This defect in appreciation of the left side of the environment is less apparent than is visual neglect, but it is no less striking when it occurs. Many patients with acute right parietal lesions are initially unresponsive to voices or noises on the left side, but the syndrome is rarely persistent. Special tests demonstrate a displacement of the direction of the perceived origin of sounds toward the right. This defect is separable from visual agnosia (see De Renzi et al); curiously, it may be worsened by the introduction of visual cues. Subtle differences between the allocation of spatial attention to sound (auditory neglect) and a distortion in its localization may be found in different cases, but the main lesion usually lies in the right superior lobule.
In summary, the effects of disease of the parietal lobes are as follows:
I. Effects of unilateral disease of the parietal lobe, right or left
A. Corticosensory syndrome and sensory extinction (or total hemianesthesia with large acute lesions of white matter)
B. Mild hemiparesis or poverty of movement (variable), poverty of movement, hemiataxia (seen only occasionally)
C. Homonymous hemianopia or inferior quadrantanopia (incongruent or congruent) or visual inattention
D. Abolition of optokinetic nystagmus with target moving toward side of the lesion
E. Neglect of the opposite side of external space (more prominent with lesions of the right parietal lobe)
II. Effects of unilateral disease of the dominant (left) parietal lobe (in right-handed and most left-handed patients); additional phenomena include
A. Disorders of language (especially alexia)
B. Gerstmann syndrome (dysgraphia, dyscalculia, finger agnosia, right–left confusion)
C. Tactile agnosia (bimanual astereognosis)
D. Bilateral ideomotor and ideational apraxia (see Chap. 3)
III. Effects of unilateral disease of the nondominant (right) parietal lobe
A. Visuospatial disorders
B. Topographic memory loss
C. Anosognosia, dressing, and constructional apraxias (these disorders may occur with lesions of either hemisphere but are observed more frequently and are of greater severity with lesions of the nondominant one)
D. Confusion
E. Tendency to keep the eyes closed, resist lid opening, and blepharospasm
IV. Effects of bilateral disease of the parietal lobes
A. Balint syndrome: visual-spatial imperception (simultagnosia), optic apraxia (difficulty directing gaze), and optic ataxia (difficulty reaching for objects)
With all these parietal syndromes, if the disease is sufficiently extensive, there may be a reduction in the capacity to think clearly as well as inattentiveness and slightly impaired memory.
It does seem reasonably certain that, in addition to the perception of somatosensory impulses that arrive in the postcentral gyrus, the parietal lobe participates in the integration of all sensory data, especially those that provide an awareness of one’s body as well as a percept of one’s surroundings and of the relation of one’s body to extrapersonal space and of objects in the environment to each other. In this respect, the parietal lobe may be regarded as a special high-order sensory organ, the locus of transmodal intersensory, integration, particularly tactile and visual ones, which are the basis of our concepts of spatial relations. In this way, parietal lesions cause disorders of specific types of self-consciousness or self-awareness that are tied to sensory modalities. This is distinctly different from the distortions of perception caused by lesions of the temporal lobes.
Authoritative references on parietal function include Critchley’s monograph on the parietal lobes and the chapter by Botez and Olivier in the Handbook of Clinical Neurology.