Anatomic and Physiologic Considerations
This part of the cerebrum, lying behind the central sulcus and above the sylvian fissure, is the least well demarcated (see Fig. 22-1). Its posterior boundary, where it merges with the occipital lobe, is obscure, as is part of the inferior-posterior boundary, where it merges with the temporal lobe. On its medial side, the parietooccipital sulcus marks the posterior border, which is completed by extending the line of the sulcus downward to the preoccipital notch on the inferior border of the hemisphere. Within the parietal lobe, there are two important sulci: the postcentral sulcus, which forms the posterior boundary of the somesthetic cortex, and the interparietal sulcus, which runs anteroposteriorly from the middle of the posterior central sulcus and separates the mass of the parietal lobe into superior and inferior lobules (see Fig. 22-1). The inferior parietal lobule is composed of the supramarginal gyrus (Brodmann area 40) and the angular gyrus (area 39). The superior parietal lobule is that remaining part of the lobe that is bounded below by interparietal sulcus, anteriorly by the postcentral sulcus, and extends onto the medial surface of the brain in Brodmann areas 5 and 7 (Fig. 22-2). The architecture of the postcentral convolution is typical of all primary receptive areas (homotypical granular cortex). The rest of the parietal lobe resembles the association cortex, both unimodal and heteromodal, of the frontal and temporal lobes.
The superior and inferior parietal lobules and adjacent parts of the temporal and occipital lobes are relatively much larger in humans than in any of the other primates and are relatively slow in attaining their fully functional state (beyond age 7 years). This area of heteromodal cortex has large fiber connections with the frontal, occipital, and temporal lobes of the same hemisphere and, through the middle part of the corpus callosum, with corresponding parts of the opposite hemisphere.
The postcentral gyrus, or primary somatosensory cortex, receives most of its afferent projections from the ventroposterior thalamic nucleus, which is the terminus of the ascending somatosensory pathways. The contralateral half of the body is represented somatotopically in this gyrus on the posterior bank of the rolandic sulcus. It has been shown in the macaque that spindle afferents project to area 3a, cutaneous afferents to areas 3b and 1, and joint afferents to area 2 (Kaas). Stimulation of the postcentral gyrus elicits a numb, tingling sensation and sense of movement. Penfield (1941) remarked that rarely are these tactile illusions accompanied by pain, warmth, or cold. Stimulation of the motor cortex may produce similar sensations, as do discharging seizure foci from these regions. The primary sensory cortex projects to the superior parietal lobule (area 5), which is the somatosensory association cortex. Some parts of areas 1, 3, and 5 (except the hand and foot representations) probably connect, via the corpus callosum, with the opposite somatosensory cortex. There is some uncertainty as to whether area 7 (which lies posterior to area 5) is unimodal somatosensory or heteromodal visual and somatosensory; certainly, it receives a large contingent of fibers from the occipital lobe.
In humans, electrical stimulation of the cortex of the superior and inferior parietal lobules evokes no specific motor or sensory effects. Overlapping here, however, are the integrative zones for vision, hearing, and somatic sensation, the supramodal integration of which is essential to our awareness of space and person and certain aspects of language and calculation (apperception), as described below.
The parietal lobe is supplied by the middle cerebral artery, the inferior and superior divisions supplying the inferior and superior lobules, respectively, although the demarcation between the areas of supply of these two divisions is quite variable.
Despite Critchley's pessimistic prediction that establishing a formula of normal parietal function would prove to be a "vain and meaningless pursuit," our concepts of the activities of this part of the brain have assumed some degree of order, in part from his own work. There is little reason to doubt that the anterior parietal cortex contains the mechanisms for tactile percepts. Discriminative tactile functions, listed below, are organized in the more posterior, secondary sensory areas. But the greater part of the parietal lobe functions as a center for integrating somatosensory with visual and auditory information in order to construct an awareness of one's own body (body schema) and its relation to extrapersonal space. Connections with the frontal and occipital lobes provide the necessary proprioceptive and visual information for movement of the body and manipulation of objects and for certain constructional activities (constructional apraxia). Impairment of these functions implicates the parietal lobes, more clearly the nondominant one (on the right).
