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crecy. Practitioner, 1915, p. 293. (97) BROWNE, SIR. THOS.: Religio Medici. London, 1915, Macmillan & Co. (98) FRIEDENWALD, H.: Ethics of Practice of Medicine from Jewish Point of View. Bull. Johns Hopkins Hosp., August, 1917, 28: 256. (99) CONI, E. R.: Necessity for code of medical ethics. Semana Med., 25: 326, March 21, 1918.

(100) ROEDER, C. A.: Bureau of Ethics and Standardization for medical profession of Nebraska. Nebraska Med. Jour., 4: 63, March, 1919. (101) EXCHAQUET, L.: Evolution of medical organization. Rev. Med. de la Suisse Rom., January, 1920, 40: 3. (102) WELCH, Wм.: Papers and addresses in 1920. Baltimore, vol. 3, p. 338. (103) IRVING, P. A.: Back to old standard of ethics. Virginia Med. Monthly, 47: 335, November, 1920.

(105) ANDERSON, A. V. M.: Lectures on medical ethics. Med. Jour. Australia, 2: 1, July 2, 1921. (106) ABBOTT, A. W.: Comparison of Medical ethics of fifty years ago and those of today. Journal-Lancet, January 15, 1922, 42: 31-33. (107) FURMAN, D.: Reflections on medical ethics. Virginia Med. Monthly, April, 1922, 49: 15.

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A

SERIOUS industrial accident

to which extensive newspaper publicity was given, has recently focussed attention upon the central nervous system manifestations of lead poisoning. Further investigation will show whether or not in the use of tetraethyl lead to promote combustion in gasoline engines we are confronted with a grave lead hazard. Nevertheless, this unfortunate occurrence has served to emphasize the clinical importance of those types of both acute and chronic lead poisoning in which the symptomatology directs. attention to the meninges and brain. Of all the forms of lead poisoning, this has received the least attention Only in France has saturnine meningo-encephalitis been properly recognized. A survey of the literature shows it to be much more common than is ordinarily believed and there can be no doubt that this condition often goes undiagnosed. Many cases are missed because of unusual and altogether unsuspected sources for the lead, so that the diagnostic hint given by the fact that the patient was obviously exposed to a lead hazard is often wanting. One of the purposes of this paper is to call attention to a few of the less commonly recognized sources of lead from which an intoxication, leading to central nervous system involvement,

has resulted. Then, by describing the protean manifestations of lead meningo-encephalopathy, the necessity of considering this possibility in the differential diagnosis of a considerabe group of cases with various combinations of convulsions, delirium and coma will be emphasized.

Cerebral accidents in association with the better known manifestations of lead poisoning were mentioned by the earliest writers on lead colic and lead paralysis. The first thorough study of lead encephalopathy, however, was that of Tanquerel des Planches (1) in 1839, who devoted to this condition an entire section, ten chapters, of his book on lead diseases. Known in this country chiefly through the translation by S. L. Dana, this remarkable description of the effects of lead upon the central nervous system is still one of the most readable expositions of this disease. Tanquerel des Planches analyzes in detail a group. of 72 cases of lead encephalopathy, which, from the standpoint of symptomatology, he considers in four groups; the delirious form, the comatose form, the convulsive form and the form showing a combination of the other three types. Taking up each of these four in detail he divides the examples of the delirious form into two subvarieties, those showing a tran

quil delirium and those exhibiting a furious delirium. Similarly, he recognizes two divisions of the comatose group, coma and sub-delirious coma. Five varieties of the convulsive type are described, characterized by partial convulsions, general convulsions, epilepsy, epileptiform movements and cataleptiform convulsions. The fourth, or combined form, he considered the type form of the disease and of the most frequent occurrence.

As additional cases were recorded and especially after examination of cerebrospinal fluid obtained by lumbar puncture became a frequent procedure, it was noted that certain cases of lead encephalopathy were characterized particularly by symptoms referable to meningeal pathology. The French clinicians, especially in the period from 1904 to 1912, developed the conception of a lead mengingitis, a meningitis saturnina. Mosny and Malloizel (2), in 1904, noted some degree of lymphocytosis in the cerebrospinal fluid of each of six patients suffering from lead poisoning and concluded that "it is possible through examination of the cerebrospinal fluid, to measure, as it were, the impregnation of the nervous system by the lead, to assign to their true cause similar nervous manifestations, and, finally, to give to the worker such advice as will enable him to safeguard his health." Three years later the same authors (3) were willing to conclude that "lead mengingitis is so frequent that one can say that it exists almost constantly in those suffering from lead intoxication, at least during the period. of colic." At this time they presented 47 clinical observations of saturnine meningitis, which they grouped, in

part, upon the basis of a division into (a) latent, (b) frustrate, and (c) active acute or sub-acute, meningitis. More than twenty papers dealing with lead meningitis were published by the French during the period mentioned and through this work it was recognized not only that there is a meningeal reaction in most if not all cases of lead encephalopathy but also that cases occur in which the entire clinical picture is determined by the meningeal involvement.

Through these developmental stages there has grown up our present conception of the effect of lead upon the central nervous system. For the complex of clinical manifestations thus produced, the newer term of lead meningo-encephalopathy is more appropriate than the older one which did not recognize the fact that the leptomeninges play an important part.

