w* - * 4? <%> • 1>- *b vA ( ^v 6* ^ 3 c> *•: **"* 4* . l ". ^ SOME PHYSIOLOGICAL FACTORS NEUROSES OF CHILDHOOD, BY B. K. "RACHFORD, M.D. Professor of Physiology and Clinician to Children's Clinic, Medical Col- lege of Ohio; Member of Association of American Physicians and American Pediatric Society, etc. lit 5M/f / CINCINNATI: >7 fa ° L THE ROBERT CLARKE COMPANY. 1895. V Copyright, 1895, By B. K. RACHFORD. PREFACE. This little book is for the most part a republica- tion of a series of papers first published in the Archives of Pediatries. In preparing these papers for republication I have thoroughly revised them and made many ad- ditions. The chapter on auto-intoxication has been entirely rewritten, so that from an unpreten- tious paragraph it has become the most important chapter in the book. B. K. Rachford, M.D. Cincinnati, Sept. 1, 1895. (iii) CONTENTS. CHAPTER I. NORMAL FUNCTIONS OF NERVE CELLS. Definition of term, " Neuroses of Childhood/' 1. Generation of nerve energy, the highest function of the nerve cell, 2. Amount of energy generated by a nerve cell depends on the degree of its functional depelopment, and on the amount of its healthful metabolism, 2-3. Discharge of energy, the second highest function of the nerve cell, 4. Nerve energy may be discharged automatically, 5 ; voluntarily, 6 ; or reflexly, 6. In- hibition of nerve energy is the third important function of the nerve cell, 7. Inhibition maybe voluntary, 8; involuntary, 9; or reflex, 9. CHAPTER II. PHYSIOLOGICAL PECULIARITIES OF THE NERVOUS SYSTEM OF IN- FANCY AND CHILDHOOD. The brain of the infant and child is morphologically and functionally immature, 11. Throughout infancy and childhood it develops slowly in weight and structure, and much more slowly in function, 12-13. Feeble inhibition of nerve energy is an important peculiarity of the nervous system of infancy and childhood, 15. Unfavorable conditions of food, heredity, and environment, may produce abnormally feeble inhibition, 16-20. Lack of sensitiveness of the motor areas in infants pro- tects against reflex neuroses, 21 ; and produces lack of tone in the sphincter muscles of the young infant, 21-23 (v) VI CONTENTS. CHAPTER III. FEVER AND THE VARIABLE TEMPERATURES OF CHILDHOOD. Definition of fever and high temperature, 24-25; of thermo- genic and thermo-inhibitory heat centers, 26. Thermogenic centers are at base of brain, 27. Thermo-inhibitory centers are in cerebral cortex, 27. Destruction and irritation of heat centers influence body temperature, 27-28. Thermogenic cen- ters are functionally mature at birth, 29. Thermo-inhibitory centers are immature at birth, 30. Immaturity of inhibitory centers is responsible for the variable temperatures of infancy and childhood, 31-34. Bacterial products, are the most import- ant of the exciting causes of fever, 35-37. Other exciting causes of fever are insolation, 38; muscular action, 38; and mechanical and reflex causes, 40. CHAPTER IV. HEAT DISSIPATING MECHANISM. We keep ourselves cool by radiation of heat from surface of the body, 42-43 ; by evaporation of water from the surface of the body. 43 ; and by evaporation of water from the air passages, 44. Loss of heat from the surface of body is three-fold greater in the infant than in the adult, 43. Polypncea may, in the in- fant, be a means of reducing high temperatures, and may be therefore a symptom of fever, 45-46. CHAPTER V. AUTOGENETIC AND BACTERIAL TOXINES. Auto-intoxication is self-poisoning, 48. Bouchard says that normal urine contains seven toxic substances, 49. It is path- ological rather than normal urine that holds the secrets of auto-intoxication, 52. Uric acid and urea are not poisonous, 52- 55 ; and are therefore not the cause of the nervous symptoms of the uric acid diathesis, 55. Paraxanthin and xanthin are CONTENTS. Vll poisonous leukoinains, present in the blood during attacks of migraine and kindred nervous disorders, 57. Leukomain poisoning is due to these and other unnamed poisonous leu- komains, 57. It is a factor in the etiology of leukomain epilepsy, 60 ; true migraine, 62 ; leukomain gastric neurosis, 63 ; neuras- thenia, 65 ; hypochondriasis, 65 ; uremia, 62 ; gout, 65 ; and lead colic, 65. Biliary toxemia is not an unimportant form of auto- intoxication, 65. Bacterial toxemia is an important factor of the neuroses of childhood, 66. It is in part responsible for the nervous symptoms of the acute infections, 67 ; for the tubercu- lous neuroses of childhood, 68 ; for the malarial neuroses, 69 ; and for the neuroses associated with acute and chronic intes- tinal fermentation, 70. CHAPTER VI. VENOUS CONDITION OP THE BLOOD. Arterial anemia and venous congestion of nerve centers produce same symptoms, 73-74. t Motor centers of cord made excitable by anemia, 75-76 ; and venous congestion, 76-77. Weak heart produces nervous symptoms by feeble capillary circulation, 78. CHAPTER VII. AN IMPOVERISHED CONDITION OF THE BLOOD. Innutrition of nerve elements results from thin blood, 81. It is not an important factor of neurotic disease in children, 82- 83. Malnutrition of nerve elements results from bad blood, 85. It is an important factor of neurotic disease in children, 85-92. The most important forms of malnutrition result from chronic anemia, 85 ; proteid and oxygen starvation, 86 ; fat starvation, 87 ; and calcium starvation, 88. CHAPTER VIII. REFLEX IRRITATION. Reflex irritation is one of the most important factors of neu- rotic disease in children, 92. It acts conjointly with other factors, 94. Overwork produces changes in the nerve cell 7 Vlll CONTENTS. 95-99. Peripheral irritation produces changes in the nerve cell, 98-99 ; and an increased excitability of the cell thus ir- ritated, 98-100. The cell recovers slowly from overwork or prolonged irritation, 98-99. This explains the slow recovery of spinal irritability after the reflex cause has been removed, 100-101 ; and gives to reflex irritation great importance as a factor of neurotic disease, 101-103. CHAPTER IX. EXCESSIVE NERVE ACTIVITY. Excessive brain work and nerve excitement are important factors of neurotic disease in delicate children, 106-114. Child is not a little man, 108. Porter demonstrated a physical basis for precocity in school children, 108-109. This is due to disease and bad heredity, 110-111. Heredity or acquired nervous weakness may be developed into actual disease, 113. Early precocity is an abnormal condition in the human infant, 113. Solitude in childhood gives independence of thought and character to the future man, 115. Play-grounds for children are greatly needed in all our large cities, 116-117. SOME PHYSIOLOGICAL FACTORS NEUROSES OF CHILDHOOD. NORMAL FUNCTIONS OF NERVE CELLS. The term " Neuroses of Childhood" is here used to cover all local and general nervous disorders which do not depend on known local pathological lesions of the nervous system. This definition of the term neuroses does not imply that these diseases have an entirely unknown pathology, but only that they can not be morphologically classified. In these diseases we know more of the symptoms than we do of the lesions, more of the effect than we do of the cause, more about the disordered functions of nerve cells than we do of the widely vary- ing pathological conditions which produce these disordered functions, and this is the reason why these diseases are incorrectly called functional nervous diseases. (1) 2 Rachford : Neuroses of Childhood. The first requisite to the study of the abnormal functions of nerve cells should be a knowledge of the normal functions of nerve cells. For this reason the following preliminary physiological out- line is introduced. Nerve cells have three important functions, viz.: to generate, to discharge and to inhibit energy. The highest function of the nerve cell is to gen- erate energy. By this is meant that the cell trans- forms and appropriates existing energy. The amount of existing energy is constant, the cell does not and can not originate energy, but in the chemical meta- bolism necessary to the life of the cell force is de- veloped which is transformed into^ that form of nerve energy which is the special function of the individual cell (Prof. J. Gad — personal communica- tion), and this nerve energy is stored up to be dis- charged in the exercise of the cell's peculiar func- tion. From this it would follow that the generation of nerve force would be directly dependent on the healthful chemical metabolism ot the nerve cell, but it does not follow that the amount of energy thus developed would always be commensurable with the physical waste or the chemical metabolism going on in the cell. This disproportion between cell activity and the amount of force developed is Rachford : . Neuroses of Childhood. 3 especially noticeable in the immature nerve cells of the child. A most marked example of the slight amount of energy developed by the cell activity of immature cells may be noted in cortical cells of the brain of the infant, and the brain of the unintel- ligent adult. In such brains the cortical cells con- cerned in the development of mental energy have going on within them an active chemical metabol- ism with the development of very little mental energy, and this failure of chemical metabolism to develop commensurate mental energy is due to the incomplete functional development of these cells. Of all the cells in the body the cell that develops mental energy is the slowest in reaching the degree of functional perfection for which it is destined, and it only does so after a judicious training in the exercise of its peculiar function throughout a long period of about twenty-three years. The functional development of the motor cell is much more rapid, and the disproportion between the amount of cell activity and force produced is not so great as in the mental cell, but nevertheless it may be stated as a fact true for all nerve cells that the amount of energy w^hich a cell is capable of generating will depend on the degree of func- tional development which the cell has attained. 4 Rachford : Neuroses of Childhood. But these facts concerning the difference in the amount of cell energy developed by different cells under the same conditions do not in any way modify the force of the statement made above that nerve energy is directly dependent on the chemical metabolism of the nerve cell. It will therefore be permissible for us to say that other conditions be- ing the same, the amount of energy developed by a nerve cell will directly depend on the amount of health- ful chemical metabolism going on within it. This point in the physiology of the development of cell energy is very important, since upon it rests the conclusion that insufficient nourishment will dimin- ish the capacity of the nerve cell for the generation of energy. The maximum amount of energy will therefore be found stored in the well nourished cell, and the minimum amount of energy in the starved cell. We shall see later that this statement which has important clinical bearing can be strongly sup- ported by experimental evidence. Discharge of nerve energy is a function of the nerve cell only second in importance to the generation of energy. The more or less constant discharge of force is an automatic function of the nerve cell, and this unconscious discharge of nerve impulse is the regulating function that controls the whole body Rachford : Neuroses of Childhood. 5 mechanism. As an example of this automatic dis- charge of nerve force one may cite the influence of the central nervous system over involuntary mus- cular tissue, whereby the " muscular tone " of in- voluntary muscles is maintained, the vaso-motor center in the medulla oblongata has such an in- fluence on the muscular coats of blood-vessels as to keep them in a state of normal contraction best adapted for the purposes which they serve, this vascular tone remains much the same at all times except when the functions of the center are per- verted by some change in the metabolism of the cells or by influences acting on the center either directly or in a reflex manner. But possibly of even greater importance to us in this study is the tonic influence of the spinal motor cells on the sphincter muscles of the stomach, the anus and the bladder, all of which are dependent on the spinal cord for their normal muscular tone. The " muscular tone " of these sphincter muscles is easily disturbed by reflex stimulation, producing on the one hand spasmodic stricture and on the other incontinence. The muscular tone of the skeletal muscles is likewise said to be maintained by an automatic discharge of nerve force, and a perversion of this function may in the same man- 6 Kachford : Neuroses of Childhood. ner produce complete relaxation or irregular spas- modic contraction of these muscles. These ex- amples on the part of the muscles are sufficient to illustrate how nerve cells, by the automatic dis- charge of nerve force regulate the whole body mechanism. It would be of no value for us to dis- cuss whether this more or less constant discharge of nerve force is purely an automatic function of the cell or whether it is due to unconscious afferent impulses producing a reflex discharge of force. It is sufficient for us to know that these phenomena exist and it is a matter of words whether we speak of them as automatic or as reflex. Nerve force may also be discharged voluntarily. This power of willing the discharge of nerve im- pulses resides in the cortical cells of the cerebrum. The influence of the will over the discharge of force, by the spinal motor cells, is a physiological fact of great clinical importance in the study of the neuroses of childhood. Thirdly and lastly and most important of all, so far as our present Btudy is concerned, nerve force may be discharged reflexly ; this reflex discharge of force occurs when nerve cells are acted on by out- side stimuli. If the stimulus be mild the reflex Rachford : Neuroses of Childhood 7 discharge of energy from the normal motor cells of the cord occurs only through the paths of least resistance, viz.: the afferent nerves in the same plane and on the same side as the nerve fiber that carried the afferent stimulus, but if the stimulus be more severe the reflex discharge of force will also occur in the same plane but on both sides of the cord. We shall see later how these simple laws of reflex action have little control over the reflex dis- charge of nerve force under certain pathological conditions. Inhibition of nerve energy is the third important function of the nerve cell. Certain cells through- out the central nervous system have the power of inhibiting energy discharged by other cells and it is also possible that some cells of high functional development may have the power of inhibiting their own energy. But however this may be it is a well established fact that inhibition does exist and that this power of inhibiting nerve energy may be either voluntary or involuntary. Voluntary inhi- bition of mental and motor force is a function pe- culiar to the cells of the cerebral cortex, but invol- untary inhibition of nerve force is a function of cells every-where distributed throughout the cen- tral nervous system, but the higher centers are 8 Rachford : Neuroses of Childhood. always the predominating centers when the nerv- ous system is intact. The spinal cord contains cells or collections of cells (centers), which are ca- pable of being excited reflexly so as to give motor expression to sensory stimulation, and inhibition can best be understood by studying the inhibitory influence of the higher centers on spinal reflex acts. The spinal reflex centers can act quite independ- ently of higher centers. Gad demonstrated that after section of the spinal cord at any point, the centers below the section are still active and capa- ble of translating sensory impressions into motor acts. But this absolute autonomy of the spinal re- flex centers does not exist when the spinal cord is in normal communication with the brain, then the reflex centers in the cord are more or less under control of other centers higher up in the cord, the medulla oblongata and the brain. These centers may influence the lower spinal centers not only in causing them to discharge force as we have above noted but also in inhibiting their reflex acts which are discharged from any cause whatsoever. Some of the inhibitory influences coining from the brain are voluntary and probably originate in the cells of the cerebral cortex, for example we can by vol- untary inhibition control the urinary bladder re- Rachford : Neuroses of Childhood. 9 flexes and prevent urination even when the mictu- rition center in the lumbar cord is strongly stimu- lated, and again there are spinal reflexes over which voluntary inhibition has no control, as for example erection, ejaculation, and movements of the iris. Of even more importance to us in the study of the neuroses of childhood are the involuntary in- hibitory centers which are distributed throughout the central nervous system. They are found in the brain, the medulla oblongata, and the spinal cord; and without voluntary effort or apparent reflex stimulation these centers seem to exert a constant inhibitory influence on the lower spinal centers. Setchenow's inhibitory center in the medulla ob- longata is an example of similar centers which we have reason to believe exist in the large ganglia at the base of the brain. The inhibitory influence of this center on spinal reflex acts has been quite sat- isfactorily demonstrated. It is also easy to demon- strate in a brainless frog that stimulation of the sci- atic nerve will inhibit spinal reflex acts. It is clear therefore that spinal inhibition may be brought about by other impulses than those that come from predominating centers in the brain and medulla oblongata, that is to say by impulses which are not 10 Ivachford : Neuroses of Childhood. in themselves of a specifically inhibitory nature, but originate in the peripheral stimulation of sensory nerves. But it is not necessary for me to narrate experiments bearing on the subject of inhibition of nerve force, for such experiments are so satisfac- torily detailed in the physiologies that I need here only say that experimental physiology teaches us to believe that there are cells every-where distrib- uted throughout the central nervous system, which have' the power of inhibiting nervous energy. It matters little to us in the present study, whether this inhibition is always the special function of cer- tain cells or whether it may also be the function of the nucleus of the cell that discharges the energy ; but it is important for us to know that inhibition exists both for mental and motor acts, and it will appear later why a clear understanding, of the in- fluences that control and disturb inhibition is of the utmost importance to us in the study of the neu- roses of childhood. If kept in mind, the above outline of the normal functions of the mature nerve cell will materially assist in the study of the functional peculiarities which are manifested by the immature cells of the rapidly developing nervous system of the child. Rachford : Neuroses of Childhood, 11 II. PHYSIOLOGICAL PECULIARITIES OF THE NERVOUS SYSTEM OF INFANCY AND CHILDHOOD. If we turn, to our text-books on physiology or diseases of children to inquire into the peculiarities of the nervous system of infancy and childhood, we shall close them with the feeling that very little is known of this important subject. While unfor- tunately this conclusion is for the most part true, yet we are not so wholly devoid of knowledge on this subject as our text-books might lead us to infer. We have at least some knowledge of a few of the physiological peculiarities of the immature nervous system of the child that have a most im- portant etiological import in the study of the neu- roses of childhood, and it is my purpose here to outline such of these peculiarities as I believe to have a bearing on neurotic disease. At birth the brain is morphologically and functionally the most immature of all the great organs of the body. From birth up to seven years of age it develops enormously in weight, in structure, and in func- 12 Rachford : Neuroses of Childhood. tion. At this time the brain has attained ninety per cent of its maximum weight (Boyd), and after this slowly increases in weight up to the age of eighteen, but increase of function does not keep pace with increase of weight, the brain of a child of eight is almost as large as the brain of an adult, but as Clouston aptly says, " the difference between what the brain of a child of eight and the brain of a man of twenty-five can do and can resist is quite indescribable. The organ at these two periods might belong to two different species of animals so far as its essential qualities go." While the rapid increase in weight of the brain does not continue after the seventh year, the rapid increase in the brain's functional development goes on and still continues long after the brain at eighteen has reached its maximum weight. Clouston says " the unique fact about the nerve cell is the extreme slowness with which it develops function after its full bulk has been attained. * * In this it differs from any and every other tissue. * * We may say that after most of the nerve cells of the brain have attained their proper shape and full size, it takes them the enormous time of eighteen or nineteen years to attain snch functional perfection as they are to arrive at." It is an important fact that Rachford : Neuroses of Childhood. 