The conceptual patterns on which complex voluntary motor acts are executed also depend on the integrity of the parietal lobes, particularly the dominant one. Defects in this region give rise to ideomotor apraxia, as discussed in Chap. 3 and further on. The understanding of spoken and written words is partly a function of the supramarginal and angular gyri of the dominant parietal lobe as elaborated in Chap. 23. The recognition and utilization of numbers, arithmetic principles, and calculation, which have important spatial attributes, are other functions integrated principally through these structures.
Clinical Effects of Parietal Lobe Lesions
Within the brain, perhaps no other territory surpasses the parietal lobes in the rich variety of clinical phenomena exposed under conditions of disease. Our current understanding of the effects of parietal lobe disease contrasts sharply with that of the late nineteenth century, when these lobes, in the textbooks of Oppenheim and Gowers, were considered to be "silent areas." However, some of the clinical manifestations of parietal lobe disease may be subtle, requiring special techniques for their elicitation.
Close to the core of the complex behavioral features that arise from lesions of the parietal lobes is the problem of agnosia. Allusion has already been made to agnosia in the discussion of lesions of the temporal lobes that affect language, and similar findings occur with lesions of the occipital lobe as discussed further on. In those contexts, agnosia refers to a loss of recognition of an entity that cannot be attributed to a defect in the primary sensory modality. The term agnosia extends to a loss of more complex integrated functions and mental symbolism as described below, a number of intriguing deficits arise. These syndromes expose properties of the parietal lobe that have implications regarding a map of the body schema and of external topographic space, of the ability to calculate, to differentiate left from right, to write words, and other problems discussed below. The fact that apraxia, an inability to carry out a commanded task despite the retention of motor and sensory function, may also arise from parietal lobe damage, and the relationship of the apraxias to language and to agnosias, exposes some of the most complicated issues in behavioral neurology. Some of the theoretical aspects of agnosia, particularly those related to the disturbances of visual processing, are discussed later in the chapter.
Cortical Sensory Syndromes
The effects of a parietal lobe lesion on somatic sensation were first described by Verger and then more completely by Déjerine, in his monograph L'agnosie corticale, and by Head and Holmes. The latter, in their important paper of 1911, noted the close interrelationships between the thalamus and the sensory cortex. Although difficult to study, it is apparent that a large lesion of the primary sensory cortex, or beneath it, results in a circumscribed loss or reduction in sensation on the opposite side of the body. When primary sensory perception is altered, analysis of more complex and integrative sensory function is rendered less accurate.
However, as pointed out in the discussion of the organization of the sensory systems in Chap. 9, the parietal postcentral cortical defect is essentially one of sensory discrimination, i.e., 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 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. 9.
Déjerine 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, e.g., 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. 9), 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.
With anterior parietal lobe lesions, there is sometimes an associated mild hemiparesis, as this portion of the parietal lobe contributes a considerable number of fibers to the corticospinal tract. Occasionally there is such a large degree of inability or disinclination to use the limb that it simulates a hemiplegia. More often, there is only a poverty of movement or a weak effort of the opposite side. The affected limbs, if involved with this apparent weakness, tend to remain hypotonic and the musculature may undergo slight atrophy of a degree possibly not explained entirely by inactivity alone. In some cases, as noted below, there is clumsiness in reaching for and grasping an object under visual guidance (optic ataxia), and exceptionally, at some phase in recovery from the hemisensory deficit, there is incoordination of movement and intention tremor of the contralateral arm and leg that closely simulates a cerebellar deficit (pseudocerebellar syndrome). While relatively rare, this type of ataxia is authenticated by our own case observations.
