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An intracranial mass thought clinically and by computed tomography and angiography to be a meningioma proved to be an inflammatory pseudotumor. The lesion was composed of sheets of mature plasma cells and lymphocytes with germinal center formation. Immunohistochemical studies revealed a polyclonal cell population, supporting a diagnosis of a reactive lesion rather than a plasma cell neoplasm. Inflammatory pseudotumor should be considered in the differential diagnosis of a sharply demarcated intracranial mass clinically and radiologically diagnosed as meningioma.

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Electron microscopic examination of a solitary soft-tissue tumor from the face demonstrated large areas with abnormal amianthoid collagen fibers in the neoplasm. The lesion was classified as a benign neoplasm of myofibroblasts and tentatively named a myofibroblastoma. The significance of the amianthoid collagen fibers is unknown. Normal native collagen fibers were found in some parts of the neoplasm.

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A pigmented choroid plexus papilloma was found in the left lateral ventricle of a 15-year-old white boy with a 10-year history of seizures. Grossly the lesion appeared finely lobular, orangish brown, rubbery, gritty, and friable. Microscopic examination revealed delicate papillary formations reminiscent of normal choroid plexus, with simple cuboidal to columnar epithelium overlying fibrovascular cores. Light- and electron-microscopic studies demonstrated that the neoplastic cell pigment consisted of both neuromelanin and lipofuscin. To our knowledge, this is the first reported case of neuromelanin pigmentation within a choroid plexus papilloma.

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A severe, generalized myopathy developed in 2 children treated with labetalol. An 11-year-old girl and a 14-year-old boy demonstrated proximal weakness and markedly elevated creatine kinase levels during labetalol therapy. Clinical improvement began immediately when labetalol administration was halted; muscle strength was normal within 2 months. Muscle biopsies were consistent with rhabdomyolysis.

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A case of cervical periosteal chondroma presenting with an enlarged neural foramen is described. Review of the literature showed that cervical chondromas are rare but that their characteristic clinical and computed tomographic findings aid in their diagnosis. The computed tomographic findings of two previously reported cases of cervical periosteal chondroma resembled those of the present case. On computed tomographic scanning, an iso-or high-density mass containing stippled calcifications and originating in a posterior cervical neural arch was observed in all three cases. Extensive spinal canal and extradural involvement was observed in five of the seven reported cases, including the one reported here.

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Electron microscopic examination of a spinal meningioma demonstrated broad zones with large amianthoid collagen fibers in the tumor. Normal native collagen fibrils were found in small scattered clumps particularly around the blood vessels in the tumor. Such abnormal large collagen fibrils have not been seen previously in meningiomas. The significance of the amianthoid fibers is unknown. The only other unusual feature of the tumor was that it had many pale-staining cells by light microscopy and was classified as a clear cell variant of meningioma.

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In a patient with nonketotic hypoglycemia, hyperammonemia, and a urinary organic acid pattern characteristic of glutaric acidemia type II, dysmorphic facial features and kidneys with multiple cortical cysts were the characteristic phenotypic findings. Electron microscopy revealed characteristic cytoplasmic, homogeneous, moderately electron-dense bodies with a limiting membrane. This specific lesion was noted in both central nervous system and renal tissues.

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Clearing of stromal cell nuclei were found in two of a series of nine cases of hemangioblastoma. The contents of the clear zones were often positive for lipoprotein by immunoperoxidase staining which suggested that the contents originated from the cytoplasm. Cytoplasmic invagination was not observed but is probable; some vacuoles had a "bubbly" appearance similar to the lipid-laden cytoplasm. The finding of these variations in two of nine cases suggests that cystic change in stromal cell nuclei may not be uncommon in hemangioblastomas.

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Within the last 18 months, we have noted the development of unexplained lymph node enlargement in otherwise asymptomatic patients with hemophilia. Because such changes are poorly understood and, in some patient groups, may be related to the acquired immunodeficiency syndrome (AIDS), we studied the enlarged lymph nodes in four patients with severe factor VIII deficiency and abnormally low peripheral blood helper-inducer/suppressor cell (OKT4/OKT8) ratios. Surgically excised lymph nodes were studied for histopathologic, electron microscopic, and chromosomal changes. Cell suspensions from these and normal nodes were also studied using monoclonal antibodies. Excised lymph nodes showed follicular hyperplasia. Electron microscopy revealed no viral particles or vesicular rosettes. Chromosomal aberrations included an acrocentric marker chromosome in one patient and monosomy 21 in another. T lymphocyte ratios (OKT4/OKT8) in lymph node suspensions were lower than those in nodes from normal controls (1.2 v 6.1) and reflected the lymphocyte ratio in peripheral blood. Mature B cell percentages were increased in the lymph nodes from patients with hemophilia (38% v 27% in controls). Patients treated with factor VIII concentrates and male homosexuals have similarities in persistent lymph node enlargement, histologic features of follicular hyperplasia, and changes in lymph node and circulating lymphocyte subpopulations.

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A 6-year-old girl with unresectable and metastatic neuroblastoma had a complete remission with irradiation to the primary tumor and systemic administration of cyclophosphamide. The patient was disease-free for 16 years but had an explosive recurrence of tumor six weeks after a hysterectomy. Although no clear cause-and-effect relationship exists between the surgery and the recurrence, this case illustrates that a recurrence is possible after a long disease-free interval. Diagnostic and therapeutic procedures in such patients should be undertaken with caution.

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Six cases of upper intestinal gangliocytic paraganglioma, five in the duodenum and one in the jejunum, are reported. Three histologic patterns, each comparable to patterns in paraganglioma, ganglioneuroma, or carcinoid-islet cell tumor, are mixed in varying proportions. The complex histologic patterns encountered within these tumors reflect the differentiation of pluripotent cells. Although the parent cell is not identified in this study, gangliocytic paragangliomas may arise from cells which normally reside in the mucosal crypts and are presumably derived from cells originating in the neural crest. Three of the six tumors contain stromal amyloid. In one case, studied by electron microscopy, dense-cored cytoplasmic vesicles almost fill some of the tumor cells. Gangliocytic paragangliomas share the features of stromal amyloid and dense-cored vesicles with other neurocrine tumors.

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The stages in the development of the Mikulicz cell in human rhinoscleroma were studied in biopsy specimens obtained from 10 patients using light, immunofluorescent and electron microscopy. The Mikulicz cell was identified morphologically as a macrophage, not a plasma cell. Acutely inflamed areas of rhinoscleroma presented abundant bacteria with a slime layer. The microorganism was infrequent and the mucopolysaccharide was scanty in rhinoscleromal tissue, where plasma cells predominated, and in cicatricial fibrous tissue. In the granulomatous stage of rhinoscleroma, the mucopolysaccharide was found within the Mikulicz cells. The vacuoles observed in the Mikulicz cells were considered to be phagosomes containing, principally, bacterial mucopolysaccharide and few bacteria and, to a lesser extent, swollen mitochondria. It was concluded that the slime layer of Klebsiella rhinoscleromatis plays an important role in the pathogenesis of the disease. It is postulated that this material is a nondigestible mucopolysaccharide that resides in the phagosomes of macrophages, increases the osmotic pressure and forms multiple hydropic vacuoles that rupture not only the phagosomes but also the cells, resulting in the liberation of the mucopolysaccharide. This would initiate a cycle that would prolong the disease in the absence of the bacteria.

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