The neuropathology of rheumatoid disease

Abstract

Patients with active rheumatoid disease may develop encephalopathy, myelopathy, peripheral neuropathy, and myopathy through a variety of tissue mechanisms. Brain involvement is usually characterized by the formation of rheumatoid nodules or by the development of vasculitis or its complications, and there is evidence to suggest that the trapping of immune complexes within the choroid plexus may be important in pathogenesis. Structural damage to the spinal cord and lower brain stem, on the other hand, most commonly results from narrowing of the bony canal, leading either to direct compression of neural tissue or to compromise of its vascular supply. The appearance of peripheral neuropathy generally signifies the presence either of inflammatory epineurial arterial disease or entrapment by neighboring anatomical structures. Skeletal muscle dysfunction may be due to vasculitis, myositis, or denervation atrophy. Both systemic and local anatomical factors, therefore, are of importance in determining the manner in which different parts of the nervous system may be affected in rheumatoid disease.