especially in the severer degrees of degeneration found in pernicious anemia, that one could rationally say the processes were the same. Putnam noted degeneration in the spinal gray in some cases in his first paper, but in his second paper with Taylor emphasis is placed upon the fact that the gray matter, the spinal ganglion, and the superficial nerves are usually not involved. In thirty-eight of Putnam and Taylor's fifty cases, six only were noted to have pernicious anemia. Of the nine cases reported by Russell, Batten and Collier, two only had pernicious anemia, and in the nine cases reported by Burr, two did not suffer from pernicious anemia. In all of these cases the spinal cord changes were practically the same, differing only in the degree of the spinal cord involvement. Indeed, Russell, Batten and Collier divide the cases clinically into three stages. The first, in which the patient is paresthetic, with possibly slight ataxia and spasticity; the second stage, in which is added an increased ataxia and spasticity, with increased knee jerks, and slight paraplegia ; and a third stage of flaccid paraplegia, with absent knee jerks, loss of sphincter control, bed sores, emaciation, etc. A patient dying in the first stage of the 'disease would show usually less marked degenerative lesions than would one of the second or of the third stage.

This division of the cases clinically, while practical for study, is one which cannot be fully maintained, for the reason that all cases do not pass to the stage of even spastic paraplegia. Case 1 of my series died with symptoms only of subjective paresthesia, and yet the spinal cord changes were sufficiently marked to have produced marked spastic, if not paraplegic, symptoms. Case 3, too, did not show flaccid paraplegia at the time of death, although the spinal cord changes, as shown by the figures, were very marked.

Spinal cord degenerative changes have been noted also in other conditions than those reported above. Williamson reports two cases of diabetes mellitus in which there was sclerosis of the nerve fibers in the posterior columns, especially in the column of Goll, with a moderate increase of neuroglia. Nonne quotes Tuczek on sclerosis of the posterior and lateral tracts in pellagra poisoning. This occurs as a symmetrical degeneration, and includes usually the column of Clarke, but the membranes of the cord remain free. It is a chronic disease, with remissions and exacerbations, and may be mistaken for amyotrophic lateral sclerosis, ataxic paraplegia, or hysteria. Nonne reports two cases of leukemia in which there was sclerosis in the middle column of Goll and Burdach, greatest in the dorsocervical region but for a few small areas in the lateral and in the

right pyramidal tract. There was no change in the spinal gray, in Clarke's column, in the root zone, in Lissauer's tract, or in the blood vessels. Nonne calls attention to the fact that this differs from the changes of pernicious anemia, in that in the latter he has always found disease of the vessels of the spinal cord. Nonne also quotes Walter Müller, who reports a case of leukemia, with spinal cord. changes similar to those described by him. E. Bloch and H. Hirschfield report a case of myelogenous leukemia, in which the cord showed moderate sclerosis of the posterior and lateral columns, greatest in the cervical region, and diminished from above downward. They quote a case by Kast of myelogenous leukemia in which there was some sclerosis in the medulla, but none in the cord. They also quote Minnich, who reported a case of myelogenous leukemia, with cord changes of a degenerative character, which he attributed to edema. consequent upon the anemia. Similar cord changes have been found in diphtheria, lathyrism, and in certain metallic poisoning, like phosphorus, lead and arsenic.

It must be evident to one who has had experience with pernicious anemia, and who is familiar with the literature of the subject of diffuse degeneration of the spinal cord as it occurs in pernicious anemia and other conditions, that there is a marked similarity of the contributory causes of pernicious anemia and of the conditions which are mentioned as causative in the production of the spinal cord lesions of other conditions. For example, in Putnam's first report he notes the age, the sex, the nutritional condition, the general feebleness and lack of vigor, the pre-existence of infectious disease, like la grippe and typhoid, the developmental fault, the neuropathic history of epilepsy, goitre, etc., and the existence of chronic gastro-intestinal disease as important factors in his cases. These very conditions are prominent elements in many of the cases of pernicious anemia. The concensus of opinion, as stated, is that pernicious anemia is due to a hemolytic toxin, and it is the universal belief, too, that the degenerative changes of the spinal cord in these different conditions are due to a toxin. It is suggestive, therefore, that possibly a toxin, which has its origin perhaps in the way suggested by Adami, may be one which may have in certain individuals a predilection for hemolysis; in another for degeneration and sclerosis of tissue which, by election, affects the liver in one case, the kidney in another, and certain parts of the spinal cord in another. We recognize tabes as a parasyphilitic disease, and believe that the toxin associated with syphilis has a predilection for the posterior columns. It affects but a small percentage

