Faculty Bibliography

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

A theory is proposed to account for unawareness of blindness, hemianopsia, and hemiplegia, and for phantom limb after amputation. It is assumed that interruption of a sensory pathway at any level--from peripheral nerve to primary sensory cortex--is not associated with any immediate sensory experience that uniquely specifies the defect. Instead the sensory loss must be discovered by a process of self-observation and inference. Discovery is easy for defects that create major functional disability, such as total blindness. Hence unawareness of total blindness occurs only in association with severe intellectual impairment, precluding the required self-observation and inference. In contrast, hemianopsia is difficult to discover because several mechanisms automatically compensate the defect effectively. Thus unawareness of hemianopsia is common, even in intellectually normal individuals. Insensate fields are often the source of suggested (false) percepts, because no information from such a field specifies the absence of a sensory stimulus. The most powerful source of suggestion is sensory activity in uninvolved portions of the affected sensory field. Thus hemianopsics may perceive complete geometric forms when only incomplete forms are shown and the missing portion falls in the hemianopsic fields. Such perceptual completion also occurs in hemianesthetic hemiplegics, creating the illusion that there are normally functioning limbs on the affected side. This perceptual completion increases the difficulty of discovery of hemianesthetic hemiplegia, but the disability is still sufficiently obvious that some additional cognitive impairment is invariably present in patients with lasting unawareness of hemiplegia. Phantom limb after amputation is the product of perceptual completion without associated cognitive impairment. The patient with phantom limb is thus aware of the illusory quality of his phantom. Some insight into the neural basis of perceptual completion and of unawareness of sensory loss may derive from considering sensory systems and associative cortex as parallel-distributed processing mechanisms

We report the clinicopathological study of an 83-year-old man who abruptly developed complex visual hallucinations, disordered sleep, and mild cognitive impairment that persisted until his death 6 months later. Postmortem neuropathological examination including serial sections through the diencephalon, midbrain, and pons disclosed isolated bilateral infarcts confined to the medial substantia nigra pars reticulata. The findings suggest that destruction of the pars reticulata may be the essential feature to the development of peduncular hallucinosis

In addition to causing visuospatial deficits, damage to the right cerebral hemisphere also impairs other cognitive abilities, including those requiring higher-order aspects of language. The present study used a standardized test battery to examine the relationship between visuospatial abilities and comprehension of narrative material in subjects having unilateral right hemisphere damage (RHD). In a series of 41 consecutively admitted RHD subjects, impairments in abstracting information from narrative passages were as prevalent and as severe in magnitude as constructional apraxia. Moreover, the extent of the visuospatial and linguistic impairments were highly correlated. Although age, educational levels, and degree of premorbid brain atrophy were all found to influence performance, analysis of a select subgroup of the population established that the covariation of visuospatial and verbal impairments is related to right hemisphere damage per se. Clinically, these findings may be of significance for understanding the pervasive cognitive impairments that are often evidenced by RHD patients

A patient with severe, lasting prosopagnosia could not get an immediate overview of a face sufficiently specific for successful identification. He also failed completely in tasks of visual closure despite adequate performances on numerous other tests of visual perception and memory. We conclude that prosopagnosia represents a loss of visual 'configural processing'--a learned skill enabling immediate identification of individual members of a class without conscious visuospatial analysis or remembering. Prosopagnosia and agnosic alexia represent two distinct defects of configural processing: Alexics cannot identify items with distinctive features that are themselves identifiable. Prosopagnosics cannot identify objects whose critical distinguishing features have no independent identities

We describe a patient with a deficit in imagery ability, following a left posterior cerebral artery infarction and possible anoxic episode. This deficit was inferred from the patient's performance on several tasks, including one in which normal adults are known to rely on imagery and two that tested imagery nonverbally, allowing us to examine the possibility of a language-imagery disconnection. In addition, we queried the patient on some cognitive capacities related to visual imagery: dreaming, geographical knowledge, and introspection regarding visual and auditory imagery. Hypotheses concerning the critical lesion site and underlying cognitive mechanism of image generation deficits are discussed in relation to this and other recent cases of impaired imagery ability with intact recognition ability, and the relevance of this deficit to the 'imagery debate' is discussed

A right-handed man suffered a left parieto-occipital cerebral infarction, causing agraphia with Gerstmann's syndrome but without major aphasia, alexia, or apraxia. Oral spelling was superior to written spelling. Experiments were performed involving (1) analysis of errors in writing, (2) tasks of visual imagery, and (3) identifying letters drawn without leaving a visual trace. The results suggest that the agraphia and Gerstmann's syndrome are due to a dissociation of language skills and visuospatial skills caused by a dominant parieto-occipital lesion

The authors used the Thought Disorder Index to measure thought disorder in 23 patients with unilateral right hemisphere cortical damage, 20 patients with bipolar mania, and 25 patients with schizophrenia. There were no differences in the total amount of thought disorder in these groups, but each showed a unique pattern of thought disorder. Patients with right hemisphere damage displayed fragmented thinking, manic patients displayed playful thinking, and schizophrenic patients displayed idiosyncratic thinking. These findings support the view that thought disorder is manifested in different forms that are relatively specific to psychiatric or neurological condition