later a true pathologic condition of all the structures in the nasopharynx. Heredity, diphtheria, scarlet fever, measles and other debilitating systemic diseases play an important role in the etiology of enlarged tonsils and adenoids, but many of the other pathologic conditions are secondary to the abnormal throat condition, as will be shown later. Symptomatology: The first and probably one of the most. troublesome symptoms of these growths is the excessive secretion of mucus in the posterior nares. Who of us has not seen any number of children, especially among the neglected classes, their posterior nares completely blocked by this mucus, and large quantities draining from their anterior nares, producing a very repulsive condition of the face to say the least? This mucus forms hard crusts, which further obstruct the child's breathing, and also prevent the secretion from dropping directly into the lower throat, where it would do little harm. Instead it is retained in the nose, degenerates into mucopus, becomes highly infected by pathologic organisms from the atmosphere and eventually lodges in the crypts and fissures of the nasopharynx, becoming a hotbed for the further development of disease germs. Finally it passes on into the stomach or lungs, where the organisms multiply still more rapidly, until we have a chronic gastritis, acute tuberculosis or intestinal infection to deal with. The child with this condition now develops an altered voice, a "nasal twang," that is, the child is said to talk through its nose, as if it had a "cold in its head," whereas, in fact, the voice becomes so because the child cannot talk through its nose. A parent will often bring forward the objection to operation that: "the child will never be able to sing as well if the tonsils are cut." They do not understand that the abnormal condition will do that very thing unless corrected and that we aim by operation to put the throat and nose back into the same condition that nature intended it to be. No normal structures are removed, only those that are diseased and so swollen that they act as foreign bodies and prevent the child from singing and talking clearly. This obstruction to free breathing soon produces a peculiar facial expression characteristic of adenoids. The child develops drooping eyelids, broadening of the nose, dropping of the lower jaw and lip. In fact all the bones and muscles of the face fall into disuse, and produce a vacant semi-idiotic expression, so that all who come in contact with the child think that it is not possessed of all its wits. Phillip D. Kernson, in the New York Medical Journal of April 21, 1896, says: "One of the most interesting problems in medicine today is the possible prevention of aural diseases in adult life, by removal of the causes in early childhood. That not infrequently the first intimation the parents have of the auditory defect of these children is the difficulty experienced in keeping abreast with classmates at school. Almost invariably there is a history of difficult respiration, mouth breathing or snoring." Of 50 children examined in Dr Wright's clinic, faucial tonsils were enlarged in all but eight, and of these 50 children, 45 showed evidences of aural disease. It is universally acknowledged by the medical profession that the dominant factor in middle ear disease is infection, and this infection could come from no other source than through the Eustachian tubes, with the possible exception of metastasis, as in systemic diseases. Clarence Blake declares adenoids responsible for 88% of deafness. McKenzie claims that the discovery of adenoids has saved thousands of cases of deafness every year. At the Central London Throat, Nose and Ear Hospital every child with aural disease is submitted to adenectomy. Streptococci and pneumococci are almost always the exciting causes of middle ear diseases. So virulent are these organisms that the entire mastoid is often destroyed in 48 hours and many operators feel justified in opening the mastoid as soon as these organisms are found in the aural discharge. In January of this year I operated upon N. W., aet. nine years, also his sister, R. W., aet. six years, both of whom had defective hearing. The brother was markedly deaf, and frequently during the past three years I had urged operation. The parents did not consent until the sister began to get deaf, and I had shown them that she possessed the same abnormalities of the nasopharynx that her brother had. They then consented to an operation, with the result that the hearing of both rapidly returned to the normal. In 1901 Mrs. L. consulted me as to why her boy was so restless at night. He would throw himself about, kick the covering off, perspire profusely, snore and have night-terrors. Upon examining the throat I found the tonsils enormously enlarged, the posterior nares almost completely blocked with adenoids and a general systemic debility. I operated upon him with a resultant cessation of all the symptoms and a rapid return to good health. Ten months later the mother came to my office and said: "Doctor we want you to come and operate upon the baby. He acts in his sleep just as Eddie did before you operated upon him." This baby was then 13 months old. As I entered the house the next morning, prepared to operate, I could hear the child breathe. from a distance of two rooms away, but when I went to see him the next morning, I was compelled to put my ear quite close to his face to hear him breathe at all. There are many other cases I could report, which showed as marked improvement, but time is limited. A chronic cough of greater or less severity is a fairly constant symptom of enlarged tonsils and adenoids. City air is nearly always laden with dust particles and these would be sifted out by the hairs in the nose, if the nasal passage were patulous. When the dust is breathed through the mouth it is deposited upon the delicate epithelial lining of the bronchial tubes, later infecting the lungs. One of the most important functions of the mucous membrane of the nares is to render the air humid as it passes to the lungs, but when the air is breathed in through