Optometry Research Today is a free monthly online journal that collates and summarizes the latest research about Optometry, including details on myopia, optometric practice, therapy.

The influence of adaptation on visual motion detection in chronic sixth nerve palsy after treatment with botulinum toxin.

Shallo-Hoffmann J, Acheson J, Bentley C, Bronstein AM

Graduate Studies Program, College of Optometry, Nova Southeastern University, Fort Lauderdale, FL 33328-2018, USA. shoffman@nsu.nova.edu

PURPOSE: To investigate changes in visual motion perception after treatment with botulinum toxin in patients with unilateral chronic lateral rectus muscle palsy. METHODS: Five patients and control subjects were asked to report the perceived drift direction of a sinusoidal grating that was initially stationary and then began to accelerate at 0.09 degrees /sec2 in a horizontal direction. The grating had a field size of 18.5 degrees and was presented monocularly with a contrast just above threshold for visibility for central vision. Both the paretic and non-affected eyes were tested. Psychophysical testing was performed under the following conditions: 1) before treatment and testing, patients occluded their paretic eye for at least three days to avoid diplopia. 2) After treatment with botulinum toxin, alignment was corrected and patients stopped occluding their paretic eye for at least three days before testing. The control subjects occluded their non-dominant eye for three days before testing. RESULTS: In condition 1, no differences in motion detection values between patients and control subjects were found. In condition 2, motion detection thresholds were raised approximately 0.15 degrees /sec as compared to pre-treatment values and compared to the control group. CONCLUSIONS: After treatment, a raised threshold for motion detection is one mechanism used to avoid oscillopsia and visuo-vestibular disorientation during head movements in patients with chronic paralytic squint. This study lends evidence that perceptual-adaptive, compensatory mechanisms develop to reduce oscillopsia and disorientation rather than being caused by abnormal cortical motion processing or defective eye muscle action.

Published 4 September 2006 in Strabismus, 14(3): 129-35.
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