pains of a rheumatic type soon followed by weakness in the legs. The paralysis extended upwards in the usual manner and soon involved the arms and the whole of the face, both sides of which became quite powerless. The muscles of mastication were not affected and those of the tongue and pharynx only to a moderate degree. The trunk muscles retained sufficient power to enable him to sit so long as he was quite erect but not if the body deviated from the perpendicular position. The intercostal muscles and diaphragm were affected but retained sufficient power to enable him to breathe without much discomfort. The functions of the bladder and rectum were not affected. The reflexes were all lost. Sensation was normal. The muscles were flaccid but there was little, if any, apparent wasting.

Six weeks later nearly full power returned to the face and to the muscles of speech and swallowing. He was able to make considerable movement of the arms and slight movement of the legs. Knee jerks were still absent.

These cases show not only the symptom-complex but also nearly all the variations met with in the course of acute ascending paralysis as first described by Landry in 1859. The picture presented by a typical case after full development is very striking. There is complete flaccid paralysis of all four extremities, of the trunk muscles, occasionally of the face, usually of the muscles of deglutition. and finally of those of respiration to which death is usually due. Sensation is usually unaffected although there may be various paræthesias such as slight numbness, tingling, areas of hpyeræthesia and pain in the back, severe in some cases, but these disturbances are temporary and the sense of touch remains unaffected. Delirium is rare, consciousness as a rule remaining clear until near death when stupor is caused by the accumulation of carbonic acid in the blood.

The reflexes are lost early, not returning in the fatal cases, and in those recovering, only after the power of the muscles has been well restored.

The bladder and rectum usually escape, but they were involved in three cases of this series, and most markedly in case 2, which ended in recovery.

The course of the disease is usually afebrile but the temperature may be high and toxic in type as in case 4, but the duration of the fever was short in all these cases.

The spleen and lympthatic glands are usually enlarged.

Although there is still much uncertainty as to the pathology of Landry's Paralysis there is scarcely room for doubt that it is due to an acute general infection. This is indicated by its onset with malaise and aching pains, the fever in some cases, and the swollen spleen and lymphatic glands. The occurrence of the fore

going cases in groups showing an endemic cause lends further support to this view. In the present winter (1906) several other cases. occurred in Toronto in the practice of various physicians. I greatly regret that an autopsy was not available in any of my fatal

cases.

With the introduction of the Marchi and Nissl methods of staining nerve tissue, much advance has been made in demonstrating the occurrence of definite changes in recent cases to account for the almost uniform course of the symptoms. Among the definite post mortem changes found, the most frequent are in the spinal cord, especially in the anterior horns. The vessels of the meninges and cord are usually engorged, frequently with capillary hemorrhages generally in the anterior horns and surrounding white substance, but also occasionally in the posterior root ganglia. In a few cases there is small round cell-infiltration into the walls of the vessels and the perivascular lymph spaces; possibly this would be found more often if the fatal termination were less rapid.

Occasionally, the pathological changes are more severe and widespread, consisting in addition to marked congestion of the cord and meninges and round cell-infiltration of the walls of the vessels and perivascular lymph spaces, of areas of softening in the cord generally limited to the anterior gray substance, the whole constituting a meningo-myelitis.

In a few cases, all that was found was degeneration of the peripheral nerves, but myelin changes in the white substance of the cord as well as of the nerves have been found. One or two cases have been reported of hyaline degeneration and thrombosis of the blood vessels, most frequently in the anterior part of the cord.

BACTERIOLOGY.

Although all these pathological changes can only be adequately accounted for by a bacterial toxine circulating in the blood the most careful search has failed to reveal, in the majority of cases, the existence of micro-organisms in either the tissues or fluids of the body. Farquhar Buzzard (Brain; Spring Number, 1903, Part C.I.), in a valuable paper, collected the records of thirty-eight cases, and in only thirteen of these were micro-organisms found by either staining the tissues or by culture methods; in the remaining twentyfive cases the examinations were negative. In these thirteen cases the micro-organisms found were nearly as various as the cases. In his own case a micrococcus was isolated from the blood, and one indistinguishable from it found in large numbers in the external parts of the spinal dura. Subdural injections into a rabbit of cultures of this coccus produced after some days a rapidly spreading paralysis, and the coccus was obtained from the blood and dura matter. In neither the man nor the rabbit was the micro

organism found in the nerve tissue or pia-arachnoid, and in both. the cerebro-spinal fluid was sterile.

