Metastases are the most common brain tumors especially in adults. Although they are generally considered a single disease entity which is universally fatal in patients with advanced cancer, brain metastases are remarkably heterogeneous both clinically and pathologically. As members of the multidisciplinary clinical team for the diagnosis and management of metastatic brain tumors, pathologists must be familiar not only with clinicopathologic features of brain metastases but also with any characteristic and clinically significant molecular findings. We discuss here the epidemiology, general gross and microscopic features of brain metastases with emphasis on how to differentiate them from primary brain tumors using immunohistochemistry (e.g., for identification of the primary site and differential diagnosis), and unique pathologic patterns of brain metastases (namely, dural metastasis, leptomeningeal carcinomatosis, miliary metastasis, ‘‘intravascular carcinomatosis’’, and tumor-to-tumor metastasis) with their clinical and radiological characteristics. We specifically address metastatic breast and non-small cell lung cancers which are the two most commonly encountered in daily practice, with emphasis on the molecular alterations related to therapy and their clinicopathologic significance.

Graft-versus-host disease (GVHD) classically involves the skin, intestines, liver, esophagus, and tongue. clinically apparent disease involving the heart, lungs, kidneys, and central nervous system (CNS) is frequently secondary to other complicating factors. This report describes a case of an infant with severe combined immune deficiency (SCID) who developed unusual manifestations of GVHD following a bone marrow transplant (BMT). These were complete heart block and respiratory insufficiency in the absence of significant pulmonary disease. He lived 133 days post-transplantation. At autopsy, the brain showed focal lymphohistiocytic aggregates which may represent a hitherto unreported lesion of GVHD.

Previous imaging studies in infants with globoid cell leukodystrophy (GLD) using computed tomography have demonstrated a reduction in cerebral white matter and increased density symmetrically in the regions of the thalami, periventricular white matter, and the internal capsules. Correlation of these findings with morphologic studies at necropsy has not been made. In particular, deposition of calcium has not been described. We have evaluated two children with GLD confirmed by the absence of leukocyte galactosylceramide beta-galactosidase activity using repeated magnetic resonance (MR) scans in each and correlated the imaging results with post-mortem analyses in one. Neuropathologic examination revealed abnormalities typical for GLD. In addition to the absence of normal myelination throughout cerebral and cerebellar white matter, MR images demonstrated the presence of a paramagnetic effect in the regions of the thalami, corona radiata, and centra semiovale. We have observed in histologic preparations from these areas a dense accumulation of globoid cells and some calcium, which we suggest may be responsible for producing the paramagnetic effect.

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Cerebral sinus thrombosis has been reported as an uncommon complication of ulcerative colitis (UC), occurring in up to 7.5% of cases. It is suspected to be a consequence of genetic predisposition and the hypercoagulable state occurring during disease relapse. We report a case of a 23-year-old male patient with one-year history of UC. He presented to the Emergency Room with left-sided progressive hemiparesis, numbness, hemiparesthesia, and pain, which followed a recent exacerbation of UC. The patient died 3 days after admission and an autopsy revealed superior and inferior sagittal sinus and cortical vein thrombosis with associated cerebral edema, hemorrhagic infarction, and herniation. The gastrointestinal tract had continuous cobblestone appearance extending from rectum to cecum, with hemorrhage and ulceration, consistent with active UC. Awareness of this rare complication of UC can contribute to early recognition and attempts at treatment of this serious and often fatal condition.

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Congenital arachnoid cysts (CAC) are benign developmental disorders. A number of theories have been proposed to explain the origin and progression to the symptomatic stage. Management strategies range from not treating the asymptomatic cysts to craniotomy, excision of cyst wall and establishment of a communication with the adjacent subarachnoid cistern or ventricle. Other lesions may resemble CAC, and can be differentiated from CAC only by a critical review of the biopsy specimen. We have reviewed our experience with true CAC and similar lesions. Based on our experience we recommend craniotomy, excision of cyst wall and establishment of a communication with an adjacent subarachnoid cistern or ventricle as the primary procedure.