Primary central nervous system lymphoma initially mimicking lymphomatosis cerebri: an autopsy case report.

A 59-year-old immunocompetent man was admitted to our hospital because of progressive dementia with concomitant bilateral uveitis. The first brain MRI revealed diffuse hyperintense lesions in the cerebral white matter of both hemispheres on a T2-weighted image and fluid-attenuated inversion recovery image. However, another MRI taken more than 1 month later revealed enhanced cohesive mass lesions in the bilateral thalami, in addition to the white matter lesions. The white matter lesions were slightly hyperintense on a diffusion-weighted image and apparent diffusion coefficient map image, suggesting vasogenic edema. One year after the onset of uveitis, he died of respiratory failure. Pathological diagnosis was diffuse large B-cell lymphoma with perivascular proliferation and diffuse scattered infiltration in the cerebrum and brainstem. Microscopically, cohesive mass lesions in the bilateral thalami were a massive cluster of lymphoma cells. This is a case of primary CNS lymphoma (PCNSL) mimicking 'lymphomatosis cerebri (LC)' at first but later exhibiting typical mass lesions, giving rise to the possibility that cases of LC might unmask features of regular lymphomas in their later course more often than believed thus far.

[Syndrome of inappropriate secretion of anti-diuretic hormone associated with limbic encephalitis due to herpes simplex virus infection--a case report].

We report a case of syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) associated with limbic encephalitis. A 79-year-old woman was admitted with a complaint of fever, disturbance of consciousness and generalized seizure. Her conscious level was E1V2M4 by Glasgow coma scale. Physical examination showed generalized seizure, neck stiffness, hyperreflexia and flaccid paralysis in her all extremities, and pathological reflexes. Blood analysis revealed hyponatremia, decrease of plasma osmolarity, spared secretion of urine sodium and increase of ADH, leading to the diagnosis of SIADH. Cerebrosponal fluid examination showed mild pleocytosis, elevated protein, and normal glucose level. Although herpes simplex virus (HSV) DNA was not detected by the polymerase chain reaction method, titers of anti-HSV IgG antibody elevated chronologically. Brain MRI revealed abnormal T2 and FLAIR high intensities in the cingulate gyrus and hippocampus bilaterally. An EEG revealed periodic synchronous discharges predominantly in the frontal areas. Based on the clinical course, laboratory data, MRI and EEG findings, we diagnosed as SIADH associated with acute limbic encephalitis caused by HSV infection. After the fluid restriction and sodium supply, plasma sodium was normalized. Administration of acyclovir and steroid was not so effective, however her condition improved gradually. Several cases of SIADH associated with limbic encephalitis have been reported; however, the pathophysiology is to be clarified. We thought that in the presented case, SIADH was caused by disturbance of the hormonal control at the hypothalamus on the pituitary gland due to the spreading of inflammation from limbic system to these areas.