was no history of syphilis and rigorous antisyphilitic treatment had no influence on the process. By removing the inner bony orbital wall access was had to the nasal structures, first on one side and at a later operation to those on the other. The morbid process was most intense at the extreme anterior extremity, where the nasal bones were pushed apart; one of these bones was necrotic and was removed. Both nasal cavities were successfully cleaned out except the posterior part of the lateral walls. Both frontal sinuses were involved. No reaction on the part of the orbital structures followed the operations, and the nasal condition was improved. The infection, however, extended upward in the diploë of the frontal bone. An osteomyelitis of a low-grade intensity spread upward and backward. After an interval of some weeks, deep subperiosteal abscesses developed in succession over the frontal eminences, the lower orbital margins, the temporal fossæ, and the vertical process of the frontal bone anterior to the coronal suture. Incision evacuated pus (streptococcus) underneath the periosteum collected in a circumscribed area, the bone in the centre showing an irregular defect in the outer table and granulations arising from the diploë. The process at no point appeared to have involved the inner table of the bone. Subsequently an abscess formed in the squamous portion of the right temporal bone about 3 cm above the mastoid fossa. On incision the entire thickness of bone was found involved and the dura lay bare covered with granulations. This wound did not do well. The temperature, which had previously varied between 100° and 101°, rose abruptly and the right suboccipital area became indurated. Involvement of the sigmoid sinus was suspected, and on enlarging the wound in the squama backward an epidural abscess was found situated over the upper knee of the sigmoid sinus. The sinus was filled with a thrombus and was completely evacuated. Signs of pyæmic extension had already become marked in the lungs. The eye-grounds presented a very marked optic neuritis with hemorrhages. Under the picture of pyæmia the patient died rather suddenly after fourteen days, or six months after the first operation.

The autopsy showed that the inner surface of the bone over the left frontal lobe was honeycombed, a dilated condition of the natural channels in the bone; the underlying dura was covered with small granulations corresponding to the depressions in the bone. There was no free pus; the process had evidently been kept in check. No meningitis.

The thrombus of the torcular was converted into an abscess. The ventricles were distended with turbid fluid. The jugular bulb was filled with a partly softened thrombus, and the jugular vein just underneath was nearly obliterated; in the neck the walls of the vein were very much thickened, and the lumen was filled with pus. This was sharply shut off at the junction with the innominate vein. The sphenoidal and maxillary sinuses contained pus. The chest cavity was not examined, but presumably would have shown the lesions of metastatic pneumonia and empyema.

In brief the morbid process began as an inflammation of all the parts of the ethmoid bone (an osteomyelitis), associated with empyema of all accessory cavities of the nose; then an osteomyelitis of the frontal bone set in, extending to the squamous portion of the temporal bone on one side and causing an epidural abscess with thrombosis of the sigmoid sinus, pyæmia, and death.

A DISCUSSION ON THE DIFFERENTIAL DIAGNOSIS AND THE TREATMENT OF OSTEOSCLEROSIS OF THE MASTOID PROCESS.'

ΤΗ

BY OTTO J. STEIN, CHICAGO, ILL.

HE mastoid process of the temporal bone in the first few years of life is composed of fine cancellated bone tissue, which gradually undergoes absorption, giving place to the presence of a series of more or less well-formed air cells (1).

These cells communicate with one another and sprout, as it were, from the parent cell or antrum. They are lined with the same delicate and highly vascular mucous membrane as that found in the tympanum and antrum.

The mucous membrane lining the mastoid cells plays a double rôle, in that it is mucous membrane to the cell cavities, and periosteal covering to the bone. The cells receive their secretion from the membrane; the bone, its nourishment.

A chronic congestion of the membrane results in a low grade of inflammation that tends, on the one hand, either to thickening or to pus formation, and, on the other hand, to an osteitis with a resulting hyperostosis, caused by the hypernutrition; or pus formation as the result of caries or necrosis.

