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T-cell large granular lymphocyte leukemia (T-LGLL) is a T-cell lymphoproliferative disorder that has recently been associated with B-cell dyscrasias on a spectrum ranging from dysgammaglobulinemia to lymphoma. To investigate the relationship between clonal B-cell and LGLL lymphoproliferations, we systematically studied lymphocytes in 57 patients with T-LGLL or NK lymphocytosis using flow cytometric methods sensitive to low-level B-cell populations. We identified 16 patients (28%) with abnormal B-cell populations; 9 (16%) of the patients had no known history of a B-cell lymphoproliferative disorder. We characterized these abnormal B-cell populations as monoclonal B-cell lymphocytosis and report a high frequency of monoclonal B-cell lymphocytosis in T/NK LGLL. Our findings suggest that certain pathologic factors may operate in patients with T/NK LGLL to drive low-level clonal B-cell proliferations. [ABSTRACT FROM AUTHOR]

Follicular lymphoma (FL) involving the spleen must be distinguished from reactive hyperplasia and from other lymphomas. A prior study reported that splenic FLs frequently lack BCL2 expression, further complicating diagnosis. We examined 16 cases of splenic FL, including 12 cases initially diagnosed at splenectomy. Two morphologic patterns were identified: one with architectural abnormalities (AA) and one with an extensive architectural preservation (AP) pattern. Newly diagnosed AP cases were associated with older age (P = .051) and grade 1 histologic features (P = .023). All cases displayed a CD10+/BCL2+ phenotype. Cytogenetics and FISH identified IGH/BCL2 or BCL6 translocations in all tested cases. Splenic FLs display phenotypic and cytogenetic findings similar to nodal FLs. However, splenic FLs frequently display an exclusively intrafollicular growth pattern resembling so-called in situ FL. Recognition of subtle FL with preserved architecture is important because patients may have overt FL at other sites or the FL may progress to overt nodal disease. [ABSTRACT FROM AUTHOR]

Temporopolar cortex plays a crucial role in the pathogenesis of temporal lobe epilepsy and subserves important cognitive functions. Because of its shape and position in the middle cranial fossa, complete electrode coverage of the temporal pole (TP) is difficult to achieve using existing devices. We designed a novel TP electrode array that conforms to the surface of temporopolar cortex and achieves dense electrode coverage of this important brain region. A multi-pronged electrode array was designed that can be placed over the surface of the TP using a straightforward insertion technique. Twelve patients with medically intractable epilepsy were implanted with the TP electrode array for purposes of seizure localization. Select patients underwent cognitive mapping by electrocorticographic (ECoG) recording from the TP during a naming task. Use of the array resulted in excellent TP electrode coverage in all patients. High quality ECoG data were consistently obtained for purposes of delineating seizure activity and functional mapping. During a naming task, significant increases in ECoG power were observed within localized subregions of the TP. One patient developed a transient neurological deficit thought to be related to the mass effect of multiple intracranial recording arrays, including the TP array. This deficit resolved following removal of all electrodes. The TP electrode array overcomes limitations of existing devices and enables clinicians and researchers to obtain optimal multi-site recordings from this important brain region. [ABSTRACT FROM AUTHOR]