syndrome

BACKGROUND: Because of denervation supersensitivity, a miotic pupil in a sympathetically-denervated eye dilates in response to a dilute or weak alpha-1-agonist drug. A reversal of anisocoria after topical apraclonidine is considered as a positive test result that diagnoses a unilateral Horner syndrome. HISTORY AND SIGNS: Two women aged 34 and 46 years with a cocaine-confirmed oculosympathetic defect (Horner syndrome) were tested with 1 % topical apraclonidine on separate days. THERAPY AND OUTCOME: In one patient, her miotic Horner pupil dilated marginally but not enough to reverse the baseline anisocoria. Additionally, the upper lid on the same side retracted. There was no discernable effect of apraclonidine on the normal, contralateral eye. In the second patient, there was no pupillary response to apraclonidine but there was resolution of her ptosis. CONCLUSIONS: Neither patient demonstrated a reversal of anisocoria, the current criterion for diagnosing a Horner syndrome using apraclonidine. Thus, these two patients with an established oculosympathetic defect were said to have a "negative test" for Horner syndrome. Yet both women showed subtle pupil and/or lid changes in response to apraclonidine that were consistent with sympathetic denervation supersensitivity. Reversal of anisocoria following topical apraclonidine does not occur in all patients with a unilateral oculosympathetic defect and more specific parameters for defining a positive test result might optimize apraclonidine's utility as a diagnostic test for Horner syndrome.     

Use of 0.5% apraclonidine solution in evaluation of blepharoptosis

PURPOSE: To evaluate the effect of instillation of a specific alpha2-adrenergic agonist, topical 0.5% apraclonidine solution, on upper eyelid position in patients with blepharoptosis. METHODS: This study included 45 eyelids of 35 adult patients with blepharoptosis. Of these, 37 eyelids had acquired ptosis and 8 had congenital ptosis. Palpebral fissure height and margin-reflex distance in the upper eyelid were measured before and after instillation of 0.5% apraclonidine, 2.5% phenylephrine, and both drugs. RESULTS: After instillation of 2.5% phenylephrine, 0.5% apraclonidine, and both drugs, the mean increases in palpebral fissure height were 2.12 mm+/-1.4 mm, 2.11 mm+/-1.4 mm, and 2.26 mm+/-1.3 mm, respectively, and the mean increases in margin-reflex distance were 1.93 mm+/-1.2 mm, 1.89 mm+/-1.3 mm, and 2.03 mm+/-1.2 mm, respectively (p=0.86 and p=0.85). The apraclonidine solution did not alter the test results in 14 eyelids in which the phenylephrine test results were negative. CONCLUSIONS: Topical 0.5% apraclonidine solution can be as effective as topical 2.5% phenylephrine in elevating a ptotic upper eyelid, and may be used for preoperative evaluation of blepharoptosis. Combined use of both drugs may not provide any additional benefit.     

Comparing efficacies of 0.5% apraclonidine with 4% cocaine in the diagnosis of horner syndrome in pediatric patients.

PURPOSE: The aim of this study was to compare the efficacy of 0.5% apraclonidine with that of 4% cocaine and to evaluate its safety in the diagnosis of Horner syndrome in pediatric patients. METHODS: This was a randomized, crossover study, wherein 10 patients with a probable diagnosis of Horner syndrome were assigned to undergo pharmacological testing with 4% cocaine and 0.5% apaconidine. The difference in the pupil diameters of each eye was recorded under dim light before and 1 h after 0.5% apraclonidine or 4% cocaine was instilled. Any adverse effects were noted during examination or reported by the patients' parents were recorded. RESULTS: The mean differences in pupil diameter before and after 4% cocaine testing were -2.08 and -2.97 mm, respectively (P = 0.0047). All patients had an anisocoria greater than 1 mm after 4% cocaine testing. The mean difference in pupil diameter before and after 0.5% apraclonidine was instilled were -2.04 and +1.08 mm, respectively (P = 0.005). All patients showed a reversal of anisocoria after 0.5% apraclonidine testing. Conjunctival hyperemia was noted in 2 patients, but systemic adverse effects were not noted during examination nor reported by the patients' parents. CONCLUSIONS: The application of 0.5% apraclonidine in pediatric patients is safe and effective in the diagnosis of Horner syndrome.     

