Parietal Lobe

PARIETAL LOBE (lobus parietalis) of the brain is bounded from the frontal lobe by the Rolandic fissure, from the limbic lobe (on the medial surface) by the posterior part of the sulci calloso-marginalis and sulci subparietalis, from the occipital lobe by the parieto-occipital fissure, the Brissau fissure and then by an imaginary line extending downward to the incisura praecoccipitalis, and finally from the temporal lobe by the Sylvian fissure (in the anterior part, while in the posterior part the boundary is not defined by morphological characteristics). The constant sulci running along the lateral surface—the postcentral and interparietal—divide the parietal lobe into three lobules: the postcentral (between the Rolandic and postcentral sulci), the superior parietal (above the interparietal sulcus, which also includes the precuneus on the medial surface), and the inferior parietal (below the interparietal sulcus). The inferior parietal lobule is divided by the Jensen fissure into an anterior part (gyrus supramarginalis), encompassing the end of the Sylvian fissure, and a posterior part (gyrus angularis), encompassing the end of the first temporal sulcus. In addition to the aforementioned constant sulci in the parietal lobe (especially in the inferior lobule), there are numerous variable sulci, differently expressed in different individuals. In this case, the left inferior parietal lobule in right-handed individuals is significantly richer in sulci than the right one. The blood supply to the parietal lobe is provided mainly by the posterior branches of the Sylvian artery fissure. The above description of the parietal lobe, accepted in macroscopic anatomy, requires significant amendments based on more precise architectonic data related to the functional significance of this area, namely: the inferior parietal lobule currently includes an extensive area below the gyrus angularis (macroscopically belonging to the temporal lobe), which, wedged between the occipital and temporal areas, extends to the basal surface of the brain. This is the so-called basal field (Brodmann's 37), having architectonic features of the inferior parietal lobule. On the other hand, the postcentral area, based on architectonic and functional characteristics, is excluded from the parietal lobe and is described separately. Thus, in the composition of the parietal lobe, we will have the superior parietal area—fields 7 and 5 according to Brodmann or PE and PA₂ according to Economo (although the latter PA₂ refers to the postcentral area), and the inferior parietal—fields 40 (area supramarginalis, PF), 39 (area angularis, PG), and 37 (area basalis, PH). Additionally, in the depth of the interparietal sulcus, there is a special formation—the Smith's band (sensory visual band). Cytoarchitectonically, the superior parietal fields belong to the second type of cortex according to Economo—of medium width, large-celled, with well-developed granular layers and a light stripe in layer V. The inferior parietal fields, differing from each other in details, are characterized by great width, multicellular, highly differentiated, with a particularly well-developed layer III, with pronounced granular layers. The cortex belongs to the third type of Economo, along with the most differentiated frontal fields. Within the inferior parietal fields, a significant number of areas (subareae) have been identified, however, it should be emphasized the indistinctness, uncertainty of boundaries not only between these subareae but also between the main fields, the abundance of transitional areas, and the enormous variability of cytoarchitecture in different individuals. Unlike other areas (with the exception of the frontal ones), the inferior parietal fields possess the most complex and variable architecture, as if not having formed into strictly fixed morphological structures. The inferior parietal fields are an exclusive feature of humans. Some rudiments of field 37 are found only in the orangutan (Gurevich), which is apparently associated with the presence of finger praxis in higher monkeys (Krol). The inferior parietal fields also develop ontogenetically later than other cortical areas (they correspond to Flexig's 'posterior associative' field with late myelination). The most important connections of the parietal area: bilateral connections with the visual thalamus, with the cerebellum through the bridge nuclei (parieto-ponto-cerebellar pathways), with the central motor cortex—the centroparietal bundle of Monakoff (fugal pathway from area 40), with the frontal cortex—fasciculus arcuatus (in particular, Quensel described a bundle connecting field 39 with Exner's place in the posterior part of the second frontal gyrus). Additionally, the inferior parietal fields are connected by association pathways with all adjacent sensory areas (temporal, postcentral, occipital). Commissural connections—through the splenium corporis callosi (forceps posterior). Upon irritation of field 7, contralateral movements of the limbs and clonic convulsions are obtained. The motor reaction is a consequence of the transmission of irritation to the posterior and central gyri, as well as to the subcortical motor centers (through the thalamus). Lesion of the superior parietal area results in 'weakening of sensitivity (especially muscle sense), disturbance of stereognosis, hemiataxia. The disturbance of sensitivity does not have a somatotopically defined character (unlike lesions of the posterior central gyrus). In cases where the epileptogenic zone is in the superior parietal area, an aura of sensory type is observed in the form of paresthesia and pains on the opposite side. With experimental irritation of the inferior parietal fields, no motor effect is obtained. With various pathological changes in these fields (40, 39, 37), very complex and diverse disorders are observed, which are mainly related to apractic and agnostic phenomena. It is characteristic in this case that we are dealing with disorders that spread to a greater or lesser degree to various functions, which however are not affected entirely, but only change and decrease to a more primitive level. In the gnostic respect, the patient can understand one thing and not understand another, can grasp a part and not recognize the whole, orient in one situation and not orient in another, etc. Similarly, in the patient's actions, partial decreases, disintegration of complex acts and skills are observed. With various localizations of lesions within the inferior parietal lobules and depending on the extent of changes, emphasis is placed on one or another disorder. Apraxia (Lipman, Krol) is observed with lesion of field 40; in this case, pure motor apraxia occurs with lesion of the white matter under the cortex of this field (Krol), i.e., with violation of the connection of this cortex with the motor fields. With violation of the cortex of field 40 itself, according to Goldstein, ideational apraxia is obtained, which however is disputed by Krol, who considers that ideational apraxia complicates motor apraxia as a result of more extensive lesions (e.g., in cerebral arteriosclerosis). Depending on the extent of the lesion and the detailed features of localization, other varieties of apraxia also occur: innervator apraxia, manifested only in the area of one limb or its part, constructive apraxia with violation of the optico-kinesthetic synthesis and the ability to reconstruct a whole from parts. In this case, the ability to draw is violated (with possible preservation of automated writing).