INCIDENCE

It is very difficult to obtain any accurate judgment as to the total incidence of lead meningo-encephalopathy. Almost all writers agree that, as compared to colic or paralysis, the incidence of central nervous system changes is very much smaller. However, close scrutiny of all cases and careful history taking may show previous epileptiform episodes, or other encephalopathic evidences, which have never been attributed to lead either by the patient or by his physician. In a group of 6638 cases of lead poisoning studied by Legge and Goadby (4) 262, or 3.9 per cent, are classified as having encephalopathic symptoms as the chief manifestation of the disease. In the same table, however, headache is given as one of the main

NALS OF CLINICAL MEDICINE, VOL IIJ, NO. 9

symptoms in 794 cases, or 11.9 per cent. We do not know what proportion of these owed their headache to meningeal involvement nor how much overlapping there may have been between the two lists, but it does appear that the lesser percentage does not properly represent the true incidence of meningo-encephalopathy. With out any knowledge of the meningeal side of the picture Tanquerel des Planches (1) listed 72 cases out of 2171 as exhibiting encephalopathy. This is 3.3 per cent, a figure according very well with those given by Legge and Goadby. If the cardinal symptoms alone are not used as the basis of the classification, it is probable that the statement of Mosny and Malloizel (3) that every case of lead poisoning has some degree of meningitis [meningo-encephalopathy] is nearer the

truth.

In respect to the age incidence of lead meningo-encephalopathy, it appears that children and young people are more apt to have this form of lead poisoning than those of more advanced years. Early statistics of occupational lead poisoning indicated this and there can be no doubt that children are especially prone to meningeal involvement. It is probable that this question is bound up with another one dealing with the incidence of meningo-encephalopathy in relation to the length of time during which the individual has been exposed to lead. There is considerable evidence to show that a short period of exposure to a rather heavy dosage of lead is more apt to give a meningo-encephalopathy than is long exposure to a more minute amount. Tanquerel des Planches (1) believed that the greater

number showing this form of lead poisoning have been exposed only a short time to lead preparations. To this, however, there are many exceptions in the reported cases. Painters, white lead workers and pottery operatives who have had repeated attacks of lead colic and lead palsy may develop convulsions after many years of exposure to lead.

The sex incidence of lead meningoencephalopathy, in so far as data are available, seems not to be significant beyond indicating that the somewhat greater general susceptibility to lead on the part of the female is true in this particular also. In the table of Legge and Goadby (4) encephalopathy was a cardinal symptom in 3.5 per cent of the cases in males, and in 6.2 per cent of the cases in females.

ETIOLOGY

In the earlier compilations the well known lead hazards such as painting, pottery glazing, white lead manufac ture, lead smelting, lead founding and file cutting furnished most of the cases of lead meningo-encephalopathy. In the more recent reports, the industrial hazards of greatest importance in this respect are lead mining and smelting, storage battery manufacture, scraping and sanding of lead paint in closed spaces and spray painting. Educational endeavor and regulative measures have reduced the risk in some of the older hazards and proof of the importance of the respiratory route, as furnished by the work of Blumgart (5), should be of great advantage in this connection. Non-industrial lead poisoning has provided many of the cases of lead meningo-encephalopathy and the diagnosis is much more apt to

be missed in these cases because the etiology is unsuspected. The wide range of possibilities may be illustrated by a few examples.

Stewart, in 1895 (6), reported a group of 16 cases of lead poisoning in which convulsions occurred. More than half of these had obtained their lead from buns or cakes colored yellow with "chrome-yellow" used at that time by certain bakers in Philadelphia. Once the true cause had been demonstrated numerous other cases of death in convulsions in children were recalled by various practitioners so that the total number of fatalities referable to this single cause must have been considerable.

Miller and Ring (7) were unable at first to find the source of the lead producing epileptiform convulsions in a female carpet weaver. Lead was demonstrated in the urine and she recovered under the administration of potassium iodide when kept away from her work. It was learned that the rag strips used in weaving were the selvage edge of window shade cloth and that this material had been painted with ordinary lead paint. In the process of weaving some of this paint was constantly dislodged from the fabric in the form of dust.

Lead containing washes and ointments have been the source in numerous instances. Hahn (8) gives case reports and reviews the literature of lead encephalopathy as occurring in young children after the application of "Hebra salve" and Norton (9) describes chronic lead poisoning with encephalitis in a breast fed child of eight months whose mother had used "Diachylon Compound" upon her eczematous breast. Here should be

considered, also, the increasing number of cases of lead meningo-encephalopathy due to lead-containing cosmetics, hair dyes, face powders and face pastes. Holland (10), in 1881, and Barron and Habein (11) forty years later, have reported cases of this sort and on both occasions the same cosmetic, a face powder known as "Flake White," was the source of lead. In the last two or three years it has been shown by Hirai (12) and by Suzuki and Kaneko (13) that the serous meningitis of infants, which is very common in Japan and which is said to be the fourth most common cause of infant mortality in Manchuria, is due to the cosmetic use of a lead-containing face paste. These workers have used this paste in experimental investigations and have produced in puppies, by administering it in milk, convulsions like those noted in infants.

Another important source of lead poisoning leading to convulsions in children has been the ingestion of lead obtained by sucking or gnawing painted surfaces. Particularly in Australia and New Zealand have convulsive seizures in children been found to be due to the ingestion of lead from painted surfaces, such as verandah railings (Turner (14)). Climatic conditions may have something to do with rendering the paint especially scaly or efflorescent. Thomas and Blackfan (15) saw a fatal case of recurrent lead meningitis in a boy of five years who had gnawed the surface of his painted crib and, more recently, Strong (16) has reported a similar clinical picture as it occurred in a child of nineteen months who had eaten the paint from a bed rail. Simi