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• 7 blood vessels in healthy areas too often were much diseased (Bastionelli, Russell, Batten, and Collier, Jacob, Moxter, Vori Voss, Putna,m and Taylor). It was likewise sho\vn that in a great many cases there was no evidence, whatever, of hemorrhage (Russell, Batten, and Collier). • Relative to the lymph stasis theory, Lene! suggests that the swelling seen in the adventitial tissue may be only a stage in the "Abbauvorgang," and thus a result, rather than a cause, of the ner\'e lesions. An entirely different explanation is advanced by Rothmann, who found hemorrhages, atrophy, and destruction of the anterior horn cells in the gray matter. These, he argues, as does Teichmueller, are the changes which initiate the cycle of disintegration, while the alterations seen in the white matter are due simply to a resulting secondary degeneration. Ile insi sts further, that although these lesions are not always demon trable micro copically, the injury is there nevertheless, and the mechanism the same. Goebel, on the other hand, though he also demonstrated changes in the gray matter, refute thi idea by saying that the changes in the gray matter are often mis ing, that the inten ity and the localization of these changes do not correspond with tho e found in the white columns, and that in longitudinal section , the commi sural fibers are found to be intact. Additional evidence was supplied by Bastionelli, who noted that the white fibers were diseased only in the peripheral portion of the cord and that the gray matter, for this reason, could not be the primary seat of the degeneration. On account of the evidences of inflammation sometimes observed, and the occa ional febrile course, it is thought by ome (Boedeke and J uliusberger) that the process taking place here i really a true myelitis of the dis eminated type. This, N onne thinks, is also true of sepsis and senility. The fact, however, that inflammatory reaction, such as cell infiltration, is too often lacking, and that the gray matter is only exceptionally involved (Billings) argue against this view. Edinger, in support of his "Ersatztheorie" performed an experiment which has a direct bearing on the point under consideration. In the spinal cords of a number of rats, in which he produced an anemia, and which he then set to work by the ingenious device of suspending them by their tails, he found exlen ive degenerative changes, while in the cords of control rats, which were not anemic, no such changes could be detected. Finally, Dana has emphasized two other factors, which may be at work in this di ea e and which may be in trumental, first, in determining the characteri tic localization, and, second, in deciding which patients are to get a combined clero i , and which are to remain
• 7 blood vessels in healthy areas too often were much diseased (Bastionelli, Russell, Batten, and Collier, Jacob, Moxter, Vori Voss, Putna,m and Taylor). It was likewise sho\vn that in a great many cases there was no evidence, whatever, of hemorrhage (Russell, Batten, and Collier). • Relative to the lymph stasis theory, Lene! suggests that the swelling seen in the adventitial tissue may be only a stage in the "Abbauvorgang," and thus a result, rather than a cause, of the ner\'e lesions. An entirely different explanation is advanced by Rothmann, who found hemorrhages, atrophy, and destruction of the anterior horn cells in the gray matter. These, he argues, as does Teichmueller, are the changes which initiate the cycle of disintegration, while the alterations seen in the white matter are due simply to a resulting secondary degeneration. Ile insi sts further, that although these lesions are not always demon trable micro copically, the injury is there nevertheless, and the mechanism the same. Goebel, on the other hand, though he also demonstrated changes in the gray matter, refute thi idea by saying that the changes in the gray matter are often mis ing, that the inten ity and the localization of these changes do not correspond with tho e found in the white columns, and that in longitudinal section , the commi sural fibers are found to be intact. Additional evidence was supplied by Bastionelli, who noted that the white fibers were diseased only in the peripheral portion of the cord and that the gray matter, for this reason, could not be the primary seat of the degeneration. On account of the evidences of inflammation sometimes observed, and the occa ional febrile course, it is thought by ome (Boedeke and J uliusberger) that the process taking place here i really a true myelitis of the dis eminated type. This, N onne thinks, is also true of sepsis and senility. The fact, however, that inflammatory reaction, such as cell infiltration, is too often lacking, and that the gray matter is only exceptionally involved (Billings) argue against this view. Edinger, in support of his "Ersatztheorie" performed an experiment which has a direct bearing on the point under consideration. In the spinal cords of a number of rats, in which he produced an anemia, and which he then set to work by the ingenious device of suspending them by their tails, he found exlen ive degenerative changes, while in the cords of control rats, which were not anemic, no such changes could be detected. Finally, Dana has emphasized two other factors, which may be at work in this di ea e and which may be in trumental, first, in determining the characteri tic localization, and, second, in deciding which patients are to get a combined clero i , and which are to remain
In the following article we desire to summarize the development of our knowledge of sensory phenomena associated with pernicious anemia and to record the sensory changes encountered in forty-one cases of pernicious anemia studied in the Elliott Memorial Hospital of the University of Minnesota and in the university service of the Minneapolis General Hospital. Nearly all these cases were also studied by the members of Dr. Rowntree's staff in internal medicine and no case appears in our list in which the diagnosis of pernicious anemia was disputed. Most of our cases belong to the Addison-Biermer type of pernicious anemia. HISTORICAL SURVEY Addison 1 (1855), in his original description of pernicious anemia, said nothing of involvement of the nervous system except that he found some fatty degeneration of a portion of the semilunar ganglion of the solar plexus. Biermer 2 (1872) referred to: weakness, giddiness and palpitation and also reported capillary hemorrhages in the brain and the retina. In 1880, Herbert W. Little 3 stated: "The indications of the nervous affection in this disease are: frequent cephalalgia, vertigo, syncope, neuralgic pains, dyspepsia, vomiting, diarrhea, mental depression, mus¬ cular weakness, pallor of the skin, reduction or rise of temperature." The author thought the nervous system the primary seat of trouble and involvement of the vasomotor system important.
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