13 should always be kept in mind that the entire ner- vous system of the normal infant and child is con- stantly undergoing structural and functional de- velopment, and that the structural development, so far as we are now able to judge by our instruments of precision, is much more rapid than is the de- velopment of function. It is also a fact that even with normal children, this development of structure and function does not always go on with the same rapidity, nor does it always follow a regular order in its development. It is quite within the limits of health that certain functions may be rapidly de- veloped and that other functions may be unusually retarded in development. The innumerable con- ditions of heredity and environment have their in- fluence on the nervous system of the child in de- veloping and retarding both structure and function, and this interference with the order of development is not an abnormal condition if within a reasonable time the delayed functions reach a normal state of development. But it is not my purpose to enter deeply into this phase of my subject. I only wish here to call attention to the following important facts : 1st. At birth the nervous system is structurally out more especially functionally immature. 14 Rachford : Neuroses of Childhood. 2d. Throughout infancy and the earlier years of childhood the brain normally undergoes rapid structural development. 3d. Throughout the entire period of infancy and childhood the brain normally undergoes rapid func- tional development. 4th. Innumerable conditions of heredity and en- vironment have much to do with the rapidity and the order of development of the functions of the nervous system of the normal child, as well as with the failure and retardation of their development in the abnormal child. 5th. The metabolism in the normal immature nerve cell of the child must be rapid enough not only to supply the functional waste, but also to supply the material for the growth and develop- ment of cells. 6th. The structural instability of the functionally weak and immature nerve cell of the child makes it much more irritable and excitable than the stable mature nerve cell of the adult. With these general considerations of some of the functional peculiarities of the nervous system of childhood, let us pass to the consideration of cer- tain special functions of the nervous system, which are not the same in childhood as in adult life. Rachford : Neuroses of Childhood, 15 The feeble inhibition of nerve energy is from a clinical stand-point the most important physiological peculiarity of the nervous system of infancy and childhood. The inhibitory function of the nerve cell is the last to be developed ; the cell first ac- quires the function of generating energy, then the function of discharging energy, and lastly the func- tion of inhibiting or co-ordinating energy. These functions of the cell are developed in the order in which they are needed. Until energy is generated there can be no occasion for a discharging function, and until energy is discharged there can be no oc- casion for an inhibiting function. Feeble inhibition is therefore one of the physiological characteristics of the immature nervous system of infancy and childhood, and it plays a most important role as a predisposing factor of the neuroses of child- hood. Otto Soltsman noted that inhibition was very feeble in young animals, and that it be- came stronger as the animal got older. The inhib- itory function of cells is therefore in this regard like the generating function, it gradually becomes stronger as the cells get older up to the time when they reach their complete functional development. But it must be remembered that the inhibitory function of a cell is always developed later than 16 Rachford : Neuroses of Childhood. that function of the cell which generates the force which is to be inhibited. In the normal order of things the function of inhibition should closely fol- low the development of the function which gener- ates the force to be inhibited. The inhibitory mechanisms which control the discharge of nerve force that regulates such vital processes as the action of the heart and the lungs are fairly well developed at birth, while those that regulate reflex phenomena are slowly developed during infancy and early childhood, and voluntary inhibition of motor and mental force does not find its complete development till long after childhood has passed. The late development of the function of inhibition is a fact of prime importance from a clinical stand-point, because this is the last function of the cell to develop and is the one that is most likely to be still further retarded in development by unfavorable conditions of heredity and environ- ment. It is therefore the abnormally feeble inhibition which occurs in the abnormal child that is such a potent factor in the production of neurotic disease in infancy and childhood. It is my belief that this functional immaturity of the inhibitory centers is most im- portant in explaining the manner in which child- hood acts as a predisposing cause of such reflex Bachford : Neuroses of Childhood. 17 neuroses as convulsions and incontinence of urine. It is evident that this cause, most potent at birth, gradually grows less as the child grows older. This is especially true of voluntary inhibition. At birth voluntary inhibition, if it exists at all, must be very feeble, and it gradually grows stronger as the higher functions of the brain are more and more developed. We have a good example of voluntary inhibition in the influence of the will over urina- tion. One wills to urinate and the impulse passes down the cord to the lumbar center that presides over urination, and it is there translated into the reflex act of micturition, or on the other hand one wills not to urinate and the impulse travels down the cord to the lumbar center, and the act of urina- tion is inhibited. But the functional immaturity of the involuntary centers is of even more importance to us as clini- cians than the voluntary, for these centers have most to do with co-ordinating and regulating spinal reflex movements, the lack of inhibition on the part of these centers would make it possible for an overflow of spinal reflex movements to occur and in this way predispose to such convulsive disorders as eclampsia, chorea and epilepsy. As previously noted the reflex discharge of energy from the 18 Rachford : Neuroses of Childhood. spinal motor cells occurs normally through the paths of least resistance, that is in the same plane and on the same side, or in the same plane and on the opposite side of the cord from where the nerve fiber entered that carried the afferent stimulus. But if the resistance to the spreading of the reflexes up and down the cord be reduced, or if the excit- ing stimulus be increased, then we may have an overflow of energy up and down the cord exciting general spinal reflex movements. As above stated, these spinal reflex movements are inhibited and an " overflow" of energy prevented by the action of involuntary inhibitory centers higher up in the cord, the medulla oblongata and the brain. The normally feeble inhibition of infancy predisposes to such an " overflow " of spinal reflexes, or, in other words, to convulsive disorders of all muscles ope- rated through spinal motor nerves. It is also easy to understand how unfavorable circumstances of environment and heredity, having their greatest re- tarding influence on the development of the in- hibitory function of the immature nerve cells of the infant and child, would still further predispose to overflow of spinal reflexes and in this way to con- vulsive disorders. By this overflow of nerve energy we may have a large number of spinal reflex move- Rachford : Neuroses of Childhood. 19 merits as the result of a single exciting stimulus. Extensive convulsive movements of almost the en- tire body may in this way be caused by some sim- ple discharging stimulus. It is one of the functions of the reflex inhibiting mechanisms to prevent this overflow, so that an impulse sent to one portion of the cord may not overflow and spread to other por- tions of the cord, but the mechanism being ineffi- cient the inco-ordinated and spasmodic muscular movements occur. This overflow of nerve force is not peculiar to spinal cells exhibiting motor energy, but it also occurs in the cortical cells exhibiting mental energy (insanity). Inhibition against this overflow is quite as important in the brain cortex as in the spinal cord. It is of clinical importance that we should here note that, not only are the reflex centers in the gray or sensory portion of the cord, but the conducting fibers by which reflex movements overflow and spread up or down the cord are also in the sensory tract of the cord, for this gives us a partial ex- planation of how certain drugs such as cimicifuga, the bromides, antipyrin, and gelsemium, by de- pressing the sensory tracts of the cord can control reflex spinal movements. But it must be remem- bered that these drugs given in this way are given 20 Rachford : Neuroses of Childhood. to relieve symptoms and do not have a curative in- fluence by removing the cause of the disease. In this connection I may quote Lauder Brun.ton, who says that " spasm is as a rule due to diminished action of the co-ordinating or inhibitory centers, rather than to excess of action in the motor cen- ters/' and " those drugs which stimulate the circu- lation and increase the nutrition of the higher nerve centers and the co-ordinating power tend to pre- vent spasm." In this we have an explanation of the benefit derived from nitro -glycerine in certain nervous conditions where the circulation is feeble and the malnutrition great. In the light of the influence of feeble inhibition as a factor in the production of spasm and other neuroses, one notorious fact demands explanation, and that is that the first half year of life, when in- hibition is most feeble, convulsive disorders are least frequent. There are a number of reasons why this is so. The most important is that the motor areas of newly born animals are not so sensitive and do not so readily respond to reflex or direct irritation as in older animals. Another reason is that the nervous system of the nursing child is not so frequently excited by reflex or direct irritants as the child that is fed on a mixed diet. Rachford : Neuroses of Childhood, 21 Lack of sensitiveness of the motor areas in in- fants has an important bearing on the study of reflex neuroses. The motor areas of the nervous system of the newly born do not respond to electrical or other stimuli as readily as in older animals. Purely reflex neuroses are therefore very uncommon in the very young infant. There is at this time in life very little need for the inhibitory control of spinal reflex acts by higher nerve centers, because the spinal reflex centers are so functionally immature that we get but a minimum reflex from a maximum excitation. The feeble inhibition of early infancy is for this reason* not so potent a factor in produc- ing disease as it is a little later on, when inhibition is found not to have kept pace with the develop- ment of cell excitability. The reflex centers very early in life take on their normal irritability while the inhibitory function is very slow in reaching fall development. In this way feeble inhibition comes to play an important role in the production of the neuroses of childhood. This lack of sensi- tiveness of motor centers in the young infant has yet another important bearing, since it is in great part responsible for the lack of tone of the sphincter muscles of the infant. I have previously noted that the muscular tone 22 Rachfokd : Neuroses of Childhood. of the sphincters was maintained by an automatic function of the central nervous system, so closely analogous to reflex action that it seems a difference of name rather than of function. Now these reflex or automatic functions of the cord are so immature in the newly born that there is a lack of tone of all sphincter muscles, that is to say an absence of the normal amount of contraction which afterward fits them for the purposes they are to serve, and which depends in great part upon the action of normal reflex centers in the cord. This lack of sensitive- ness of the reflex centers of the cord in the infant is in my opinion, a most important'factor in produc- ing the incontinence which is characteristic of in- fantile sphincters. The incontinence of infantile sphincters passes away with the functional develop- ment of the centers whose function it is to main- tain in them the normal amount of muscular tone that fits them for the purposes they are to serve. Abnormal conditions of heredity and environment may much delay the functional development of these centers and for this reason a complete or par- tial incontinence may continue long after the pe- riod when it should normally disappear. During this period, when involuntary inhibition is so feeble, voluntary inhibition is of great service in Rachford : Neuroses of Childhood. 23 preventing, as it usually does, the diurnal inconti- nence. But at night when the will is asleep a minimum reflex will overcome the feeble involun- tary inhibition and cause a relaxation of the sphincters. Besides this any abnormal conditions of heredity or environment which increase the irri- tability of these reflex centers will also make it possible for slight reflex causes to disturb the "muscular tone" of sphincters and cause either spasmodic stricture or incontinence. The patho- logical conditions therefore which produce feeble inhibition and excitable nerve centers are sufficient explanation, for the not infrequent condition of in- continence of sphincters during childhood, and it is not necessary to invoke a cause which does not as a rule exist, viz., insufficient muscular develop- ment. 24 Rachford : Neuroses of Childhood. III. FEVER AND THE VARIABLE TEMPERATURES OF CHILD- HOOD. It is a well-known fact that children are more prone to fever than adults, and it is also well known that the temperature is more variable in the fevers of infancy and childhood than it is in the fevers of adults. Why this is so, is a question which we now wish to study from a physiologic stand-point. But first let us clearly understand what we mean by the terms high temperature and fever. By high temperature is meant an increase of the body heat, whether it be due to increased heat pro- duction or diminished heat dissipation. When high temperature is due to increased heat produc- tion it is a symptom of fever, but when it is due to diminished heat dissipation it is not a symptom of fever. By fever is meant an abnormal increase of those tissue changes by which the normal heat of the body is produced, that is to say an abnormal in- crease of the chemic changes which result in disor- ganizing tissues and breaking them up into car- Rachford : Neuroses of Childhood. 25 bonic acid, water, urea and other products of retro- grade metamorphosis. The fever process is characterized by a chain of symptoms with which every clinician is familiar, the most characteristic of these symptoms is in- crease of body temperature. But it must be re- membered that the height of the body temperature does not always mark the severity of the fever pro- cess, and that even a severe and wasting fever may exist with a subnormal temperature. One may note at least two reasons why the temperature is not an index of the severity of the fever process. First : increased heat production is but one of the symptoms of fever, which is ordinarily but not nec- essarily produced by the same causes that produce fever. Second : even should heat production keep pace with the severity of the fever process, heat dissipation may be so rapid or so variable that the body heat at any given time would not be an index of the fever process. With this understanding, the terms fever and temperature will be used as above defined, and we can proceed to study the influence of the nervous system on these processes. Increased tissue metabolism, which is the one great cause of increased heat production (fever), is under the direct control of the nervous system, and 26 Rachford: Neuroses of Childhood, the centers which control this metabolism and in- directly the production of body heat are called heat centers.* Certain of these heat centers have the function of discharging force which will increase tis- sue metabolism and thereby increase the body heat, they are for this reason called thermogenic centers. Other so-called heat centers have the power of inhibiting or controlling the discharge of force from the thermogenic centers, and they are for this reason called ther mo -inhibitory centers. These thermo-inhibitory centers have no direct influence over the processes whereby the body heat is pro- duced ; yet they are of the greatest clinical impor- tance because of their control over the thermogenic centers. The thermogenic and thermo-inhibitory centers have their functions so nicely balanced in the nor- mal adult nervous mechanism that, with the aid of the heat-dissipating centers, they are able to main- tain the body at almost an uniform temperature under the most adverse circumstances, and this temperature equilibrium can only be disturbed by some maladjustment of this nervous mechanism, which would produce either increase or decrease of the body temperature. * Metabolism centers might be a better name for these centers. Rachford : Neuroses of Childhood. 