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THE PYRAMIDAL TRACT Its Status in Medicine By A. M.
Professor of Anatomy Boston University School of Medicine Boston, Massachusetts
CHARLES C THOMAS • PUBLISHER Springfield • Illinois • U. S. A.
Publication Numbe, 233
AMERICAN LECTURE SERIES®
The BANNERSTONE DIVISION of AMERICAN LECTURES IN ANATOMY
OTTO F. KAMPMEIER, Ptt.D., M.D. Professor of Anatomy and Head of Department, 1928-1951 Professor of Anatomy, Emeritus, 1953 Professor of Medical History, 1951-1953 University of Illinois College of Medicine, Chicago Head of Department of Anatomy Schooi of Medicine, College of Medical Evangelists Loma Linda, California
CHARLES C THOMAS • PUBLISHER BANNERSTONE HousE 301-327 East Lawrence Avenue, Springfield, Illinois, U.S.A.
Pub/ished simultaneous/y in the British Commonwealth of Nations by BLACKWELL SCIENTIFIC PUBLICATIONS, LTD., OXFORD, ENGLAND
Pµbli.rhed simultaneously in Can4da by THE RYERSON PRESS, TORONTO
This monograph is protected by copyright. No part of it may be reproduced in any manner without written permission from the publisher. Copyright 1954, by CHARLES C THOMAS • PUBLISHER Library of Congress Catalog Card Number: 54-10787
Printed in the United States of America
OLIVE A. IRVINE, M.
Contents A. INTRODUCTION .
B. EVENTS LEADING TO THE DISCOVERY OF THE PYRAMIDAL DECUSSATION-460 B.C.-1710 A.D.
C. GROSS ÜBSERVATIONS (1710-1870)
D. NORMAL HISTOLOGICAL STUDIES
E. STUDIES IN SECONDARY DEGENERATION (PATHOLOGY)
F. INVESTIGATIONS IN RETROGRADE DEGENERATION
G. RESULTS OF ELECTRICAL STIMULATION
H. SIGNS AND SYMPTOMS •
1. SURGICAL ÜPERATIONS lNVOLVING PYRAMIDAL TRACT
RESULTS OF ANIMAL EXPERIMENTATION .
K. A CONSIDERATION OF THE AFFERENT SYSTEM
L. THE STATUS OF THE PYRAMIDAL TRACT IN MEDIONE
N. CHRONOLOGICAL ÜUTLINE OF BASIC PYRAMIDAL TRACT
lNVESTIGATIONS IN MAN
Ü. CHRONOLOGICAL ÜUTLINE OF SUBHUMAN EXPERIMENTS ON PYRAMIDAL TRACT
Introduction MovEMENT, or the ability to propel through space, is characteristic of the biological world. There are some authorities who are convinced that the central nervous system has evolved primarily to produce motion. Although the pyramidal tract is universally regarded as being concerned with innervating volun tary muscles, all chordates below mammals (pisces, amphibia, reptilia and aves) are able to make adjustments to their respec tive environments without it. The motor behavior in sub-mam malian species varies but evolves from simple undulating swim ming actions to hopping, to walking, climbing and running, and finally to flying. The problems for those interested in broad research on the pyramidal tract would be probably tc:i find what its true anatomical, physiological, pathological and clinical role may be in mammals. lt is the purpose of this monograph to collect and correlate the known facts on the pyramidal bundle in an attempt to ascertain its true status in medicine. There are about a half-dozen pathways in the central nervous system about which much is known and can be written. The pyramidal belongs to this group. The reasons for this are inher ent in the tract itself. lt was one of the first fasciculi to be ob served in man and to excite general curiosity. lt was assigned a major function and the results of a continuous series of investi gations over a period of many years did not materially alter the original conceptions of it. Further, no other group of fibers in the central nervous system resembles it in respect to its length, its varying position from the surface, its square area, its fiber . constituents, its splitting into bundles, its crossing characteristics
and its blood supply. It has been regarded as the most vulnerable division in the brain and spinal cord on the basis of the fre quency with which voluntary motor paralysis, a debilitating symptom, is encountered clinically. Therefore, the pyramidal tract should have considerable applied signifi.cance. This pathway has apparently been of investigative interest principally to medical men. Most of the fundamental facts regarding its status in man were contributed before 1900. The majority of publications have emanated from the countries of Britain, the U. S., Germany, France and Italy. These five nations have published about 95 % of all the articles listed under the heading of "pyramidal tract" in the Medical Index as far back as can be traced. Very few investigators have devoted their full time and energies to investigating it so that the studies, on the whole, have been scattered, heterogeneous and little cor related. Every neurological investigative approach has been utilized in studying the origin, course and termination of pyramidal neurons. The following is an outline of the methods employed: A. Anatomical. I. Gross dissection. II. Embryological-the myelinogenetic method. III. Histological-including biometrical studies. B. Physiological. I. Electrical and strychnine stimulation. II. Effect of lesions-experimental, diseased processes and surgical. C. Pathological. I. Studies of secondary degeneration-experimental and pathological. Involves the use of such stains as silver, myelin sheath, cellular and Marchi. II. Retrograde degeneration. D. Clinical-studies of signs and symptoms in man.. All the general methods were applied, in one form or another,
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before the year 1909. Of the categories listed above, the physio logical has been apparently the most popular. The gross dissec tion and myelinogenetic approaches have enjoyed but a short vogue. Probably the biggest gap in our over-all knowledge of the pyramidal tract in man exists in the neuropathological field because few exact scientific studies have been made since the original pertinent investigation of Bouchard in 1866. Great reliance and confidence have been placed on certain specific rnethods of investigation. For example, the results of retrograde degeneration have to be regarded as important since they were initially judged to prove unequivocably that the pyramidal fibers arise from Betz cells. In rnore recent years, the application of silver stains in studying degeneration in the fibers and their end bulbs as well as oscillographic recordings following stimula tion of the tract fibers have been added to the array of research procedures. On checking and comparisons, it is noticeable that there are hardly any two investigations on the pyramidal tract, using identical technics, which harmonize in all essential facts. Every neurological method seems to have some inherent weakness. There is no one stain, for instance, which acts on all the com ponent parts of a pyramidal neuron. All the approaches utilized for studying function are crude by comparison with what goes on normally in the brain and cord. Besides, there is a human factor which depends upon the background, skill and interpreta tive ability of the contributing investigators. Although the foundational studies were made on man, the pyramidal tract has been investigated broadly. Sorne animals have been observed more than others. Certain species, because of their restricted and remote geographical location from the important neurological laboratories, have not been analyzed from the standpoint of their motor systems; in this category can be placed such groups as edentates ( ant-eaters), insectivores ( moles), cetacea ( whales) and chiroptera ( bats) . Base of ob-
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tainance has undoubtedly been a factor in the selection of such animals as the rat, cat, dog and monkey. Such investigations as have been made show that the pyramidal tract is a relatively late phylogenetic addition to the central nervous system, that it is not cast on any standard mold and that there is a gap in our knowledge of its anatomy and physiology in marine and air mammals. From the medical point of view, research on the pyramidal tract of sub-human mammals would be probably classified as basic. The question arises as to what practical value results from studies on lower ranking mammals. The great concept of cere bral motor localization began with a emde, electrical experiment on the cortex of the dog (Fritsch and Hitzig, 1870) and this approach has been popular and influential ever since; the phylo genetic age of the pyramidal tract is thought by some clinicians to be of significance in its susceptibility to diseased processes and actual physical and chemical differences have been prognos ticated for it on this basis ( Brouwer, 1920) . Observations on sub-humans have also been taken into consideration by clinicians in respect to the type, character and permanency of the paralysis produced by pure lesions in the pyramidal tract. From the phylogenetic aspect, pyramidal neurons have been investigated in some mammals in respect to their origin, course and termination. Attention has been paid to the lower extent of the bundle, the position it may occupy in the funiculi of the spinal cord and whether it subdivides into component parts. Since it has been found that the constant feature of the pyrami dal tract is its passing, in relative isolation, through the anterior pyramids of the medulla oblongata, this region has been chosen as a site to make biometrical measurements. Its square area, the determination of the size of the individual fibers and the total number of axons as weil as its degrees of myelinization have been studied in the pyramids. There have been a few attempts to correlate the physio-