—With lesion of the cortex of field 40, astereognosis is observed without other changes in sensitivity (difference from violations of stereognosis with superior parietal lesions).—Aphasia observed with lesions of the inferior parietal fields manifests differently; the most indisputable is amnestic aphasia, relating to the basal field. Other forms of aphasia described by various authors cause objections: total parietal aphasia (Marie, Foix), according to Monakoff, requires participation of temporal fields; parietal aphasia described by Head (field 39) is characterized by the fact that patients understand speech but do not fully grasp its complete meaning, getting stuck in details and being unable to form concepts from what is heard, to connect what is said into a unity. This form undoubtedly goes beyond the speech disorder and is complicated by changes in thinking; finally, conductor aphasia with paraphasia and disturbance of word repetition (field 40) is also disputed by many as an independent form with this localization. Agraphia occurs with foci in two places: in field 39 on the border with the visual fields—Dejerine's place, and on the border with the temporal area—Pick-Wernicke's place. In Dejerine's agraphia, alexia, amnestic aphasia, sometimes hemianopia, disturbances of direction, and no word deafness are usually observed; in Pick-Wernicke's agraphia, there is word deafness, without alexia and hemianopia (German and Petsch). Additionally, optokinetic nystagmus is disturbed in the first case, preserved in the second (Krol). Both parietal forms of agraphia differ from pure motor frontal agraphia of Pitres in that with them the function of writing is disturbed with any organ, not only the right hand (due to disturbance not of the movement itself, as in the frontal form of agraphia, but of the corresponding formulas and sensory prerequisites). Sometimes with parietal lesions, writing is disturbed only in the sense of direction—mirror writing, vertical.

These disorders form the basis for the assumption that in the lower parietal area there are mechanisms determining direction, the disruption of which affects not only writing but also optico-gnostic functions and spatial orientation. The mechanisms of direction are probably also connected with the vestibular apparatus, which apparently has its cortical representation in the lower parietal area. -Furthermore, when the angular gyrus is affected, the following are observed: alexia with preserved copying (a difference from pure verbal blindness of occipital type), acalculia, and disorders of spatial and temporal gnosis. When there are lesions in the depth of the intraparietal sulcus, geometric-optical disorders (metamorphopsias), changes in body schema (see Body schema) with disorientation in one's own body (autotopagnosia of Pick), in the right and left, etc., are observed. This also includes symptoms of foreignness of parts of one's own body and one's own voice, painful asymbolia, anosognosia of Babinski (loss of perception of painful changes in one's body, e.g., hemiplegia), finger agnosia of Gerstmann (however, the latter Pötzl and Kroll attribute to innervatory apraxia). When the schema of one's own body is disrupted, the gnosis of another's body is sometimes also impaired, as a result of which a sculptor with autotopagnosia loses his skill, a patient with agnosia of his own face cannot draw a human face, and a patient with finger agnosia cannot draw a hand (Engerth).-Finally, when the lower parietal fields are affected, a peculiar dementia is observed. Patients recognize individual objects in their surroundings but not the entire 'situation,' they have simple judgments but not complex inferences, they are unable to combine multiple impressions; they find it difficult to switch from one type of thought or action to another, to turn successive into simultaneous (i.e., to create a unified representation from a sequential series of impressions). Conceptual, abstract thinking (categorical according to Goldstein) is disrupted. These disorders, along with amnesic phenomena and the various symptoms described above, render such patients helpless and unable to work, but they usually maintain external correctness of behavior (unlike cases with frontal lesions). Most of the described disorders are usually associated with lesions of the left P. l., which is definitely dominant over the right (in right-handed individuals), but undoubtedly many disorders are also observed with right-sided lesions, especially agraphia, disorders of body schema, acalculia, and partly apraxia, etc. However, the question of the distribution of functions between the left and right parietal areas is unclear. In general, the study of parietal areas began relatively recently, and much in this matter is controversial and not established. It is only certain that the lower parietal fields, located between the main sensory areas (postcentral, occipital, and temporal), are the site of complex sensory synthesis, as a result of which when these specifically human fields are affected, gnosis and complex movements, characteristic exclusively of humans, are disrupted. The motor disorders here are secondary (unlike frontal ones), resulting from partial shutdowns of the corresponding synthetic sensory prerequisites. Therefore, this area can be called psychosensory (just as the frontal is psychomotor).-Taking into account that localization of a disorder does not yet prove localization of functions, which rely on many systems and are disrupted when various links in these systems are affected, and considering in particular the impossibility of localization of complex psychic functions, connected with the activity of the brain as a whole and even of the entire organism, we must nevertheless recognize that in the lower parietal fields, as specifically human formations, there are particularly important reference points for these functions; therefore, when these fields are affected, psychic activity is often impaired to a greater or lesser degree. Lesions of the parietal fields are possible in arteriosclerosis, brain tumors, skull injuries, etc. Characteristic is their almost constant selective involvement in Pick's disease. There are data on involvement of this area in schizophrenia. Finally, it should be mentioned that in skull defects in the parietal area, Pötzl, Hoff, and others were able experimentally (by freezing, etc.) to induce some of the symptoms described above (disruption of body schema, alexia, disorders of direction, etc.).