Pathoarchitectonics

PATHOARCHITECTONICS, a concept introduced by C. and O. Vogt to designate pathological changes in the central nervous system concerning its architectonic structure. Although the facts related to this were known earlier, they were first systematically and detailedly developed in the well-known work of the Vogts. Since pathoarchitectonics deals with systemic changes, this concept is closely connected, on the one hand, with the concept of topistics and, on the other hand, with the concept of pathoclise. By topistics, C. and O. Vogt understand "the doctrine of unities united on the basis of common properties or features." These morphologically functional unities can correspond to topographical areas. In this case, topistics coincides with the doctrine of localization. But these unities can also be systemic, uniting areas, although spatially distant from one another, but possessing one or another common property. Furthermore, the unities singled out by topistics can be subdivided into supracellular and infracellular. The former encompass complexes of neurons, the latter only individual parts of specific neurons. In both groups, one can further encounter more elementary and more complex unities. The characteristics of each department of the nervous system are so diverse that for topistic definitions one can choose either one of them or another and thus isolate various topistic unities containing the same elements. The very features on the basis of which the isolation of topistic unities proceeds can be of a physiological, pathoclinic (see below), or anatomical character. Examples of topistic unities: the area gigantopyramidalis represents a unity of a physiological character, since only it reacts with special tonic movements to minimal stimuli; the area striata forms a unity of a different, namely, anatomical-systemic character, since it receives all corticopetal pathways from the lateral geniculate body. The fields singled out by architectonics, as well as the individual layers of each field, represent architectonic unities. Examples of topistic unities of varying degrees of complexity: a cortical layer represents a relatively elementary unity, an architectonic field a more complex unity, the entire cerebral cortex a unity of an even higher order. But topistics should not be limited only to the isolation of topistic unities. Its tasks also include the study of the interdependence of such unities, which can explain many data of experimental physiology and clinical symptomatology. In some cases, such dependence is negligible; for example, visual acuity does not change from deafness that has occurred at a late age, etc. In other cases, it is expressed very sharply. Thus, with a sudden lesion of known topistic unities, the function of others, which are in close functional connection with the first, suffers greatly—what C. Vogt designates as a dislocation of functions, and Monakow as diaschisis (see). Furthermore, an already smoothed-out defect of a particular topistic unit is revealed anew if "auxiliary topistic units" are damaged. Finally, remaining unaffected topistic unities can act compensatorily upon the lesion of other units standing in close relations with them. The lesion of a particular topistic unity or a complex of such unities by a particular pathogenic agent constitutes the subject of study of pathoarchitectonics. In this regard, the concept of pathoclise is of fundamental importance. Pathoclise is the tendency of a certain anatomical formation to react with a special pathological process to a known harmful agent. Such a special pathoclise is demonstrated, for example, by the pallidum, which reacts with the formation of necrotic foci and cysts to carbon monoxide poisoning, while the striatum, which is in very close connection with it, and the adjacent internal capsule do not show any changes in this regard. The striatum exhibits the exact same special pathoclise; thus, in the case of Wilson's disease described by Bielschowsky, it was exclusively a matter of a lesion of the putamen. But pathoclise can also be general rather than special. If we compare the number of harmful moments to which the striatum reacts with the number of those leading to disease of the pallidum, we come to the conclusion that the striatum is generally much more vulnerable or, in other words, that the striatum is characterized in comparison with the pallidum by a general pathoclise. This general pathoclise can lead to very different diseases, as can easily be seen from the example of the striatum. Such a general pathoclise is called nonspecific. But within the framework of such