However, as pointed out in the discussion of the organization of the sensory systems in Chap. 8, the parietal postcentral cortical defect is essentially one of sensory discrimination, that is, impairment of the ability to integrate and localize stimuli that is reflected by an inability to distinguish objects by their size, shape, weight, and texture (astereognosis); to recognize figures written on the skin (agraphesthesia); to distinguish between single and double contacts (impairment of two-point discrimination); and to detect the direction of movement of a tactile stimulus. This type of sensory defect is sometimes referred to as “cortical,” although it can be produced just as well by lesions of the subcortical connections. Clinicoanatomic studies indicate that parietocortical lesions that spare the postcentral gyrus produce only transient somatosensory changes or none at all (Corkin et al; Carmon and Benton). In other words, the primary perception of pain, touch, pressure, vibratory stimuli, and thermal stimuli is relatively intact in lesions of the parietal cortex that does not involve the postcentral gyrus.
The question of bilateral sensory deficits as a result of lesions in only one postcentral convolution was raised by the studies of Semmes et al and of Corkin and their associates. In tests of pressure sensitivity, two-point discrimination, point localization, position sense, and tactile object recognition, they found bilateral disturbances in nearly half of their patients with unilateral lesions, but the deficits were always more severe contralaterally and mainly in the hand and therefore the ipsilateral effect is rarely evident in clinical work. These disturbances of discriminative sensation and the subject of tactile agnosia are discussed more fully in Chap. 8.
Dejerine and Mouzon described the sensory syndrome in which touch, pressure, pain, thermal, vibratory, and position sense are lost on one side of the body or in a limb. This syndrome, typically the result of a thalamic lesion and not of a parietal one, may nonetheless occur with large, acute lesions (infarcts, hemorrhages) in the central and subcortical white matter of the parietal lobe. In this case, the symptoms partially recede in time, leaving more subtle defects in sensory discrimination. Smaller lesions, particularly ones that result from a glancing blow to the skull or a small infarct or hemorrhage, may cause a defect in cutaneous–kinesthetic perception in a discrete part of a limb, for example, the ulnar or radial half of the hand and forearm; these cerebral lesions may mimic a peripheral nerve or root lesion (Dodge and Meirowsky).
A pseudothalamic pain syndrome on the side deprived of sensation by a parietal lesion has been described (Biemond). In a series of 12 such patients described by Michel and colleagues, burning or constrictive pain, identical to the thalamic pain syndrome (described in Chap. 7), resulted from vascular lesions restricted to the cortex. The discomfort involved the entire half of the body or matched the region of cortical hypesthesia; in a few cases, the symptoms were paroxysmal.
Head and Holmes drew attention to a number of interesting points about patients with parietal sensory defects: the easy fatigability of their sensory perceptions; the inconsistency of responses to painful and tactile stimuli; the difficulty in distinguishing more than one contact at a time; the disregard of stimuli on the affected side when the healthy side is stimulated simultaneously (tactile inattention or extinction); the tendency of superficial pain sensations to outlast the stimulus and to be hyperpathic; and the occurrence of hallucinations of touch. Of these, the testing of sensory extinction by the presentation of two tactile stimuli simultaneously on both sides of the body has become a component of the routine neurologic examination for parietal lesions. In modern parlance, these are “cortical sensory” defects of extinction of double simultaneous stimulation—astereognosis and agraphesthesia.