In a remarkable case ending fatally, reported by Gordinier (Albany Medical Annals; January, 1904), a careful bacteriological examination gave negative results. The illness began with symptoms of general infection from intestinal origin, thirteen days before the onset of the paralytic symptoms which developed rather suddenly and death occurred nine days later from respiratory paralysis. Widespread degeneration of the peripheral neurones was found at the autopsy.

In this last case had life been prolonged sufficiently there must have followed marked atrophy as in cases of acute poliomyelitis, a case of which it would doubtless have been regarded. It is a question whether all cases of Landry's Paralysis should not be regarded as identical pathologically with acute poliomyelitis. However, it is remarkable that in the cases of Landry's Paralysis terminating in recovery there is not permanent injury such as paraylsis and atrophy. The following case may be quoted to show the close resembl ance, if not identical nature, of the two affections. A child, female, aged ten years, presented the symptoms of a moderately acute infection, with the enlarged spleen and lymph glands, followed in a few days with increasing paralysis, first of the legs and then extending to the trunk and arms. When I saw her a few days later all four extremities were completely paralysed; the diaphragm was quite weak but the intercostal muscles were little affected. Swallowing was somewhat difficult. The face was normal. Occuring at a time when a case of Landry's Paralysis was under observation the child's case was regarded as one of the same disease. The subsequent history proved it to be poliomyelitis; when seen some weeks later there was atrophy affecting all four extremities, almost complete of the legs and very marked of the arms, chiefly of the muscles of the shoulder girdle; the trunk muscles recovered fairly well. A year later she was able to sit in a chair and use the arms sufficiently to enable her to take easily managed food, but her power over the legs was limited to a little swinging movement. Had the nerves supplying the diaphragm and intercostal muscles and those of the medulla escaped with less injury in Gordinier's case, so as not to have ended fatally, the ultimate result should have been practically identical with that of this case. The case, at least, shows that it is not always possible to differentiate the two affections.

151 Bloor Street West.

Proceedings of Societies.

PRELIMINARY PROGRAMME OF THE SEVENTY-FOURTH ANNUAL MEETING OF THE BRITISH MEDICAL

ASSOCIATION.

EXECUTIVE OF THE TORONTO BRANCH BRITISH MEDICAL Asso

CIATION.

President.-IRVING H. CAMERON, M.B., F.R.C.S., Eng., and Edin., LL.D., Edin., Toronto.

Vice-President.-ADAM H. WRIGHT, M.D., Toronto.

Honorary Secretary.-WILLIAM B. THISTLE, M.D., 171 College Street, Toronto.

BRANCH COUNCIL.

ALLEN BAINES, M.D., ALEXANDER MCPHEDRAN, M.B., RICHARD ANDREWS REEVE, M.D.

TUESDAY, AUGUST 21st.

PROGRAMME OF MEETING.

8.30 a.m. Clinic.

9.30-12.30 a.m. Meetings of Sections.

1.00 p.m. Luncheon for Visiting Ladies.

2.00 p.m. Address of Welcome, Introduction of Guests, Delegates, etc., and President's Address.

4.30- 6.00 p.m. Reception and Garden Party, by His Honor the Lieutenant-Governor and Mrs. Clarke at Government House.

6.30 p.m. President's Dinner.

8.00 p.m. General Meeting.

8.30 p.m. Address on Obstetrics, Dr. W. S. A. Griffith. 9.30 p.m. Reception by the President and Mrs. Reeve in the University Quadrangle.

WEDNESDAY, AUGUST 22nd.

8.30 a.m. Clinic.

9.30-12.30 a.m. Meetings of Sections.

1.00 p.m. Luncheon by invitation of the Dominion

Alliance.

2.30 p.m. Address on Medicine, Sir James Barr, M.D.