154 THE THYROID, THE THYMUS, AND THE ADRENALS. 



and persistent terminal vomiting, as to the gastro-intestinal 

 tract; and glycosuria, albuminuria, acetonuria, excess of urea, 

 as to the general metabolic processes. 4. By the eye-symp- 

 toms: the slow descent of the upper eyelids (von Graefe's 

 sign), due to paresis of the orbicularis; increase of the palpe- 

 bral fissures and infrequent winking (Stellwag's sign), due to 

 muscular paresis plus exophthalmos, ascribable to paresis of the 

 ocular muscles, and reaching sometimes to complete ophthal- 

 moplegia. 5. By the insufficient cardiac stimulation, as shown 

 by the weak, rapid (sometimes 200), and irregular heart- 

 beat, air-hunger, and cyanosis (cardiac dilation with muscular 

 degeneration is usually found post-mortem in such cases). 6. 

 And, finallyj by numerous evidences of impaired nutrition, 

 softness of the bones, atrophy of the uterus, degeneration of 

 the arterial walls, etc., etc. 



It is important to bear in mind, in this connection, how- 

 ever, that the symptoms of suprarenal insufficiency are the 

 result of an excessive supply of thyroid secretion, the supra- 

 renal glands finally lapsing into this condition as they would 

 under the effects of any toxic, through overstimulation and 

 exhaustion of their cerebral centers. As is well known and 

 as herein sustained, a deficiency of thyroid secretion gives rise 

 to another disease: i.e., myxoedema. 



The above list only includes the main symptoms of the 

 disease: i.e., those that emphasize most strikingly the physio- 

 logical and pathological connection between the thyroid and 

 the adrenals. The manner in which all the symptoms of over- 

 stimulation and insufficiency of the adrenals are reproduced 

 seems to clearly show that exophthalmic goiter is the result 

 of an excess of suprarenal secretion, due primarily to increase 

 of thyroid secretion. 



Doubt has been expressed, however, that excessive thy- 

 roid secretion could occur as the only pathogenic factor. Thus, 

 Ord and Mackenzie 11 contend that, "if overactivity or over- 

 secretion of an hypertrophied thyroid gland were the whole 

 disease, it ought to be possible to produce it by administration 

 of large quantities of thyroid gland. No one has yet succeeded 



11 Ord and Mackenzie: Quoted by Godfrey Carter, Edinburgh Medical Journal, 

 Oct., 1899. 



