Lesions of the skull are, with a few exceptions, quite similar to those of other bones in the body, while those ansmg in the brain, its coverings and appendages, are not duplicated elsewhere in the human anatomy. As bony tissue, the cranial vault is liable to injuries, anomalies, and deformities; inflammations and repair, and newgrowths, both primary and secondary. Injuries (1) will not be considered here except to mention that the secondary or late effects may be of more clinical importance than the immediate results. Anomalies of the skull, especially as to size and shape, are rarely of importance, unless one classifies turricephaly, scaphocephaly, oxycephaly, etc., under this heading. These terms are misleading, being descriptive only, without a suggestion as to etiology or causation. They would be grouped better under the heading “synostosis cranii” (2), which indicates that the trouble is due to early closure of the sutures, with a consequent marked increase in intracranial pressure as the expanding brain pushes against the unyielding skull (Fig. 1). The most bizarre appearances may result, but the key to the situation remains the same—recognition of the fact that one or more of the sutures are, or were, tightly closed during the period ordinarily devoted to growth. For example, the coronal suture may close and thus cause a deep furrow or constriction across the head as the adjacent bones yield slowly to the continually increasing pressure, or all of the sutures may close except the sagittal, which may be spread apart, giving an unroofed appearance. An interesting but rare anomaly is that associated with diabetes insipidus, where the X-ray occasionally reveals large defects in the membranous bones of the skull. Only eight such cases have been reported to date (3). With osteomyelitis, which is fortunately rare in cranial bones, we have the various stages of destruction and bone production similar to those seen elsewhere, but of course in flat bones. Under inflammation and repair one might classify Paget's disease (osteitis deformans) (Fig. 2), which ordinarily produces a typical picture of alternate areas of absorption and production of bone, with an actual increase in the diameter of the involved area, and the typical cottony appearance as described in text books (4). In passing, it is wise to remember that osteogenic sarcoma may and frequently does arise in a bone affected with osteitis deformans (5). Possibly similar in origin but different in expression is the peculiar apparent decalcification of the bones descriptively named by Schuller as “osteoporosis” (6). It may well be that this is simply the absorptive or destructive phase of Paget's disease at work, with the productive phase held in abeyance (Fig. 3). Similarly, if the formative half of the disease alone were present, we might get the appearance known as “leontiasis cranii,” where the bone is tremendously thickened. without any evidence of rarefaction.