Cerebral Blindness

Abstract

Cerebral blindness, often called "cortical" blindness, may be defined as bilateral absence of light perception (under the usual conditions of testing) caused by disease of the cerebral hemispheres. The lesions involve the retrogeniculate portions of the visual system on both sides, either the optic radiations or the calcarine cortex or both. For the purpose of this study, fulfillment of the following clinical criteria was required: 1. The patient was totally blind. 2. The eyes themselves (that is, media, retina, and optic nerve) were normal or showed only minor abnormality, incapable of causing blindness. 3. The pupillary light reactions were normal.4. There was other evidence of bilateral cerebral disorder, either at the time the blindness developed or in the past. The limitations of these criteria will be discussed later.This entity is well known, and many cases have been reported since the classical paper of F\l=o"\rsterin 1890.11 These reports have usually emphasized the pathology of this condition, and many concerned themselves with the denial of blindness (Anton's syn¬ drome) that frequently occurs. Although denial of blindness was once believed to be a specific dysfunction relating to the visual system. Redlich and Dorsey24 and, more recently, Weinstein and his associates33·34

Restitution of visual function in patients with cerebral blindness.

“…Perimetric "blind" or impaired visual field areas may fluctuate in sensitivity (Bender and Teuber, 1946). Recovery of visual function has been observed in patients with postchiasmatic lesions although return of vision is rarely complete (Bergmann, 1957;Symonds and Mackenzie, 1957). Reappearance takes place in a definite temporal order: sensation of light and motion, form perception, colour perception (Poppelreuter, 1917;Riddoch, 1917).…”

Cortical Blindness as a Manifestation of Basilar Artery Occlusion

“…The appearance of cortical blindness in an occlusion of the basilar artery is more likely to occur if a preexisting circulation impairment in the 'anterior' circulation result in an inadequate collateral flow to the occipital lobes [Reese, 1954]. Another explanation would be the development of a thrombus or the lodgement of an embolus at the junction of the basilar and posterior cerebral arteries with its extension beyond the posterior communicating arteries [Bergman, 1957]. It is, however, rather unlikely that the throm bus at the tip of the basilar artery will extend into both posterior cere brals, and reach beyond the posterior communicating arteries at the same time.…”

“…There was no abnormality in the eyes capable of producing blindness and blinking re flex to menace was absent. One of the most outstanding features of cortical blindness, which dis tinguishes it from mere bilateral homonymous hemianopia is the visual agnosia, the inability to recognize blindness [Symonds and Mackenzie, 1957;Bergman, 1957;Silverman et al, 1961;Sugar, 1965]. The cal carine cortex, Brodmann's area 17, serves as the primary visual cortex.…”

Prognostic Value of Visual Evoked Potentials in Occipital Blindness following Basilar Artery Occlusion

“…The lesion involves either the posterior part of the optic radiation or the occipital cortex, or both, leaving eye movements, structures, and pupillary light reaction unaffected. Occlu sion of the basilar artery or both posterior cerebral arteries are the most frequently found cause; injury, inflammation, tumor or others are found less frequently [5].…”