Next to the peripheral nerve degenerations, to be later considered, the most important lesions are found in connection with the heart. All chambers of the heart show a dilatation with hypertrophy as well as dilatation of the right ventricle in cases that have lasted for some time. The heart muscle has the faded-leaf appearance indicative of fatty degeneration. Microscopically there are segmentation and vacuolation of the fibres. The lungs show congestion and at times present the characteristics of pulmonary oedema. The kidneys are congested but show only exceptionally parenchymatous or interstitial changes. As would be expected, the back pressure in the right heart gives a dilatation of the central vein of the liver lobules which at times is productive of atrophy of the adjacent liver cells. The muscles supplied by the affected peripheral nerves show more or less atrophy according to the duration of the disease. Microscopically, the affected fibres show a loss of striation with a colloid degeneration. These changes are more marked in beriberic residual paralysis. The key to the disease is in the changes present in the peripheral nerves. While these may appear normal yet histological examination shows varying nerve degenerations from slight medullary degeneration in a few fibres to complete destruction of the nerve, giving a Wallerian degeneration (vacuolation and formation of myelin droplets in the medullary sheath with fragmentation of the axis-cylinder). While it is usually stated that the central nervous system (brain and cord), remains uninvolved yet we note axonal degeneration in the cells of the nuclear centres of the affected peripheral nerves as shown by convexity of the cell sides, dislocation of the nucleus and disappearance of the tigroid substance. The striking feature of the pathology of beriberi is the involvement of the vagus nerve and there is evidence of degenerative changes in the cells of the vagal origin in the floor of the fourth ventricle. Various investigators have shown that in fowls marked peripheral neuritis can exist long before clinical manifestations appear and that typical cases of beriberi may show striking improvement following vitamine administration, notwithstanding the continued existence of peripheral nerve degeneration. For such reasons Vedder thinks the more important changes to probably belong to cells of cord and brain. McCarrison has noted striking changes in the endocrine glands in avian polyneuritis, particularly hypertrophy of the adrenals and atrophy of the other glands of internal secretion. He attributes the oedema to increase in adrenalin content. Shimbo has reported adrenal hypertrophy in 14 human cases of beriberi. SYMPTOMATOLOGY