In instances of cortical sensory disturbance, the outstretched hand may display small random "searching" movements of the fingers that simulate playing a piano (pseudoathetosis); these are exaggerated when the eyes are closed. Fixed dystonic postures and asterixis have also been described after parietal lesions with sensory loss, but these are most often the result of thalamic damage.
A conceptual inability to recognize objects, persons, or sensory stimuli in the absence of a primary deficit in the sensory modality is termed agnosia, derived from the Greek for lack of knowledge. It was included as a form of loss of insight as part of the confusional state in Chap. 20.
The idea that visual and tactile sensory information is synthesized into a body schema or image (perception of one's body and the relations of bodily parts to one another) was first formulated by Pick and elaborated by Brain. Long before their time, however, it was suggested that such information was the basis of our emerging awareness of ourselves, and philosophers had assumed that this comes about by the constant interplay between inherent percepts of ourselves and of the surrounding world.
The formation of the body schema is considered to be based on the constant influx and storage of sensations from our bodies as we move about; hence, motor activity is important in its development. A sense of extrapersonal space is central to this activity, and this also depends upon visual and labyrinthine stimulation. The mechanisms of these perceptions are best appreciated by studying their derangements in the course of neurologic disease of the parietal lobes.
Denny-Brown and Banker introduced the idea that the basic disturbance in all these defects is an inability to integrate a series of "spatial impressions"—tactile, kinesthetic, visual, vestibular, or auditory—a defect they referred to as amorphosynthesis. Examples of the loss of concept in their schema include finger agnosia, right-left confusion, acalculia, and all the apperceptive losses that attend damage of integrative sensory areas of the brain. The theoretical problem presented by agnosia is taken up in a later section.
Anosognosia and Hemispatial Neglect (Anton–Babinski Syndrome)
The observation that a patient with a dense hemiplegia, usually of the left side, may be indifferent to a paralysis, or is entirely unaware of it, was first made by Anton; later, Babinski named this disorder anosognosia. It expresses itself in several ways. For example, a lack of concern regarding paralysis was called anosodiaphoria by Babinski, an interesting term that is now little used. The term "denial" was introduced by Freud to explain the problem but is laden with psychic and psychoanalytical meaning and is less precise than "neglect."
With regard to parietal lobe disease, the term "anosognosia," using "anos," disease, is used to describe a group of disorders in which there is an unawareness of a deficit. While used most frequently to describe a lack of recognition, neglect, or indifference to a left sided paralysis or even to ownership of the limb, the term anosognosia is appropriate to denote the inability to perceive a number of deficits based on cerebral disease including blindness, hemianopia, deafness, and memory loss. Anosognosia is usually associated with a number of additional abnormalities. Often there is a blunted emotionality. The patient is inattentive and apathetic, and shows varying degrees of general confusion. There may be an indifference to performance failure, a feeling that something is missing, visual and tactile illusions when sensing the paralyzed part, hallucinations of movement, and allochiria (one-sided stimuli are felt on the other side).
The patient may act as if nothing were the matter. If asked to raise the paralyzed arm, he may raise the intact one or do nothing at all. If asked whether the paralyzed arm has been moved, the patient may say "yes." If the fact that the arm has not been moved is pointed out, the patient may admit that the arm is slightly weak. If told it is paralyzed, the patient may deny that this is so or offer an excuse: "My shoulder hurts." If asked why the paralysis went unnoticed, the response may be, "I'm not a doctor." Some patients report that they feel as though their left side had disappeared, and when shown the paralyzed arm, they deny it is theirs and assert that it belongs to someone else or even take hold of it and fling it aside. The mildest form of anosognosia is reflected by an imperfect and reduced appreciation of the degree of weakness. On the other extreme of the conceptual negation of paralysis are instances of self-mutilation of the paralyzed limb (apotemnophilia). It should be pointed out that the loss of body schema and the lack of appreciation of a left hemiplegia are separable, some patients displaying only one feature.