the mouth, it extracts the natural moisture of the larynx trachea and bronchi, keeping the mucous membrane dry and irritated and producing a dry, rasping cough, with its consequent debilitating influence upon the general health and resultant reflex nervous symptoms. It may now be easily seen how readily a tuberculous infection may take place. It is a well established fact that many tuberculous patients state that the trouble was preceded by a chronic catarrhal inflammation of the throat and nares. One patient in my own practise had suffered from chronic catarrh for years which eventually developed into tuberculosis. There is no question in my mind but that this man would never have had tuberculosis had his nasopharynx been in a normal condition. The time is not far away when we shall consider tuberculosis a rare disease, because we now teach the laity the early signs of the disease, and the means of prevention. We teach the parents that many children are born with conditions which, unless corrected, will produce such invalidism as will wreck their happiness, and possibly necessitate their being sent to public institutions for the blind, deaf or feeble minded. E. H. White (American Journal of Medical Sciences, August, 1907) summarizes his study in 75 cases of adenoids, with especial reference to tuberculosis. In five there were histologic evidences of tuberculosis. In four of these five, the disease was primary in the adenoids, making a percentage of 5.3. He quotes McBride and Turner as finding 3%, Dreulafar 20%, Pludar and Fisher 15%, Nicholl and Latugan 16%, Wood, out of 1675 cases, 5%. He advises operation in all cases of primary tuberculous infection of the adenoids with a favorable prognosis as to cure. Watson Cheyne (British Medical Journal, February, 1899) reports that out of 27 autopsies on subjects that had died. of pulmonary tuberculosis, 26 had involvement of the cervical glands. It could not be determined where the primary infection took place, but no doubt in not a few it was in the throat, the infection in the glands and lungs being secondary. So that in all cases of cervical adenitis the nasopharynx should be first examined. If adenoids are found, the first step in the treatment of the adenitis should be the removal of the adenoids as a probable source of the primary infection. Exophthalmic goiter is not an infrequent result of enlarged tonsils and adenoids. In 1899, I removed the tonsils and adenoids in a little girl 10 years old, who had a large goiter but not the exophthalmic type. Six months after the operation the goiter had entirely disappeared. W. H. Wingram (Lancet, December, 1903) reports a case of a man 21 years of age, who complained of persistent redness and enlargement of the nose. He was of temperate habits, used tobacco only moderately, there was no marked obstruction to breathing, but the supranasal vein was varicosed and very prominent. Anterior rhinoscopy revealed no abnormalities, but posterior rhinoscopy and palpation with the finger revealed a large mass of adenoids. Their removal was soon followed by the disappearance of the varicosity of the supranasal vein, and of the hypertrophy of the nose. The cure was complete and permanent. Diagnosis: Kernson says that: "Bilateral retraction of the drum membranes in a child of 10 years or less is pathognomonic of one condition only, viz., nasopharyngeal obstruction." This retraction is seldom discovered until later in life, then the patient remains chronically deaf. The catarrhal discharge, the facial expression and a history of disturbed sleep will usually enable us to make a diagnosis. This may be confirmed by posterior rhinoscopy and the finger. Very soon after operation the child feels so much better that it seems as if nature was delighted to get rid of the offending material. The child acts as if a great burden had been lifted from its shoulders, the flesh becomes pink and firm, the eyes regain their lustre, the face assumes a happy, intelligent expression, hearing becomes more acute, the child sleeps better, eats better, learns more rapidly and grows faster. Hypertrophic and atrophic rhinitis, headache, asthma, epistaxis, nightmare, night-sweats, convulsions, rickets, anemia, pigeon-breast, round shoulders, pallor, vertigo, sneezing, loss of smell and taste, aphonia, salivation, stammering, enuresis, chorea, rheumatism, heart disease and indigestion are common sequelæ. Surely there is no other act that we can do in our professional capacity that wins such praise and gratitude from the parents of these little ones as the removal of diseased adenoids and tonsils. 532 Rose Building. Types of Paranoia By H. H. DRYSDALE, M. D., Cleveland, Ohio Paranoia is a chronic form of mental derangement characterized by an elaborate system of fixed delusive conceptions unaccompanied by any disturbance of the logical or syllogistic faculties. In tracing the development of the malady a morbid heredity will be found in almost every case. Krafft-Ebing has never seen a paranoiac free from neuropathic or psychopathic taint. Many of these cases present anthropologic degenerative stigmata. The disease preeminently is a disorder of the intellect and the false ideas that completely dominate the subject have their origin in the emotive nucleus. In the evolution of the personality, the fundamental emotions, ambition, pride, suspicion and fear, shape the order of thought and action but when their development exceeds the normal measure of intensity, they exercise complete dominion over the mental patrimony, disturbing the perceptive and associative functions and provoking a current of thought unrelated to reality. From this cause reason is dethroned and the subject throws himself without consideration into ruinous undertakings, indulges in a line of conduct that is mystic and incoherent and becomes a firm believer in the world of chimeras. In years gone by. paranoia was erroneously known as "reasoning insanity" from the fact that most of these patients are able to conceal cunningly their delusions and defend their Read before the Clinical and Pathological Section of the Cleveland Academy of Medicine, June 5, 1908 |