Meningeal and intracranial vascular lesions were observed in two cases of rheumatoid arthritis. Granulomas of the meninges were present and histologically identical with subcutaneous rheumatoid nodules. Arteritis similar to that occasionally seen in systemic rheumatoid disease was found in all types of intracranial vessels.
Lesiones vascular meningee e intracranial esseva observate in duo casos de arthritis rheumatoide. Granulomas del meninges esseva presente e histologicamente identic con subcutanee nodulos rheumatoide. Arteritis simile a ill0 incontrate a vices in systemic morbo rheumatoide esseva observate in omne typos de vaso intracranial.
HE EXTRA-ARTICULAR mesenchymal lesions associated with rheuma-T toid arthritis have been studied extensively. Sinclair and Cruikshank' suggested that the term rheumatoid arthritis should be reserved for nonspecific inflammatory lesions confined to joints, and that cases in which other tissues are involved should be called rheumatoid disease.
Cruikshank2 undertook an extensive study of the rheumatoid lesions in skeletal muscles and peripheral nerves, and Hart et al.3 studied the neuropathy of rheumatoid disease in detail.
Bauer and Clark,4 in reviewing the central nervous systems of 44 patients with rheumatoid arthritis, found no specific lesions in the brain or spinal cord. Alterations attributable to aging were more pronounced in arthritics than in a control group of similar age distribution. Two reports of rheumatoid lesions of the dura mater appeared in 1954. Ellman et al.5 described, in their case of systemic rheumatoid disease, chronic inflammatory changes of the cranial aspect of the pachymeninges with formation of rheumatoid nodules. Maher6 presented a case of rheumatoid nodules of the dura. In neither instance was there any evidence of leptomeningeal or cerebral involvement.
The following cases illustrate various aspects of rheumatoid lesions in dura, leptomeninges and intracranial vessels.
CASE REPORTS
Case I.-Mr. G. M., a 32 year old man developed rheumatoid arthritis at the age of 16. The condition was rapidly progressive and over the next 3 years he became bedridden with -evere deformities of his peripheral joints. His disease then became quiescent for 13 years. Treatment during this time consisted of aspirin, physiotherapy, various orthop-dic procedures and gold injections (discontinued because of dermatitis). In 1955 he was started on cortisone. One year following this, while the dosage of cortisone was being reduced, his disease flared up with the development of subcutaneous nodules and cardisc signs, namely sinus tachycardia, bundle branch block and a systolic murmur. He was admitted to the Toronto General Hospital in January, 1957, with symptoms of tlysphagia and constipation.