The lesion responsible for the various forms of one-sided anosognosia lies in the cortex and white matter of the superior parietal lobule. Rarely, a deep lesion of the ventrolateral thalamus and the juxtaposed white matter of the parietal lobe will produce a similar contralateral neglect. Unilateral asomatognosia is many times more frequent with right (nondominant) parietal lesions as with left-sided ones (seven times more often according to Hécaen). The apparent infrequency of right-sided agnosic symptoms with left parietal lesions is attributable in part, but not entirely, to their obscuration by an associated aphasia.
Another common group of parietal symptoms consists of neglect of one side of the body in dressing and grooming, recognition only on the intact side of bilaterally and simultaneously presented stimuli (sensory extinction) as mentioned above, deviation of head and eyes to the side of the lesion (transient), and torsion of the body in the same direction. The patient may fail to shave one side of the face, apply lipstick, or comb the hair only on one side.
Unilateral spatial neglect is brought out by having the patient bisect a line, draw a daisy or a clock, or name all the objects in the room. Homonymous hemianopia and varying degrees of hemiparesis may or may not be present and interfere with the interpretation of the lack of application on the left side of the drawing.
Clinical observations indicate that patients with right parietal lesions show variable but lesser elements of ipsilateral neglect in addition to the striking degree of contralateral neglect, suggesting that, in respect to spatial attention, the right parietal lobe is truly dominant (Weintraub and Mesulam). Damage of the superior parietal lobule, in addition to producing agnosias and apraxias, may interfere with voluntary movement of the opposite limbs, particularly the arm, as pointed out by Holmes. In reaching for a visually presented target in the contralateral visual field, and to a lesser extent in the ipsilateral field, the movement is misdirected and dysmetric (the distance to the target is misjudged).
Another subtle aspect of parietal lobe physiology revealed by human disease is the loss of exploratory and orienting behavior with the contralateral arm and even a tendency to avoid tactile stimuli. Mori and Yamadori call this rejection behavior. Denny-Brown and Chambers attributed the released grasping and exploring that follow frontal lobe lesions to a disinhibition of inherent parietal lobe automatisms but there is no way of confirming this. It is of interest that demented patients with prominent grasp reflexes tend not to grasp parts of their own bodies, but if there has been an additional parietal lesion, there is "self-grasping" of the forearm opposite the lesion (Ropper).
Conventional treatments for hemispatial neglect use prismatic glasses and training in visual exploration of the left side. Another approach demonstrates improvement by the application of vibratory stimulation to the right side of the neck, as reported by Karnath and colleagues, or of the ipsilateral labyrinth by caloric or electrical means (a similar treatment has been successful in some cases of dystonic torticollis, see Chap. 6). Based on the work of Ramachandran and colleagues, mirrors have been used to assist recovery of the side with agnosia. With a mirror in the right parasagittal plane, the patient observes the mirror image of their neglected hand and space and is induced to use that side more naturally. The larger problem is that these patients may not respond to rehabilitation if they lack an innate body schema.
Ideomotor and Ideational Apraxia
As discussed extensively in Chap. 3, patients with parietal lesions of the dominant hemisphere who exhibit no defects in motor or sensory function, lose the ability to perform learned motor skills on command or by imitation. They can no longer use common implements and tools, either in relation to their bodies (e.g., brushing teeth, combing hair) or in relation to objects in the environment (e.g., a doorknob or hammer). The patient holds the implement awkwardly or seems at a loss to begin the act. It is as though the patient had forgotten the sequences of learned movements. The effects are bilateral. When defects of apraxia are intertwined with agnosic defects, the term apractognosia seems appropriate. A special type of visuospatial disorder, separable from neglect but also associated with lesions of the nondominant parietal lobe, is reflected in the patient's inability to reproduce geometric figures (constructional apraxia). A number of tests have been designed to elicit these disturbances, such as indicating the time by placement of the hands on a clock, drawing a map, copying a complex figure, reproducing stick-pattern constructions and block designs, making three-dimensional constructions, and constructing puzzles.
