Laws, Edward R.

Abstract Between 1935 and 1974, 3598 episodes of head trauma among Olmsted County, Minnesota, residents resulted in 1097 skull fractures. Of these, 53% were simple, 16% were depressed, 12% were compound, and 19% were basilar. The age- and sex-adjusted incidence of skull fractures was 44.3 per 100,000 person-years overall, was somewhat greater in the urban than in the rural areas of Olmsted County, and was relatively stable for the final 30 years of the study. Age-specific incidence rates were highest for the very young, and simple linear fractures were the predominant type of skull fracture in this age group and among the elderly. The male:female ratio of incidence rates varied from 2.1:1 to 4.5:1 depending on fracture type. Motor vehicle accidents accounted for 38% of the skull fractures and were a particularly important cause among young males. Falls accounted for 37% of the skull fractures and were the major cause of fractures in the elderly and pediatric age groups. The results of this population-based study may be helpful in formulating recommendations for the evaluation and management of head-injured patients.

Abstract The pathogenesis of postlaminectomy spinal deformity and instability in children was evaluated by reviewing appropriate roentgenographic findings. First, we reviewed spine roentgenograms of patients below 40 years of age who underwent spinal fusion for deformity and instability of the spine developing after a multiple level laminectomy. Two types of deformity were recognized on the roentgenograms: increased mobility between the vertebral bodies and wedging deformity of the ventral aspect of the vertebral bodies. Second, we did a follow-up study of another group of patients who had undergone laminectomy. We found the same two types of deformity in children, but not in adult patients. The incidence of deformity was higher after laminectomies of the cervical or cervicothoracic region than after lumbar laminectomies. Our data suggest that postlaminectomy spinal deformity can develop in children without irradiation or facet injury. The deformity is due to a wedging change in the cartilaginous portion of the vertebral body and to the viscoelasticity of ligaments in children. When treatment of this complication becomes necessary, anterior fusion may be effective in arresting progression. Prophylactic measures against the development of deformity are discussed. Our hypothesis concerning the mechanism of development of this complication supports the rationale of osteoplastic laminar resection and reconstruction instead of laminectomy, particularly in the management of children.

AbstractSuccessful therapy for pituitary apoplexy depends on prompt recognition of the clinical syndrome, accurate anatomic evaluation of the lesion with the CT scan, intensive steroid replacement therapy, and effective transphenoidal decompression of the tumor. Successful long‐term management of patients who have suffered pituitary apoplexy requires recognition by the complex interrelationships of the pituitary with adrenal, thyroid, gonadal, pancreatic, and gut physiology. Such patients often require multiple medications for replacement therapy. Surgical treatment is often supplemented with radiation therapy, and prolactin‐ and growth hormone‐secreting adenomas may require long‐term management with bromocriptine. Careful follow‐up evaluations and appropriate post‐surgical therapy enable most of these patients to live normal lives.

ABSTRACT OBJECTIVE To determine the clinical presentation, imaging characteristics, microscopic and ultrastructural characteristics, and treatment outcomes of patients with clinically silent pituitary corticotroph adenomas. METHODS All silent corticotroph adenomas diagnosed at the Mayo Clinic during the years 1975 through 1997 were selected from the files of the Mayo Tissue Registry. RESULTS We studied 23 cases, occurring in 16 male and 7 female patients (age range, 11–79 yr; mean age, 48 yr), who presented with headaches (50%), visual field defects (61%), extraocular muscle paresis (13%), hypopituitarism (26%), and galactorrhea/amenorrhea (43%/29% of the female patients). No patients exhibited clinical hypercortisolism. All tumors were macroadenomas (2.4 ± 0.8 cm; range, 1.5–4.0 cm) and exhibited suprasellar extension in 87% of the cases and hemorrhage, necrosis, and/or cystic changes in 61%. All tumors stained were variably periodic acid-Schiff-, adrenocorticotropic hormone-, and β-endorphin-positive, particularly Subtype I lesions. Ultrastructural classification was performed in 19 cases. In a comparison of Subtype I and II tumors, differences were observed with respect to sex (male/female, 1.4:1 versus 6:1), preoperative hyperprolactinemia (5 of 16 versus 0 of 6 cases), preoperative hypopituitarism (9 of 16 versus 5 of 7 cases), radiographic or gross invasion (7 of 16 versus 5 of 7 cases), and partial or total postoperative pituitary failure (6 of 16 versus 6 of 6 cases). The overall median postoperative follow-up period was 4.9 years (range, 0.3–16.6 yr); 54% of the patients had persistent or recurrent tumors. CONCLUSION Clinically silent corticotroph adenomas behave in an aggressive manner and are characterized by the following: lack of clinical signs or symptoms of Cushing's syndrome and normal cortisol levels; no or only minor elevations of serum adrenocorticotropic hormone levels; macroadenomas with hemorrhagic infarction; and presentation dominated by mass effect symptoms. The high persistence/recurrence rate underscores the need for long-term follow-up.