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the infection was primary, no other lesions due to the organism having been found. In but one of the recent cases was the infection primary in the meninges, and even here the accompaniment of an acute nephritis suggests a preceding acute infection. In six cases the infection was secondary to otitis media and mastoiditis: in one case it was secondary to an infection of a tumor of the sphenoid ; in one case it was associated with the streptococcus, secondary to fracture of skull and operation; in on e case it was secondary to abscess of the prostate ; in one case it was secondary to acute infection of ethmoid, “ the pores of right cribi form plate contain tibrinous pus in continuity with exudation about right olfactory lobe,” in two cases it was secondary to acute croupous pneumonia, in four cases it was secondary to acute bron chopneumonia and pleurisy, and in two cases it was secondary to acute pneumococcus endocarditis.

In but few of these cases did the infection appear to be embolic; in most cases the extension to the meninges was by continuity or by the lymphatics. In its general pathogenic properties, th pneumococcus attacks tissues from mucous surfaces and extends in the body by surfaces. I believe that the frequency of pneu mococcus meningitis is greatly overestimated, and especially its frequency secondary to pneumonia.

Vital statistics with regard to the occurrence of disease are not worth much, owing to errors in diagnosis. The deaths froin meningitis and pneumonia in Massachusetts have been taken during a period of five years in order to cover slight inequalities in different years, commencing in 1898, the year following the epidemic of cerebro-spinal meningitis. If there is any marked relation between meningitis and pneumonia it should be shown in the inter-occurrence of the diseases. The greatest number of deaths from what are described as other forms of meningitis occur in August, when the mortality from pneumonia is lowest. It is very possible that the high number of cases in March, April and May is due to confusion of these cases with primary meningitis due to the diplococcus intracellularis, for these months show the highest mortality in epidemics and in sporadic cases due to this organism.

There were eighteen cases of streptococcus infection, and in one the infection was primary. In seven cases it was secondary to fracture or operation wound of the skull; in eight cases it was secondary to otitis media and mastoiditis, in one case it was secondary to acute streptococcus endocarditis, and in one it was secondary to acute bronchopneumonia and acute cystitis. We see from this analysis that, in the two hospitals mentioned, fata I sporadic cases of meningitis are equally divided between the three organisms which are to be regarded as the main etiologic factors. Of the remaining four cases, two were produced by the staphylococcus pyogenes aureus, one was secondary to trauma with following operation, and one was secondary to empyema. In two cases

the nature of the infection was not determined. In one of the cases reported in 1898 the meningitis was produced by the anthrax bacillus and was secondary to a primary lesion on the face. We have never had any cases due to the typhoid bacilli.

The pathologic process in meningitis due to the diplococcus intracellularis consists in inflammation, with purulent, sero-purulent and fibrino-purulent exudation. The most marked lesions are found at the base of the brain, extending from the optic commissure backward over the cura, the pons and medulla. On the convexity of the brain the exudation is usually most intense on the lateral surface, little or none being found in the meninges of the longitudinal tissure. The meninges of the cerebellum are always involved and often the greatest mass of the exudation is found on the upper surface of this structure. In the most acute cases, those dying a few days after the onset, there may be a little more than intense hyperemia of the vessels of the meninges and cortex. In the more advanced cases, dying from five to twelve days after the onset, the amount of exudation is much greater and has a tough, rather gelatinous character. In the chronic cases, in which death has occurred in from fifteen to thirty days from the onset, there is edema and general thickening of the meninges, which is most marked at those localities where the acute process is most evident. In one case, the duration of which was apparently over thirty days, the entire medulla was embedded in a dense mass of connective tissue. In the cord the exudation is most marked along the posterior surface and may be found here in large amount, while the anterior surface may show only cloudiness and injection. There is usually more exudation along the dorsal and lumbar cord than along the cervical.

