IT IS GENERALLY accepted that Sydenham's chorea, or chorea minor, is a manifestation of rheumatic fever. It was only logical, therefore, that McCulloch1 (1938) should use the term "encephalitis rheumatica" for Sydenham's chorea, as had been done before him by Poynton and Paine 2 and by Greenfield.8 Greenfield studied the pathologic features of chorea minor in patients who died during the acute stage of the illness. He observed round cell infiltration, consisting of lymphocytes and plasma cells, within the perivascular spaces. More impressive, however, than the infiltration of elements of the blood was the glial reaction of the brain tissue around the perivascular spaces. Sometimes there was present only this spotty glial reaction, which resembles that seen in poliomyelitis and von Economo's (lethargic) encephalitis. There was a great increase in vascularity, with congestion of the capillaries and even subpial hemorrhages. Greenfield expressed the belief that the picture resembled the acute stage of encephalitis lethargica. In less severe cases the involvement of the brain is not so damaging, and McCulloch pointed out that acute rheumatic encephalitis is one of the exudative manifestations of rheumatic fever, rather than a proliferative one. In less severe cases no structural change of the type of rheumatic nodules or scars were observed in the brain. This is prob¬ ably the reason that chorea is commonly not followed by permanent paralysis, weakness or other neurologic alteration. McCulloch sug¬ gested, therefore, that the encephalitis of rheumatic fever is similar in its anatomic process to the arthritis, the acute pericarditis and the myocardial changes of an acute attack of rheumatic fever. The first changes