Adverse effects of apraclonidine used in the diagnosis of Horner syndrome in infants.

Apraclonidine, a selective alpha(2)-agonist, was developed to lower intraocular pressure and minimize the systemic side effects associated with the use of its parent drug, clonidine.(1) An investigation of the site of action of apraclonidine incidentally uncovered a reversal of anisocoria in patients with absent sympathetic innervation of one pupil (Horner syndrome) due to its alpha(1)-effect on a pupil with denervation supersensitivity.(2) It has been used as a diagnostic test for Horner syndrome.(3,4) We report adverse effects of topical apraclonidine when used in the diagnosis of Horner syndrome in infants.     

Effects of 0.5% apraclonidine on optic nerve head and peripapillary retinal blood flow

AIMS—To examine the effects of 0.5% apraclonidine on optic nerve head (ONH) and peripapillary retinal blood flow by scanning laser Doppler flowmetry (SLDF).
METHODS—ONH and peripapillary retinal blood flow of 17 healthy subjects were measured by SLDF before and 1 hour and 3 hours after unilateral administration of 0.5% apraclonidine. The fellow eyes were treated with balanced salt solution and the examiners were masked as to which eye was treated with apraclonidine. On each occasion, three scans were obtained and haemodynamic variables (volume, flow, and velocity) were analysed at eight locations, four in the neural rim and four in the peripapillary retina, avoiding ophthalmoscopically visible vessels. The statistical significance of changes from the baseline value of variables and the differences in the measured quantities between apraclonidine treated eyes and fellow eyes at each time point were evaluated using Wilcoxon signed rank test.
RESULTS—The intraocular pressure was reduced significantly in apraclonidine treated eyes by 15.0% (p=0.001) at 1 hour and 30.0% (p=0.000) at 3 hours after administration. In the volume, flow, or velocity of ONH and peripapillary retinal blood flow, there were no significant changes from the baseline values at 1 hour and 3 hours after apraclonidine administration in either apraclonidine treated eyes (p >0.4) or fellow eyes (p >0.2). Also, no significant differences were found in the measured quantities between apraclonidine treated eyes and fellow eyes at each time point (p >0.1).
CONCLUSION—A single dose of topical apraclonidine 0.5% in healthy subjects does not have adverse effects on the ONH and peripapillary retinal blood flow.

     

The sensitivity and specificity of 0.5% apraclonidine in the diagnosis of oculosympathetic paresis

AIMS: To evaluate the sensitivity and specificity of 0.5% apraclonidine test in the diagnosis of oculosympathetic paresis (OSP). METHOD: Apraclonidine (0.5%) was administered to 31 eyes, nine with a diagnosis of Horner syndrome (HS), 22 with bilateral OSP caused by diabetes, and to 54 control eyes. All were confirmed with the cocaine test. The effects on pupil diameter and upper eyelid level were observed 1 hour later. RESULTS: Apraclonidine caused a mean dilation of 2.04 mm (range 1--4.5) (p<0.001) in the pupils with OSP and it caused pupillary constriction in the control eyes with a mean change of -0.14 mm (range 0.5 to --1) (p<0.05). It caused reversal of anisocoria in all HS cases. Its effects on both pupil diameters and upper lid levels differed significantly between the groups (p<0.001). The mean elevation in the upper lid was 1.75 mm (range 1--4) in the OSP group (p<0.001) and 0.61 mm (range 0--3) in the control group (p<0.001). CONCLUSION: The effect of the apraclonidine (0.5%) test on the pupil diameter was diagnostic for OSP and had at least the same sensitivity and specificity as the cocaine test for the diagnosis of OSP.     