In eight of thirty-five cases on which autopsies were made in the epidemic studies, there were definite microscopic lesions in the brain, consisting of hemorrhages in the white matter. No ab-cesses were found. The cranial nerves were affected to a greater or less degree in all cases. Those most affected were the second, fifth, seventh and eighth. They were embedded in the exudation which extended along them, and on section they were found to be swollen and reddened. The gasserian ganglia were examined in a number of cases, and in all they were found swollen and softened. The spinal nerves were also affected; the nerve roots were embedded in the exudation and the spinal ganglia were red and swollen. The exudation was also found around the nerves of the cauda equina.

Microscopically, the exudation in the most acute cases was purulent and the leucocytes were exclusively polynuclear. The absence of eosinophile cells was remarkable. In more advanced cases the number of cells in the exudation was greater and the fibrin was abundant. As the process advanced, large, endothelial, phagocytic cells became increasingly numerous, and in some cases made up a large part of the exudation. They often contained from

one to several polynuclear leucocytes enclosed in vacuoles and showing varying degrees of disintegration.

In the chronic cases the exudation was mainly represented by degenerated

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cells. In these chronic cases there were also numbers of plasma and lymphoid cells.

Microscopically, lesions of the tissue of the brain and cord were absent in but few cases. They were most evident in those cases in which from five to ten days elapsed from the onset of the disease until death. The blood vessels of the convexity were injected. The cortex appeared redder and the tissue edematous. In places there was circumscribed infiltration of the tissue with pus cel Is, which extended downward from the infiltration in the meninges. This infiltration was usually most marked in the outermost lay er of the cortex above the ganglion cells, but in some places it extended among the ganglion cells and even into the white matter. Single pus cells were often found in the brain tissue, apparently remo te from the areas of infiltration. In two cases extensive softening, with purulent infiltration and hemorrhage, was found in the cortex of the cerebellum. These pus cells in the brain were irregularly distributed in the tissue, and were found both in places which appeared to be altered by infiltration of edematous Auid and in those in which the intracellular material seemed to be normal. The pus cells in the tissue were often distorted in shape, sometim es extending in long lines, the shapes resembling those seen in pus cells wandering in the tissue of the cornea. Their situation and shape did not seem to indicate the existence of preformed spaces. They were but rarely found around the ganglion cells.

In certain areas in the cortex, particularly about the vesse 1 s, large numbers of large endothelial cells resembling those in the meninges were often found. They were apparently formed by pro liferation of the cells in the adventitial tissue. They extended often for some distance in the tissue around the vessels where this showed evidence of disintegration, but they seemed to have little or no power of wandering into tissue which was comparatively normal. The presence of these cells is important in relation to the neuroglia cells. Proliferative changes in the neuroglia were con stantly present. In the chronic cases there was a distinct increase in neuroglia fibrils, together with increase of cells, which was chiefly marked in the tissue of the ventricles and in the outermost layer the cortex. In several of the more acute cases numerous nuclear figures were found in the cells of the neuroglia. These were pa rticularly marked in one case. The proliferating neuroglia cells somewhat resemble the large endothelial cells. There is an increase of nucleus with the formation of evident protoplasm about it. The nuclear figures are well marked, showing spindles and centrosomes. Often large cells with several nuclei result from such proliferation. In one specimen in which this was most marked, nuclear figures were also found in the so-called Trabant cells adjoining the ganglion cells.

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Analogy with other tissues would indicate that such changes in the intercellular tissue consisting of proliferation of fixed tissue elements and exudation of leucocytes would be accompanied by degeneration of the specific cells of the tissue, namely, the ganglion cells. The most evident changes in the ganglion cells were found in those places where disintegration of the tissue was best marked, and consisted in disintegration of the cell protoplasm. It is difficult to distinguish such conditions from artefacts. Degeneration of nerve cells is not of the saine character as degeneration of parenchymatous cells in other organs. The state of our knowledge with regard to structure of ganglion cells and arrangement of granules is not sufficiently definite to enable us to determine with certainty their degenerations.