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logical results obtained on motor studies in lower mammals with the anatomy of the tract. Most of the functional work has been clone by means of either electrical stimulation, abla tions of the motor cortex or section of the pyramic:ls. The last two named methods have been the most influential and in late years the results obtained in apes have been instrumental in raising questions regarding spastic or flaccid phenomena. Both morphological and physiological results indicate that the tract assumes more importance in its evolution from lowest to highest mammals. Although the pyramidal tract offers an opportunity for studies in experimental pathology, only several investigations have been made. These have been concerned with determin ing the sensitivity and reaction of the large, intermediate and small-sized neurons in response to trauma of their cells of origin. The advantage of the experimental method in sub-human mammals lies in the fact that accurate circumscribed lesions can be made in some portions of the pyramidal tract and their effects studied. The disadvantages from the clinical viewpoint are the following: Comparatively speaking, lower mammals do not have a well-developed pyramidal tract, their postures are not erect and their voluntary movements are less skilled. Investigations restricted to man alone have the handicap that they must concern themselves largely with the experiment of disease, the lesions of which may not be accurately localized. lt may be, however, that the key to the understanding of the pyramidal tract in man lies in ascertaining the meaning of its varied morphological and physiological characteristics through out the phylogenetic scale. By continued research, the question may be solved as to whether it basically changes its function as the mammalian phylogenetic scale is ascended. There exists a tremendous volume of literature revolving around the pyramidal tract in man. Some of this is off the
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beaten highways and is to be found objectively in general articles or isolated case reports. There is an extensive bibli ography on the sign of Babinski alone. A review shows that human paralysis has been known and speculated upon for thousands of years; the anatomy, physiology and pathology of the pyramidal tract has been studied for about a century. The view which developed quickly in the mid-nineteenth century and became firmly crystallized in the minds of medical men is that the pyramidal tract is the great motor fasciculus and that when involved by pathological lesions there develops a definite syndrome. This involves interference with movement, tone, and reflexes. The classical symptomatology usually given is the following: paralysis of voluntary motion, the presence of spasticity, the absence of atrophy in the muscles, the ability to respond actively to electrical stimulation of peripheral nerves in spite of paralysis and finally a host of abnormal reflexes among which the Babinski is regarded as the most important. Not all the muscles are said to be affected equally by pyram idal lesions, some being more vulnerable. lt is only in recent decades that some of these traditional concepts have been questioned. Throughout the years, numerous scientific terms have been selected to describe pyramidal lesions producing paralysis of voluntary motor muscles such as hemiplegia, paraplegia, diplegia, monoplegia, tetraplegia, brachioplegia, acroplegia and others. These are based on the location of the parts exhibiting motor deficits and imply maximal paralysis. No scientific termi nology has been formulated regarding variations in the degree of musclar deficiencies outside of the term paresis which means a milder form of paralysis. Few case reports need to be studied to learn that it is possible to have pathological involvement of the central nervous system so that the symptoms vary from simple or maximal deficits. For example, the Babinski sign may be the only evidence of disturbance present, or altered ten-
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don reflexes, or interference with tone, or any possible degree of paralysis or, finally, any combination of these. One of the controversial issues revolving around the pyram idal tract syndrome is its relation to muscular tonicity both under normal and pathological conditions. Whether spasticity or flaccidity occurs in man following degeneration in its fibers is a problem that is being explored in both experimental and clinical fields of research. The status of reflex activity has been extensively studied for many years in patients exhibiting voluntary motor paralysis. Alterations have been noted in skin reflexes affecting the big toe and in the abdominal and cremaster muscles. The most im portant sign in neurology is regarded by some as the Babinski reflex. Other pathological signs of a somewhat similar nature are manifold and include such well-known ones as the Oppen heim, Schaefer, Allen and Cleckley, Chaddock, Gonda, Wein berg and the resistant reflexes. The question arises as to whether any correlation has been made between any or a combination of these motor abnormal ities with observed involvement of the pyramidal tract. The syndrome is only as good as the pathology or experimental evidence which supports it. External signs and symptoms are much easier to study than their causes within the brain and cord. The pyramidal syndrome appears to be a phenomenon occurring largely in man in the phylogenetic scale and it is known to follow such pathological entities as neoplastic, vas cular, traumatic, inflammatory, toxic, sclerotic and congential processes in the central nervous system. Just how each of these conditions affect the pyramidal neurons is an unexplored field. Surgery has been performed in the past few years to alleviate the presence of tremors by sectioning of pyramidal fibers. The theoretic basis for this procedure is that the tract, in these cases, is thought to conduct abnormal impulses of a release nature. So far, the surgical lesions in man have been made in ap-
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proachable sites, the spinal cord below and the motor regions above. There has been a minority group of theorists and investiga tors during the past hundred years who have refused to con sider the pyramidal tract as a self-sufficient, autonomous unit. They have taken the afferent system into account in attempts to explain what initiates, directs, modifies and dominates the pyramidal impulses leaving the cerebral cortex. Their conclu sions are presented in the text in the belief that the sensory aspects of motor behavior have been neglected and underrated in the considerations of the mechanism behind efferent phys iology. lt is the belief of the author that the pyramidal tract, from the broad viewpoint, is such that it constitutes an enigmatic and challenging pathway. Since 1850, medical men have re garded it as the most important in the central nervous system. In the past two decades, there has been a revival of scientific interest in certain aspects of its anatomy, physiology, pathology and clinical significance. These recent results and interpreta tions are such that some traditional views have been questioned. Some attempt is here made to cover the major facts in its evolutionary history and to present the story of the pyramidal tract with emphasis on man.