27 Where are these heat centers located ? Ott, Richet, Sachs, Aronson, Wood, Reichert, Girard, Ba- ginski and White agree that the dominating thermo- genic or heat producing centers are situated at the base of the brain in or near the corpus striatum. Eulenberg, Landois, Wood, Ott, Reichert and White agree that important thermo-inhibitory cen- ters are located in the cerebral cortex, and they are known as the cruciate and Sylvian centers. As a prelude to the use of these physiologic data in the explanation of some important clinical phe- nomena associated with the diseases of infancy and childhood, let us first inquire, what should one ex- pect, in the light of these facts, would be the influ- ence on the body temperature of disease or injury of the parts of the brain containing these centers? 1st. Destruction of that portion of the cerebral cor- tex containing the cruciate or Sylvian inhibitory heat centers should cause a rise of temperature be- cause the inhibitory influence of these centers on the basal thermogenic centers would be wholly or partially withdrawn. Experimental physiology confirms this deduction. This is probably the ex- planation of the fever that follows cerebral haem- orrhage into the cortex, and a partial explanation of the fever of insolation. 28 Rachford : Neuroses of Childhood. 2d. Irritation of these cortical inhibitory centers should cause a sub-normal temperature by strength- ening the inhibitory control which they exercise over the thermogenic centers ; this is also evidenced by physiologic experiments. We have here an ex- planation of the sub-normal temperature which may result from cortical meningitis and from haemorrhage, foreign bodies or depressed bone, all of which may first act by irritating these cortical centers (sub-normal temperature), and later by de- stroying them (increase of body temperature). 3d. Destruction of the basal thermogenic centers should cause a decrease of the body heat. But clinically there is little opportunity to observe the effect of destructive lesions of this portion of the brain, since any lesion sufficiently severe to destroy the basal heat centers would cause immediate death by the involvment of adjacent centers controlling vital processes. In shock we possibly have an ex- ample of sub-normal temperature from partial par- alysis of these centers, and in the compression stage of basilar meningitis we may have a sub-normal temperature due to enfeeblement of these centers. 4th. Irritation of the basal thermogenic centers should cause an increase of body heat, this fact which is proven by physiologic experiment is the Rachfokd : Neuroses of Childhood, 29 explanation of the increased temperature that ac- companies the specific fevers. When are the heat centers developed? The answer to this question is in great part the answer to the question why are infants and children more prone to high temperatures than adults? The heat dissipating centers situated in the medulla oblongata are well developed at birth, but these centers be- cause of their special clinical importance in infancy and childhood will be given separate consideration later on. Here it is my purpose to note and es- pecially emphasize the time of functional develop- ment of the heat-producing and the heat-inhibiting centers. Before birth the thermogenic centers are in a state of immature functional development. In the human infant born prematurely they are so imper- fect that artificial heat is necessary for a time to keep the body heat up to the normal. In this re- spect the immature human foetus resembles cold blooded animals who are more or less dependent on their surroundings for their body heat. But as the foetus matures, the thermogenic mechanism reaches a state of fair development, so much so, that one may say that the thermogenic centers are functionally competent at birth ; this of course must 30 Kachfokd : Neuroses of Childhood. be so, since the formation of body heat is a vital process, and is as we have seen probably controlled by the same mechanism that controls the all im- portant process of tissue metabolism. While the thermogenic heat centers have a fair degree of de- velopment at birth, they are yet immature and un- stable, and are therefore like all the nerve centers in the unfinished brain of the child, more easily ex- cited to abnormal action, than are the mature heat centers of the adult brain. All the nerve cells of the rapidly growing brain of the infant and child are in a state of more or less structural instability since the metabolism going on within them must not only be rapid enough to supply waste but also to furnish material for the growth and development of new cells. This structural and functional insta- bility of the cells makes them more irritable and ex- citable than the nerve cells in the finished brain of the adult. For this reason one would expect to find the thermogenic heat centers of the child more excitable than those of the adult, and such in fact is the case. This is one important reason why the temperature of the infant is so variable and unsta- ble under slight disturbing influences and why like causes produce higher temperatures in the infant and child than in the adult. Rachford : Neuroses of Childhood, 31 But important as this normal excitability of the immature thermogenic centers of the child may be, yet of far greater importance, from a clinical stand- point, is the greatly increased irritability from un- favorable conditions of heredity, nutrition and en- vironment. The thermogenic heat centers of the nervous, anemic, delicate child are in a state of ab- normal excitability, so that a slight excitation may produce an abnormal discharge of force resulting in fever and high temperature. But after all probably the most important cause of the instability of temperature in infants and children is to be found in their feeble cortical thermo-inhibitory centers. The thermo-inhibitory centers, like other cortical inhibitory centers pre- viously spoken of, have very imperfect functional development at birth, so that at this time they do not exert a very strong controlling influence over the basic thermogenic centers, and are not able to inhibit these centers from discharging increased en- ergy under slightly increased excitation ; for this reason slight causes may produce an elevation of temperature in the infant. Hale White says in speaking of the thermo-inhibitory centers : " In the human adult they are fairly competent and active as is proven by our pretty constant temperature/' 32 Rachford : Neuroses of Childhood. "In the lower animals and in children they are probably not so completely evolved fori have found that the normal temperatures of rabbits varies sev- eral degrees, and rapid fluctuations of temperature are common with children when slightly ill." Ott in a recent personal communication says : "It seems to me that children are more prone to high temperatures because of a loss of control of the cor- tical centers." It is on the whole a justifiable conclusion from all the evidence in our possession that the high and variable temperatures of infancy and childhood are in part due to the normal immaturity and insta- bility of the cortical thermo-inhibitory centers. But as I have previously noted the feeble inhibi- tion in the normal child is not of so much clinical importance as the abnormally feeble inhibition of the abnormal child, this is as true of the heat reg- ulating mechanism as it is of all other nervous mechanisms. The inhibitory part of the heat mechanism in its feeble and unstable state is the portion of this mechanism which suffers most from disease, and in its development is still further re- tarded by unfavorable conditions of heredity and environment. McAlister says : " The inhibitory is the first portion of the heat regulating mechanism Rachford : Neuroses of Childhood. 33 to fail under injury or disease. " All of this is quite in accord with the general observation pre- viously made that the amount of energy developed by a nerve cell will depend directly on the amount of healthful chemical metabolism going on within it. The maximum amount of energy being stored up in the well-nourished cell and the minimum amount of energy in the starved cell. One can readily un- derstand then how a malnutrition of the nerve ele- ments resulting either from heredity, impoverished blood or bad hygiene can still further weaken the physiologically incompetent cortical ther mo-inhibi- tory centers of the child, so as to make it more prone to variable and to high temperatures from slight causes than the normal child is, since in this condition the energy from the thermogenic centers would be discharged under much less restraint from the inhibitory centers than it is in the normal child. It may not be out of place here to state that the best explanation we have for the rapidly varying un- stable temperature that not infrequently occurs in hysterical women is, that it is due to the instability of the cortical thermo-inhibitory centers which have given way under the combined influence of envi- ronment, bad heredity, bad hygiene and impov- erished blood, 34 Rachford : Neuroses of Childhood. From what has been said the following summary may be made of the reasons why children are more prone than adults to high and variable tempera- tures : 1st. In normal children the thermogenic centers are more unstable and therefore more easily excited than in the adult. 2d. In normal children the thermo-inhibitory centers are weaker, more excitable, and therefore more incapable of exercising proper control over the thermogenic centers, than they are in adults. 3d. In nervous, anemic children the thermogenic centers are far more excitable than in the normal child, such children are therefore more prone to high and variable temperatures. 4th. In nervous, anemic children the thermo-in- hibitory centers are even weaker than in the nor- mal child, and therefore still more incapable of re- straining the discharge of force from the thermo- genic centers; this is a most important reason for the variable and high temperatures of such chil- dren. Exciting causes of fever and high temperature in infants and children. Having studied the pecu- liarities of the nervous mechanism which controls the body temperature of the infant and child, we will Rachford : Neuroses of Childhood, 35 now inquire what are the causes most likely to dis- turb this mechanism so as to produce an increase or decrease of body temperature. Or in other words, we will ask what are the usual exciting causes for the high and variable temperatures which are so likely to occur in infancy and childhood ? These causes may be classed as follows : 1. Bacterial products. 2. Insolation. 3. Muscular action (convulsive). 4. Mechanical and reflex causes. 1st. Bacterial products are by far the most im- portant of the exciting causes of fever and high tem- perature in children. The variations in tempera- ture accompanying the acute infections, including all forms of external and internal bacterial toxe- mias, are due to the action of bacterial products on the heat centers. Bacterial products capable of producing fever and variations in temperature may be formed by bacterial action either within the blood and tissues of the animal or outside the blood and tissues of the animal, in wounds, or in cavities, such as the intestinal canal, which com- municate with the external air. But wherever these bacterial products may be formed the soluble ones are absorbed and produce fever and variable 36 Rachford : Neuroses of Childhood. temperature by their direct action on the nervous centers. As a rule the soluble bacterial products which produce fever also produce increase of body temperature and the increase of temperature is often a valuable indication as to the severity of the fever process, but this is a rule which unfortunately has many exceptions, as is shown by the subnormal temperature that occasionally attends pneumonia, malaria, typhoid fever, influenza, scarlatina, and other acute infections. The subnormal tempera- ture which occasionally occurs in these fevers has not been satisfactorily explained. Very recently Centanni investigated seventeen pathogenic species of bacteria and found in cultures of all of these germs a substance, not a peptone, which when in- jected into animals caused fever with the following symptoms, high temperature, prostration, emacia- tion, and finally death. Omitting further discussion I will say that the evidence justifies the conclusion that bacterial products excite fever by acting di- rectly on the fever* centers and the variations in temperature that accompany fever are due to the action of bacterial poisons on the heat * centers. *The fever and heat centers are probably identical since ex- perimental physiology has not been able to differentiate be- tween them. Rachford : Neuroses of Childhood. 37 Why do bacterial products produce fever and variable temperature so much more readily in children than they do in adults ? This question has in part been answered by our previous study of the pecularities of the heat mechanism in child- hood. (a) The thermogenic centers being more unstable and irritable in the child are more readily excited by bacterial products. Fever and increased tem- perature are therefore more easily produced. (b) The thermo-inhibitory centers being imma- ture and feeble in the child they exercise but a weak restraining influence over the discharge of force from the thermogenic centers which are being excited by bacterial products. For this reason fever and increased temperature are more easily pro- duced by bacterial products in the child than in the adult. (c) Still another possible reason why microbic poisons produce fever and increase of temperature more readily in the child than in the adult was suggested to me by Prof. Charles Richet in a per- sonal communication. This explanation depends on the potency of the fever poison and not upon the peculiarities of the nervous mechanism. Richet asks : " Is it not possible that the microbic fever pro- 38 Rachford : Neuroses of Childhood. ducing toxins may be stronger or more toxic when they are produced in young organisms that are not protected by previous attacks of acute infections?" That is to suggest that in infants and children who have not had previous microbic infection and who are not therefore protected against these diseases pathogenic microbes may develop more potent fever producing toxins than they can later in life. 2d. Insolation is an important cause of fever and high temperature in infancy and childhood. The best explanation of the fever of insolation is that the feeble inhibitory heat centers of the child are still further weakened by the heat so that practi- cally no restraint is exercised over the heat produc- ing centers. Cases of insolation in infancy and childhood are ordinarily classed as cholera infan- tum, or other forms of summer complaint, and this classification greatly obscures the direct etiological importance of heat in these cases. Forchheimer has for many years taught that many of the cases of so-called cholera infantum were cases of insola- tion, and that in such cases the intestinal fermenta- tion is primarily a symptom rather than a cause of the disease. 3d. Convulsive muscular action is not an infre- quent cause of increased temperature in infants and Rachford : Neuroses of Childhood. 39 children. The manifestation of muscular energy is always accompanied by the evolution of heat and the production of carbonic acid, and excessive mus- cular action such as occurs in general convulsions is always accompanied by increased production of heat. And this is a factor of the increased tem- perature that occurs in general spasms. But a por- tion of the increased body heat that occurs in this condition may be attributed to the increased fric- tion of the muscles, tendons and articular surfaces which transform kinetic energy into heat. It should be remembered therefore that excessive muscular action may be a factor in producing increase of body heat and that this source of heat production is quite distinct from that which results from the normal metabolism constantly going on in the muscles, etc., at rest, and from the abnormal metabolism going on in the muscles, etc., during fever. I do not wish to convey the idea that in- creased muscular action is the most common or most important cause of the increased body tem- perature that occurs during muscular spasm, but only to impress the fact that violent muscular action is a factor in producing the increased body heat rather than that the increased body heat is a factor in producing the spasm. 40 Rachf ord : Neuroses of Childhood. When the spasm is purely reflex in origin the excessive muscular action is then no doubt the most important cause of the increased body heat, but when the spasm results from microbic poisons, as it usually does, then no doubt the increase of temperature is chiefly due to the action of these poisons on the heat centers. For these reasons one would expect to find the temperature during reflex spasm not so high as it is in spasm due to microbic infection. 4th. Mechanical and reflex causes of fevers and the variable temperatures of infancy and childhood. In speaking of the heat centers I have already in- dicated how foreign bodies, growths, and exuda- tions could act directly oh the heat centers to dis- turb the body temperature, so that there now only remains the consideration of the reflex causes of variations in the body temperature of infants and children. Ott says : " After the use of large doses of atropine I have seen the temperature rise greatly upon sciatic irritation. * * It was also found that this increase of temperature was accompanied by an increased production and augmented dissipation of heat." In these experiments we have proof that not only high temperature but also fever may be produced reflexly. Rachford : Neuroses of Childhood. 41 Gall stone fever, which is classed by physiologists as a reflex fever, has been studied by Wood, who found that in the " fever produced by gall stones, elevation of temperature did increase urea elimina- tion. 7 ' Here again is an instance of both fever and increased temperature from a purely reflex cause. It is my belief that variations in the body tem- perature in infancy and childhood are not infre- quently of reflex origin, and that the intestinal canal and the genitalia are the sites where reflex irritation is most likely to produce this symptom. Increased temperature may occur in the infant and child from the cutting of a tooth, from worms, un- digested food, and other foreign bodies in the in- testinal canal. The irritating products of an in- testinal fermentation may also produce increase of temperature unaided by the soluble bacterial poisons previously spoken of. It is a matter of every day experience with clinicians that the removal of such simple causes as are here narrated will ofttimes cause the temperature of the sick child to fall to normal and all the other symptoms of fever to dis- appear. It will be well therefore, in these days when chemistry and bacteriology are dominating medical pathology, for us to remember that a purely reflex fever can and does sometimes occur during infancy and childhood. 