_Beriberic Residual Paralysis._—Hamilton Wright has used the term beriberic residual paralysis to indicate cases which, in the course of convalescence and favorable regeneration of axis-cylinders and more or less return to a normal condition, become subject to some factor lowering the vital forces and body resistance and experience a return of the beriberi manifestations. To use a common expression the patient has a set-back and the favorable progress to complete recovery is temporarily in abeyance. Symptoms in Detail _Nervous Symptoms._—The most common symptoms are those connected with degenerations involving the peripheral nerves of the extremities. The motor nerves are more involved than the sensory ones, there being rarely complete anaesthesia, but rather a blunting of sensation as though a piece of cloth were interposed between the examining instrument and the skin. At first there is weakening of the muscle power as shown by the grip of the hand or weakness of foot muscles. In more advanced cases we may have foot and wrist-drop. Hyperaesthesia of the muscles is prominent, especially that of the calf muscles. The unsteadiness of gait is not true ataxia as the patient does not clearly show the Romberg sign. It is muscular weakness rather than incoördination. The Argyll-Robertson pupil is absent. The gait is the steppage one of peripheral neuritis, the patient walking as if extracting one foot after the other from clinging mud. Later on, when other muscles than the foot extensors are involved, the gait becomes a shuffling one. The mind is entirely clear. The vasomotor phenomena are often marked as shown by patchy or most extensive development of oedema and serous exudates. The knee-jerk is usually absent. Fibrillary twitchings may be observed in beriberi as well as in progressive muscular atrophy. The extensors of arms and legs are more markedly affected than the flexors. The cardiac symptoms are really connected with vagal involvement. _The Cardio-respiratory Symptoms._—Owing to involvement of the vagus the inhibitory apparatus is deranged so that we have palpitation and rapid pulse rate both of which are markedly increased by the slightest exertion. The blood pressure is below normal. Shortness of breath is the earliest feature of respiratory trouble. This may go on to marked thoracic oppression and dyspnoea. Aphonia may be present in acute pernicious beriberi and probably indicates laryngeal palsies. Such cases are usually fatal. Pulmonary congestion and oedema always accompany the terminal right side dilatation of the heart which is responsible for the cyanosis, pulsating jugulars and various murmurs. The pulmonic second sound is accentuated and may be reduplicated. The rhythm of the heart sounds is replaced by the equal spacing of embryo-cardia. The diaphragm may be paralyzed as may also happen to the intercostal muscles.