Events Leading to the Discovery of the Pyramidal Decussation 460 B.C.-1710 A.D. MEDICAL men have lang been interested in the manner and frequency in which the voluntary muscles of man can be af fected by disease of the brain and spinal cord. In the earliest times, paralysis was the only symptom known for involvement of the central nervous system. Hippocrates ( 460-377 B.c.) knew that disease of one side of the brain produces motor deficits on the contralateral half of the body. As far as is known, this was the first step in cerebral localization. How ever, he thought that paralysis was caused by phlegm blocking the channels which transmitted the pneuma. lt took twenty-two centuries after the time of Hippocrates before the observations of pioneering investigators on the human brain-stem suggested an explanation for the presence of paralysis opposite to the side of the lesion. Much of this tardiness in progress can be explained on the basis of the universal restrictions placed on human dissections. During this scientifically retarded era, only a f ew publications were made on this subject. The first of these was by Galen ( 131201 A.D.) regarded as the founder of experimental physiology. Although he was considered to be the most skillful practitioner of his time and must have observed many cases of human paralysis during his wanderings from capital to capital, he is best known for his investigations on animals. He may have
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been the first to produce experimental injuries in the central nervous system, using apes and swine. Some of bis contribu tions to motor neurology are the following: a complete tran section of the spinal cord produces a total paralysis whereas a hemisection affects the same side; by contrast, a longitudinal incision is not followed by a loss of movement. Galen ap parently did not mention the crossed effects of brain lesions. As an anatomist, he left many excellent descriptions of the motor system. Much of the work, however, was faulty and inaccurate in its application to man. The first theoretical explanation of an anatomical nature for the crossed paralysis occurring in head injuries appears to have originated from Aretaeus of Cappadocia, who is thought by some to have lived in Alexandria, Egypt, about the second half of the first century A.D.; by others he is placed in the early second century. This physician is acclaimed by Mettler ( 1947) as the greatest after Hippocrates. He believed that a decussation of each of the peripheral nerves from its point of origin in the central nervous system to the opposite side could best account for crossed paralysis. In modern terms, this would mean a lower motor neuron crossing in the spinal cord and brain-stem instead of a decussation of the upper or pyramidal. In spite of bis being wrong in the light of our present knowl edge, the idea of Aretaeus was an enlightened one for bis time and is based on sound theoretical reasoning. Other early ideas as to the etiology of voluntary motor paralysis were that it is due to the clogging of the motor nerves by thick, viscid humors ( Aetius of Amida, Fl. 380 A.D.) or that the responsible phenomenon is a stoppage of the flow of animal spirits caudally ( Caelius Aurelianus, Fl. 400 A.D.). Although apoplexy was known as a clinical syndrome for many centuries, it wasn't until 1658 that Wepfer defined it as being due specifically to vascular insult, thus placing its pathology for the first time on a hemorrhagic basis. In bis
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treatise, which has been regarded as historically important, he stated that the opposite muscles are mostly affected but felt that some lesions produce unilateral effects. Some, but not all, historians credit Domenico Mistichelli ( 1709), professor of medicine at the University of Pisa, as being the one who discovered and first described the decus sation of the human pyramids. The latter was clone in a treatise on apoplexy which has become a rare work. In it, he explains the contralateral paralysis by a new concept. He stated that the "medulla is on the outside interwoven with fi.bers, which by their criss-cross superposition, resemble a woman' s braid, whence it comes that many nerves which branch out on one side, have their roots on the other." He believed that the cra nial and spinal· nerves arose from the pia mater instead of the nerve tissue underneath. lt would seem that Mistichelli had very little understanding of even the most primitive neurologic concepts involved in the phenomenon of crossed motor con duction. However, he must have searched for an explanation of contralateral paralysis and dissected the human medulla oblongata. Having noticed the pyramidal decussation, he in ferred that it was the answer to the question which had puz zled medical men for centuries. Thomas ( 1910), in his histor ical inquiry into the decussation of the pyramids, says it is remarkable that Mistichelli is spoken of as the discoverer of this part of the nervous system. Just one year later, the much less equivocal results of the investigation of Petit were published in a pamphlet entitled Lettres d'un Medicine, etc. Namur, (1710). Two hundred copies were made, none of which have been found in America. In his study of the pyramidal decussation, he used three ap proaches combining the clinical, experimental and anatomical methods. This was unique considering the scientific atmosphere of the early eighteenth century. Petit observed on patients that brain injury, usually abscess,
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resulted in paralysis of the opposite side. Experimentally, he trephined over the middle of the parietal lobe in dogs and then inserted a scalpel to various depths and extents. Removal of the central portion of the hemisphere by this procedure al ways produced a contralateral paralysis. lt was more profound the deeper the lesion, reaching its maximum when the corpus striatum was injured. Lastly, he discussed the anatomical factors involved and gives a beautiful figure of the medulla and upper part of the spinal cord which clearly shows the pyramidal decussation. His description of this part is as follows: "each pyramidal body divides at its inferior part into two !arge handfuls of fibers, more often three, sometimes four. Those of the right side pass to the left and vice versa." Petit' s contribution is an admirable one and it can be judged to be on a much sounder scientific basis than that of Mis tichelli' s published just one year earlier. SUMMARY
For 22 centuries after the time of Hippocrates, speculations were made as to the reasons why paralysis occurred opposite to the side of the head injudes. The only theory which can be mentioned on neurological grounds is that of Aretaeus ( second half of first century) who believed that each of the peripheral nerves decussate from one side to the other within the brain stem and spinal cord. Other views revolved around the possible functions of phlegm, pneuma and humors. lt remained for Petit in 1 71 O to demonstrate strikingly that the pyramidal de cussation is the nerve mechanism which may be involved in crossed paralysis. He presented evidence on anatomical, exper imental and clinical grounds.