42 Rachford : Neuroses of Childhood. IV. HEAT DISSIPATING MECHANISM. In the previous chapter the consideration of the heat dissipating mechanisms was purposely omitted because it was thought that certain clinical phe- nomena dependent on the peculiarities of this mechanism during infancy and childhood could best be studied in a separate chapter. The heat dissipating mechanism is the mechanism by which we keep ourselves' cool. This may be done in three ways : (1) By radiation and conduction of heat from the surface of body. (2) By constant evaporation of water from the surface of body. (3) By evaporation of water from the air pas- sages. Dissipation of heat by radiation from the surface of the body is by far the most important means of heat dissipation. In this process the vaso-motor nervous mechanism is all important. When un- Rachford : Neuroses of Childhood, 43 usual heat loss is demanded the vaso-motor nerves dilate the blood-vessels of the skin and in this way expose more blood to the lower temperature of the air. Loss of heat by evaporation is dependent on the activity of the sweat glands which are controled by sudoriparous nerves and sweat centers. When unusual heat loss is demanded these centers respond by increasing the activity of the sweat centers which cover the surface of the body with fluid and the temperature is lowered by its evaporation. Both the dominating vaso-motor and sweat centers are located in the medulla oblongata and have reached good functional development at birth. But in the infant and child they respond more readily and energetically to the demands for heat reduction than they do in the adult. It must also be kept in mind that heat loss from both radiation and evaporation is greater in the infant than in the adult because its area of sur- face is greater in proportion to its body weight, the infant has in fact a three-fold greater radiation. These are the reasons therefore why the high tem- peratures of infancy and childhood are so readily reduced by the heat dissipating mechanisms. The increased activity of the heat dissipating mechan- 44 Rachford : Neuroses of Childhood. ism acting on a proportionately larger surface compensates for the increased activity of the ther- mogenic centers. In the play of function between the heat generating centers and the heat dissipating centers we have an explanation of the rapid varia- tions of temperature so characteristic of the fevers of infancy and childhood. Evaporation of water from the air passages is a means of heat dissipation which we have yet to consider. And it is the special purpose of this chapter to study this function in its relation to clinical phenomena. In certain animals, the dog for instance, who do not sweat, the evaporation of water from the air passages is the chief means of reducing the body temperature. Richet calls the rapid respirations of the panting dog Polypnoea. By these rapid respi- rations, amounting to as many as 400 in a minute, the heat of the body is rapidly given off. Richet located the polypnceic center in the medulla ob- longata. Ott later located it in the tuber cinerium. Richet proved that the polypnceic center was not affected by the amount of carbonic acid or oxygen in the blood, and that it was solely for the purpose of heat dissipation. In answer to the question, How is the polypnceic Rachford : Neuroses of Childhood, 45 center excited to activity? we have the experiments of Sihler demonstrating that increased respirations of an animal exposed to heat is due to two causes, warmed blood and stimulation of the skin by the heat, and that skin stimulation is the more im- portant factor. Gad and Mertschinsky also demon- strated that increased temperature of the blood stimulates the respiratory centers and causes an increased number of respirations, and Ott pro- duced polypnoea by electrical stimulation of the tuber cinerium. Does the polypnoeic center exist, and is it func- tionally active in infancy and childhood? The answer to this question has most important clinical bearings. Ott says, " In infants we see a polypnoea during fever, the respirations rise in frequency with the rise in temperature." Every physician must have seen many cases of rapid respiration in children that could not be accounted for by pulmonary disease. It not infrequently happens that a child with fever will have 60, 80 and 100 respirations per minute, without presenting any sign or symptom of lung trouble. Polypnoea is to my mind the only explanation of this phenomenon. Very rapid breathing is a common symptom of summer complaint, and in many cases means 46 Rachford : Neuroses of Childhood. nothing more than nature's attempts at heat dissi- pation. The importance of recognizing polypncea as a symptom of fever in infancy and childhood, is very great. If we do not do this we may often be led, by the rapid breathing, away from the real cause of the disease. Fortunately for us as clini- cians there is a marked difference between the character of the polypnceic breathing and the rapid respirations due to lung or heart disease. In polypnoea the breathing is regular, easy and rapid, but is not as it is in lung and heart disease irreg- ular, labored and accompanied by cyanosis. Rachford : Neuroses of Childhood, 47 AUTOGENETIC AND BACTERIAL TOXINES. The qualitative and quantitative changes in blood supplying nerve tissues are, from a clinical stand- point, the most important causes of the neuroses of childhood. The importance of blood changes as a cause of neurotic disease depends, not only upon the fact that they are most potent factors, but more because they are factors which can as a rule be removed by treat- ment, and as clinicians we are especially interested in the remediable causes of disease. For convenience of study, one may say that there are four important blood changes related to neurotic disease : 1st. The presence of autogenetic toxines in the blood. 2d. The presence of bacterial toxines in the blood. 3d. A venous condition of the blood. 4th. An impoverished condition of the blood. 48 Kachford : Neuroses of Childhood. The above named blood changes do not, as a rule, exist as separate pathological conditions ; but should rather be considered as factors of a com- plex blood condition which is very commonly etiologically related to the neuroses of childhood. The above classification is given that it may fur- nish topics for discussion. Auto-intoxication. Auto-intoxication is one of the most important and certainly one of the least understood of all the causes of neurotic disease both in adults and children. The poisons of this class are not of microbic origin, but they are for the most part either substances which are formed by the various organs of the body to serve some phys- iological purpose, but which are toxic when ab- normally accumulated within the blood and tissues, or they are substances which are either normally or abnormally formed in the tissue changes incident to the functional activity of muscles and other or- gans. The poisons which produce auto-intoxica- tion are therefore as a rule substances which are normally produced in the body in such quantities that they can readily be disposed of by the tissues or be eliminated by the intestinal canal, the kidneys, liver, lungs and other excretory organs. In this way these bodies may be excreted as rapidly as they Rachford : Neuroses of Childhood. 49 are formed, so that under normal conditions they do not accumulate in sufficient quantities to pro- duce nervous or other symptoms. But in certain pathological conditions there may be such an accu- mulation of these poisons that they become most important factors in the production of disease; this may result either from a perverted metabolism, which causes an increased production of these poisons, or from disease of the kidneys, liver, or other excre- tory organs, which will cause their accumulation from defective elimination or defective neutraliza- tion. But vast and important as is this field of the re- lation of auto-intoxication to nervous disorders, yet it is so confused and so full of misinformation that it seems almost presumptuous to write upon it- One begins to realize what an important disease producer auto-intoxication is, when told that it is the most important etiological factor of acute and chronic uremia, of gout, migraine, migrainous gastric neurosis, migrainous epilepsy, neurasthenia, hypochondriasis, neuralgia, myalgia and possibly other nervous disorders. The importance therefore of this field, as well as the darkness which shrouds it, are my excuses for attempting its exploration. Bouchard, in his " Lectures on Auto-intoxica- 50 Rachford : Neuroses of Childhood. tion," proves that normal human urine is toxic, when injected in large quantities into the veins of rabbits; he found on the average that it requires forty-five cubic centimeters of urine to kill one kil- ogram of rabbit. From this Bouchard estimates that, " On an average of two days and four hours man makes a mass of urinary poison capable of in- toxicating himself." Bouchard's experiments were conducted with sufficient care to prove that normal urine contains toxic bodies ; but the large quantity of urine necessary to produce intoxication also proves that the poisonous bodies in normal urine either exist in minute quantities, or have a very low degree of toxicity. Bouchard from his researches concludes that there are seven toxic principles in normal urine. 1st. "A diuretic substance," urea, which, by rea- son of this property, " plays a useful role in the economy." While urea in " an enormous dose " may be said to be toxic, yet " there are few bodies in the urine so feebly toxic as urea, if we except albumen and water which naturally exist in the blood." " Sugar is more toxic than urea." " Urea has almost the toxicity of the most inoffensive salts." These observations concerning urea are in accord with the well established physiological fact, Rachford : Neuroses of Childhood. 51 that urea is not sufficiently poisonous to play any part in the production of urinary toxemia. 2d. An unnamed narcotic body, which has not been separated from the urine, and which is thought to be the cause of the narcosis produced by the in- jection of normal urine. 3d. An unnamed sialogogic body which has not been separated from the urine. It is presumed to exist in minute quantities in human urine, because under certain conditions urine produces salivation. 4th. An alkaloidal body " endowed with the property of causing convulsions." This body has not been named or isolated. 5th. An organic substance which contracts the pupil, and causes convulsions. It has not been named or isolated, but is thought to be a coloring substance. 6th. An organic substance which " reduces heat," not named or isolated. 7th. The potash salts, u whose convulsive proper- ties have long been known," play an important part in the production of urinary toxemia. Bouchard believes that the above named bodies play an important role in uremia, and other auto- intoxications. But important and valuable as this work is, it really gives very little definite kuowl- 52 Eachford : Neuroses of Childhood. edge except that normal urine is feebly toxic, and that it contains a number of unnamed and uniso- lated toxic bodies, which are so feebly toxic, or ex- ist in such small quantities, that it requires " on an average of two da}^ and four hours for a man to make a mass of urinary poison capable of intoxicat- ing himself." On the whole one may say that Bouchard's work is a valuable contribution to the study of auto-in- toxication, but it falls far short of giving a satisfac- tory explanation of the symptoms of " uremia " or of other auto-intoxications. It is my belief that pathological, rather than nor- mal urine, holds the most important secrets of auto- intoxication, and I would ask attention to a phase of this subject to which I have given much study, viz., the relation of the uric acid diathesis to ner- vous diseases. On this subject I wish to speak emphatically, in the hope and belief that what I shall say will throw a ray of light into one of the darkest fields in medical pathology. At the pres- ent time there is no fallacy so deeply rooted in the medical mind, as that uric acid and urea can, by their direct action on the nerve centers, produce nervous disease. This belief has been so firmly fixed in the medical mind, that it was considered al- Eachford : Neuroses of Childhood. 53 most too trite a fact for medical discussion, and even now it seems almost heresy to proclaim that uric acid and urea do not produce nervous symptoms, since the ingenious theory of.Haig, that migraine and kindred nervous disorders are commonly due to an excess of uric acid in the blood, is now very gener- ally accepted by the profession. In the field of pediatrics we have blamed uric acid with causing paroxysmal gastric neuroses, mi- graine, convulsive disorders, and other neurotic dis- eases ; while against urea has been charged certain convulsive symptoms. But I wish here to empha- size the fact, that both urea and uric acid have, in this regard, been falsely accused, and convicted upon circumstantial evidence. They are innocent, non- poisonous bodies, not capable of producing the severe nervous symptoms, which accompany the excessive elimination of uric acid and the dimin- ished elimination of urea. Bouchard injected experimentally in the blood thirty centigrams of uric acid for each kilogram of animal without apparent injury. In one instance he injected sixty-four centigrams for each kilo- gram of animal, without injury to the animal. Roberts says : " Uric acid and its compounds are deleterious simply because of their sparing solubil- 54 Rachford : Neuroses of Childhood. ity in the body media." In fact all experimental evidence is opposed to the idea that uric acid or its compounds can, in any other than a mechanical way, produce nervous symptoms. Uric acid has been accused and convicted of producing certain nervous disorders, on the circumstantial evidence that it was present in excess in the urine immediately before, during, or after an attack of these diseases. But its innocence is now thoroughly well established, and the same may also be said of urea. In the light of our present knowledge, we can only consider the increase of uric acid and the di- minution of urea in the urine as valuable signs, in- dicating the approach, or presence of a nervous attack, due, in all probability, to auto-intoxication, but of which they are entirely innocent. Sir Alfred Garrod, Sir Dyce Duckworth, M. Lecorche, Sir William Roberts, Murchison, Alexander Haig and many other observers have conclusively shown that there is a definite relation between the quantity of uric acid excreted and the paroxysms of gout ; and several of these observers have also called attention to the relation existing between the amount of uric acid and urea excreted and certain paroxysmal nerv- ous diseases, such as migraine, epilepsy, spasmodic asthma and uremic manifestations. But no one Rachford : Neuroses of Childhood. 55 has given so much time and careful study to the re- lation that exists between nervous diseases and the presence of urea and uric acid in the blood as has Alexander Haig. The term uric acid diathesis is, therefore, rightly used to describe the condition in which, either from increased production, or deficient elimination, there is an excess of uric acid and its compounds either in the blood or in the tissues, which are closely as- sociated with gout, migraine and allied diseases. In some disorders, such for example, as gout and gravel, which belong to the uric acid diathesis, the distressing symptoms are, no doubt, due in part to the precipitation in the tissues, or elsewhere, of the comparatively insoluble urates ; but in other dis- eases, such for example, as migraine which may also under the above definition be classed as coming un- der the uric acid diathesis; the uric acid, although it may occur in excess in the blood or urine in these cases, has nothing whatever to do with the production of nervous symptoms. In accepting the non-toxicity of uric acid and its compounds, one must not forget that, by reason of their insolubil- ity, these substances may be important patholog- ical factors in gravel and articular gout, and that they may, in a reflex way, even produce nervous 56 Rachford : Neuroses of Childhood. symptoms; and it should also be remembered that, by their presence in excess in the urine,, they may serve as important signs or signals to announce the presence or the approach of migraine and allied nervous diseases. In the light of the above facts we are left abso- lutely without any explanation of the constitutional symptoms which occur in the uric acid diathesis, and which have heretofore been ascribed to the toxic influence of this body on the nervous cen- ters. In this condition of affairs, one may there- fore be pardoned for suggesting, that the poisonous bodies so closely allied to uric acid, and named and classified as leukomains, may be in part re- sponsible for the nervous symptoms that have here- tofore been attributed to uric acid. For it seems altogether possible that, along with the increased excretion of uric acid, there might also be an in- creased excretion of uric acid leukomains, since these bodies belong to the same chemical group, and are probably formed by the same, or a like metabolism. It also seems possible that a perverted metabolism, or a defective elimination, might result in these leukomains being present in the blood in such abnormal quantities as to make them in part responsible for the nervous symptoms. Some Rachford : Neuroses of Childhood. 57 of these leukomains, notably paraxanthin, gerontin, and xanthin, are very poisonous, and quite capable of producing nervous symptoms if they occur even in small quantities in the blood. The uric acid leukomains are a group of bodies closely related to uric acid, of which paraxanthin, xanthin, and ge- rontin are poisonous, and xantho-creatinin is a poi- sonous leukomain of the creatinin group. It is quite possible that all of these poisonous leukomains, as well as other unnamed poisonous leukomains, may contribute to the production of the complex of symptoms which I shall here class under leuko- main poisoning ; but in this study I shall only at- tempt to show that paraxanthin and xanthin are etiologically related to the group of nervous dis- orders above noted as being manifestations of leukomain poisoning. Paraxanthin is by far the most poisonous of all known leukomains. Salomon thus describes paraxanthin poisoning in the mouse. If one-half milligram of paraxanthin be intro- duced into the peritoneal cavity of a mouse the following symptoms will result: " The reflexes are increased to a tetanus, followed by a rigor-mortis like contraction of the muscles ; marked dyspnoea is a constant symptom which continues till death/' Xanthin is very much less poisonous than parax- 58 Eachford : Neuroses of Childhood. anthin, but according to Filehne it produces in the frog a decided muscular rigor and paralysis of the spinal cord. In brief, we may note the following facts concerning xanthin and paraxanthin as bear- ing on this subject : 1st. Paraxanthin and xanthin are poisonous leu- komains of the uric acid group, capable of produc- ing the most profound nervous symptoms. They are readily soluble in water, urine and blood. 