A 70-year-old man who suffered from osmotic demyelination syndrome (ODS) is presented. Dyspnea, pseudobulbar palsy and motor weakness were seen. MRI in the acute stage revealed focal abnormal high-signal lesions in the pons, thalamus and bilateral cortical areas on Tl-weighted and FLAIR images. With corticosteroid therapy he recovered from his dyspnea and severe pseudobulbar palsy, and the spastic quadriplegia gradually improved. One year later the brain lesions had disappeared on T1-, T2-weighted and FLAIR images. To detect the cortical or subcortical lesions in ODS, FLAIR imaging should be performed routinely. (Internal Medicine 42: 867-870, 2003)

A 55-year-old man suffered from nasal obstruction, swelling of the salivary glands, and diplopia caused by markedly enlarged lacrimal glands. The diagnosis of primary Sjogren's syndromewas madeby a positive Schirmer's test and nasal mucosal biopsy with severe lymphocyte infiltration. He was also found to have swelling of the whole pancreas and increased wall thickness in the commonbile duct and the gall bladder. His serum was positive for an anticarbonic anhydrase II antibody. Since carbonic anhydrase II is present in the ductal cells of various exocrine organs, this autoantibody is considered to be related to the pathogenesis of primary Sjogren's syndrome with a marked swelling of multiple exocrine organs. (Internal Medicine 41 : 749-753, 2002)

A 74-year-old man developed fever, somnolence, hyponatremia, and life-threatening sinus bradycardia for three weeks. He showed a slight elevation of lymphocyte count and protein level in the cerebrospinal fluid. A brain CT scan revealed a diffuse low density area around the hypothalamus which was identified as a high intensity signal by flair MR imaging. Marked sinus bradycardia developed with no abnormality in the echocardiograph or cardiac enzymes. Over the next 6 weeks he became alert and normal sinus rhythm resumed. The results of endocrine tests were compatible with hypothalamic insufficiency with partial hypopituitarism and the syndrome of inappropriate secretion of ADH. (Internal Medicine 40: 805-807, 2001)