THE PARIETAL LOBES

The primary sensory (somesthetic) cortex (S1; areas 3, 1, and 2)

The secondary somatosensory cortex (S2)

The interparietal sulcus extends posteriorly from the midpoint of the postcentral gyrus and divides
the remainder of the parietal lobe into the superior parietal lobule above and the inferior parietal
lobule below and these The superior and inferior parietal lobules are sensory association areas.

Functions –

The functions of the parietal lobe are essentially those of reception, correlation, analysis, synthesis,
integration, interpretation, and elaboration of the primary sensory impulses received from the
thalamus.

1 S1 is the initial reception center for afferent impulses, especially for tactile, pressure, and
position sensations. It is necessary for discriminating fi ner, more critical grades of sensation
and for recognizing intensity.
Stimulation produces paresthesias on the opposite side of the body, with tactile and
pressure sensations, numbness, tingling, sensations of constriction and movement, and
occasional thermal sensations, but rarely pain. Such sensations may precede or
accompany Jacksonian convulsions as part of a seizure ; the spread of the
sensory disturbance follows the same general pattern as in the motor area.
2 The sensory association areas are essential for the synthesis and
interpretation of impulses, appreciation of similarities and differences, interpretation of
spatial relationships and two-dimensional qualities, evaluations of variations in form and
weight, and localization of sensation. Overactivity of these areas causes minimal
symptoms, for example, vague paresthesias or hyperesthesias on the opposite side of the
body.
Destructive lesions affect mainly the gnostic (knowing, recognition) aspects of
sensation. Simple appreciation of primary sensations remains, but associative functions are
impaired. (These deficits are discussed further in Chapters 10 and 35.)
3 Parietal lobe lesions produce abnormalities of higher-level sensory functions,
which require association cortex: stereognosis, graphesthesia, two-point discrimination, and
tactile localization. Patients with nondominant parietal lobe lesions may display various
forms of apraxia, hemiinattention, hemineglect, and denial of disability, culminating in the
striking syndrome of anosognosia, in which patients may deny owning their contralateral
limbs (see Chapter 10).
The parietal lobes, through connections with the temporal and occipital lobes,
integrate somatosensory with visual and auditory information.
The inferior parietal lobule—especially the angular and supramarginal gyri and the
areas in close proximity to the occipital and temporal lobes—are functionally associated
with the visual and auditory systems.
4 The angular and supramarginal gyri of the dominant hemisphere are
important in relation to language and related functions. Lesions in these areas may cause
aphasia, agnosia, and apraxia; these are discussed in Chapter 10.
5 The optic radiations course through the deep parietal lobe to reach the visual cortex. A
deeply placed parietal lesion may cause either an inferior quadrantic or
hemianopic visual fi eld defect.
6 Parietal lesions have been reported to cause contralateral muscular atrophy and
trophic skin changes.
7 Deafferentation may produce hypotonia, slowness of movement—especially of the
proximal muscles—ataxia, updrift and pseudoathetoid movements (sensory wandering) of
the opposite side of the body .
8 Inco-ordination of movement due to sensory loss from a parietal lobe lesion may mimic
cerebellar ataxia (pseudocerebellar syndrome).
9 Dystonia has also been described. Focal motor seizures and partial paralysis involving the
contralateral parts of the body can occur with parietal lesions. These may be due to
impaired communication with areas 6 and 4, or they may indicate that the parietal lobes
also possess some motor function.