The lesions of the nervous system in the Trypanosomiasis Cruzi are quite frequent and are not only limited to the encephalo-spinal-axis. Actually, they are much more common in the peripheral representations of the autonomic nervous system, resulting in the so-called enteromegalies (mega-esophagus, megacolon, etc.) so frequent in Brazil. However, only the clinical manifestations due to the encephalic and spinal lesions have been included in the neurological aspects of Chagas' disease (as formerly contended for by Carlos Chagas). In the acute phase of the central nervous system infestation, the Trypanosoma cruzi,as leishmanias, is found in cellular elements of the neuroglia (microglia, astroglia) and may be isolated from the peripheral blood and cerebrospinal fluid (inoculation in sensitive animals). The corresponding clinical manifestations are the severe difuse meningo-encephalo-myelitis with a high degree of lethality and also signs of infection, hepatomegaly and splenomegaly. The infants from endemic areas are much more compromised. The clinical-pathologic as well as experimental confirmations on that acute phase of the disease are numerous and irrefutable. In the chronic phase of the disease, the neurological manifestations are not very clear. Early in 1909, Chagas, impressed with the great number of cases of infantile encephalopathy found in infested regions, imputed to the T. cruzithe etiology of such cases of encephalopathy and considered them as pertaining to a chronic phase of the disease. This has not been confirmed by other investigations, and even if the etiologic agent were the T. cruzithe clinical manifestations have no evolutive character and seem more sequelae than symptoms of a real chronic nervous phase. Even experimentally it has not been possible to demonstrate the presence of parasites in the nervous system of infested animals after clearing of the signs of the acute phase. In patients with chronic Chagas' disease with lesions in several organs and with nervous symptoms (especially mental disturbances) it has not been possible to get positive results from the complement fixation test (Machado-Guerreiro's reaction) when performed using cerebrospinal fluid, yet this test is positive in about 97% of the cases when blood is used instead. Recently, Köberle and coworkers have shown a great diminution in the number of nerve cells in the intramural plexuses of hollow viscera and in the cerebellum and spinal cord of men and experimental animals with Chagas' disease. It is hoped this approach using neuronal countings will in a near future show which are the true cases of chronic Chagas nervous disease. Regarding the embolic phenomena of Chagas heart disease, they do not have particular symptomatological aspects, except the high degree of mortality. Theoretically, cerebral thrombotic phenomena may also develop under the same etiology, but they have not been demonstrated through a pathological study.