From the above descriptions, it is evident that the left and right parietal lobes function differently. The most obvious difference, of course, is that language and arithmetical functions are centered in the left hemisphere. It is hardly surprising, therefore, that verbally mediated spatial and praxic functions are more affected with left-sided than with right-sided lesions. This is ostensibly because language function, sited in the left hemisphere, is central to all cognitive functions. Hence cross-modal matching tasks (auditory–visual, visual–auditory, visual–tactile, tactile–visual, auditory–tactile, etc.) are most clearly impaired with lesions of the dominant hemisphere. Such patients can read and understand spoken words but cannot grasp the meaning of a sentence if it contains elements of relationship (e.g., "the mother's daughter" versus "the daughter's mother," "the father's brother's son," "Jane's complexion is lighter than Marjorie's but darker than her sister's"). There are similar difficulties with calculation. The recognition and naming of parts of the body and the distinction of right from left and up from down are learned, verbally mediated spatial concepts that are disturbed by lesions in the dominant parietal lobe.
This syndrome, caused by a left (dominant) inferior parietal lesion, provides the most striking example of what might be viewed as a bilaterally manifest agnosia (the previously mentioned asomatognosia of Denny-Brown and Banker). The characteristic tetrad of features is (i) inability to designate or name the different fingers of the two hands (finger agnosia), (ii) confusion of the right and left sides of the body, (iii) inability to calculate (acalculia), and (iv) inability to write (dysgraphia). One or more of these manifestations may be associated with word blindness (alexia) and homonymous hemianopia or a lower quadrantanopia. The lesion is in the left inferior parietal lobule (below the interparietal sulcus), particularly involving the angular gyrus or subjacent white matter of the left hemisphere.
There has been a dispute as to whether the four main elements of the Gerstmann syndrome have a common basis or only an association. Benton states that they occur together in a parietal lesion no more often than do constructional apraxia, alexia, and loss of visual memory and that every combination of these symptoms and those of the Gerstmann syndrome occurs with equal frequency in parietal lobe disease. Others, including the authors, tend to disagree and have the experience that right–left confusion, digital agnosia, agraphia, and acalculia have special significance, possibly being linked through a unitary defect in spatial orientation of fingers, body sides, and numbers. The relationship between the finger agnosia and the inability to enumerate is especially intriguing and relates to other arithmetic difficulties, discussed below. Attempts to clarify a common or fundamental source for all the elements of the Gerstmann syndrome by functional imaging have been difficult to comprehend. In healthy subjects, Rusconi and colleagues were unable to find a shared cortical substrate that could give rise to the features of the Gerstmann syndrome.
Dyscalculia has attracted little critical attention, perhaps because it occurs most often as a by-product of aphasia and an inability of the patient to appreciate numerical language. Primary dyscalculia is usually associated with the other elements of the Gerstmann syndrome. Computational difficulty may also be part of the more complex visuospatial abnormality of the nondominant parietal lobe; there is then difficulty in the placing of numbers in specific spatial relationships while calculating. In such cases, there is no difficulty in reading or writing the numbers or in describing the rules governing the calculation, but the computation cannot be accomplished correctly with pencil and paper. Hécaen has made a distinction between this type of anarithmetia and dyscalculia. In the latter, the process of calculation alone has been disturbed; in the former, there is an inability to manipulate numbers and to appreciate their ordinal relationships. Recognition and reproduction of numbers are intact in both. An analysis of how computation goes awry in each individual case is therefore required.
Visual Disorders with Parietal Lesions
A lesion deep to the inferior part of the parietal lobe, at its junction with the temporal lobe, involves the geniculocalcarine radiations and results in an incongruous homonymous hemianopia or an inferior quadrantanopia on the opposite side; but just as often, in practice, the defect is complete or almost complete and congruous. If the lesion is small and predominantly cortical, optokinetic nystagmus is usually retained; with deep lesions, it is abolished, with the target moving ipsilaterally (see Chap. 14).