Traumatic ptosis and mydriasis masking Horner syndrome from an internal carotid pseudoaneurysm

A 46-year-old woman presented after blunt facial trauma for evaluation of bilateral orbital floor fractures, which were confirmed by clinical and radiographic examination. In addition, findings of right traumatic mydriasis and left traumatic ptosis were seen. On close investigation, miosis was noted on the side of the traumatic ptosis. Therefore, a workup for Horner syndrome was obtained, including neuro-ophthalmic consultation and magnetic resonance angiography of the neck. The magnetic resonance angiography showed an internal carotid pseudoaneurysm, an uncommon but potentially fatal complication of blunt carotid injury. The authors describe an interesting case where a life-threatening diagnosis was nearly masked by more common, benign pathology.     

Brimonidine 0.2% versus apraclonidine 0.5% for prevention of intraocular pressure elevations after anterior segment laser surgery

OBJECTIVE: To compare the efficacy of brimonidine 0.2% with apraclonidine 0.5% in preventing intraocular pressure (IOP) elevations after anterior segment laser surgery. DESIGN: Double-masked, randomized clinical trial. PARTICIPANTS: Sixty-six patients underwent either laser peripheral iridotomy, argon laser trabeculoplasty, or neodymium:yttrium-aluminum-garnet laser capsulotomy. INTERVENTION: Eyes received either one drop of brimonidine 0.2% or apraclonidine 0.5% before laser surgery. MAIN OUTCOME MEASURES: Intraocular pressure, heart rate, and blood pressure were measured before laser surgery and at 1 hour, 3 hours, 24 hours, and 1 week after laser surgery. RESULTS: Before the laser treatment, 33 patients (50.0%) received brimonidine 0.2% and 33 patients (50.0%) received apraclonidine 0.5%. Eight of 33 patients (24.2%) in the brimonidine-treated group and 9 of 33 patients (27.3%) in the apraclonidine group had postoperative IOP increases of 5 mmHg or more. This was not statistically different (P = 0.80). By the time of last follow-up examination, 3 of 33 patients (9.1%) in the brimonidine-treated group and 3 of 33 patients (9.1%) in the apraclonidine group had IOP increases of 10 mmHg or more. This was also not statistically different (P > or = 0.95). The mean IOP reduction from baseline in the brimonidine group (-2.8 +/- 2.8 mmHg) was not statistically different (P = 0.55) compared with the mean IOP reduction in the apraclonidine group (-3.6 +/- 3.3 mmHg). There were no statistically significant changes in mean heart rate or blood pressure in either group except for a slight reduction in diastolic blood pressure at 1 hour (P = 0.005) in the brimonidine group (-5.2 +/- 7.4 mmHg) compared with the apraclonidine group (-0.2 +/- 6.4 mmHg). There were no clinically significant side effects noted in either group. CONCLUSIONS: A single preoperative drop of brimonidine 0.2% is as effective as apraclonidine 0.5% in preventing IOP elevation immediately after anterior segment laser surgery.     

Brimonidine 0.15% versus apraclonidine 0.5% for prevention of intraocular pressure elevation after anterior segment laser surgery

PURPOSE: To compare the efficacy and safety of brimonidine 0.15% with those of apraclonidine 0.5% in preventing intraocular pressure (IOP) elevations after anterior segment laser surgery. SETTING: Massachusetts Eye and Ear Infirmary, Glaucoma Service, Boston, Massachusetts, USA. METHODS: This double-masked randomized trial 80 eyes of 80 patients who had laser peripheral iridotomy, argon laser trabeculoplasty, or neodymium:YAG laser capsulotomy. Eyes received 1 drop of brimonidine 0.15% or apraclonidine 0.5% before laser surgery. Intraocular pressure, heart rate, and blood pressure were measured before laser surgery and at 1 hour, 3 hours, 24 hours, and 1 week after laser surgery. RESULTS: Before laser treatment, 41 patients received brimonidine 0.15% and 39 received apraclonidine 0.5%. Thirteen (31.7%) patients in the brimonidine group and 11 (28.2%) in the apraclonidine group had postoperative IOP elevations of 5 mm Hg or more (P = .5). Four patients (9.8%) in the brimonidine group and 3 (7.7%) in the apraclonidine group had IOP increases of 10 mm Hg or more (P = .5). There were no statistically significant changes in mean heart rate or blood pressure in either group except a slight reduction in diastolic blood pressure at 1 hour in the brimonidine group (-4.7 +/- 9.2 mm Hg) compared with that in the apraclonidine group (-0.1 +/- 9.1 mm Hg) (P = .01). No clinically significant side effects were noted in either group. CONCLUSION: A single preoperative drop of brimonidine 0.15% had similar efficacy and safety as apraclonidine 0.5% in preventing IOP elevations immediately after anterior segment laser surgery.     

