OPTOKINETIC nystagmus (OKN) was introduced as a clinical tool by Barany1 in 1921, but in spite of intensive study and investigation, knowledge of the mechanisms underlying the phenomenon and the anatomic substrates involved in its production is incomplete. An "optokinetic center" has been assumed to exist mainly on the basis of analysis of optokinetic dysfunction in patients with lesions more or less well localized on clinical grounds. This hypothesis, while consistent with classical anatomic conjecture, has not proved fruitful in understanding the phenomenon. Witness the fact that little agreement has been reached regarding the location of the so-called "center."2-5
Although it is generally agreed that disturbances of optokinetic nystagmus are frequent in patients with intracranial pathology, the clinical value of optokinetic testing has been disputed. While some authors have insisted that a unilateral defect in OKN is virtually diagnostic of a parietal lobe lesion,4,6 others have taken
DAVIDOFF RA, ATKIN A, ANDERSON PJ, BENDER MB. Optokinetic Nystagmus and Cerebral Disease: Clinical and Pathological Study. Arch Neurol. 1966;14(1):73–81. doi:10.1001/archneur.1966.00470070077009
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