March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
Development Of Pupillary Adrenergic Supersensitivity After Pharmacologic Induction Of Oculosympathetic Defect
Author Affiliations & Notes
  • Christopher A. Kirkpatrick
    University of Iowa Carver College of Medicine, Iowa City, Iowa
  • Randy H. Kardon
    Ophthalmology and Visual Sciences, University of Iowa, Iowa City, Iowa
  • Footnotes
    Commercial Relationships  Christopher A. Kirkpatrick, None; Randy H. Kardon, Consultant for Novartis (C), Steering committee for OCTiMS multicenter trial (C)
  • Footnotes
    Support  Department of Veterans Affairs Center for the Prevention and Treatment of Visual Loss, the Pomerantz Family Chair Endowment, and the Mintzer Family Research Fund in Ophthalmology
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 4899. doi:
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      Christopher A. Kirkpatrick, Randy H. Kardon; Development Of Pupillary Adrenergic Supersensitivity After Pharmacologic Induction Of Oculosympathetic Defect. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4899.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Interruption of oculosympathetic nerve activity induces the development of adrenergic supersensitivity of end-organs. Evidence suggests that this receptor upregulation takes 3-5 days after denervation, but some report as few as 36 hours. Brimonidine is a selective alpha-2 agonist and will produce a pharmacologic oculosympathetic deficit by inhibiting presynaptic sympathetic neurotransmitter release. Apraclonidine is an alpha-2 agonist with weak alpha-1 agonistic properties that will manifest if end-organ supersensitivity is present. This study seeks to investigate the time course for development of adrenergic supersensitivity by monitoring pupil size in response to apraclonidine after the induction of a pharmacologic oculosympathetic defect using brimonidine.

Methods: : In this cohort study, 10 healthy subjects were prospectively studied by administering one drop of 0.2% brimonidine to the right eye twice daily for 5 days to induce a unilateral oculosympathetic defect. The left eye was used as a control. Adrenergic supersensitivity was assessed by measuring the pupillary response of both eyes to one drop of 0.5% apraclonidine daily.

Results: : 9 of 10 subjects developed an anisocoria 2 days after initiation of unilateral brimonidine that persisted throughout all study days. This anisocoria was reversed in 8 of 9 subjects by the third study day, 45 minutes after administration of one drop of apraclonidine bilaterally. 1 subject never developed an anisocoria with daily brimonidine dosing and 1 subject had a baseline dilation reaction to apraclonidine and could not be included in analysis.

Conclusions: : The results of this study suggest that detectable adrenergic supersensitivity of end-organs develops in as few as 48 hours from the onset of the functional sympathetic denervation, induced in normal subjects with brimondine, and that apraclonidine can be utilized as a diagnostic aid for detecting oculosympathetic defects in an acute setting of 48 hours from onset.

Keywords: pupil • receptors: pharmacology/physiology • neuro-ophthalmology: diagnosis 

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