Another who saw the disease in Algeria and described the symptoms found in ten cases observed that they came on suddenly, in damp weather, with some pains in the loins, trembling, motor paralysis and exaggerated reflexes. He attributed these phenomena to an acute transverse myelitis with degenerative changes in the cord. A German writer states that the drug produces disturbances of nutrition of the muscles of the lower extremities, paresis, and that the muscles of the trunk and neck and face remain unaffected. Sensation remains normal. It seems to produce a sclerosis of the pyramidal tracts of the cord. In animals the same condition is found; namely, paralysis of the hind legs. Pigs drag their hind legs and horses give out. AGGRAVATED SYMPTOMATOLOGY. From all the sources which I have been able to find, the following seem to be the symptoms caused by the drug: Sudden loss of power in the lower extremities, from the waist down. Tremulous, tottering gait. Great exaggeration of the reflexes. Stiffness and lameness of the ankles and knees. Excessive rigidity of the legs; flexion difficult; spastic gait, the legs becoming interlocked, and walking is difficult or impossible. Sudden onset of the trouble, and apparent aggravation in cold and damp weather. Emaciation of the gluteal muscles also observed. Those having taken it walked on the metatarso-phalangeal articulation, the heel not touching the ground. Impossible to stand steady; swayed from side to side, but closing the eyes had no effect. This with the exaggerated reflexes would exclude its use in locomotor ataxia. Debility and tremors of the legs. Rigidity of the adductors of the thighs. Staggering gait, with eyes fixed on the floor. Could not extend or cross the legs when sitting. Sensibility unimpaired. CORRESPONDENCE TO SPINAL DISORDERS. From these symptoms it will be seen that the effects of the drug correspond to many spinal symptoms, but more especially to what is known as spastic paraplegia. Indeed, Struempel asserts that it produces a perfect picture of this disease. It is not so often that such a perfect picture of a disease can be had as in this instance. The disease itself is easily recognized by the stiff, spastic gait; the spasm of the adductors, causing the knees to strike each other, or to become locked, causing the patient to fall; the shuffling of the feet; the excessive muscular rigidity and the other well-known symptoms of paraplegia. Therefore, reasoning from our law we would expect the drug to be of service in such cases, and although our pathogenesis of it is coarse we may be permitted to apply it to a disease whose symptomatology is of the coarse order; for it is often difficult to elicit any fine and characteristic symptoms in diseases like ataxic and spastic paraplegia.