Gross Observations (1710-1870)
OR A CENTURY after the discovery of the pyramidal decussation by Mistichelli ( 1709), and Petit ( 1710), little or no progress was made toward an understanding of the pathway or pathways concerned with nervous control of striated mus cles. During the early part of this period, some additional gross observations were made on dissections of normal human pyramids and different interpretations were given as to the possible function of the crossing. Correlations between cerebral atrophy and changes in the size of the pyramids were made later as autopsy restrictions were gradually lifted. Joseph-Guichard Duverney, Professor of Anatomy, in Paris, was one who was aware of the decussation of the pyramids but it is thought that the crossing was pointed out to him by his pupil Petit. He described the decussation in a post humous publication twenty years after Petit' s report in 1710. In 1739, Giovanni Domenico Santorini, Professor of Anat omy at Venice, demonstrated the decussation of the human pyramids and made comments on the original observation of Mistichelli ( 1709). He thought the latter' s investigation ob scure and said that it was doubted by many of his contem poraries. In respect to his own findings, he felt that he had proven conclusively the status of the cross connections in the lower medulla. During the past two centuries, the view that an inju� to one side of the head is followed by paralysis of the opposite muscles has been designated frequently as the "Valsalva doc trine.'' This originated from a publication of Antonio Maria 15
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Valsalva ( 1666-1723) of Imola, Italy, an early investigator in pathology. Some students of neurology have argued, prob ably erroneously, that this was the first treatise referring to the decussation of the pyramids. One of the most interesting figures of his time, Albrecht von Haller, prolific physiologist, regarded the medulla oblongata as the source of all motor power. In his book on physiology (1754), one of his 13,000 publications, he stated that trans verse fibers are detected as proceeding from side to side both in the medulla oblongata and upper spinal cord. He thought this could account for crossed paralysis but also described it as a contrivance which was supplied by nervous energy from both sides of the brain. To him, this explained the fact that injury to the cerebral hemisphere did not always paralyze. Still another view regarding the decussation of the pyramids was held by Vicq d' Azyr ( 1786), regarded as the greatest com parative neuro-anatomist of the 18th century. He made general studies on the morphology of the brain in numerous mammals and described the pyramidal crossing. However, he thought it was commissural in function. As can be seen, little was actually known at the beginning of the 19th century regarding the neurology of the motor mechanism in man or lower mammals. Between 1700 and 1800, probably the best and most authoritative investigation was that of Petit on the pyramidal decussation ( 1 71 O) . This work apparently attracted little attention so that the significance of this part was generally unknown up to the turn of the cen ury. The individual who again called attention to the crossing was the well-known Gall, so-called founder of the school of phrenology. Gall's pupil Spurzheim supported him in this field and together they traveled over Europe in 1805 lecturing on the relation of the conformation of the skull to mental faculties. Most of the modern writers dealing with Gall pre sent him sympathetically and claim that he was an able invest-
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igator far ahead of his generation. Gall and Spurzheim pub lished the Anatomie et Physiologe du Systeme Nerveux en General et du Cerveaux en Particulier, etc., Paris, 1810. For the first time Gall and Spurzheim went beyond the confines of the decussation and dissected the pyramidal tract upwards in humans to the cerebral cortex where they thought it receives fibers from the central region. They present a beau tiful picture of the crossing and upper portion of the tract, probably the first illustration of its kind. Further, they designate it as motor. Gall and Spurzheim were acquainted with Petit's important work but gave Mistichelli credit for the discovery of the decussation. Some texts on anatomy of this period, such as those of Beclard ( 1823), John and Charles Bell ( 1826) and Homer ( 1830) mention nothing more of the tract than the pyramid and its decussation. Shortly after Gall, Sir Charles Bell ( 1830), famous Scotch physiologist, anatomist and surgeon, made a thorough gross dis section of the pyramidal tract. He traced it upward through the brain-stem to the internal capsule and found it spreading out fan-like to the gray matter of the central area of the cere brum. He called it "that grand tract which furnished the nerves of motion," and he thought it gave origin to the ven tral roots of the spinal cord. In his text on The Anatomy of the Human Body, published in 18 5 3, Cruveilhier lists those writers for and against the existence of a pyramidal decussation. Those who favored its presence were Santorini, Winslow, Lieutad, Duverney, Scarpa and Sömmering. The opposite opinion was maintained by Mor gagni, Haller, Vicq d' Azyr, Sabatier, Cuvier, Chaussier, and Rolando. He claims Gall and Spurzheim did not have a de cided opinio1;1 on this point. Cruveilhier studied medullas either hardened in alcohol, boiled in oil or in a solution of salt. On these medullas he directed a jet of water, tl1e force the size of which was varied in order to more easily separate the
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fibers. By this means, he traced the left pyramidal bundle to the right, backwards and downwards into the lateral column but could not account for a direct corticospinal component. The credit for being the first to correlate cerebral atrophy, pyramid shrinkage and crossed paralysis apparently goes to Jean Cruveilhier. His original contribution was in 1835, the year he was selected to fill the newly created chair of pathology at the University of Paris, having previously been professor of anatomy. In the cases he studied, he could not notice any signs of degeneration in the opposite half of the spinal cord but he assumed it might be involved. Shortly following Cruveilhier' s contributions, several inves tigators reported on the gross changes occurring in the pyram idal tract in cases of cerebral atrophy. These include Charcot and Turner (1852), Kolk (1852), Turner (1856), Gubler (1859), Cornil (1863) and Vulpian (1866). Their reported observations all harmonized to the extent that their cases ( a total of about twelve) with cerebral atrophy showed atrophic changes in what had come to be called the "motor tract" in the brain-stem. Some also detected loss of nerve substance in the lateral column of the opposite half of the spinal cord. SUMMARY Slight progress in the general. understanding of the pyram idal tract developed between 1710 and 1850. The only method of investigation was by gross observation and dissection. For the first time, the bundle was dissected up to the cerebral cor tex. Opinion was .almost equally divided as to whether a true decussation of the pyramids exists. Unilateral atrophy of the pyramid in cases with cerebral atrophy became more commonly observed during the latter 'half of the 19th century and this part gradually became designated as the "nrotor tract."