Brinzolamide 1% versus apraclonidine 0.5% to prevent intraocular pressure elevation after neodymium:YAG laser posterior capsulotomy

PURPOSE: To compare the efficacy of brinzolamide 1% with that of apraclonidine 0.5% in preventing intraocular pressure (IOP) rise after neodymium:YAG (Nd:YAG) laser posterior capsulotomy. SETTING: Department of Ophthalmology, Akdeniz University, Antalya, Turkey. METHODS: One hundred fifteen patients who had Nd:YAG laser posterior capsulotomy for posterior capsule opacification were prospectively randomized to receive brinzolamide 1% (57 patients) or apraclonidine 0.5% (58 patients) approximately 1 hour before laser surgery. A masked observer measured IOP by Goldmann applanation tonometry before treatment and after treatment at 1, 2, and 3 hours and 7 days. RESULTS: The mean IOP changes from baseline were not statistically different between the study groups at 1, 2, and 3 hours and 7 days (P =.109, P = .764, P =.275, and P =.879, respectively). The incidence of IOP elevation of 5 mm Hg or higher was 12.2% (7 of 57 eyes) in the brinzolamide group and 10.3% (6 of 58 eyes) in the apraclonidine group (P = .743); IOP elevations of 10 mm Hg and greater occurred in 3.5% (2 of 57 eyes) and 1.7% (1 of 58 eyes) (P = .618), respectively. There were no IOP elevations greater than 20 mm Hg in either group. CONCLUSION: Brinzolamide 1% and apraclonidine 0.5% given prophylactically before Nd:YAG laser capsulotomy were effective in preventing IOP spikes after treatment.     

Reversal of intraocular pressure increases with 0.5% apraclonidine after dilated fundus examination in patients with chronic open-angle glaucoma.

BACKGROUND: Apraclonidine 1.0% has been shown to reverse the potential intraocular pressure (IOP) increase after pupil dilation IOP increases in patients with chronic open-angle glaucoma. However, it is only approved for preventing IOP spikes after laser surgery. The purpose of this study is to determine the effectiveness of 0.5% apraclonidine in reversing IOP increases after pupillary dilation in patients with chronic open-angle glaucoma. METHODS: Twenty-two patients with chronic open-angle glaucoma were found to have an increase in post-dilation IOP of at least 4 mmHg from pre-dilated levels (baseline) in both eyes. IOP was measured 1 hour after dilation, after which two drops of 0.5% apraclonidine were instilled in one eye and the IOP was remeasured 15 minutes later in both eyes. Instillation of 0.5% apraclonidine in one eye was continued every 15 minutes and IOP was measured 15 minutes after each instillation, until the pressure returned to baseline levels. RESULTS: The IOP of the initially treated eye of all 22 patients returned to within levels clinically insignificant from baseline IOP within 90 minutes. By comparison, the IOP of the control group (untreated eye) remained elevated. Once the initial treatment eye returned to baseline levels, the control group was then treated with 0.5% apraclonidine, resulting in a lowering effect of the IOP in similar fashion to the initial treated group. CONCLUSIONS: Apraclonidine 0.5% appears to be effective in reduction of post-dilated IOP increases in patients with chronic open-angle glaucoma.