2d. Paraxanthin is found in normal urine in such small quantities that its poisonous properties are lost in dilution. Salomon found only 1.2 gm. in 1,200 litres of urine. This quantity is so minute that its presence can not be satisfactorily demon- strated in such quantities of normal urine as can conveniently be obtained from patients. In a re- cent personal communication Salomon says : " Nine litres of normal urine is a very small quantity to prove the presence of paraxanthin if one has not previously worked with larger quantities so as to master the details of the work, and very much harder would it be to prove the presence of parax- anthin in four litres of normal urine, as I know from experience. ... I would advise that not less than ten litres of normal urine be used to demonstrate the presence of paraxanthin." My own Rachford : Neuroses of Childhood. 59 experience is in accord with Salomon's. In pre- vious papers I have recorded my failure to demon- strate the presence of paraxanthin when working w x ith as little as four litres of normal urine ; and, since these papers were written, I have made a large number of examinations of normal and other urines, and I have always failed to de- monstrate the presence of paraxanthin in four litres of normal urine. Upon this evidence I have concluded that paraxanthin is present in abnor- mally large quantities when I can find it in less than four litres of normal urine. Xanthin also, as a rule, requires more than four litres of urine to demonstrate its presence, but I have frequently found small quantities of xanthin where I could not find paraxanthin in working with four litres of urine. 3d. Paraxanthin and xanthin are not formed in the kidney. They are excreted from the blood by the kidneys. The presence, therefore, of large or small quantities of xanthin bodies in the urine means that these bodies were present in large or small quantities in solution in the blood previous to their elimination by the kidneys. With the above facts in mind concerning xanthin and paraxanthin, we are better prepared to study 60 Rachford : Neuroses of Childhood.. leukomain poisoning, which, I believe, is the most important form of auto-intoxication. Leukomain Poisoning. In the Medical News, Philadelphia, May 26, 1894, I published a paper on " Paraxanthin as a Factor in the Etiology of Cer- tain Obscure Nervous Conditions." That paper was based on the study of a patient who had. migraine all her life till she was past sixty years of age, at which time the migrainous attacks were superseded by epileptoid paroxysms, which came at about the same interval of time as the migrain- ous attacks had previously come. These epilep- toid attacks were very severe, and very sudden in their onset ; almost immediately the muscles would become rigid and the breathing would be labored, gasping and irregular; the heart's action was rapid but would remain regular and strong. These at- tacks would last from twenty minutes to an hour and unconsciousness would continue from the begin- ning to the end. In the interval between these at- tacks the patient was well mentally and physically. By a careful study of this case, both before and after (See Medical News, Philadelphia, November 3, 1894, and Medical Record, New York, June 22, 1895) the publication above referred to, I have demonstrated that the epileptoid symptoms of this Rachford : Neuroses of Childhood. 61 patient were caused by the direct action of poisonous uric acid leukomains on the nerve centers. I found that the urine of this patient passed during and just after an attack of epilepsy contained an excess of uric acid, and that in color, quantity and other particulars it corresponded to the urine of the epileptoid cases which Alexander Haig and others have thought to be due to uric acid ; but I also found, a fact of much greater importance, and one that has previously been overlooked in the study of these cases, viz., that along with the excess of non-poisonous uric acid compounds excreted during and after these attacks, there was also excreted in the urine a very great excess of paraxanthin and other poisonous uric acid leukomains. The paraxanthin solution obtained from the urine of this patient, when injected into rats and mice, produced epileptoid symptoms very similar to those from which my patient suffered when this same paraxanthin was circulating in her blood just prior to its excretion by the kidneys. From the study of this and other so-called mi- grainous epilepsy cases I am convinced that there is a form of epilepsy which begins as a rule in middle life, either alternating with or taking the place of migrainous attacks of previous years, which 62 Rachford : Neuroses of Childhood. has as its most important etiological factor the presence in the blood of the very poisonous leuko- main paraxanthin. This form of epilepsy is an auto-intoxication — a true leukomain poisoning. A further study of these cases leads me to believe that many of the hystero-epilepsy cases are leu- komain epilepsies, and are therefore more amenable to medical than to surgical treatment. It is impossible at the present time to say just what part paraxanthin poisoning plays in the pro- duction of puerperal and other eclampsias of uremic origin, but it is not improbable, in fact it is my belief, that the poisonous leukomains are in part re- sponsible for uremic symptoms. True migraine is perhaps the most common of the well marked forms of auto-intoxication due to leu- komain poisoning. In the Medical News, Philadel- phia, November 3, 1894, and the Medical Record, New York, June 22, 1895, 1 have published a study of a number of cases of true migraine, in which I demonstrated that attacks of migrainous headache were always immediately followed by the excretion of an excess of uric acid in the urine of these patients; this fact has been fully worked out by Alexander Haig and other English writers who have unjustly accused the non-poisonous uric acid Rachfokd : Neuroses of Childhood. 63 of producing the complex of nervous symptoms so characteristic of migrainous attacks. But these and all other investigators have up to the present time overlooked the fact demonstrated by me in the papers above referred to, viz., that along with an excess of uric acid, there is excreted, in the urine passed just after an attack of migraine, a very great excess of xanthin and paraxanthin, and that the solution of these leukomains, obtained from such patients, produces in rats and mice the characteristic symptoms of paraxanthin poisoning. From my researches it is plain that attacks of migrainous headache are coincident with an excess in the blood of uric acid leukomains. The conclu- sion therefore seems justifiable, that migraine is a manifestation of leukomain poisoning, and is not, as Haig and others have thought, due to uric acid and its compounds which are also present in excess in the blood during these attacks. There is a leukomain gastric neurosis, the study of which has been of more interest and more value to me than any other phase of leukomain poi- soning. In the Medical Record, New York, June 22, 1895, I have published a careful study of one of these cases, in which I demonstrated that the gastric attacks were followed by the excretion in the urine 64 Rachford : Neuroses of Childhood of an excess of uric acid and its compounds, and of a great excess of xanthin and paraxanthin ; and in this case I also demonstrated the presence of xanthin in the mucus which was discharged in great quantities from the stomach during these attacks. In leukomain gastric neurosis there is almost al- ways a personal history of migraine. The gastric attacks often take the place of migrainous head- aches, or the patient may suffer from both of these manifestations of leukomain poisoning at the same time. The day before a gastric attack the patient may be uncomfortable, with slight pain in the stomach, and eructation of gas, and the urine may be very scant and high colored. These warning symp- toms may be more or less distinct, and then the at- tack bursts with great fury. At once the patient has great pain in the stomach, and vomiting comes on at the same time. The pain and vomiting con- tinue and a large quantity of glairy mucus is dis- charged from the stomach. In severe cases, eructa- tion of gas, pain in the stomach, and vomiting of mucus continue in paroxysms till they are relieved by the hypodermic injections of morphine. The frequency of these attacks and the relief obtained from morphine gradually induces the opium habit Rachford : Neuroses of Childhood. 65 in the unfortunate victims of this phase of leuko- main poisoning. It is therefore of the very great- est importance that physicians every- where should recognize that these gastric attacks are of leukomain origin, in order that they may be relieved by proper treatment and saved from the morphine habit. Fortunately many of the cases of leukomain gastric neurosis are much less severe than the type of cases just described. In some instances the attack is terminated by the first paroxysm of vomiting, and in others there may be no vomiting at all. In the cases where there is no vomiting patients often complain of periodic diarrhea, with more or less constant pain in the stomach, and with well marked symptoms of hypochondriasis or neurasthenia. It is my belief that the importance of leukomain poisoning as a disease producer is not half told by the above outline, but it would not be profitable to attempt to predict the findings which may come from this field of work. In this connection, how- ever, I shall say that- 1 have unpublished experi- mental evidence that causes me to believe that the gastric attacks in lead poisoning, and the arthritic paroxysms of true gout are due to leukomains. Biliary toxemia is a form of auto-intoxication re- sulting from the absorption of bile. Bouchard has 66 Rachford : Neuroses of Childhood. shown that the biliary salts and the biliary coloring matters are active poisons, the latter being much the more poisonous. These substances when in- jected into the veins of rabbits are very active pois- ons, killing in convulsions. From his experiments on rabbits, Bouchard estimates that man forms in eight hours enough biliary poison to kill himself. But these experiments are not fully substantiated by clinical experience, since the absorption of con- siderable quantities of bile may go on over a long period of time, producing a well marked jaundice, without causing very pronounced symptoms of auto- intoxication. The simple jaundice of infants and the catarrhal jaundice of children do not, as a rule, have well defined symptoms which can be ascribed to the toxic influence of bile. But children suffer- ing from the more severe forms of jaundice may be irritable, and may even have convulsions; or they may be drowsy, stupid and pass into coma; but it is impossible to say what part the biliary toxemia plays in producing these symptoms. In the present state of our knowledge, the further discussion of this subject would not be profitable. Bacterial toxines. Bacterial toxines play an im- portant role in the etiology of the neuroses of childhood. We know from both laboratory and Rachford : Neuroses of Childhood. 67 clinical observations that bacterial products can, by their direct action on nerve elements, produce most profound nervous symptoms. In a previous chap- ter we have seen that bacterial products are by far the most important of the exciting causes of fever and high temperature. These bacterial poisons produce this efiect by their direct action on the heat centers. High temperature is therefore a nervous symptom which is, for the most part, pro- duced by the physiological action of certain bacte- rial products on the heat centers. Centanni has isolated this fever producing toxine from pure cult- ures of a large number of pathogenic bacteria. The toxines produced by the tetanus bacillus were shown by Brieger to be the cause of the profound nervous symptoms of that disease. From pure cultures of the tetanus bacillus he isolated bacterial products capable of producing tonic and clonic muscular spasm. Poisonous bacterial products ca- pable of producing marked nervous symptoms have also been isolated from pure cultures of a number of other bacteria, including those of diph- theria, cholera, tuberculosis, typhoid fever, septi- caemia and other acute infections, so that clinicians have now very generally come to believe that the nervous symptoms of the acute microbic diseases 68 Kachford : Neuroses of Childhood. are, in great part, due to the action of bacterial toxines on the nervous system. But these acute bacterial toxemias do not properly come within the scope of my subject, and we are therefore not so much interested in them, as we are in those chronic blood intoxications which result from such chronic microbic diseases, as tuberculosis, malaria, summer complaint, rheumatism and syphilis, since these are the chronic diseases, which are so inti- mately associated with the neuroses of childhood. Hysteria, incontinence of urine, night terrors, chorea and other neuroses, are very commonly as- sociated with tuberculosis in childhood. In the Archives of Pediatrics, May, 1893, under the head- ing " Tuberculous Neuroses of Childhood," I noted the fact that, in my clinic, chronic glandular tuber- culosis was, of all diseases, the most intimately as- sociated with the neuroses of childhood. How then is tuberculosis etiologically related to these neuroses ? We know that the tubercle bacillus pro- duces a toxine which, when introduced into the body, causes fever and other well marked nervous symptoms; the inference therefore is unavoidable that this tuberculous toxine is a factor of that com- plex blood condition which results from chronic Rachford : Neuroses of Childhood. 69 tuberculosis and which is etiologically related to many of the neuroses of childhood. Chronic malaria is etiologically closely related to the neuroses of childhood, and this relationship is no doubt, in part, due to the production of nervous symptoms by malarial toxines. It has been demon- strated that toxic substances are produced in ma- larial disease, and that these substances are elimi- nated in large quantities, in the urine during a malarial paroxysm ; and what is of more impor- tance to us in our present study is that it has been proven that the urine in chronic malaria is at all times more toxic than normal urine. These mala- rial toxines, eliminated in the urine, when injected into the veins of animals, will produce well marked nervous symptoms. These experiments corroborate the well grounded clinical belief that the many neuroses of childhood, so commonly associated with chronic malarial diseases, are, at least in part, due to the direct action of malarial toxines on the nerv- ous tissues ; and they also afford an explanation for the fact that such neuroses as neuralgia, night sweats, hysteria, incontinence of urine, night ter- rors, and chorea are occasionally cured by the specific treatment for malaria, viz., quinine and arsenic. 70 Rachford : Neuroses of Childhood. Intestinal fermentation is very frequently etio- logically related to the neuroses of childhood, and there can be no doubt but that intestinal toxemia is one of the links which unite these two condi- tions. There is perhaps no fact better established by experimental and clinical medicine, than that very active poisons, capable of producing the most violent nervous symptoms, can be produced by a putrid fermentation of albuminous material either within or without the intestinal canal. Booker, Vaughn, and others have demonstrated that intes- tinal toxemia, producing the most violent nervous symptoms, can result from bacterial products formed in, and absorbed from the intestinal canal. These acute intestinal intoxications are factors in producing the greater number of the convulsions which occur in infancy and the frequent rise of temperature so common at this period of life. These are facts known and taught every-where, and therefore need not here be enlarged upon. But in a study of the etiology of the neuroses of childhood it is of especial importance to call at- tention to chronic intestinal toxemia as one of the most important factors in producing these nervous conditions. It is my belief that the continued ab- sorption from day to day of bacterial and other Rachford : Neuroses of Childhood, 71 toxines from the intestinal canal is a very impor- tant and much underestimated cause of neurotic disease in children. Chronic intestinal toxemia in childhood is, as in the adult, very commonly asso- ciated with both constipation and diarrhoea. If this fact be kept in mind we shall often be able to cure hysteria, night terrors, neuralgia, headache, neurasthenia and the convulsive neuroses by diet, cathartics, and intestinal antiseptics. Stomachal toxemia may also be a factor in producing neurotic disease in childhood. An important fact not to be overlooked in this connection is that the toxemia is not the only change in the blood, resulting from chronic intesti- nal fermentation, which is etiologically related to neurotic disease. Forchheimer has shown that in- testinal fermentation is a hemoglobin destroyer and an anemia producer ; this would result in a general malnutrition which, as we shall see in the next chapter, is closely related to neurotic disease. 72 Rachford : Neuroses of Childhood. VI. VENOUS CONDITION OF THE BLOOD. It is a striking fact that the nervous symptoms resulting from a venous condition of the blood, sup- plying nervous centers, are quite the same as the symptoms produced by an arterial anemia of the same centers, due to a complete or partial closure of the arteries supplying these centers. The rea- sons for this are plain, since following the ligation of arteries we have not only an arterial anemia of the nerve centers, but also a compensatory venous congestion, so that in both artificial venous con- gestion and arterial anemia we have the nerve cen- ters bathed in venous blood. It is thought by Landois and Sterling "that the stimulation of the nerve centers which results from the ligation of arteries, is due to the sudden inter- ruption of the normal exchanges of gases between blood and tissues." But it must be remembered that a venous condition of the blood means not only a decrease of 0, and increase of C0 2 , but it Rachford : Neuroses of Childhood. 73 also means more urea, more uric acid and more of all the effete products of retrograde tissue meta- morphosis. That is to say, that the nerve tissues are not only deprived in part of all those substances which are necessary for their nutrition and health- ful action, but they are also exposed to the irritating and poisonous influence of the effete products pre- viously noted. It seems therefore a safer explana- tion of the symptoms, which result from experi- mental arterial anemia or venous congestion of nerve centers, to say that they are caused not only by an interruption in the normal exchange of all substances, necessarv to the nutrition and healthful action of nerve tissues, but also by the presence in the blood of C0 2 , and other effete and poisonous products. In this connection we may note the following physiological facts concerning the influence of the above-named blood conditions on important nerve centers. A venous condition of the blood in the medulla oblongata will stimulate the vaso-motor centers and cause constriction of the small arteries ; this has been thought to be due to the direct stimulation of the centers by C0 2 (Landois and Sterling)., The 74 Rachford : Neuroses of Childhood. same result may also be produced by arterial anemia of these centers due to ligation of arteries. In the medulla oblongata there is a center whose stimulation causes general spasms. This center may be excited either by a venous congestion or an ar- terial anemia of the medulla oblongata. The respiratory center may also be excited by either a venous condition of the blood or by an arterial anemia. Lauder Brunton cites the following experiment to show the relation existing between convulsive movements, and a venous condition of the blood, supplying nerve centers : " In fowls killed by Cobra poison the convulsions come on at the mo- ment the comb becomes livid, and when artificial respiration is begun, the convulsions disappear as the comb again regains its normal color." Brun- ton believes this to be an instance of asphyxia! convulsions, due to irritation of the higher brain centers, thus diminishing their co-ordinating or in- hibiting action on the lower centers of the cord. He also says that " drugs which stimulate the cir- culation and increase the nutrition of the higher nerve centers, in this way strengthen their co-or- dinating power and tend to prevent spasm ; alco- hol and ether act in this way." That this weaken- Rachford : Neuroses of Childhood. 