Normal Histological Studies THE RESULTS of histological investigations on the pyram idal tract, directed at morphology, have helped in crystallizing the view that pyramidal neurons are motor in function. Numer ical investigations have been instrumental in casting doubt on the established view that all pyramidal fibers arise from the Betz or giganto-pyramidalis cells of the motor cortex. The fiber diameters of the pyramidal tract have been established giving clues as to their speed of conduction. 1. THE BETZ CELLS
The Betz cells are the best known cells of the cerebral cortex. Their size, morphology and exact location have been inves tigated by numerous individuals and much speculation has arisen regarding their role in motor physiology. For years, they were unequivocally accepted as being the sole source of pyramidal tract fibers. The discovery of these giant cells in the human precentral cortex was made by Vladimir Betz, Russian histologist, in 1874. They have since been studied specifically in man by Lewis and Clarke (1876); Campbell (1905); Brodmann (1909); Econo mo and Koskinas (1925); Hammarberg ( 1895) and Lassek (1942). The typical Betz cells are located in the fifth layer of the posterior portion of the precentral gyrus, now designated as the motor cortex or area 4 of Brodmann. The region of their dis tribution forms about 2.8% of the surface of the human brain (Michails and Davison, 1930). Their morphological resem blance to the anterior horn cells of the spinal cord led 19
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Campbell ( 1905) to classify them as true motor cells and the ones giving origin to pyramidal tract fibers. He was influenced in this opinion by the investigation of Grünbaum and Sherring ton ( 1901) who localized the excitable cortex to the Betz cell region on the basis of their results with electrical stimulation in apes. Variable dimensions for these elements have been given by the above named histological investigators, the extremes be ing from 30-96 Microns in length by Lewis and Clarke ( 1878) to 50-120 Microns by Economo and Koskinas (1925). Tue largest, on the average, are found in the paracentral lobule. In shape, they are described as pyramidal or pyriform multi polar cells giving off numerous stout and knotted dendrites, some of which extend to the surface of the cortex. The nucleus is spherical and relatively !arge possessing a well defined nucleolus. Characteristic of these cells is the presence of numer ous, !arge Niss! granules. Formation of Betz cells in groups or clusters is well-developed in man. Campbell ( 1905) enumerated 25,000 Betz cells, without giving any scientific criteria as to what he considered these cells to be, whereas Lassek ( 1940) specifically counted 34,000 between the size limits of 900 and 4,100 square microns. These values are far less than that obtained for the number of pyramidal tract fibers in the pyramids (Lassek and Rasmussen, 1939). Seventy-five per cent of the Betz cells are in the leg area, 17.9% in the arm region and 6.6% in the head center. Eighty-two per cent are buried in the anterior wall of the cen tral (Rolandic) sulcus. Of the 18% on the visible cortex, Lassek ( 1940) found none in the lower one-half of area 4. The excitable properties of area 4 with its low threshold to electrical stimulation, the discrete muscular responses ob tained and the fast conduction from area 4 have been attributed to the presence of Betz cells (Foerster, 1936; Fulton, 1949). Walshe ( 1942) in a critical review on the possible role of the giant cells of Betz, the motor cortex and the pyramidal tract in motor physiology states that in his opinion the cells do not
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constitute a specific morphological and physiological category and that they defy scientific description. He points out the striking · discrepancy between the estimated totals of Betz cells and the numerical analysis of the pyramidal tract. II.
THE FIBER COMPONENTS OF THE PYRAMIDAL TRACT
The investigations which have been made on the fiber com ponents of the pyramidal tract give information as to how the bundle maturates ontogenetically and also as to its fiber spec trum. The former should give indication as to when it be comes morphologically mature and the latter as to its speed of conduction and possibly as to its reaction to pathological lesions. The pyramids of the medulla oblongata, where the tract is most isolated, constitute an excellent site for examining the neurons of the pyramidal tract. Duncan (1940) found the size of the pyramidal tract in this region to vary from 8. 16 to 13. 7 sq. mm. in 128 specimens. This makes it one of the largest bundles in the central nervous system. Descending through the pyramids are about one million axons (Lassek and Rasmussen, 1939). In a biometric analysis of 30,000 myelinated pyramidal tract fibers in two young adults, Lassek (1942) showed that 89.6% are between 1-4 Mu in diameter, 8.7% are 5-10 Mu whereas only 1.7% are }arger than 10 Mu. Over one-half of the fibers are approximately one Mu in thickness. This suggests that most of the pyramidal fibers in man are slow conductors and that the majority of the cells of origin should be small to cor respond with the fiber diameters. This would not harmonize with Foerster's (1931) view that the pyramidal tract is a "fast train" conductor because of its uninterrupted course from cor tex to lower lying centers. Tower (1940) has found exper imentally that the pyramidal tract may play a role in the main tenance of vascular tone and reflexes. If this is true, it is possible that the fibers regulating these vascular functions would be of small caliber.
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There are indications that fiber diameter in the pyramidal tract may have pathological significance. In cases of amyotroph ic lateral sclerosis, Wohlfart and Swank ( 1941) report the loss of the largest fibers in the bundle whereas the smallest survive the pathological process. Lassek ( 1948) likewise found the largest axons to be more sensitive, for they were the first to disappear from the field in nine cases with acute cerebral lesions ( vascular and abscess) . Man is susceptible to pathological involvement of his motor system at all ages but particularly early and late in life. The mechanical hazards of the birth process may injure the pyram idal pathway and in senility the tract is in a vulnerable position in cases of vascular insults. Collier ( 1924) stated that in the majority of cases of cerebral birth palsies, the clinical and pathological evidence indicates pyramidal involvement. From the physiological viewpoint, the postnatal changes in the per formance of striated muscles in man must depend on concomi tant alterations in the efferent structures of the nervous system including the pyramidal tract. A knowledge of the year-by year changes in pyramidal neurons during individual growth might be of basic value in the fields of human pathology and physiology. The pyramidal tract is a late developing tract. At birth, it measures 1.9 sq. mm.; at eleven months, 5.4 sq. mm.; at two years, 5 .8. sq. mm.; at twenty-two years, 11. 7 sq. mm. and at eighty years, 7.3 sq. mm. (Lassek, 1942). Thus, between birth and maturity, it increases in area about six times; between two years and maturity it doubles its size and in old age its cross sectional area is decreased. Throughout life, changes occur in the caliber of certain axons in the pyramidal tract. During the first eight months, the fibers are uniformly small, closely packed together and they are less responsive to the stain used. This period appears to be a quiescent one with little increase in the area or magnitude of
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the fibers. lt may be that this histological picture is associated with non-motor physiology. At eleven months of age, a few predestined fibers begin to grow more rapidly than others. The !arger fibers may myelinate first. This is characteristic at the time walking is attempted. At two years, the fibers resemble those of an adult but in miniature form. There is definite dif ferentiation into small, medium and large axons but the big gest are only about one-fourth to one-third the size of similar mature fibers. Growth, characterized by an increase in length and diameter, continues between two years and maturity while motor movements become more refined and skilled. The picture in the adult shows a few large, more medium and many small axons. lt appears that the ontogenetic development of the pyramidal tract repeats its phylogenesis since the presence of more and more large fibers appears as we go up the mammalian scale from marsupials to man (Lassek, 1940). The following factors develop as a unit during the growth stage in the pyram idal tract: increase in length and diameter of axons, change in chemical nature, myelination and integration of function. The early microscopic picture of the axons in the pyramids is not incompatible with that reported for the infant motor cortex by Conel ( 1939). At this age, the Betz cells are rounder, smaller and have a less differentiated Nissl substance. Very little change in the morphology occurs until some time later ( Conel, 1941). One of the most influential investigations clone in the pioneering days of neurology was that of Flechsig ( 1876) who used the myelogenetic method. His results were important be cause they were universally taken into consideration by clin icians interested in the concept of cerebral localization, but especially by Charcot. The procedure is based on the fact that all the fibers of the tracts of the spinal cord receive their myelin sheaths at or shortly after birth. The exception is the pyramidal tract. Flechsig traced the location of the path (by its absence in
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newborns) from the anterior and posterior central gyri and paracentral lobule of the cerebral cortex. The Weigert stain, then new, was employed. He added much to our knowledge of the variations in the decussation. The lateral or crossed com ponent was followed to the lower sacral region and the ventral or direct bundle to an ending sometime in the middle cervical enlargement, in others to the upper thoracic but most com monly to the mid-thoracic level. Occasionally, he found it ex tending to the lumbar enlargement. SUMMARY
Both the known cells of origin (Betz cells) located in area 4 and the fiber components of the pyramids have been studied histologically at various ages in man. The Betz cells have been measured for size, counted, local ized and studied morphologically. On the basis of the results obtained in these categories, they are large, multipolar elements with well-developed Nissl substance. They are definitely re garded as motor and as a partial source of pyramidal tract :fibers, possibly the largest ones. Physiologists have regarded them as eo-extensive with area 4 and responsible for its excit able properties, for its low threshold to electrical stimulation, for the discrete muscular responses obtainable and :finally that they are designed for speedy conduction. The fiber components of the pyramidal tract are almost thirty times more numerous than the Betz cells and they are mostly of small diameter indicating primarily slow conduction. There are some axons of intermediate size and a few of !arge caliber. The area of the tract augments about six times between birth and maturity. During maturation of the pyramidal fibers, there is an increase in length and diameter, a possible change in chemical nature, a latent myelination and an integration of function. The ontogenetic development of pyramidal neurons appears to repeat their phylogenesis.
