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Volume 117, Issue 1, Pages 175-179 (January 2010)


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Pupillographic Investigation of the Relative Afferent Pupillary Defect Associated with a Midbrain Lesion

Aki Kawasaki, MD1, Neil R. Miller, MD2, Randy Kardon, MD, PhD3Corresponding Author Informationemail address

Received 14 April 2009; received in revised form 1 June 2009; accepted 23 June 2009. published online 17 November 2009.

Objective

To identify clinical and pupillographic features of patients with a relative afferent pupillary defect (RAPD) without visual acuity or visual field loss caused by a lesion in the dorsal midbrain.

Design

Experimental study.

Participants and Controls

Four patients with a dorsal midbrain lesion who had normal visual fields and a clinically detectable RAPD.

Methods

The pupil response from full-field and hemifield light stimulation over a range of light intensities was measured by computerized binocular pupillography.

Main Outcome Measures

The mean of the direct and consensual pupil response to full-field and hemifield light stimulation was plotted as a function of stimulus light intensity.

Results

All 4 subjects showed decreased pupillographic responses at all intensities to full-field light stimulation in the eye with the clinical RAPD. The pupillographic responses to hemifield stimulation showed a homonymous pattern of deficit on the side ipsilateral to the RAPD, similar to that observed in a previously reported patient with an optic tract lesion.

Conclusions

The basis of a midbrain RAPD is the nasal-temporal asymmetry of pupillomotor input that becomes manifest when a unilateral postchiasmal lesion interrupts homonymously paired fibers traveling in the contralateral optic tract or midbrain pathway to the pupillomotor center, respectively. The pupillographic characteristics of an RAPD resulting from a dorsal midbrain lesion thus resemble those of an RAPD resulting from a unilateral optic tract lesion, but without the homonymous visual field defect.

Financial Disclosure(s)

The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Available online: November 17, 2009.

1 Hôpital Ophtalmique Jules Gonin, Lausanne, Switzerland

2 The Wilmer Eye Institute, Johns Hopkins Medical School, Baltimore, Maryland

3 Department of Ophthalmology and Visual Science, University of Iowa and Veterans Administration Hospitals, Iowa City, Iowa

Corresponding Author InformationCorrespondence: Randy Kardon, MD, PhD, 200 Hawkins Drive, Iowa City, IA, 52242

 Manuscript no. 2009-523.

 Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article.

 Supported by a Merit Review and Rehabilitation Award from the Veterans Administration, Washington, DC (RK); and by Research to Prevent Blindness, Inc., New York, New York. Dr Kardon is the recipient of a Lew Wasserman Scholar Award from Research to Prevent Blindness, Inc., and the Pomerantz Chair in Ophthalmology at the University of Iowa and Veterans Administration Hospitals. Dr Kawasaki was supported by the Swiss National Foundation (grant no.: 32 66319.01), Bern, Switzerland.

PII: S0161-6420(09)00699-X

doi:10.1016/j.ophtha.2009.06.053


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