In this section the postcentral gyral cortex will not be considered, as it is more accurately included in the central, or Rolandic, cortex than the bulk of the parietal lobe cortex. Hence, the reader is referred to Chap. 8 regarding this cortex.

When one views the registries of epilepsy cases from many institutions, there is often a relative paucity of cases of parietal lobe epilepsy. While there is some variety in the percentage of parietal lobe epilepsy (PLE) cases, nevertheless many figures fall beneath the 10 % mark. I suspect that parietal lobe epilepsy is more common than is normally appreciated in these registries. One of the reasons for this is that this cortex cannot be considered “eloquent” in the way that it is defined and utilized in this book (see Sects. 3.​1 and 4.​1). Some refer to this as “association” cortex. Thus, it is not uncommon to have parietal foci in the mid- to posteroparietal cortex that comes to notice when the epileptic discharge spreads to juxtaposed cortices, which do represent eloquent cortex the stimulation of which exhibits clinically recognizable altered neurological function, e.g., visual, Rolandic, post-Sylvian temporo-occipitoparietal dominant cortex, etc. Under these circumstances clinical observations of the epileptic semiology lead to these epileptic foci being more likely attributed clinically to these eloquent cortices, than to the clinically silent (i.e., non-eloquent) association cortical foci in the parietal cortex, per se. This is exemplified in various parts of the literature. The statement “It has been long recognized that clinically similar seizures may arise from epileptic foci at different sites and that a focus at a particular site may give rise to a variety of seizure types by virtue of differing pathways of seizure spread” was the initial sentence of the very excellent paper devoted to a consideration of parietal and occipital lobe epilepsies by Sveinbjornsdottir and Duncan (1993). The publications of Williamson et al. (1992) and Salanova et al. (1995) are also good descriptions in dealing with PLE. The latter describes the patients with parietal lobe epilepsy who were investigated at the Montreal Neurological Institute over a 50-year period.

The Montreal series of patients with parietal lobe epilepsy was similar to many epilepsy centres, in that a great number of their epileptic cases had primarily Rolandic semiology, either alone or with associated features such as “dizziness, cephalic sensation, conscious or unconscious contraversion, epigastric sensation, dysphasia, or automatism” (Rasmussen 1975b).

The medical students who were educated before the waning years of the twentieth century will remember learning that the parietal lobe cortex, posterior to the postcentral sulcus, was involved in numerous activities, such as dressing, distinguishing between right and left sides of the body, agnosia associated with the identification of fingers, etc. In large part the origin of these neurological deficits was attributed to the parietal cortex, posterior to the postcentral gyrus, by Critchley in his The Parietal Lobes (1955). However, it is now known that this is perhaps more the result of the destruction of the white matter underlying the mid- to posterior parietal cortex, as Rasmussen has shown that the removal of this cortex, per se, posterior to the postcentral sulcus, may infrequently be associated with mild, transient sensory deficits, but never associated with a permanent sensory neurological deficit (Corkin et al. 1970; Rasmussen 1975a, p. 298). That is to say, a pure “decortication” of this posterior parietal cortex results in no clinically demonstrable permanent defect. However, Mattingly et al. with the currently available much more sophisticated investigative technology have more recently demonstrated evidence of complex alterations in movements as determined by subtle unilateral neglect in patients with inferior parietal lobule (IPL) lesions (1998).

I will add to the immediate foregoing a paragraph in a letter that Dr. Rasmussen wrote to me in 1984: “In regard to the parietal cortical excisions, we have not seen the “parietal syndrome” from excisions in either the dominant or the non-dominant parietal lobe. I am sure this syndrome which is most clearly seen in patients with stroke is actually due to damage to projection fibers from the depths of the parietal lobe, and does not occur when the parietal lobe excisions are carried out the way they do for epilepsy. We have not seen this even when we have removed the posterior third of the non-dominant hemisphere up to the postcentral gyrus.”