Minor salivary gland inflammation in Devic's disease and longitudinally extensive myelitis.

Devic's disease is often considered as a variant of multiple sclerosis (MS). However, evidence suggests that Devic's disease may be distinct from MS. Devic's disease can coexist with connective tissue diseases, particularly Sjögren's disease, but this association is rare with MS. Diagnosis of Sjögren's disease in patients with neurological symptoms is often difficult. During early stages of Sjögren's disease, patients may not fulfill all criteria for Sjögren's disease. A high percentage of patients with Sjögren's disease have inflammatory infiltrates in minor salivary glands, and this may be a reliable indicator of early or subclinical disease. We show high prevalence (80%) of salivary gland inflammation in Devic's disease and longitudinally extensive transverse myelitis (LETM). We diagnosed 16 patients with Devic's disease, and 2 of these satisfied criteria for Sjögren's disease as did 2 of 9 patients with LETM. Anti-SSA/B titers were infrequently elevated. Although most did not satisfy criteria for Sjögren's disease. 9 of 12 Devic's disease patients and 7 of 8 LETM patients had severe salivary gland inflammation. Thus: (1) patients with Devic's disease or with LETM who have positive labial biopsies but do not satisfy criteria for Sjögren's disease could have subclinical Sjögren's diseases. Alternatively, (2) as patients with Devic's disease have elevated titers of several autoantibodies, so there may exist a set of antibodies that react with antigens in minor salivary glands and cause inflammation. Minor salivary gland biopsy is more sensitive than anti-SSA/B serology in providing histological evidence for possible Sjögren's disease with CNS lesions.

Vascular and Alzheimer-type pathology in an autopsy study of African-Americans.

The authors studied 13 autopsy brains from a larger cohort of 270 African-Americans with a clinical diagnosis of Alzheimer disease (AD), vascular dementia (VaD), or stroke without dementia. Two subjects exhibited changes of pure VaD, 5 had pure AD, and 6 showed a mixture of AD pathology and strokes. Overall, there was good agreement between the pathologic diagnoses and the clinical diagnoses.

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with hypertrophic spinal radiculopathy mimicking neurofibromatosis.

This report illustrates a case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) masquerading as neurofibromatosis due to multifocal enlargements of spinal nerve roots. The patient initially complained of intermittent numbness of the hands and leg weakness at age 62. Nerve conduction velocities were reported to be abnormally slow, suggesting a diagnosis of demyelinating neuropathy. A complaint of progressive lower back pain 4 years later prompted a lumbar CT myelogram, which demonstrated bilateral nerve root enlargements. A biopsy of an enlarged lumbar root obtained during decompressive laminectomy was interpreted as consistent with a plexiform neurofibroma. He suffered recurrent paraparesis, at times with a sensory level indicating spinal cord compression, which responded to corticosteroid therapy. An autopsy 15 years after the onset of symptoms revealed hypertrophic radiculopathy and peripheral neuropathy due to CIDP with no evidence of neurofibromatosis. This case illustrates how the hypertrophic neuropathy accompanying CIDP can be mistaken for neurofibromatosis.

Crystal and molecular structure of a new cobalt complex of quinine.

A new cobalt complex of quinine, C20H25Cl3CoN2O2, was obtained from a mixture of saturated alcohol solutions of CoCl2 6H2O and quinine. The X-ray structure analysis of a single crystal revealed that the complex is a zwitterion in which the positive charge is localised on the protonated nitrogen atom, N1, of the quinuclidine fragment and the negative charge is shared by the three chlorine atoms. The cobalt atom coordinates the chlorines and the nitrogen atom, N13, of the quinoline fragment. Each chlorine atom is engaged in intermolecular hydrogen bonds. One of them is an acceptor of the proton of the hydroxyl group, while the two others share the proton of the quinuclidine nitrogen atom, N1, in a bifurcated hydrogen bond. Quinine has open conformation typical for Cinchona alkaloids forming intermolecular hydrogen bonds in the crystalline state.