4 QUATERCENTENARY STUDIES IN PATHOLOGY 



in aggravating the symptoms, and indeed are often associated with their 

 commencement. 



On the other hand, evidence continues to accumulate in favour of the 

 primary implication of the thyroid gland. Mobius (Die Basedow'sche 

 Krankheit, Wien, 1896), Gauthier (Lyon med., 1895, Ixxx., 5-12), Renaiit 

 (Courrier med., Paris, 1895, xlv.), Greenfield (British Med. Journ., 1893, 

 Dec. 9), and Kocher (Mitteil. aus den Grenz. der Med. und Chirurg., 

 1902, Bd. ix., p. i) all support this view. 



Certain pathological alterations are invariably found in the gland, 

 whether the enlargement be evident or slight. The number of glandular 

 elements becomes vastly increased, and the secreting epithelium changes 

 its character. The whole appearance of the gland suggests " a prolifera- 

 tion for the performance of increased function " (Greenfield). The older 

 theory that the goitre was probably due to dilatation of the vessels has 

 not received support from the numerous examinations made of its 

 structure. Of course, with this increase in its tissue, and probable 

 increase in its function, the gland becomes more vascular, still extreme 

 vascularity is rarely an outstanding feature, and hence the enlargement 

 of the gland can in no sense be regarded as due primarily to this cause. 

 Edmunds (" Pathology and Diseases of the Thyroid Gland ") has pointed 

 out that when a portion of the thyroid gland is removed, the remaining 

 part undergoes compensatory hypertrophy. The vesicles enlarge, and 

 tend to become oval or branched ; the lining membrane becomes 

 convoluted ; the secreting cells, instead of maintaining their cubical 

 shape, become columnar. These changes are almost identical with those 

 found in the goitre of Graves' disease, and would certainly appear to point 

 to an increased activity of the organ. With the hyperplasia of glandular 

 tissue there is usually some change in the microscopic characters of the 

 colloid in the vesicles ; it appears to become more mucinoid. According 

 to Greenfield, fibrous overgrowth may ultimately ensue, which, in 

 advanced cases, may spread from the septa into the lobules, and 

 produce e'xtensive atrophy. 



The hyperplasia of glandular tissue and the evidence of increased 

 activity of function suggest the probability that the disease is due to 

 excessive formation of thyroid secretion, and much clinical evidence can 

 be brought forward in favour of this view. The striking contrast between 

 the symptoms of Graves' disease, and those of myxoedema, would lead 



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