75 ing of the inhibitory power of the brain and medulla oblongata may result from arterial anemia as well as from venous congestion is shown by the following experiment: If the arteries going to the brain be ligatured so as to paralyze the medulla oblongata, then, on ligaturing the abdominal aorta, spasms of the lower limbs occur, owing to the anemic stimulation of the motor ganglia of the spinal cord (Sigm. Meyer). That the anemic condition of the cord produced by ligaturing the abdominal aorta is incapable of pro- ducing spasms, when the medulla oblongata is in normal condition, is a striking example of the in- hibitory influence of the oblongata centers on the motor centers of the cord. V. Aducco made a series of valuable experiments on dogs. He produced anemia of the nerve centers by cutting off a portion of the blood supply from the spinal motor centers. He compared the ex- citability of these centers before and after the artificial anemia thus produced, and in this way he determined "the effect that partial anemia exer- cised on the motor centers of the cord." Aducco concludes his paper as follows : " The researches I have just described have led me to draw the following conclusions : in anemia, that is 76 Rachford : Neuroses of Childhood. to say when the flow of blood is diminished, the active elements of the nerve centers are found in a state of great excitability. In this condition, ex- citants from the exterior act much more ener- getically than in the normal condition, and this state of excitability increases, very probably, dur- ing the entire duration of the anemia. It seems to me that one should, within certain limits, admit that there is an inverse relation between nutrition and the excitability of the nerve elements. This latter augments during the time that the nutrition diminishes." In these conclusions, Aducco wrongly interprets artificial arterial anemia to mean a simple innutri- tion^ and concludes that the excitability of the nerve centers is due to this innutrition rather than to the numerous blood changes which we have previously shown to accompany arterial anemia. I have repeated Adueco's experiments and quite agree with him that the excitability of the nerve centers increases with the duration of the arterial anemia ; but I have also shown by a series of ex- periments, made upon rabbits and dogs, that the complete closure of the veins, returning the blood from the spinal motor centers, will produce the Rachford : Neuroses of Childhood. 77 same symptoms that are produced Ky the ligature of the arteries supplying the same spinal centers. In these experiments, I studied the increase in the electrical excitability in the muscles of the hind le^s as well as the increase in the reflex excitability of these parts ; and always obtained practically the same results from ligatures of arteries as from liga- tures of veins supplying the same nerve centers. From the observations cited in this chapter, the following inferences may be made : 1st. Both arterial anemia and venous congestion can produce an excitable condition of the nerve centers, and may therefore be factors in the pro- duction of nervous symptoms. 2d. The nervous symptoms resulting from arterial anemia are very similar to those resulting from venous congestion, and this is because in both con- ditions there is a venous condition of the blood sup- plying the nerve centers. 3d. Arterial anemia and venous congestion pro- duce nervous symptoms by producing a malnutri- tion rather than a simple innutrition of the nerve centers. 4th. Arterial anemia and venous congestion weaken the inhibitory centers, and this results 78 Rachford : Neuroses of Childhood. in the discharge of force from reflex centers on comparatively slight excitation. 5th. Arterial anemia and venous congestion make more excitable both the reflex centers in the cord, and the more important reflex centers in the medulla oblongata. The above outline will be of assistance in ex- plaining many obscure nervous symptoms, and the following examples may be cited to indicate the important relationship existing between a venous condition of the blood and the neuroses of child- hood : 1st. The venous condition of the blood, resulting from a weak or crippled heart, is at least a partial explanation of the relationship which exists be- tween this condition of the heart and certain neuroses, such as chorea, hysteria and general nervous irritability. 2d. Rheumatism, scarlet fever, diphtheria, and other acute diseases, which ofttimes produce a weakened condition of the heart, may in this way be indirect factors of neurotic disease; (from what has been said in the previous chapter, it is scarcely necessary here to note that these diseases may also act in another way in producing nervous symptoms). Rachford : Neuroses of Childhood. 79 3d. Tuberculosis, chronic intestinal catarrh, and other diseases, that produce a profound chronic anemia and resulting malnutrition of the nerve centers, may be powerful factors in producing many of the neuroses, such for example as hysteria, in- continence of urine, chorea and spasm. 80 Rachford : Neuroses of Childhood. VII. AN IMPOVERISHED CONDITION OF THE BLOOD. In previous chapters I have noted certain blood conditions which produce nervous symptoms by their direct irritant or poisonous action on the nerv- ous centers ; and now I wish to inquire what nerv- ous symptoms may be produced by an impover- ished condition of the blood, producing either innu- trition or malnutrition of nerve elements. It is most important in this study that one should always keep in mind that innutrition and malnutrition represent very different types of nutritive disturbance. By innutrition of nerve elements is meant a simple starvation of nerve elements, such as would result from a simple quantitative reduction in all the nu- tritive elements of the blood, which are necessary to the development and healthful action of nerve tissue. By malnutrition of nerve elements is meant a bad nutrition or a qualitative change in the blood, such as a diminished amount of fat, of albumen, of Rachford: Neuroses of Childhood. 81 calcium or of some other important constituent of the blood. Innutrition of nerve elements, such as may result from a simple quantitative reduction of all the nutritive elements of the blood, rarely, if ever, exists as an unaided cause of disease, except possi- bly such an uncomplicated condition may be pro- duced by actual complete starvation or by repeated hemorrhages. But while a simple innutrition of nerve elements may very rarely exist as an uncom- plicated factor of disease, yet nerve innutrition in some more or less modified form is a constant ac- companiment of all the blood conditions, which poison, irritate, or mal-nourish nerve elements ; and medical writers have always thought that the in- nutrition of nerve elements was in great part re- sponsible for the nervous symptoms which are asso- ciated with all these abnormal blood conditions. For these reasons, it is most important that one should inquire into the exact role played by a simple innutri- tion of nerve elements in the production of nervous symptoms. After a careful study of this question, and numerous consultations with physiologists, it was decided that the best method of studying this question experimentally in animals, was by subject- ing them to repeated bleedings or by starvation, or 82 Rachford : Neuroses of Childhood. by both methods combined. Following out this idea, a number of rabbits were starved and bled into a condition of profound innutrition. In these experiments the rabbits were given all the water they would take, and as little food as possible con- sistent with life. These rabbits were kept for two or three weeks almost at the point of complete starvation, before they finally starved to death. It was found that the innutrition of nerve elements, which must necessarily have resulted from this star- vation, had very little influence in producing nerv- ous symptoms. After two or three weeks of star- vation, the spinal reflexes were not noticeably ex- aggerated, and the electric excitability of the mus- cles was actually diminished. It would seem, there- fore, from these experiments that a simple innutri- tion of nerve centers, when not assisted by other factors of neurotic disease, has little influence in producing nervous symptoms ; and, it is moreover, here worthy of note, that this conclusion, drawn from physiologic experiments, is in keeping with the physiologic law noted in chapter first of this series of papers; viz., " other conditions being the same, the amount of energy developed by a nerve cell, will depend directly on the amount of health- ful chemical metabolism going on within the celL Rachforp : Neuroses of Childhood. 83 The maximum amount of energy will be found stored up in the well nourished cell, and the mini- mum amount of energy in the starved cell." For the above reasons, I am led to believe that a simple innutrition of nerve centers leads to such a diminu- tion of stored up energy in the cells of these centers, that any increase of irritability which may result from the simple innutrition of these cells, is of little moment in the production of reflex neuroses. The diminished amount of stored up energy in starved nerve cells will offset the influence of their increased irritability in the production of nervous disorders. But whether or not this is the true ex- planation of the observed phenomena, the fact re- mains, that experimental innutrition of nerve cen- ters does not increase the reflex phenomena pre- sided over by these centers. Clinical medicine also furnishes evidence that a simple innutrition of nerve elements is not an im- portant factor of neurotic disease, since it is a fact not infrequently observed, that long and repeated hemorrhages may produce a profound innutrition without causing any pronounced nervous symp- toms. It is also a notable fact, that the starvation experiments which have been made, for notoriety and pecuniary benefit, by a number of persons 84 Rachford : Neuroses of Childhood. within recent years, did not produce any increase in their nervous irritability. All of these facts are in evidence to prove the truth of the proposition that innutrition of nerve elements is not an important factor of neurotic disease in children. The clinical importance of this physiologic propo- sition is great, and must not be neglected. If clinicians would keep this fact in mind, it would always suggest to them the importance of care- fully inquiring into the exact blood conditions present in nervous disorders. It is " bad " blood, not "thin " blood, that is a most important factor in producing neurotic disease in children. Malnutrition of nerve elements, such as may result from a diminished amount of fat, albumen, calcium, oxygen or some other important con- stituent of the blood, very commonly exists as a factor of neurotic disease in children. This condi- tion, which Christopher has described as a " partial starvation " of nerve elements results in making the nerve cells much more irritable, so that they discharge their force much more readily than stable, normally nourished cells would do. Such qualitatively starved cells are yet sufficiently well Rachford : Neuroses of Childhood. 85 nourished to store up considerable nerve energy to be thus fitfully discharged. While we are reasonably certain that malnutri- tion in the restricted sense here used is an im- portant cause of nervous disease in children, yet, we have very little accurate knowledge upon this subject. We have reason to believe that a mal- nutrition of nerve elements is in part responsible for the nervous symptoms which result from the chronic blood intoxications referred to in previous chapters; but in these instances it is impossible to separate the symptoms produced by the malnutri- tion from those produced by the toxemia. Notwith- standing the very great difficulty of studying this subject from a clinical stand-point, jet its import- ance demands that we should make an attempt at conclusions from clinical observations, even though they may not have the force of deductions from clean physiologic experiments. Chronic anemia is a term used to express an in- constant and very complex blood condition, which is one of the most common causes of general mal- nutrition and nervous disease in infancy and child- hood. The chronic anemias of infancy and child- hood are due to a great variety of causes, the most important of which are tuberculosis, rheumatism, 86 Rachford : Neuroses of Childhood. malaria, syphilis, intestinal diseases, improper food and bad hygiene. The blood in chronic anemia is weak in proteids and hemoglobin, and such a con- dition must necessarily produce an oxygen and pro- teid starvation of the nerve cells, and there can be little doubt but that this proteid and oxygen starva- tion of nerve tissue is an important factor in pro- ducing the nervous symptoms of chronic anemia in childhood. But as previously stated, chronic anemia is a very complex blood condition, which may comprehend not only a diminished amount of proteids and hemoglobin, but it may also mean a diminished quantity of fat and of inorganic salts, or an increase of the poisonous and irritating pro- ducts previously referred to; yet, these accessory conditions are probably not so constant in chronic anemia as the diminution in proteids and hemo- globin, and there is, therefore, good clinical grounds for the belief that a proteid and oxygen starvation will increase the irritability of nerve elements, and in that way act as important factors in producing the various neuroses of childhood. In this we have an explanation of the well-known clinical fact that iron, and a food rich in easily digested proteids, will, as a rule, relieve the nervous symptoms of Rachford : Neuroses of Childhood. 87 chronic anemia by raising the percentage of cor- puscles and hemoglobin. Pat starvation, as a form of malnutrition, can best be studied in rachitis, which of all diseases is the most closely related to the neuroses of infancy. The work of Cheadle and others clearly demon- strates that fat starvation is one of the important causes of rachitis; and the feeding of some easily digested fat is now accepted as a most important means in the cure of this disease. It must not be understood that the blood condition in rachitis is described by saying there is a diminution in the amount of fat, since there is always present more or less chronic anemia, as described in the previous paragraph, and also possibly a diminished quantity of calcium and phosphorus; but by far the most important blood condition is the dimin- ished quantity of fat, since this is a constant condi- tion, and one that we know is etiologically related to rachitis, and especially to its nervous symptoms. The inference therefore is probable that fat starva- tion is a form of malnutrition, which may predis- pose to laryngismus stridulus and other local and general convulsive neuroses, so common in rickety babies. It must be remembered, however, that fat starvation is not the only factor in producing the 88 Rachford : Neuroses of Childhood. malnutrition of rachitis, any more than oxygen and proteid starvation are the only causes of malnutri- tion in " chronic anemia" from other causes. Just the part that calcium starvation plays in the etiol- ogy of rachitis, is a question in sharp dispute, and one that can not here be discussed. Calcium starvation may be studied to some ad- vantage from the very careful experiments of W. H. Howell, who demonstrated that the normal irri- tability of nerve and muscle tissue is in great part dependent upon the proper supply of calcium to these tissues. If the heart be deprived of calcium salts, by feeding it with blood deprived of its cal- cium salts, it stops beating very soon, and this action is so rapid that it could only result from nervous influence. The most plausible explanation of this fact is that the nerve ganglia of the heart, in the absence of calcium, fail to discharge the nerve force which stimulates the heart muscle to contraction. If, on the other hand, the heart be fed with a calcium solution in distilled water, it will continue to beat for a long time. In this in- stance, the calcium keeps up the irritability of the cardiac ganglia, so that they continue to discharge nerve force into the cardiac muscle, and the heart's action continues. In this explanation, which I Rachford : Neuroses of Childhood. 89 have taken the liberty to make from Howell's ex- periments, I have attributed to calcium an impor- tant influence over the discharge of nerve force from automatic centers ; the presence of calcium in normal quantities causes these centers to discharge their nerve force into the cardiac muscle, as they normally do ; and the absence of calcium inhibits the discharge of nerve force from these automatic centers, and as a result the heart stops. If a certain amount of calcium is necessary to the normal irritability of nerve centers, and if the absence of calcium inhibits the discharge of force from nerve centers, then it is reasonable to infer that a diminished amount of calcium would have an influence on the irritability of nerve centers, which would find expression in clinical manifesta- tions. That an insufficient quantity of calcium in the blood may produce nervous symptoms, is, I think, proven by Howell's experiments. He says : " When a frog is irrigated with oxylate solutions, that is to say calcium free solutions, the muscles are affected quickly and in a peculiar manner, * * * twitching movements of toes begin in a few minutes, and soon extend to muscles of the leg and trunk. In some cases these movements were violent; strong convulsive contractions of 90 Kachford': Neuroses of Childhood. muscles and limbs followed each other rapidly, and were often so violent as to throw the animal out of the position in which it was lying, The convul- sions resembled those caused by strychnia, the vio- lent tetanic contractions had the appearance of being caused by stimulation of the cord." This extremely excitable condition of the reflex nervous mechanism was followed after a time by the com- plete loss of irritability of this mechanism. These observations by Howell seem to me to show that be- tween the stage of "the normal irritability of this re- flex mechanism, when the calcium salts are supplied to it in normal quantity, and the complete paralysis or loss of irritability of this mechanism, due to the more or less complete absence of calcium salts, which have gradually been washed away by the cal- cium free circulating fluid, there is a stage of ex- treme irritability, and reflex excitability of this re- flex nervous apparatus, which corresponds to the period when this nervous mechanism is supplied with a diminished amount of calcium salts ; that is to say, there is a partial calcium starvation of the nerve elements. This explanation of Howell's ex- periments is supported by his further experiments. In animals, in which the irritability of the reflex nervous apparatus had been destroyed by calcium Rachford : Neuroses of Childhood. 