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Bitemporal Hemianopia Associated With Fusiform Dilatation of the Anterior Cerebral Arteries

George F. Hilton, MD; William F. Hoyt, MD

JAMA. 1966;196(11):1018-1020.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

IN A REVIEW of the blood supply to the optic chiasm published in 1958, Hughes implied that arteriosclerosis in the elderly patient can, on rare occasions, cause a classical chiasmal syndrome (optic atrophy, bitemporal field -defects, and a normal sella turcica).¹ He referred specifically to the case of a 74-year-old man with generalized arteriosclerosis who suffered the abrupt onset of uppertemporal-field defects, and he deduced from findings in this case and from findings in "a few related cases" that the responsible occlusive vascular changes had occurred in small prechiasmal vessels derived from the anterior cerebral arteries.

In 1960, Walsh and Gass called attention to a direct effect of sclerotic anterior cerebral arteries on the chiasm.² They showed a necropsy specimen (Fig 1) in which they found compression and distortion of the chiasm and optic nerves by sclerotic, elongated, and prolapsed anterior cerebral arteries. They had no information regarding . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Ophthalmology and the Division of Neurological Surgery, University of California Medical Center, San Francisco.

Footnotes
Reprint requests to Division of Neurological Surgery, University of California Medical Center, Parnassus and Third, San Francisco 94122 (Dr. Hoyt).

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