Studies in Secondary Degeneration (Pathology) °WiAT HAPPENS to the individual neurons comprising the various tracts in the central nervous system of man follow ing injury has not been extensively studied in the pathological specialty. The pyramidal tract is, perhaps, the one exception to this statement. Cognizance and acceptance of some of the re sults of pioneering investigators in this field might have materially altered the traditional concepts which were for mulated regarding the pyramidal tract and led to new avenues of research. Almost all of the pertinent investigations in sec ondary degeneration were clone either before 1875 or within the last decade. The results of this method have been of im portance in settling the controversial question as to the course and divisions of the bundle, in giving clues as to the region of its origin from the cortex and how the neurons are affected individually and en toto by the different pathological lesions. A pioneering landmark in this field · was the investigation of Türck, able neurologist of Vienna, in 1851. At a time when some texts were still denying the existence of a pyram idal decussation ( Le., Craigie, 1851), Türck published the results of bis studies in long-standing cases of hemiplegia. By a new method of investigation, he established the fact that Wallerian degeneration can occur in the pyramidal tract and thus in the central nervous system. His technic consisted of cutting thin sections of spinal cord and brain-stem with a fine curved scissors and putting them in alcohol. He noticed that 25
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when definite parts of the cerebrum are destroyed there de velop distinct bands of diseased fibers in the internal capsule, in the base of the cerebral peduncles, in the ventral part of the pons, in the medulla oblongata and in the spinal cord. The early manifestations of the process are manifested by the for mation of numerous fatty particles in the bundle followed later by atrophy. The cause of the changes, he thought, was due to interruption of nerve conduction. He inclined to the view that the direction of the flow of impulses can be detected on the basis of which side of the lesion degeneration occurs. Türck also initially reported the presence of a direct, uncrossed tract ( still occasion· ally called by his name) . The crossed component was named the "pyramidal-lateral-tract" and the shorter direct one the "capsular-anterior-column tract." He speculated erroneously that the descending bundle originates from the central gray mat ter rather than from the cerebral cortex. By contrast, his ob servations on the course and subdividing of the tract are ac curate. One of the best neuropathological investigations made on the pyramidal tract was published by Bouchard in 1866. He was the first to use a combination of hardening ( alcohol) and staining ( Carmine) along with thin sectioning of nerve tissue. Basically he confirmed and extended Türck's work. The essence of Bouchard's investigation was the study of 32 cases of old hemiplegics. In these, he noted the type and loca tion of lesions in the cerebrum and brain-stem which cause secondary degeneration. In some, he observed the onset in the motor tract and correlated it with the beginning of the paralytic symptoms. He also made observations on the status of tone in the muscles and advanced a reason for the presence of spasticity. The initial signs of breakdown were detected by Bouchard as early as the sixth day in the pyramidal tract following apoplexy.
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He never was able to see any signs of retrograde degeneration above the level of lesions. One of the findings of Bouchard which is significant is that some pathological lesions causing paralysis are not followed by fiber changes in the motor tract. He classified his cases into some which do not cause neuronal disappearance, some which produce only slight deterioration and those which are character ized by severe loss. The heaviest damage, he found, occurs in hemorrhagic lesions in the corpus striatum and internal capsule. Bouchard thought that spastic contractions in the muscles were due to scar formation in the tract. As to the strength in the muscles during hemiplegia, he judged them as follows: very feeble, feeble, strong, quite strong and very strong. One out of his 32 cases had a flaccid type of paralysis. Bouchard feit that there are some essential differences be tween secondary degeneration in the spinal cord and in the peripheral nervous system. The pyramidal fibers of the cord, he said, are more sensitive, more easily compressed and the gran ules remain longer so that the time of deterioration is pro longed. In cerebral hemiplegia some fibers in the spinal cord distribution of the pyramidal tract always retain their structure. Either these have been respected by the injury or they arise from other parts of the central nervous system than does the motor fasciculus. As glia forms in the injured tract, he further stated that these normal remaining fibers gradually become varicose and so affected functionally as to modify their vitality. The observations of Bouchard' s pioneering investigation were of such significance that no less an authority than Charcot called his publication a classical memoir in the field of neu rology. J. Hughlings Jackson, probably the greatest and most in fluential theorist in the field of modern neurology, was familiar with the pyramidal bundle and referred to it as the "motor tract." He felt that in epileptic seizures irritative impulses are
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discharged over it. According to him, the nerve fibers compris ing it could have changes of a nondestructive nature which in hibit normal function. This, he said, was true in cases of hem iplegia which develöp following epileptic attack, the cause be ing exhaustion of nerve fibers. The pyramidal tract, he thought, might be squeezed in many instances instead of being actually destroyed. In cerebral tumors, destruction of fibers occurs, at most, slowly and they may act indirectly in causing paralysis. A small quantity of the tract can be lost without producing obvious motor symptoms as can be proved at post mortem. Finally, he stated that there are few nervous diseases which cause cells and fibers to disintegrate directly. Nearly all begin in the connective tissue or blood vessels. The nervous tissues are innocent but suffer. In contrast to the English school, which concentrated on studies of electrical stimulation of the cortex and the anatomy of the cells in what was considered to be the motor area, the French were more concerned with pathological and clin ical investigations. After the first of the studies on morbid anat omy by Bouchard in 1866, the next figure to stand out in France was Jean Martin Charcot ( 1825-1893), one of the most distinguished of all neurologists. From small beginnings, he created one of the greatest neurological clinics of modern times at the Salpetriere, Paris. At first suspicious, Charcot later enthusiastically threw bis weight behind the conception that the pyramidal tract is con cerned with voluntary motion. Judging by the lectures which he presented to his students in 1878 (published in 1883), it would seem that he had a more profound knowledge on the subject than any of his contemporaries. There is indication that he was familiar with the literature covering the field. He claimed that he spent 15 years studying the motor tract with anatomical, physiological, pathological and clinical observations on 200 patients. In his pathological studies on the motor tract, Charcot was