a nonspecific general pathoclise, specific subgroups can also exist. For example, progressive status fibrosus of the striatum can arise under the influence of various pathogenic factors. We thus have, within the limits of the nonspecific general pathoclise of the striatum, a specific general pathoclise expressed by the tendency to react to a whole series of various insults with the same pathoarchitectonic process of elective cellular necrosis. Also, status marmoratus by C. Vogt must be understood as a reaction to very different pathogenic moments and at the same time as a manifestation of a specific general pathoclise as well. Both special and general pathoclise can affect a single topistic unity. In such cases, one speaks of monotopic pathoclise. But pathoclise can affect many topistic unities simultaneously and sometimes even those that are not in close functional connection with each other. In such cases, one speaks of a polytopic form of pathoclise. In polytopic pathoclise, topistic unities can fall ill one after another in an irregular sequence. In such cases, we are dealing with metabolic polytopy. Thus, in paralysis agitans, either the striatum or the pallidum falls ill first. But the sequence of involvement of individual topistic units in the disease process can also be very regular. In such cases, it is a matter of so-called eunomic (i.e., having a regular sequence) polytopy. In the region of the striatal system, this would take place if the pathological process that began in the striatum spread for pathoclinic reasons to the pallidum. Finally, there is yet another division of pathoclises according to a completely different principle. A harmful agent can affect a fully developed individual and cause a pathological change in a known topistic unity. In such cases, it is a matter of a non-hereditary disease, and C. and O. Vogt speak here of somapathoclises; for example, the reaction of the pallidum to carbon monoxide with total necrosis serves, according to C. and O. Vogt, as an example of such a somapathoclise. But a harmful agent can also act on the germ plasma and alter specific genes within it. In all such cases, hereditary diseases arise, and the authors speak here of "Generj-Pathoklise". An example of such a pathoclise is precisely status marmoratus.—Between normal and pathological phenomena, abnormal phenomena that do not yet cause disease should be included. Correspondingly, C. and O. Vogt, alongside the concept of pathoclise, single out the concept of propathoclise. Such propathoclinic phenomena can be observed in the pallidum, which already in normality and in young people exhibits calcium deposits in the media of blood vessels. From here, all transitions to proper pathological phenomena are already possible. Of great interest are attempts to explain the essence of pathoclise. C. and O. Vogt consider a whole series of possibilities presented here. One can explain the preferential lesion of a given topistic unity by unfavorable blood supply conditions. Kolisko, for example, explained the symmetrical softening of the pallidum on both sides in carbon monoxide poisoning by the fact that the pallidum is supplied by very narrow and non-anastomosing arterioles. Anton explained the softening of the striatum in chorea by features of blood supply, and Mott explained the localization of the cortical process in progressive paralysis assumed by him. Another explanation given is a reference to Edinger's wear-and-tear theory—concerning the primary death of neurons due to an existing disproportionality between synthesis and decay processes. The predominance of decay is explained either by excessive tension of normal neural tissue or by the normal work of elements that are constitutionally weak or weakened by diffuse intoxication. Such an explanation is clearly mechanistic, just like another explanation—by the action of mechanical causes. Thus, Bielschowsky attempts to explain the general pathoclise of the third layer of the cerebral cortex by a special lack of resistance of this layer to mechanical stretches (in the second layer there are strong glialous fibers, from the fourth downward—resistant myelin fibers). Belonging here is also the attempt to explain the lesion of Ammon's horn cells and fasciae dentatae in epileptics, known since Meynert, as a consequence of increased intracranial pressure. The cited explanations, minus their small factual substantiation, cannot satisfy also because in their logical development they lead to the recognition of the irreparability of neuropsychiatric diseases, to fatalism, and to the irreversibility of certain pathological processes.