91 starvation as in the above experiments, it was found, that if calcium solution was added to the circulat- ing fluid of the muscle, the primary effect was to again produce a twitching movement of these mus- cles, " lasting for a short while," to be followed by a more or less distinct return of the muscle to its normal irritability. I have taken the liberty of drawing the above conclusions, which I believe to be correct, from the work of Howell and others, but to which I do not wish to commit Dr. Howell, as he made no such deductions from his experi- ments. The small amount of calcium, which first reached the muscle, resulted in a partial restoration of the nerve muscle irritability, and made possible the same convulsive movements which were above noted as being due to too little calcium in the circu- lating fluid, and these convulsive movements sub- sided when the nerve and muscle elements had re- ceived sufficient calcium to place them in a state of normal irritability. From these, and other ex- periments along the same line, I conclude that cal- cium starvation of nerve elements may be a factor in the production of the convulsive neuroses of childhood. The application of this conclusion to clinical medicine will, I believe, in the near future be recognized as something of real importance. 92 Rachford: Neuroses of Childhood. VIII. REFLEX IRRITATION. Reflex irritation is one of the most important etiological factors of the neuroses of childhood. Many able pediatrists in recent years have waged an active crusade against this proposition, which previously was thought to be one of the axioms of medical knowledge. While these men have not been able to convince the medical world that re- flex irritation is an unimportant factor of neurotic disease, they have very much modified the view, which so long obtained, that reflex irritation was the all important factor in producing these diseases. In the proposition, as stated at the beginning of this chapter, I have taken position between these extreme views, and it will be the purpose of this chapter to show that the influence of reflex irritation in producing nervous diseases in childhood has been as much underrated in recent years as it was exaggerated by earlier writers, who taught that al- most every nervous disease was caused by some re- Rachford : Neuroses of Childhood. 93 flex act. It is a matter of common clinical ob- servation that such neuroses as hysteria, inconti- nence of urine, night terrors, chorea, convulsions, fever and headache are etiologically related to some form of reflex irritation, and this relationship is not infrequently absolutely demonstrated, when re- moval of the reflex irritation cures the neurosis. The common sights of reflex irritations, which are recognized factors of nervous diseases in chil- dren, are the genito-urinary organs, the gastro- intestinal tract, the eye, the ear and the nose. The importance of this subject does not end with recog- nizing that reflex irritations from all of the above- named sights are common factors of neurotic dis- ease, but it is of equal importance that we should recognize that, as a rule, reflex irritation acts con- jointly with other factors in producing the neuroses of childhood. It is a well-known fact that reflex irritation, of apparently a severe type, may exist without producing nervous symptoms. In such in- stances, the center which is the most important part of the reflex arc is normal, stable and not easily excited to discharge its stored up nerve en- ergy. It is most important, therefore, that we should recognize the fact that the reflex irritation, which excites neurotic disease, is made potent by 94 Rachford : Neuroses of Childhood. reason of its connection with an abnormally irritable reflex center. In previous chapters we have studied the influence of heredity, sex, age, environ- ment and various blood conditions, in producing an increased irritability of nerve centers; and it is chiefly with the aid of these factors of neurotic dis- ease, that reflex irritation can produce such a wide range of nervous symptoms. The study of this subject embraces, therefore, not only how each of these factors may act in producing nervous symp- toms in children, but it must also inquire into the inter-dependence and relationship of these factors in producing these symptoms. The fact that reflex irritation is commonly asso- ciated with other factors does not in the least di- minish its importance as a factor of neurotic dis- ease, since the removal of the reflex excitant very commonly cures the neurosis, even though the other factors remain, and since our best efforts at removal of other factors of neurotic disease, as a rule, are futile for good, so long as the reflex ex- citant remains to constantly excite the nerve centers. The explanation of these clinical facts is, that reflex irritation does not act simply as an ex- citant in discharging nerve force from irritable centers, but it also acts by keeping up the irritabil- Rachford : Neuroses of Childhood, 95 ity of these centers, and, if long continued, by pro- ducing changes in the nerve centers recognizable under the microscope, which make these centers more irritable and more susceptible to reflex exci- tation. If this be true, then, reflex irritation at once as- sumes a commanding position among the factors of neurotic disease in children; such a position as, in recent years, has not been accorded to it, and it is the special purpose of this chapter, to replace reflex irritation in the high position which it merits among the factors of neurotic disease in children ; in that position which it formerly occupied, and from which it has been unjustly removed. The microscope has gradually revealed to us the fact, that all cellular activity is accompanied by definite chemical .and morphological changes in the cell itself. The tired cell differs from the rested cell, not only in morphological changes which can readily be noted in nucleus and cell protoplasm, but also in the reaction of both cell protoplasm and nucleus to coloring matters. The changes which result from the functional activity of cells may be called fatigue changes, and it is evident that the longer the cell is worked, the more marked will be these changes. It is also 96 Kachford : Neuroses of Childhood. a physiological fact, that fatigue changes in the tired cell will disappear after a period of rest, and the cell will again be found morphologically and chemically a rested cell, but it requires a longer period of time for a cell to return to its rested con- dition than it does for the same cell to tire under ordinary work. The fatigue changes, resulting from the func- tional activity of glandular epithelium are, as a rule, very pronounced. These changes, while not the same in all gland cells, may be noted in the shrunken condition of both nucleus and cell proto- plasm and in the changed reactions to coloring matters of both nucleus and cell protoplasm. Fatigue changes in the tired muscle cell are also shown in the shrunken and vacuolated condition of its protoplasm. And both the tired muscle cell and the tired gland cell are only restored to their rested condition by a period of prolonged rest — the period of rest required being considerably longer than the period of activity. The nerve cell, like the gland and muscle cell, shows marked morphological and chemical fatigue changes. C. F. Hodge, in a very clever piece of work, has shown that definite changes occur in the nerve cells of the brain and spinal ganglia of cer- Rachford : Neuroses of Childhood, 97 tain birds and bees as a result of their normal daily activity. He compared the nerve cells of sparrows and swallows, shot in the early morning, with the nerve cells of sparrow r s and swallows, shot in the evening, after a day of hard flight. Experi- ments of this kind on birds and bees invariably showed fatigue changes in the nerve cells tired from the day's work. Hodge also found definite changes to occur in the spinal ganglion cells of the frog, the cat and the dog, under electrical stimula- tion, and these changes were very similar to the changes which he had observed to result from the normal daily activity of nerve cells. These fatigue changes in the nerve cells, whether resulting from normal daily activity or electrical excitation, are as follows : Nucleus was " much smaller, and had a jagged, irregular outline. It took a darker stain, and lost its reticular appearance." Cell protoplasm " did not take stain so readily, and was much shrunken. In spinal ganglia it was vacuolated." Hodge also observed that the nerve cell recov- ered much more slowly than it tired, and that the recovery of the nerve cell might be represented by a curve, quite similar to the curves obtained by 98 Rachford : Neuroses of Childhood. Mosso and Lombard, for the muscle cell in its re- covery from fatigue. He concludes that " indi- vidual nerve cells, after electrical excitation, re- cover if allowed to rest for a sufficient time, but the process of recovery is slow. From five hours' stimulation, recovery is scarcely complete after twenty-four hours' rest." The changes above noted in nerve cells, as re- sulting from electrical stimulation and normal fa- tigue, have a plain bearing on the study of the changes which occur in the spinal ganglion from reflex irritation, since reflex irritation can do noth- ing more than greatly exaggerate the functional activity of these cells, and must, therefore, result in changes within the cells similar to those above de- scribed. Satovski, in a careful research on " Changes in Nerve Cells Due to Peripheral Irritation," has made an important advance in our knowledge of this subject. He irritated a peripheral nerve by liga- ture, and thereby caused a peripheral, but not a central, degeneration of the nerve. In this way, he produced a chronic reflex irritation of that por- tion of the cord to which this nerve belonged, and on microscopical examination of the cord, at this point, he found on the injured side, using the unin- Rachford : Neuroses of Childhood, 99 jured side for a control, many cells exhibiting great vacuolation, and shrinking of the protoplasm from the capsule. The nuclei of these cells were oval instead of round, they stained easily, and were sometimes so much shrunken that they were zig- zag in outline, and left a space between the proto- plasm and the nucleus of the cell. Mrs. Ternowski, in a research on " Changes in the Spinal Cord from Stretching the Sciatic Nerve, 5 ' found changes very similar to those previously noted by Satovsky. From the observations quoted, it is plainly evi- dent that chronic reflex irritation can produce very marked changes in the nerve cells of the spinal ganglia, and that the longer and more violent this irritation is, the more pronounced will these changes be. It is also plain that a considerable length of time must be required to restore to their normal condition, cells which have been subjected to reflex irritation for months and years. It has even been noted that nerve cells, under electrical stimulation, can be so exhausted that the nuclei will entirely disappear, and the cells be unable to recover their normal condition, even after the removal of the stimulus which produced the change. Here we have an explanation of the ofttimes slow recovery 100 Rachford : Neuroses of Childhood, of an irritable spinal cord, after the removal of the reflex cause which brought about the irritability. In the application of these facts to clinical medi- cine, we must remember that the spinal cord has but two functions, viz., conduction and reflex action. We must also remember that a reflex irritation of an afferent nerve, carrying impulses to any one of the many special reflex centers of the cord, does not confine its morbid influence to that center, but, by reason of the physiological law of " overflow of reflexes," the impulse spreads up and down the cord, producing changes in the cells of adjacent centers; and if the reflex irritation be severe and long continued, the impulses may spread through- out the cord involving all its centers, and produc- ing a general spinal irritability, and in this way predisposing the individual to all kinds of reflex nervous diseases. In some recent experiments made upon rabbits, I have been enabled to demonstrate, that a chronic reflex irritation can produce a most extreme irrita- bility of the nervous centers in the cord of this an- imal. In these experiments, the abdominal cavity of the rabbit was opened and the large intestine stitched into the abdominal wound. These rabbits quickly recovered from the operation, and for a Rachford : Neuroses of Childhood. 101 week or ten days seemed normal in every way. At this time the reflexes, which in the normal rab- bit can scarcely be brought out at all, began to be very perceptible. In these experiments the knee jerk, and a reflex, which is produced by letting the finger slip over the anterior superior spine of the ilium, were studied, and it was found that from the tenth day onward, there was an increase in the reflex excitability of the cord, as determined by an increase in the above-named reflexes. The reflex excitability of the cord continued to increase for about six weeks ; after this period of time, the cord was so excitable that it was impossible to make out whether the excitability was increased or not, since a slight touch would produce a maximum reflex. These experiments clearly show that chronic re- flex irritation, unassisted by any other cause that could be made out by careful post-mortem exam- ination, can produce in the rabbit a most extreme irritability of the spinal motor centers. The post- mortem examinations of these rabbits, one of which was killed three months after the operation, showed no evidence of peritonitis or other disease, other than the attachment of the large intestine to the abdominal wall. The spinal cord of the rabbit. 102 Rachford : Neuroses of Childhood. killed at the end of the third month, was examined microscopically, a number of sections being made from the lumbar and dorsal regions. In all of these sections changes in the ganglion cells, similar to those described by Satovski, were found. The nu- clei were irregular in size and outline, many were oval and many had a jagged outline, many of the nuclei were small and had a shrunken appearance, and all of them took the stain more deeply than does the rested (normal) nucleus. The protoplasm of the cells did not take the stain as it normally does, and in many instances it took the stain so faintly that the outline of the cells could not be made out. In some instances only the small, deep- stained nuclei were visible. In the above observations, we have not only a physiological, but also a morphological explana- tion, of how and why a chronic reflex excitation may be an important factor in producing a general spinal irritability, and we have also a sufficient explanation of the fact that the removal of the reflex cause, which has been acting for years in producing spinal irritability, may not at once be followed by the cure of the spinal irritability, and that it may even require years of comparative rest for the irritable spinal centers to become Rachford : Neuroses of Childhood. 103 stable (normal), even after the removal of the reflex cause which produced the irritability of these centers; and these observations also justify the belief that reflex irritations, acute and chronic, are among the most important causes of neurotic disease in children. In the study of the influence of reflex causes in producing the neuroses of childhood, one important question must be answered, viz.: Why is it that chronic reflex irritation is so much more important, as a factor, in producing nervous diseases in chil- dren, and in girls, than it is in men? The oculist will testify that eye-strain is a much more potent factor in producing headache, chorea and gen- eral nervous irritability in children, and in young women, than it is in men. The surgeon will tes- tify that diseases of the genito-urinary apparatus, which produce the most profound nervous symp- toms in women and children, have little or no such influence in men. The physician will testify that irritation from disease of, or foreign bodies in, the intestinal tract will produce convulsive and other nervous disorders in children, while the same conditions have little influence in producing nervous symptoms in men. The gynecologist is prone to believe that disease of the female generative organs 104 Rachfokd : Neuroses of Childhood. is the most important of all the reflex causes of nervous disease ; and every clinician has observed the predisposition to nervous disease, which accom- panies the growth and functional development of these organs. In fact every department of medical science lends testimony to the fact, that age and sex are among the most important of the predis- posing factors, which assist reflex irritation in pro- ducing neurotic disease; and the reasons for the potency of reflex causes in producing neurotic disease in children and girls are not altogether ob- scure. The following facts may be noted : 1st. In children, (a) Reflex causes are more frequent than in adults, such for example as uncor- rected eye-strain, adherent prepuce, balinitis, etc. (6) The nervous system of the child is more irritable and unstable by reason of its incomplete functional development, (c) The inhibitory control of higher nerve centers on spinal reflex movement is feebly developed in the child, (d) Blood changes are much more common allies of reflex disturbances, in producing nervous disease, in children than they are in adults. 2d. In girls, (a) Reflex causes are very much more frequent than in boys or in female adults, Rachford : Neuroses of Childhood. 105 (the approach of puberty, with the functional de- velopment of ovaries and uterus, is a source of constant reflex disturbance; after the full func- tional development of these organs, the reflex ex- citation is intermittent and confined to a period just before and during a menstrual period), (b) Inhibi- tory control of the spinal motor centers more readily gives way in young girls than in boys of the same age. (c) The social conditions and habits of life of the young girl predispose her to nervous disease, (d) Blood changes, which produce nervous irritability, are very much more common in girls than in boys. The above are some of the factors which assist reflex causes in producing neurotic disease in chil- dren and in young girls, but which have little influence in producing disease in male adults. In these observations we have an answer to the ques- tion : Why does reflex irritation produce nervous disease more readily in the child and young girl, than it does in the male adult? 