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can bear criticism or warrant conclusions. But while we must distrust the old data, we may well accept those which in these latter years have been carefully collected by authors who under stand the exigencies of the anatomo-clinical method. By taking their stand upon these, clinicians have been able to formulate the propositions to which I am now to call attention, and which form the groundwork of topographical diagnosis in the pathol ogy of the brain. In this summary statement I intend absolutely to avoid reference to facts that are not perfectly estab. lished, for instance, those bearing on sensitive localizations. I will mention only such as may be regarded as firmly and defi nitely settled.
When a brain lesion, whether cortical or of any other sort, is accompanied by motor paralysis, the seat of the paralysis is always on the side opposite to that of the lesion. This proposition is universally accepted by physicians, and in clinics it may be said to have the force of a law. I would not have referred to this elementary truth had not some physiologists in these latter days ventured to call it in question, or at least sought to lessen its diagnostic value by citing in opposition to it alleged contradictory facts. But when these observations are subjected to criticism, it is easily seen that they have no such force as they have been credited with. In the record of a clinical case there may easily occur an error as to the side affected-"right" instead of "left," and vice versa. To some such lapsus, as I can show, is to be referred the apparent anomalousness of some, at least, of the facts alleged in opposition to the law of chiasm; hence, in my opinion, no weight is to be attached to cases, even modern cases, in which authors have not taken pains to insist explicitly on this anomaly.
And even were it proved that in a few cases, that are surely exceptional, the paralysis and the lesion producing it are both on the same side of the body, it would be necessary, before drawing an inference from such facts, to make sure that they are not to be explained by an abnormal arrangement of the nerve conductors. This calls for a few words of explanation. We know that the centrifugal, or motor, fibers proceeding from the brain decussate, those of the right crossing those of the left side at a
certain point in their course before they enter, first, the spinal cord and then the muscles. This decussation takes place at the level of the pyramids of the bulb; it gives the reason why a lesion of the right side of the brain produces paralysis of the left side of the body, and vice versa. But normally the decussation is incomplete; for though most of the motor fibers that constitute the pyramid pass into the spinal cord of the opposite side, some of them take the straight course and enter the anterior spinal cord of the same side. These fibers are, under ordinary conditions, very few in number. But it may happen, in case of an exceptional anatomic arrangement, that the fibers taking the straight course are more numerous than those which cross. Of course in such a case a lesion of the brain would be explained by an anomaly of structure, but that would give no ground of inference against the law of decussation, which still holds good in the immense majority of cases. Even granting, therefore—a thing that has yet to be proved-that this law is subject to exceptions, these exceptions are so rare that, as far as clinical diagnosis is concerned, we may leave them out of account, and hold it for a well-established truth that a paralysis of cerebral origin presupposes a lesion of the hemisphere of the opposite side. If I have mentioned incidentally the objections brought against a proposition long since become classic in nerve pathology, it was in order to show the danger of accepting theories, for so a man may be led to question the most indisputable clinical facts.
Turn we now to the study of disorders consequent on lesions of the cortex. Hemiplegia, i. e., paralysis of the movements concerned with the face and with the two members of one side of the body, is often the consequence of these lesions. But not all lesions of the cortex are accompanied by hemiplegia; they are so only when certain conditions as to the extent of the lesion, and particularly as to its seat, are present.
Now, anatomo-clinical research shows that even considerable alterations in the gray matter of the brain cause no motor disturbance when they are localized in certain regions. These regions include the sphenoidal, occipital, and inferior parietal lobes of the pli courbe and of the insula, the orbital lobule, and the anterior portion of the first, second, and third frontal con
volutions. These portions of the brain may be destroyed by softening, may be compressed or irritated by tumors, by bony splinters, or by effusion of blood, without in the least affecting the motility. The case is totally different if the region de stroyed is that corresponding to the two ascending frontal and parietal convolutions and the adjoining replis, viz., the paracen tral lobule, the foot of the first three frontal convolutions, and of the superior and inferior parietal lobules. In such cases we always find hemiplegia of the side opposite to that of the lesion. Here, then, we have a striking contrast between the gravity of the symptoms produced by lesions of this zone and the marked harmlessness, at least the latency of effects as regards the phenomena of movement, in the case of lesions to other portions of the cortex.
This contrast has been so often noted and verified in clinics that we can have no hesitation in admitting the existence, now well established, of a motor zone in the cortex. This zone occupies, as we have seen, pretty nearly the middle portion of the external surface of each hemisphere; the region anterior or posterior to this does not, directly at least, control movements.