These conditions, of course, may co-exist or occur independent of one another. The hyperostosis may exist as an idiopathic disease, the result of a previous inflammatory

1 Read before the eighth annual meeting of the Academy of Ophthalmology, and Oto-Laryngology, held at Indianapolis, Ind., April 9, 10, and 11, 1903.

condition of the tympanum or antrum, but developing itself after the latter had subsided; and, on the other hand, it may develop as an accompaniment to an active morbid condition within the tympanum or antrum, or both.

In the hyperostosis we have the formation of new bone cells from the periosteum and also from the medullary spaces. This proliferative process may continue so that all of the cells may be obliterated, the new bone tissue finally becoming so compact and hardened as to merit the name of "ivory-" or "ebony-like." This process is known as osteosclerosis or eburnification of the mastoid bone.

It is very easy for us to trace the development of our knowledge on this subject, because it is a knowledge of but comparatively few years.

The first recorded reference to the subject that I could find is in the early writings of Schwartze and Politzer. Vague, incomprehensive, and perhaps doubtful as they may have seemed, they nevertheless directed the inquiring and progressive otologic mind in the direction that has developed into a knowledge that to-day gives to the subject a distinct and individual place in the pathology of mastoid disease. What the subject still lacks, though, is a clinical picture that will awaken in the mind of the otologist the necessity of differentiation between conditions productive of similar symptoms, which, thoroughly understood, gives to him the requisite conviction to apply a remedy potent with decided and prompt relief.

Schwartze (2) says: "Sclerosis is a frequent sequence of chronic purulent inflammation of the middle ear, the cells gradually contracting and finally disappearing."

In the report of the American Otological Society of 1870, Dr. C. R. Agnew (18), of New York, probably makes the first recorded reference to this condition, in the following words: "Caries is not the invariable and immediate result of mastoid-cell disease, but sometimes there may be, instead, an osteitis, with hyperplasia of the bone, filling a few or all of the cells."

From this time on several investigators followed up the subject very carefully, and in 1873 Buck (3), in an article on

mastoid disease, referred to the condition under the head of Hyperostosis of the Mastoid Process.

Shortly following upon this time, 1876, J. Orne Green (4), of Boston, Mass., as is shown in the Report of the International Otological Society of 1876, and in the Transactions of the American Otological Society of 1880, attempted to diagnose a specific mastoid disease known as Hyperostosis of the Mastoid Process; and three years later Dr. Arthur Hartmann (5), of Berlin, published in the ARCHIVES OF OTOLOGY, 1879, a paper in which he sets forth a statement recognizing that an idiopathic disease of the mastoid process may exist as an osteosclerosis with definite symptoms.

In all the four cases reported by Green, in 1876, in connection with his article on Hyperostosis of the Mastoid, there was present a chronic purulent inflammation of the tympanum, associated with the hyperostosis of the mastoid, and sudden acute symptoms arising, operations on the mastoid were carried out, with the result that nothing but a hyperostosed condition was found, although complete relief from pain was brought about by the operations.

In three cases reported by Buck (6), in 1883, all were associated with running ears in their early history. One case was lost sight of, the others were operated upon solely for the mastoid pain, the discharge having stopped for years, and complete relief was afforded after the patient had suffered for several months.

A most excellent exposition of the condition is given by J. A. Lippincott (7), of Pittsburg, Pa., in his report of "A Case of Mastoiditis Interna Chronica with Sclerosis," before the seventeenth annual meeting of the American Otological Society, 1884. In this case, like the two cases reported by myself (8), the chief symptom was pain, without any marked evidence of existing middle-ear disease that would otherwise demand relief. This case, like my own, made an excellent recovery after trephining the mastoid process.

From the foregoing remarks it will be seen that there are two varieties of this condition: one where the sclerosis is associated with a suppurating process within the tympanum or antrum, and the other without any associated suppura