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A review of the literature on suppuration of the petrous pyramid reveals the fact that the symptoms and signs now associated with this condition were known to pioneer otologists.

In the last few years increasing emphasis has been placed on that portion of the field of otologic surgery which might be considered to concern itself with efforts to prevent intracranial extension of middle ear and mastoid suppuration. It is understood, of course, that the surgical treatment of the infected ear and mastoid is in itself an attempt along these lines. However, with the increase of our knowledge of the spread of infection from the ear and mastoid there has developed pari passu a broadening of the limits of surgical exploration so that exenteration of the cells in the mastoid does not always suffice. While it is true that in most instances of mastoid disease the complete removal of all cellular elements is all that is essential for recovery, there are instances in which further exploratory measures must be instituted.It must be obvious that in order to establish a rational basis for the exploration of structures beyond the mastoid, we must lay as a foundation a thorough understanding of the pathologic changes and the pathways along which these changes progress. The literature contains comparatively few such studies.Realizing the importance of this problem, we have, for the past four years, carefully prepared and studied histologically a considerable number of temporal bones illustrative of the various pathways of intracranial extension. Occasionally in the routine removal of temporal bones we obtained specimens that demonstrated possible pathways of infection, such as dehiscences in the bony jugular dome ( fig. 1) and middle fossa, open sutures (fig. 2) and erosion of the facial canal (fig. 3) in patients who died of entirely unrelated diseases.An infection beginning in the middle ear may extend through various routes and involve a variety of structures. Thus middle ear or mastoid disease may involve the intracranial contents by bone necrosis or through sutures, dehiscences, perforating vessels or lymphatics.When we have accumulated sufficient material to be able to make authoritative statements, we mean to divide the presentation anatomi-

No comprehensive discussion of any phase of labyrinthitis should be undertaken without at least mentioning the contributions of such pioneers as Duverney,1 who in 1684 described pus in the middle ear, vestibule, semicircular canals and cochlea; of Leschevin,2 who fifty years later noted caries of the labyrinth and superior surface of the petrous pyramid, that went on to meningitis; of Morgagni,3 who described suppuration in the tympanum with caries of the facial canal and the semicircular canals and a collection of pus between the dura and the posterior surface of the petrous pyramid, and of Itard,4 who first noted the association of vertigo and vomiting with aural disease. In 1827 Saissy 5 reported two cases in which he found pus in the inner ear. In these earliest communications we have the foundation for both the pathology and symptomatology of labyrinthine infections; a foundation on which the superstructure of therapy in labyrinthine disease has been built.

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