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particularly interested in the questions of its cerebral local ization and the phenomenon of secondary degeneration which he called "descending sclerosis." There were three factors that were important to him: the site of the lesion, its extent and lastly whether it is destructive to the tract. Charcot insisted that · an indispensable requirement for fiber deterioration is that cerebral injuries must be destructive. Tumors, he maintained, did not interrupt the continuity of pyramidal tract fibers, they merely displaced and separated them. Yet, he feit this type of lesion was inclined to produce more permanent and increasingly severe motor symptoms by compression. Restitution of function is more likely in hemorrhagic or inflammatory conditions which destroy quickly. If the lesions are destructive then there are certain re gions which, when involved, invariably cause a descending secondary degeneration in the motor fasciculus according to Charcot. These sites are as follows: the anterior two-thirds of the internal capsule, the centrum ovale near the root of the corona radiata and the deeper parts of the cortex involving the pre- and postcentral convolutions. However, destructive injuries located in the caudate or lentiform nuclei or thalamus can pro duce paralysis, without evidence of secondary degeneration, by means of compression. Another fact noticed by Charcot, is the absence of retrograde changes in the pyramidal tract above the level of lower-lying lesions. Some attempts were made by Charcot to explain the pres ence of paralysis on the same side as the lesion which he had noticed. His explanation of this was that either no crossing of the pyramidal tract occurs in the medulla oblongata or there was a double decussation, the second occurring in the cord. One of the characteristics Charcot emphasized is that con tractures of muscles occur only when there is actual sclerosis in the pyramidal tract and that this feature of paralysis becomes decisive in the second or third month following an attack. The early results and conclusions of Türck ( 1851), Bou-
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chard ( 1866), Charcot ( 1878) and others from studies of sec ondary degeneration were such that the medical world accepted the pyramidal tract as being the great voluntary motor pathway of the central nervous system. Apparently, the :first observation of a homolateral tract in man was made by Pitres in 1884. In 40 cases of long-stand ing hemiplegia, he reported it present in 10. Not all inves tigators have accepted the entity of a distinct homolateral pyramidal tract as a fact. Hallopeau ( quoted by Barker, 1900) suggested that the degeneration of the homolateral bundle de pends upon pressure effects from the swelling of degenerating fibers which acts on normal fibers at the point where they cross in the decussation in the medulla. The aberrant fasciculi leaving the pyramidal tract in man have been noticed a number of times. Beginning with the in vestigation of Pick ( 1890), this investigator described a recur rent bundle leaving the pyramidal decussation which proceeds dorsolaterally to the - facial nucleus with a few fi.bers entering the restiform body. The same group of fibers has been traced by Barnes ( 1901 ) and Stern ( 1908) who added nothing new. A distinct circum-olivary fascicle has been recognized as a common variation of the pyramidal tract by Barnes ( 1901 ) , Hajos ( 1914), Smith ( 1904), and Swank ( 1934). The last named found such a bundle present in nine of 8 5 human brains and he traced the fibers around the inferior margin of the olive to the pontobulbar body and lateral reticular nucleus. The pontobulbar body, located in the restiform body, he be lieves is homologous with the pontine nuclei, and he favors the view that both Pick' s and the circum-olivary bundle belong to the corticopontine system of motor fi.bers. One of the major concepts which was universally accepted before the year of 1900 was that paralysis of voluntary muscles can occur from indirect pressure effects exerted upon the pyramidal tract without destruction by lesions in the central
THE PYRAMIDAL TRACT
nervous system. Others besicles Bouchard ( 1866) and Charcot (1878) mentioned this possibility. Bennet (1840) said that recovery occurs when the cause of the pressure is removed. Strümpell ( 1893) stated that transitory symptoms might last several days, weeks or months from pressure on the pyramidal tract. Those which outlasted six months, he regarded as direct. According to Marie ( 1895), compression from cerebral tumors or meningeal lesions can cause paralysis without signs of sec ondary degeneration in the pyramidal tract. He emphasized that the lesions must be destructive for loss of fi.bers to make an appearance. In the opinion of Ranney (1890), hemiplegia re sults from any lesion which interferes with the free action of the motor tract. Gowers ( 1888) stated that pyramidal neurons are remarkably tolerant of morbid processes that develop grad ually. Tumors and abscesses act in such a manner that the nerve elements are displaced rather than destroyed even though they might be located right in the motor path. Pearce ( 1904) stated that brain compression may cause paralysis due to edema, in creased blood pressure or malnutrition. Many other references could be cited in support of this concept. Periodically, between 1900 and the present, there have been investigations on man the results of which tend to further neutralize the concept that the neurons of the pyramidal tract must be destroyed to cause motor symptomatology. Spiel meyer ( 1906) reported two cases of hemiatrophy and hemi plegia associated with an intact pyramidal tract. He attributed the hemiplegia as due to loss of ganglion cells of the cortex other than the Betz. type. Rhein ( 1913) described two cases of spastic diplegia without demonstrable anatomical findings. Bielschowsky ( 1916) and Finkelnberg ( 1913) likewise found intact pyramidal tracts in cases with classical motor deficits. Railton ( 1892) published results of a study of a case of an idiot three years of age that had double spastic hemiplegia. The pyramidal tract in the pons, medulla and cord was judged
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to be normal. In the motor area, there was a diminution in the number of large ganglion cells and some increase in neuroglia. Monakow ( 1915) made an extensive experimental and clinical study of the effect of cortical lesions on secondary de generation in the pyramidal tract. In man, he believed that complete degeneration occurs only when the internai capsule or deeper parts of the corona radiata are destroyed, whereas sur face injuries in the two central gyri produce an incomplete loss of fibers. Employing the Weigert, Carmine and Marchi methods he judged that cortical involvement of the head and arm regions in the Rolandic area cause only the mildest sort of destruction in the pyramidal tract. He felt that a consider able portion of this bundle had an extra-Rolandic origin and particularly the direct pyramidal tract which is distributed primarily to the anterior horn cells innervating the arm muscles. More recently, Lassek ( 1950) reported on an analysis of 331 human paralytic cases, caused by various pathological entities, in which the pyramidal tract had been studied quan titatively at autopsy. Twenty-six of these showed complete de generation of the bundle, 59 had severe but not complete loss of fibers, in 58 there was only slight damage to pyramidal neurons and finally in 188 no signs of fiber injury could be detected. Tumors, he agreed, are prone to produce paralytic symptoms without causing a breakdown of these fibers. There are other evidences that paralysis may be produced by phenomena which do not destory pyramidal neurons. Monoplegia, hemiplegia or central ocular palsy, usually regres sive, but occasîonally permanent, may follow an epileptic seizure. Acute massive hemorrhage or chronic loss of blood in any portion of the body may cause paralytic symptoms. Other instances where temporary hemiplegia or more general paralysis may develop are the following: extremely low blood pressure, cerebral air embolism, an oversensitive carotid sinus reflex,