This fact, resulting from a careful comparison of the symp toms observed during life and of the necroscopic lesions of the cortex, is further confirmed by anatomo-clinical observations of another order. The fact is well known that a nerve fiber degenerates when separated from its trophic center, which, in the case of motor fibers, is the motor cell whence these fibers emanate. On the other hand, we know that, as a sequel of certain cerebral lesions, there is developed in the peduncles, bulb, and spinal cord a degenerescence of the centrifugal or motor nerve tubes. Turck first brought this to light in 1851. Soon afterward I verified the exactitude of this observation in my researches with Vulpian. The labors of my pupils, Bouchard, Pitres, Brissaud, in France, and those of Flechsig, in Germany, have settled the determining conditions and the topography of this degenerescence-"secondary " degenerescence, as it is called. Now, not all lesions of the cortex are equally capable of producing secondary degenerescence. This special point I distinctly called attention to in one of my lectures in 1876. I attach the more importance
to what I said then, because the question of cortical localizations in man had not yet been raised, and there could be no suspicion that my statement was put forward to strengthen a theory. I said:
"Cerebral lesions en foyer, considered with respect to the seat they occupy, are not all equally capable of determining the production of consequent scleroses. Thus, among these lesions there are some which are never followed by descending sclerosis, while others are dead certain, so to speak, to produce it.. It results from my observations that extensive superficial softening, when it occupies either the occipital lobe, or the posterior portions of the temporal lobe, or the sphenoidal lobe, or, finally, the anterior regions of the frontal lobe, is not followed by consecutive fasciculated sclerosis; while such sclerosis, on the contrary, regularly appears when the foyer compromises the two ascending convolutions (ascending parietal and ascending frontal) and the contiguous parts of the parietal and frontal lobes."
Research has, during the past ten years, confirmed the exactitude of the foregoing propositions. We may, therefore, hold it as certain that secondary degenerescence is never seen except after cortical lesions; that when these lesions are in the zone which we have called the motor zone, that fact of itself suffices to prove that there is no direct relation between the motor conductors and the regions of the gray matter of the brain which we have called the latent zone, destruction of which does not cause paralytic effects.
I might cite more arguments to prove the reality of the motor zone of the cortex; in particular, I might recall the fact, demonstrated by Betz, Mierzezewski, and other authors, that its structure differs perceptibly from that of the adjoining regions, and that this zone has a mode of development peculiar to itself, as shown by Parrot. But whatever the force of these new proofs, I do not dwell upon them here, wishing to stand on the ground of clinical observation exclusively. On that ground the reality and the independence of a motor zone are universally recognized and accepted to-day.
The question now arises whether this zone is functionally homogeneous, or whether, on the contrary, it is not resolvable into distinct centers, each concerned with the movements of some special part of the body. Let us see what is to be learned on this point by the anatomo-clinical method. Motor paralyses
resulting from lesions of the cortex do not always assume the form of hemiplegia. They may affect the face, the arm, or the leg; in that case there is "monoplegia," or, as Nothnagel terms it, "parcellary paralysis." We must observe that monoplegia does not necessarily depend on lesion of the cortex. Besides cases of monoplegia due to hysteria there are some that are due to affections of the motor conductors at points in their course more or less distant from the convolutions. But we, of course, have to do only with monoplegia caused by lesion of the cortex. Now can we, from the localization of a monoplegia, infer the seat of the affection which produces it? In 1883 I was led to conclude, from researches made in conjunction with Mr. Pitres, that the cortical motor centers for the two members of the opposite side are situate in the paracentral lobule and in the superior two-thirds of the ascending convolutions; that the centers for the movements of the lower part of the face are situate in the upper third of the ascending convolutions, near the fissure of Sylvius; that very likely the center for the isolated movements of the arm lies in the middle third of the ascending parietal convolution of the opposite side. Nothnagel reached these same conclusions through a close analysis of a multitude of facts, and they are confirmed by observations published since 1883. This is specially true as regards the motor center of the inferior members, the localization of which has been determined with the utmost exactitude. Sundry recent facts, particularly those, at my instance, collected by one of my pupils, Mr. G. Ballet, have, in fact, shown that the paracentral lobule, with the uppermost part of the frontal and ascending parietal convolutions, has specially to do with the motility of the femur and crus. Hence, when a case occurs of monoplegia of the inferior member referable to a lesion of the cortex, we can affirm that a lesion localized at the points mentioned is the cause.
Paralysis is not the only manifestation which enables us to diagnose a lesion of the cortex and to point out its seat. Alongside of the "deficit" symptoms, so called, must be ranged the "excitation" symptoms, which are also of the very highest diagnostic value in nervous clinics. The symptoms of this