While not denying the greater or lesser vulnerability of individual systems, and consequently their susceptibility to pathological processes, one cannot possibly agree with the proposition that logically leads to the conception of pathoclisis as a kind of predetermined mechanism of "wear and tear." Such a mechanistic understanding reduces to nothing the peculiarity of local processes and their role in compensatory mechanisms arising as a reaction of the holistic system to a pathological process of a local nature. The following explanation, which reduces the phenomena of pathoclisis to the phenomena of heredodegeneration (Schaffer), is subject to criticism primarily from the standpoint of the untenability of this latter concept. As an explanation, reference is also made to the inverse proportionality existing between the vulnerability of individual systems and their onto- or phylogenetic age. Phylogenetically and ontogenetically younger units should be more vulnerable, i.e., exhibit the phenomena of general pathoclisis. Thus, for example, Schaffer assumes that in progressive paralysis, it is chiefly those fields of the cortex that myelinate later that are affected, and therefore, for example, the special vulnerability of the third layer could be linked to the circumstance that it reaches its full development only comparatively late. Such an explanation is closer to the truth if one has in mind not the entire process as a whole, but one of the conditions entering into it. C. and O. Vogt reduce all pathoclinic phenomena to differences in the physical chemistry of individual topistic units or their genes. This view is based on the circumstance that in the overwhelming majority of cases, pathoclises occur in such topistic units which, already on the basis of physiological, architectural, and similar traits, are distinguished as such. The indicated authors see confirmation of their view in Ehrlich's doctrine of receptors for known toxins. If various tissues possess various receptors, then differences in metabolism within them are a direct consequence of this. Finally, C. and O. Vogt believe that their explanation of the nature of pathoclisis finds very great justification in the circumstance that pathoclinic phenomena can be regarded as a special case of a much broader group of phenomena, namely, the phenomena of physioclisis, "governing all variation of living beings." By physioclinic phenomena, O. Vogt understands "exogenously conditioned reactions, the character of which is determined by the physico-chemical differences of individual parts of the organism." The factual material used by C. and O. Vogt as the basis for the doctrine of patho- and physioclisis can by no means be recognized as exhaustive in any way. The attempt to ascribe "selective" vulnerability to topistic units in the Vogt sense still has a far from sufficient factual basis. Even less substantiated by facts are the considerations of Vogt (as well as Bielschowsky) on the pathogenesis of this vulnerability. Completely unacceptable are the theoretical foundations of Vogt's doctrine of pathoclisis, which contain, on the one hand, the vulgar materialist assertion that "the physiological features of the cortical field are reduced in the final analysis to its physical chemistry," and on the other hand, an idealistic attempt to depict the fact of a certain sequence in the spread of the pathological process to various cortical layers ("eunomia" according to Vogt)

as allegedly proof against Darwin's doctrine of the role of chance in biological development, as an argument in favor of the presence of "eternal, primordial, great laws" predetermining our existence. In inseparable connection with the doctrine of C. and O. Vogt on pathoclisis stands their doctrine on the essence of neuropsychiatric diseases. From the fact that electrical stimulation of various areas of the cortex gives a different motor or sensory effect, the mechanistic conclusion is drawn that mental functions of any complexity are also strictly localized to specific, limited cortical areas. Likewise, this is asserted regarding psychotic syndromes. From this point of view, psychosis turns out to be necessarily an expression of the inferiority of a known topistic unit, and this inferiority, again, is necessarily rooted in the genotype and sooner or later brought to light by exogenous factors. The features of the genotype are said to fatally predetermine both the disease itself and its specific form. Thus, to discover pathoclisis means, according to Vogt, to uncover both the etiology, and the topics, and the pathophysiology, and the clinical picture of a neuropsychiatric disease and, moving along this path, to resolve the complex problem of neuropsychiatric classification. The indicated construction has nothing in common with the only scientific dialectical-materialist understanding of disease. In the Vogts' doctrine, the constitutional features of the organism are identified with the features of its genotype, mechanically contrasted with the influences of the environment, which appears as something allegedly external to the organism. The concrete historical formation of the personality under certain social conditions, its consciousness, its character, its physiological features are ignored—that is, precisely that question the study of which alone constitutes in medicine a truly reliable basis for approaching the etiology, pathogenesis, and clinical manifestation of diseases, their varying resistance to disease and varying ability to overcome it once it has arisen. To account for this most important side of the problem, the authors of the doctrine of patheoarchitectonics prefer far-fetched references to the laws of "variation of living beings" and, moreover, laws derived from observation of lower representatives of the animal world. From this—from a logical standpoint—flows the simplicity of conceptions regarding the connection between etiology and the form of manifestation of diseases, regarding the principles of their classification. The bourgeois nature of these views and their suitability for use for reactionary political purposes are entirely obvious.