Faculty Bibliography

A 59-year-old man developed problems with reading and driving. When first examined, he had great difficulty locating and identifying items by sight. Visual acuity was normal, but contrast sensitivity for low spatial frequencies was severely impaired. The peripheral visual fields were moderately constricted with depressed flicker fusion frequencies, more on the right. Color identification was preserved. The difficulties in identifying and locating objects by sight were aggravated by increasing the complexity and multiplicity of the items in the field of vision and by changing the ambient illumination. Intellect and memory were relatively intact, except for difficulty with calculations. Over a 12-year course the visual defects steadily worsened, and eventually memory and language skills failed. Social manners, perseverance, and affect remained normal. Postmortem examination showed cortical atrophy, predominantly posterior, with abundant neurofibrillary tangles and senile plaques. The density of the tangles was correlated with the severity of the atrophy, being highest in the occipitoparietal areas and lowest in the frontal lobes. Alzheimer's disease can preferentially affect the posterior cerebral hemispheres and cause a dementia presenting with, and dominated by, visual disturbances

We compared patients with unawareness of hemiplegia lasting more than 1 month after right hemisphere stroke with other patients with right hemisphere stroke who became aware of hemiplegia within a few days after onset. Patients with persistent unawareness invariably had severe left hemisensory loss and usually had severe left spatial neglect. They were almost always apathetic; their thought lacked direction, clarity, and flexibility, and they had at least moderate impairment of intellect and memory. Their right hemisphere strokes were large and always affected the central gyri or their thalamic connections and capsular pathways. In addition, there was evidence of at least mild left hemisphere damage, most commonly caused by age-associated atrophy. The pathogenesis of anosognosia for hemiplegia may involve failure to discover paralysis because proprioceptive mechanisms that ordinarily inform an individual about the position and movement of limbs are damaged, and the patient, because of additional cognitive defects, lacks the capacity to make the necessary observations and inferences to diagnose the paralysis. We discuss the implications of this 'discovery' theory and contrast it with other explanations of anosognosia

We present a patient with Balint's syndrome who complained of fading of the scenes under visual fixation. When he intentionally blinked, the faded visual percept reappeared. The disappearance of the visual percept may be explained as the result of either unstable visual fixation or of saturation of the visual pathways. The role of blinking in reviving the visual percept may be explained accordingly as causing a refixation of the target under visual fixation or as resetting the visual pathways for visual processing