of syphilitic cases. Our want of knowledge of the nature of the toxin or toxins makes a discussion of this part of the subject purely theoretic, and of no value, although perhaps interesting. It is clear, however, that the future study of these degenerative processes must lie in the direction of an attempt at discovering the source and nature of the probable toxin, not only of pernicious anemia, but of the degenerative changes of the cord in other conditions.

are:

CONCLUSIONS.

The conclusions which one may draw from a study of the subject

1. That there is a well established relation of diffuse cord degeneration with pernicious anemia.

2. It seems probable that the hemolysis and the cord changes are due to the same toxin.

3. While the source of the toxin is unknown, the fact that gastro-intestinal disturbance is so common in the disease would lead one to suppose that it is of intestinal origin.

4. The diffuse degenerations of the spinal cord which occur in conditions without pernicious anemia do not appear to differ essentially from those of pernicious anemia.

5. It is possible that a common blood circulating poison exists which may expend its force upon the blood in one individual, upon the nervous apparatus in another, and coincidently upon the blood. and spinal cord in others.

FIBLIOGRAPHY.

Lichtheim: Congress f. Inn. Med., 1887.

Minnich, W.: Inaug. Dissert., Munich, 1891.

Minnich, W. Zeitschrift f. Klin. Med., 1892, p. 25, and Vol. 22, 1893,

1 бо.

Putnam: Journal of Nervous and Mental Diseases, Feb., 1891. Bastianelli: Bullettinio della R. Academia Medica di Roma Ano, 1896. Putnam and Taylor: Journal of Nervous and Mental Diseases, Jan. and Feb., 1901.

Adami, J. G.: Chicago Medical Recorder, Vol. XIX, p. 157. Nonne, M.: Verhandlung Deutsche Aertze, Wiesbaden, 1887. Nonne, M.: Deutsche Zeit. f. Nervenheilkunde, Leipzig, 1894-5. Nonne, M.: Deutsche Zeit. f. Nervenheilkunde, Leipzig, 1897, Vol. X, page 165.

Russell, Batten and Collier: Brain, Vol. XXIII, Spring, 1900.

Dana, C. L.: Journal of Nervous and Mental Diseases, Feb., 1891; April, 1891, and January, 1899.

Burr, C. W.:

University Medical Magazine, April, 1895.

Minnich, W.: Nothnagel, loc. cit., p. 135.

Bloch and Hirschfeld: Zeit. f. Klin. Med., Berlin, 1900, p. 32.

Müller: Inaug. Dissert., Berlin, 1895.

Williamson: Brit. Med. Journal, Feb. 24, 1894.

Schauman and Tallquist: Nothnagel, loc. cit., p. 96.

Nothnagel, H.: Special Pathology and Therapy, Vol. VIII, p. 100. Lloyd, J. H.: Journal of Nervous and Mental Diseases, 1893. Juliusberger: Archiv. f. Psychiatrie, Berlin, 1898. Vol. XXX, p. 975. Jacob and Moxter: Deut. Med. Woch., 1898, No. 24, 152.

Tallquist Octavo Volume, Berlin, 1900.

Hughes, W. E.: Philadelphia Med. Jour., 1901, Vol. 1, p. 1207.

Clark, J. M. Brit. Med. Jour., 1897, Vol. 2, p. 325.

von Voss, G. E. Deut. Archiv f. Klin. Med., 1897, Vol. 58, 487. Boedecker and Berger: Centralbl. f. Nervenheilkunde und Psychiatrie, Leipzig, 1896; New Fasciculis, Vol. 7, p. 315.