Visual neglect is a typical feature of posterior parietal lesions on either side, more prominent with right-sided lesions. The problem that often arises is of distinguishing visual hemineglect (particularly of the left side) from a hemianopia. In its more severe forms the neglect is evident from casual observation of the patient's behavior or in drawings made by the patient that omit features on the left side; but here a more pervasive syndrome of hemispatial neglect, discussed earlier, may underlie the visual behavior. Occasionally, severe left-sided visual neglect results from a lesion in the right angular gyrus (see Mort et al). Visual neglect can also occur after focal lesions in the posterior medial temporal lobe (supplied by a branch of the posterior cerebral artery, in contrast to the middle cerebral artery supply of the angular gyrus of the inferior parietal lobule).
With posterior parietal lesions, as noted by Holmes and Horrax, there are deficits in localization of visual stimuli, inability to compare the sizes of objects, failure to avoid objects when walking, inability to count objects, disturbances in smooth-pursuit eye movements, and loss of stereoscopic vision. Cogan observed that the eyes may deviate away from the lesion upon forced lid closure, a "spasticity of conjugate gaze."
A common disorder of motor behavior of the eyelids is seen in many patients with large acute lesions of the right parietal lobe. Its mildest form is a disinclination to open the lids when the patient is spoken to. This gives the erroneous impression that the patient is drowsy or stuporous, but it will be found that a quick reply is given to whispered questions. In more severe cases, the lids are held shut and opening them is strongly resisted, to the point of making an examination of the pupils and fundi impossible.
Visual Disorientation and Disorders of Extrapersonal Space (Topographic Localization)
Spatial orientation depends on the integration of visual, tactile, and kinesthetic perceptions, but there are instances in which the defect in visual perception predominates. Patients with this disorder are unable to orient themselves in an abstract spatial setting (topographagnosia). Such patients cannot draw the floor plan of their house, a map of their town, or of the United States and cannot describe a familiar route, as from home to work, for example, or find their way in familiar surroundings. In brief, such patients have lost topographic memory. This disorder is almost invariably caused by lesions in the white matter deep to the inferior and superior parietal lobules and it is separable from anosognosia as summarized by Levine and colleagues.
A clever mental experiment posed to patients by Bisiach and Luzzatti has suggested that the loss of attention to one side of the environment extends to, or perhaps is derived from, the mental representation of space. Their patient with a right parietal lesion was asked to describe from memory the buildings lining the Piazza del Duomo, first as if seen from one corner of the piazza and then from the opposite corner. In each instance, the description omitted the left side of the piazza from the observer's perspective.
An important and not infrequent disorder of visual agnosia, a disorder of visually directed reaching with the hand, difficulty directing gaze, and simultanagnosia, is given the name Balint syndrome. It is, strictly speaking, a bilateral disorder of the parietal lobes but we discuss it below for convenience in order to append it to the clinically similar entity of cortical blindness.
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:
Effects of unilateral disease of the parietal lobe, right or left
Corticosensory syndrome and sensory extinction (or total hemianesthesia with large acute lesions of white matter)
Mild hemiparesis or poverty of movement (variable), poverty of movement, hemiataxia (seen only occasionally)
Homonymous hemianopia or inferior quadrantanopia (incongruent or congruent) or visual inattention
Abolition of optokinetic nystagmus with target moving toward side of the lesion
Neglect of the opposite side of external space (more prominent with lesions of the right parietal lobe; see later)
Effects of unilateral disease of the dominant (left) parietal lobe (in right-handed and most left-handed patients); additional phenomena include
Disorders of language (especially alexia)
Gerstmann syndrome (dysgraphia, dyscalculia, finger agnosia, right–left confusion)
Tactile agnosia (bimanual astereognosis)
Bilateral ideomotor and ideational apraxia (see Chap. 3)
Effects of unilateral disease of the nondominant (right) parietal lobe
Topographic memory loss
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)
Tendency to keep the eyes closed, resist lid opening, and blepharospasm
Effects of bilateral disease of the parietal lobes
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.