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free blood in the subarachnoid space, brain edema, many gen eral inflammatory processes and numerous miscellaneous conditions (Lassek, 1944, 1945). Many findings, therefore, indicate that the majority of cases where the pyramidal tract has been quantitatively studied at autopsy show little or no degeneration. It must be assumed that in these and probably in most instances there is some other cause for the paralysis than disappearance of pyramidal fi.bers. Early observations on secondary degeneration in the pyram idal tract played an initial role in developing the concept of cerebral localization of fonction. Charcot (1883), who accord ing to the records probably studied more cases of hemiplegia than any other neurologist up to the current period, stated that in his cases ( possibly 200 in number) the cerebral lesions in variably involved one or the other of the pre- and postcentral convolutions and often the two at the same time. All of the neurological texts I have been able to examine written before the year 1900, state that at least the two central convolutions, anterior and posterior, contribute fi.bers to the pyramidal sys tem. As examples, Buck (1889) gives the two central gyri, the posterior parts of all the frontal gyri, the rostral portion of the superior parietal lobule, the pai;acentral lobule and the precuneus gyrus as areas from which the pyramidal tract arises. Ferrier (1890) collected data on 483 cases of localized cortical and subcortical lesions and stated there was no doubt that lesions of the pre- and postcentral gyri were invariably followed by paralysis of volitional movements. Herter (1892) gave the two central gyri, the superior parietal and paracentral lobules and Edinger ( 1899) and Marie (1895) the two central gyri and paracentral lobule. The last named considered the subject of the origin of the pyramidal tract as being exhausted before 1895. Dejerine (1901) believed that pyramidal fibers degenerate from the premotor, pre- and postcentral gyri follow ing cortical lesions.
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A study of the segmental distribution of the pyramidal tract in the spinal cord was made by Weil and Lassek ( 1929) . In 10 cases of hemiplegia showing degeneration in the tract, they calculated that 50% of all pyramidal tract fi.bers supply the cervical, 20% the thoracic and 30% the lumbar segments. The muscles of the neck and trunk receive from three to six times as many fi.bers as those which innervate the extremities. The band muscles, concerned with skilled motor fonctions, are no better supplied with pyramidal fi.bers than are the remainder of the arm and shoulder. The upper extremity, however, re ceives approximately twice as many fi.bers per unit of muscle weight as the lower extremity. Minckler et al. ( 1944) traced the course of fi.bers arising from the premotor area in man distally in the pyramidal tract by means of the Marchi technic. In the posterior limb of the internai capsule, they were situated one centimeter from the genu; in the basis pedunculi and pons, they occupied the media! portion of the tract; in the pyramid they were scattered through out its area and in the spinal cord they descended in the position of the direct or ventral corticospinal tract. It was assumed that they crossed in the anterior white commissure of the cord. That the pyramidal tract may originate solely from cells in the cerebral cortex in man is indicated by the investigation of Lassek and Evans (1946) who observed complete descending degeneration in the pyramid following hemispherectomy which · spared the basal ganglia. SUMMARY
Sorne of the best pathological investigations on the pyram idal tract were made before the turn of the century. The results of investigations in secondary degeneration since 1850, using fixing, sectioning and staining methods, have shown its course and relationships from brain to spinal cord. Clues have been obtained by this approach as to the region of its origin from
a central portion of the cerebral cortex and in general its termination in the brain-stem nuclei and the gray matter of the spinal cord. The decussation of the pyramidal tract in the lower medulla was definitely proved to the satisfaction of ail. Half of its fi.bers disappear in the cervical segments of the spinal cord, 20% in the thoracic and 30% in the lumbosacral. The hand muscles are no better supplied with pyramidal .fi.bers than arm and shoulder. Before 1900, numerous correlations were made between the degree of pathology in the pyramidal tract and the symptom· atology particularly by the French school of neurologists. Since the bundle is the only one which could be found descending from the cortex to the cord, it became readily accepted as the motor tract. In the early half of modern neurology, it was widely held that certain diseased conditions, especially those which de· velop slowly, such as tumors or abscesses, can produce marked motor deficits without causing any secondary degeneration or depletion of .fi.bers in the pyramidal tract. More recent quan titative investigations indicate that there are few cases on record showing complete degeneration of this bundle and that the majority with cerebral paralysis show no or minimal neuronal loss. Pressure effects acting on pyramidal neurons and blockage of afferents have been advanced as explanations to explain the preservation of pyramidal .fi.bers in paralytic cases. lt seems evident that some other factor or factors besicles secondary de generation of pyramidal tract .fi.bers must account for paralysis in a considerable proportion of cases.
Investigations in Retrograde Degeneration THE RESULTS obtained from studies of retrograde degen eration of the pyramidal tract have been the most influential in crystallizing the view that its fi.bers arise solely from the giant or Betz cells of the motor cortex. Possible changes in the cells of the cerebral cortex have been investigated following lesions of various types and dura tions located in the internal capsule, brain-stem and spinal cord. The speed and intensity of the reaction have been co ordinated with both the distance and acuteness of the lesion. The investigators who have added to our knowledge of this in humans incfode the following: Dotto and Pusateri (1897); Marinesco, 1899, 1900 and 1910; Sano, 1900; Parhon and Goldstein, 1901; Monakow, 1905; Holmes and May, 1909; Schroder, 1914; and Wohlfahrt, 1932. In general, the pioneering investigators found that retro grade degeneration, consisting of pigmentation and atrophy of Betz cells, results from lesions located in any portion of the pyramidal tract. The doser the injury may be to the cortex, the faster and more pronounced is the reaction. The cellular•· changes are also more advanced when the injury is chronic. A rule was formulated early that retrograde reactions always re sult from fi.ber destruction in the brain and spinal cord whereas this is not necessarily true in the peripheral nervous system. The research of Holmes and May (1909) on retrograde changes following pyramidal injury can be considered a classic. 36
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They studied this reaction in cat,