Brown, Langdon and Wolfstein: Journal Amer. Med. Assoc., March 2, 1901, Vol. 36, p. 502.

Campbell, A. W.:

Liverpool Medico-Chirurg. Jour., 1898, Vol. 18, 218.

Neusser: Wiener Klin. Woch., 1899, 12, 388.

Mott, F. W.: The Lancet, London, 1900, Vol. 1, June 23 and 30; Vol. 2, July 7 and 14.

100 STATE STREET.

CASE OF FUNNEL PELVIS WITH CAESAREAN SECTION.

BY CHARLES B. REED, M. D. CHICAGO.

History. On May 4th, 1900, I saw, in consultation, a patient, aged 19, in her first confinement. She had been in labor twentyfour hours, the membranes had ruptured and dilatation was complete. The unengaged head presented, mobile above the inlet in L. Ô. A. and the woman was nearly exhausted by her long labor. The external measurements of the pelvis were small and the conjugata diagonalis could not be obtained. The outlet seemed contracted, but an estimation of the size of the child's head did not apparently preclude its passage and with the usual preparations and precautions a combined external and internal version was done. The anterior foot was seized and brought down and the extraction followed directly. No trouble was experienced until the head reached. the inlet and refused to enter. Under the combined use of pressure from above (on abdomen), the Walcher position and the SmellieVeit method of delivery, the head slipped through the inlet, passed rapidly, and without difficulty through the excavation to the bony outlet where its progress was stopped.

In spite of our utmost efforts the attempts to complete the delivery failed. The child was asphyxiated, craniotomy was done through the roof of the mouth and the mutilated head passed the contracted outlet with some difficulty.

In Oct., 1901, she reappeared, pregnant for the second time, but Chicago Medical Society, Dec., 1902.

with no knowledge of the date of conception. She did not remember when her periods were interrupted, nor when she first felt life.

From examination it seemed probable that labor would occur about Feb. 1st, 1902, and appreciating the difficulties which the case presented, her own and her husband's consent was secured for the performance of any operation which would most nearly promise a living child.

Labor began at two o'clock A. M., Feb. 16th, and at 8 A. M. she went to Wesley hospital and was immediately prepared for Caesarean section. No internal examination was made. The operation began three hours later with the courteous assistance of Dr. Watkins and the hospital staff. Through the usual median celiotomy incision the uterus was delivered, the blood supply manually compressed and a median longitudinal incision made in the uterus through which the child was easily extracted by the anterior foot. Contraction of the uterus was secured by massage and hot applications and the placenta was delivered. The opening in the uterus was closed by through and through sutures of chromicised catgut. After direct measurement of the inlet the abdominal wall was closed.

The thoroughly mature male child was cared for by Dr. Farrell and cried lustily. The head was well ossified and non configurable; a small caput was found over the left eye. The child weighed 3,400 grms. (71/2 lbs.) and gave the following measurements: Length, 52 cm.; Bitem., 7.5 cm.; Bipar., 9.75 cm.; occ-front, 12.5 cm.; occ-mental, 13.75 cm.; subocc-breg., 10.0 cm.; occ-front. circum., 37.0 cm.; subocc-breg. circum., 33.0 cm.

The involution progressed rather slowly and at the time of the removal of the sutures the uterus was found to be adherent to the abdominal wall throughout the entire line of the wound, resulting in an involution, which took place laterally, but hardly at all longitudinally the uterus being long and narrow in form and extending to the umbilicus.

The convalescence was interrupted by a slight pleuritis, but at the end of the fourth week she left the hospital with her babe in excellent condition. Examination about three months later showed the condition practically unchanged.

IDENTIFICATION.

The measurements in this case are very interesting as showing a pure type of the "funnel pelvis" (masculine or infantile pelvis), by which is meant a pelvis with normal or only slightly contracted inlet and high lateral walls which converge strongly downwards to a markedly contracted outlet. In the identification of this pelvis, it is necessary to exclude certain anomalous pelves wherein the contracted outlet exists only in association with characteristic deformity of the vertebral column such as kyphosis and spondylolisthesis