[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.197.142.219. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Citations 0
Letters to the Editor
August 2001

Ocular Motor Apraxia and Ataxia-Telangiectasia

Arch Neurol. 2001;58(8):1312. doi:

Dr Dawson's discussion of ocular motor apraxia (OMA) in his recent editorial1 was largely accurate, but some of his statements require further clarification. As he indicated, OMA is characterized by an impaired initiation of saccadic eye movements. When this deficit is severe, thrusting head movements are observed during attempted gaze shifts that appear to partially normalize the defect in saccade initiation.2 While the anatomic basis for the congenital form of OMA remains uncertain, those cases that are associated with congenital or acquired structural abnormalities are typically caused by lesions in the brainstem or the cerebellar vermis,3 not the cerebral hemispheres. Furthermore, since the defect in OMA is impaired initiation of saccades, slowing of saccades is not a feature of the syndrome.2

First Page Preview View Large
First page PDF preview
First page PDF preview
×