The most marked changes in the nerves were found in the second, fifth and eighth ; the lesions of the nerves represent an extension of the inflammatory process from the meninges.

The dural covering of the optic nerve in the orbit showed little change save dilatation of vessels. The subdural space was dilated and the exudation was found in the pia arachnoid of the nerve. From the meninges the infiltration extended more or less into the nerve itself. In both the optic and olfactory nerves, proliferation of the neuroglia cells was shown similar to that in the brain. The exudation may extend along the optic nerve into the eye.

In acute cases, section of the eighth nerve showed it embedded in a mass of pus, its sheaths softened, broken up and in places entirely gone. The nerve was infiltrated with numbers of pus cells, partly in the form of lines running through it, partly in a more diffuse infiltration. The seventh nerve often showed as great a degree of infiltration as the eighth. Longitudinal section of the fifth nerve extending into the gasserian ganglion showed intense neuritis in the nerve on the cerebral side of the ganglion. Similar changes of the nerve roots and ganglion of the spinal cord were found in all cases which were examined. In some of the more chronic cases, lesions of the nerve roots of the spinal cord were more marked than in the acute cases

In the chronic cases there was marked thickening of the meninges due to connective tissue formation and a marked increase of the neuroglia of the cortex. There was little evident exudation, circumscribed yellowish foci marking the remains of it. The meninges at the base were opaque, and were enormously thickened, and there were bands of organized tissue extending from point to point. In one of the most chronic cases, in which the duration of the disea-e could not be ascertained with any accuracy, owing to the mental condition of the patient when brought into the hospital, the meningeal changes simulated general paralysis. The only evidence of exudation was in the ventricles, in which masses of partly organized fibrin were found adherent to the lining. In another case the entire medulla was so embedded in a dense mass of connective tissue that it was difficult to remove it. Chronic hydrocephalus is

not uncommon in such cases. It is due to closure of the foramen of Magendie by organization of the exudation about the cerebellum.

There is some difference in the character of the lesions due to pneumococcus and streptococcus, as compared with those due to the diplococcus intracellularis, but no difference between le-ions due to the pneumococcus and streptococcus. Endovascular lesions, consisting in cellular infiltration behind the endothelium, were found in both arteries and veins in meningitis due to the pneumococcus and streptococcus. The endothelium was preserved and of ten formed festoons projecting into the lumen of the vessel, with the cell accumulations behind it. The endothelial cells were swollen, but otherwise unaltered. I do not believe that the large cells arise from proliferation of the endothelium, but they seem to reach their position by emigration from the interior of the vessel. In meningitis due to these organisms there is also less tendency to invol veinent of the tissue of the brain and cord, nor is the extension along the nerves so marked. The cases of these forms of meningitis h ave not been so numerous nor has their anatomic study been so thairough as in the cases due to intracellularis. ---Journal of the A. MA.

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Chronic Myositis Rheumatica and Its Treatment by Massa ge. -G. Norstrom discusses this condition, which lie says is not, as is generally believed, a rare disease, but is, on the contrary, of the most frequent affections of the human body, though as it is seldom diagnosed, it is but little known. The principal f eatures of the malady are inflammatory deposits in the substa nce of the muscle, which may vary greatly in size and may become as hard as cartilage, and pain, mostly resembling that of chronic rheumatism. The errors in diagnosis to which the condi tion may give rise are very numerous, and illustrative cases are

described in which what had been considered to be rheumati sm, renal calculus, growing pains, Bright's disease, ,

tortico 1 lis, migraine, neuralgia, cystalgia, writer's cramp, sciatica, tarsal gia, etc., proved to be chronic myositis. The treatment consists

in massage, more or less energetic, according to the consistenc age of the deposit. Great patience is necessary on the part the patient and operator, as long standing cases in old people may require several months of energetic friction. In order to prevent relapses the treatment should be continued until paluable changes are completely removed, although in young people may leave a small residue which by the treatment has been duced to a soft condition, in the hope that nature will remove it.

Medical Record March 11th, 1905.

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