106 Rachford : Neuroses of Childhood. IX. EXCESSIVE NERVE ACTIVITY. There is a- well-grounded and wide-spread medi- cal opinion that excessive nerve activity, (the term including brain work and nerve excitement) is an important factor in the production of nervous disease in children, but notwithstanding the preva- lence of this belief among medical men, very little has been done to educate those, who have the rear- ing and tutorage of the young, on this subject, which, I believe, is one of almost vital importance to the state itself. It is a fact which should be heralded every- where that the vast army of neurasthenics and hysterics, which now inhabit our cities, is yearly being in- creased by subjecting the immature nervous sys- tems of young children to the almost constant ex- citement, strain and mental activity with which our social order has surrounded them. An all impor- tant question, therefore, to pediatrists, who should be especially interested in making of the child Eachford : Neuroses of Childhood. 107 the strongest possible man, is : How can these influ- ences, which are playing such havoc w T ith the nerv- ous systems of children, be guarded against ? How can they be counteracted? How can parents, guardians, nurses and teachers be made to compre- hend the importance of this subject ? If these questions are to be answered; if the campaign against the evil of constantly subjecting children to the nervous strain, resulting from the artificial conditions which obtain in all cities, is to be, in any degree, successful, then the whole sub- ject must be placed upon a more exact physiologi- cal basis than it has ever been before, so that those who have charge of the young may be told not only that nervous strain is an important cause of neurotic disease, but they may also be told why this is so. And in the series of papers which this chapter concludes, I have attempted to outline some of the physiological facts by which this goal is to be approached. The teachers and guardians of the young must be told that the nervous system of the child differs very materially from the nervous system of the adult; they must be told that the child, especially in his nervous organization, is not a little man; that his nervous system is structurally and functionally 108 Eachford : Neuroses of Childhood. immature ; that it is excitable, unstable and under feeble inhibitory control ; that the sources of reflex irritation in the child are many, and that the nerve centers discharge their force more fitfully and readily than in the adult ; that the period corre- sponding with the onset and establishment of the reproductive function in girls, is a time when they are especially predisposed to nervous disease. And they must also be told that these, and other physi- ological peculiarities of the nervous system of childhood, are made much more potent for evil when they are associated with the various " blood conditions," which in previous chapters, I have shown to be etiologically related to the neuroses of childhood. In order to approach this subject in a physiologi- cal way, I shall call attention to a recent very ex- tensive research by Dr. "W. Townsend Porter, which has, I believe, great practical importance in the study of the influences of school life in produc- ing the neuroses of childhood. Dr. Porter demonstrated that children who are advanced in their studies, are, on the average, heavier, taller and of larger girth of chest, than less advanced children of the same age. Thus, boys aged eleven, were found in Grades I, II, III, Rachford : Neuroses of Childhood. 109 IV, V and VI, of the St. Louis Public Schools. The average weight of the four classes was re- spectively 64, 66, 68, 71, 72 and 74 pounds. The ability to succeed in school life is, in the average, a measure of mental power, and if successful scholars are, as a rule, better developed physically than the less successful, it follows that mental ability is, in the average, greater in large children than in small children of the same age. Dr. Porter makes a practical deduction from the law thus established. The entrance to any grade in a graded school system is guarded by examina- tion, and the children found in that grade are such as have passed the entrance examination, and have, in this way, shown their capacity to do the mental labor exacted in this grade. The greater number of these children are of the same age. The work of this grade is, then, normal for this age, and the average height, weight and girth of chest of this age, form the physical development most often found in children able to do the work of the grade. No child younger than the average age of any grade should be permitted to enter it, until a phys- ical examination has shown that his strength shall probably be sufficient. In determining this, the relation of weight and girth of chest to height is 110 Rachford : Neuroses of Childhood. of special importance. Abnormal height is un- doubtedly a disadvantage, yet such children may be strong, provided their physical development is in proportion to their height. If the contrary is the case, the child will be much less able to resist the strain of school life. Dr. Porter points out the importance of frequent weighings of growling children. Persistent loss of weight in an adult is a matter of grave concern. The failure of a child to make the normal gain in weight is no less grave, and should lead to an in- quiry into his school tasks, for the effects of pro- longed overwork are very serious in children, and often irremediable. It is my belief that if there was a rule, such as Dr. Porter suggests, guarding every grade in our public school system by a physical as well as a mental examination, it would prevent the develop- ment of a considerable portion of the neurotic disease, which is now so prevalent among school children. With children of good physical devel- opment, working in the public schools within the limitations of their proper grades, there is almost no danger that a moderate amount of school work will in any way assist the development of neurotic disease, provided always that the hygienic condi- Rachford : Neuroses of Childhood. Ill tions of the school, especially the light and venti- lation, are good. But the strain of ordinary school work is a very different matter with children »of poor physical development, many of whom are, unfortunately, precocious. A large number of these children, by reason of bad heredity, are neurotic, poorly nourished and anemic, and many of them have tuberculous, rheumatic or syphilitic inheri- tance, while others, from accidental causes, such as bad hygiene, improper food, etc., are below the normal in physical development. The nervous systems of such children are in a condition of malnutrition, and are, therefore, not capable of doing the ordinary work of their grades in the public schools, and if they are permitted to do this work, or if, as is often the case, these chil- dren are encouraged to push on into higher grades than the one to which their years and strength should assign them, disastrous consequences will surely follow, and their nervous systems may be injured beyond repair. These children, under the mental strain of school work, may develop chorea, hysteria and other neuroses. The important duty, therefore, of every physician is to advise against much school work in children of feeble physical development, and to 112 Eachford : Neuroses of Childhood. explain to parents and teachers why such children as these should first have their physical defects looked after, and should then be placed in a grade lower than that to w T hich their age and intelligence should assign them. It is my belief that a normal dwarf, with no bad hereditary influences behind him, may, without in- jury to himself, keep pace in mental development with fellows of his own age; the dwarfish body is not of itself an indication that school work might be injurious, if there is every other evidence of perfect physical development. Dwarfishness of body in school children of good physique does not mean dwarfishness of mind. But dwarfishness among children, as indicated by weight and chest development, is, as a rule, the result of disease and bad heredity, and this is the reason why children who are under weight and have poor chest develop- ment, are, as a rule, incapable, without injury to their nervous systems, of doing the same amount of school work as their fellows of the same age. It is my belief, therefore, that the physical basis of precocity and dullness in children depends upon the facts that bad heredity and disease are the chief causes of abnormal dwarfishness or poor physical development in the young. It is also my Rachford : Neuroses of Childhood. 113 belief that children of this class are, as a rule, anemic and poorly nourished, and that their nerv- ous systems are therefore in a condition of mal- nutrition, and not capable of doing an amount of work in keeping with the age of the child. The reasons, then, are clear why we should not allow a child of poor physical development to be pushed to rapid brain development. If we do, their nervous systems will surely suffer from the strain, and whatever predisposition they may have to neurotic disease will be greatly increased. In dealing with individual cases, it will be of the utmost importance to the physician to know the child's heredity ; if the child has a bad family history, it should be the imperative duty of the physician to protect it against mental overwork. We can not, of course, change the child's ancestry, but we can speak out against the crime of pushing children with hereditary physical defects to rapid brain development, and in this way developing an hereditary or acquired nervous weakness into actual disease* School work may therefore be classed as a cause of neurotic disease in children of poor physical development, and it acts chiefly in calling out hereditary defects of the nervous system. In speaking of the school work as a cause of neurotic 114 Rachford : Neuroses of Childhood. disease in children, it must be understood that this term embraces not only brain work, but also the mental excitement which attends examinations, and the eye strain which results from imperfect vision and bad light, the latter being one of the most common causes of reflex nervous disease in children, and one of the physical defects which should be promptly removed. It must be remembered that what is here said of the physical basis of precocity and dullness is a matter of proof, and not of opinion, and that it ap- plies to children only, and has nothing whatever to do with the question of whether, in adult life, a healthy body adds strength and capacity to the nervous system. In this demonstration of the injury which results to the nervous system of the delicate child from the nervous strain of school life, we have a most im- portant warning against the pernicious habit of en- couraging mental precocity in early childhood. It is a matter of almost daily experience to see a poorly nourished tuberculous child brought forward for the purpose of demonstrating its u wonderful" precocity. The proud mother and over zealous nurse commence the process of mental cramming Rachford : Neuroses of Childhood. 115 even before infancy has passed into childhood. From this time on, children are daily being taught, apparently with the idea of destroying their child- hood, and making of them little men and women. And this unphysiological process is not infrequently a factor in the production of the nervous disorders of late childhood, puberty and adult life. Mothers must be told that early precocity is an abnormal con- dition in the hitman infant, which, if encouraged^ may result in actual disease and permanent mental impairment. They must be told that vegetation is the ideal life of infancy and early childhood. Look to the physical, and retard the intellectual develop- ment of the child. It must not be taught, it must not be trained. It must have plenty of exercise, fresh air, proper food and, if possible, a large portion of the year should be spent in the country, away from the clamor and excitement of city life. In the country, also, the child can have a certain amount of solitude, the importance of which can scarcely be overestimated in giving independence of thought and character to the future man. It is mv belief that the nurse and the governess in the modern home are doing much to destroy the development of individuality in children. The 116 Rachford : Neuroses of Childhood. modern child has some one to do his thinking, some one to minister to his every want, and is almost constantly being trained. He has no time to him- self, and a very small portion of his day is spent in play with his intellectual equals. If there is one crying evil common to all of our large cities it is the absence of play-grounds for children, and the attention of humanitarians should be called to this fact. If our generous citizens would pause long enough in the building of hospitals, libraries and places of learning, to realize that there is a field al- most totally neglected by the humanitarian, and one of as much importance to the welfare of our communities as the building of hospitals, libraries and institutions of learning; then possibly a por- tion of the vast sums of money annually spent in this way would be spent in providing play-grounds for children. These play-grounds should not be covered with beautiful grass plots, guarded by po- licemen, but they should be play-grounds in the best sense of these words — places where ball, tennis, and all kinds of healthful sport could be enjoyed. And I believe the day is not distant when the physiological importance of the physical, as op- posed to the mental development of children, will Rachford : Neuroses of Childhood. 117 be so generally recognized that some philanthro- pists will prefer to hand their names to posterity associated with " play-grounds," rather than with fountains, art museums, music halls and other worthy enterprises. INDEX. PAGE Aducco, V 75 Age and sex, How, predispose to neurotic disease 104-5 Anemia, chronic, Kelation to neurotic disease of 85-6 Arterial anemia, How, produces nervous irritability 77-8 Auto-genetic and bacterial toxines 47 Auto-Intoxication, Bouchard's work on 50-1-2 " " Definition of 48 " from bile 66 " " from leukomains v 60 " " from poisons in normal urine 51 Bacterial products, How, produce fever 35 Bacterial toxines, How, produce neurotic disease 67-8 Biliary toxemia 66 Blood changes related to nervous disease 47-8 Blood, Venous condition of 72 " Impoverished condition of 80 Brain, Influence of heredity and environment upon the functional development of 13 Brain, Morphological and functional development of 11-12 " Order of functional development of 13 Brunton, Lauder 20, 74 Calcium starvation 88 Changes in nerve cells due to peripheral irritation. : 98 in spinal cord from stretching the sciatic nerve. . 99 " in spinal cord from reflex irritation 99, 102 Child is not a u little man " 108 Christopher, W. S 84 Convulsive muscular action, How, produces fever 38 Clouston, T. S 12 Destruction of heat centers. Influence on body tempera- ture of ' 27 Discharge of nerve energy 4 Dwarfishness of body and dwarfishness of mind 112 Early precocity an abnormal condition 115 Evaporation from surface of body . 43 (119) 120 INDEX. Evaporation from air passages 44 Exciting causes of fevers and high temperatures in infants and children 35 Fat starvation 87 Fatigue changes in nerve cells 97-8 Fever and the variable temperatures in childhood 24 Fever, Definition of 24 Fever, How bacterial products produce 35 Fever, How convulsive muscular action produces 38 Fever, How insolation produces 38 Forchheimer, F 71 Functions of normal nerve cells 1 Gad, Prof. J 2 Gallstone fever 40 Gout, an auto-intoxication 65 Heat centers, Thermogenic . ." 26 " " Thermo-inhibitory 27 Location of 27 " " When developed 29 Heat dissipating mechanism 42 Hereditary nervous weakness developed into actual dis- ease 113 Highest functions of nerve cells 2 High temperature, Definition of 24 Hodge, C. F 97 Howells, W. H 88 Hypochondriasis 65 Hystero-epilepsy 62 Incontinence of urine 22, 68 Influence on body temperature of irritation of heat cen- ters 28 Inhibitory function, Development of 15 Inhibitory mechanism, Development of 16 Inhibition, Abnormally feeble, of nerve energy 15-16 Inhibition, Development of voluntary 7-8 Inhibition, Reflex 9-10 Inhibition, Involuntary 9-17 Insanity 19 Insolation, How, produces fever. 38 Intestinal toxemia not an auto-intoxication 70 Intestinal fermentation, chronic 70 Intestinal toxemia, chronic 71 Involuntary inhibition 9-17 Lead poisoning, How, produces auto-intoxication 65 Leukomain epilepsy 61 Leukomain gastric neurosis 63 INDEX. 121 Leukomain headache 62-3 Leukomain poisoning 60 Malaria chronic, How, related to nervous diseases 69 Malaria, Urine in 69 Mechanical and reflex causes, producing fever 40 Migraine 62 Motor areas in infants, sensitiveness of 21 Muscular action, How, produces fever 39-40 Muscular tone 5 Nerve activity, Excessive 106 Nerve cell, Immature 3 Nerve cells, Functions of normal 1 Nerve cells, Highest functions of 2 Nerve elements, Innutrition of .81, 84 Nerve elements, Malnutrition of 84 Nerve energy, Abnormally feeble inhibition of 15-16 Nerve energy, discharged refiexly 6 involuntarily 6 " " " voluntarily 6 Nerve energy, Generation of 2 " " Inhibition of 7 " " Involuntary inhibition of 8 " " Law governing : 4 " . " Mental 3 " " Motor 3 " " Overflow of 19 " " Reflex inhibition of 17 Voluntary inhibition of 8 Nervous irritability, How arterial anemia produces 77-8 Neurasthenia 65 Neuroses of Childhood, Definition of 1 Neurotic disease, Relation of chronic anemia to 85-6 Neurotic disease, How age and sex predispose to 104-5 Neurotic disease, How bacterial toxines produce 67-8 Ott, Isaac 32, 40 Overflow of nerve energy 18, 19 Paraxanthin, the most poisonous leukomain 57-8 Paraxanthin poisoning in the mouse 57 Paraxanthin in normal urine 58 Physical examination to guard entrance to school grade. . . 109 Physiolggical peculiarities of the nervous svstem of child- hood 11 Play grounds for children 11 6-1 1 7 Polypncea 44 Polypnoeic center, Does it exist in infancy and childhood ? 45 Polypncea, Symptoms of 46 Porter, W. T 107 122 INDEX. Porter's law . „ . . 109 Rachitis 87-8 Radiation of heat from the surface of the body 42 Reflex inhibition .- 9-10 Reflex irritation 92 " " Common sights of 93 " " Importance of 94-5 " " as a factor in neurotic disease 100-1 " " Changes in the cord from 99, 102 Rheumatism 86 Richet, Chas 37, 44 Salomon, G 57, 59 School grade, Physical examination to guard entrance to. . 109 Skeletal muscles, Tone of 5 Soltsman, Otto 15 Sphineter muscles, Tone of 5 Spinal reflex centers 8 Spinal irritability from reflex irritation 101 Temperatures of children, High and variable 34 Temperature, Influence of destruction of heat centers on. 27 Temperature, Influence of irritation of heat centers on 28 Toxic principles in normal urine 50-1 Tuberculous neuroses 68-9 Urea is non-toxic 53 Uremia 62 Uric acid diathesia 55-6 Uric acid leukomains 56, 57, 58 Uric acid is non toxic 53-4 Uric acid, a sign of leukomain poisoning 54-5 Urine, Paraxanthin in normal , . . . 58 Urine in malaria 69 Vascular tone 5 Voluntary inhibition, Development of 7, 8 at birth 17 Xanthin 58-9 H"98 «3 „ r « ♦ v *%lRir« «C*' «i» • ^"s^* * •# •' * 4 °^ "^Si^V .» u ^ ^ BV. ^~ ^ Infill- ^* •«SP3K2«- ^ ^o 1 «5^ -v. •f » ^ V ^ . « * < * -¥ ^ovl £ 4 °* ••••' A °A *•«• A "^ "' •<*' w ^ "••' A w ^ v v fV % m ^*~* - ^ -ay o » *** W^ • »'».. ^J-. ^ &> » • » ~<* - • • » . w 4 .♦jsS^'. «.,