Rheumatic Brain Disease as a Cause of Convulsions

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THE classical symptoms of acute rheumatic fever have been recognized for many years, but the other manifestations of this protean process were long interpreted as simply sequelae of the acute infection. It is now universally agreed that the endocardium harbors primary lesions,22 but it is not so commonly realized that the brain may be similarly affected. Certainly the details of the etiology of rheumatic fever are not yet understood. It does appear, however, that the disease is basically an inflammatory condition of fibrous connective tissue. As such the brain cannot be excluded as a potential site. Indeed, rheumatic lesions have been found in lungs,2,28 kidneys,10,24 spleen, ovaries,24 testes,24 pancreas,24 coronary arteries,12,15 in peripheral arteries24 and in the brain.

Many theories of the pathogenesis of brain complications have been proposed; most have assumed that the lesions were secondary to rheumatic heart disease. Some investigators have said that cardiac valvular lesions brought on circulatory changes in the brain causing stasis and ischemia. Evidence against this theory is the fact that the majority of patients with rheumatic brain disease, including those presented here have no history of congestive heart failure. It has also been conjectured that minute emboli may detach from rheumatic vegetations and lodge in vessels of the brain, but the cohesive properties of these vegetations speak against this mechanism. It is true, in patients with mitral stenosis and auricular fibrillation, mural thrombi may beget emboli, but pathologists deny that such emboli form foci for the endarteritic changes which characterize rheumatic brain. . .



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