DYSTKOPHIA ADIPOSOGENITALIS 903 



incidence of the disease; therefore, from a pathogenetic standpoint the 

 causes may be grouped as neoplastic and aneoplastic. 



There are unquestionably many mild cases formes frustes belong- 

 ing to the second group, which do not present a complete clinical picture 

 of the classical syndrome, but which nevertheless come under the caption 

 of dystrophia adiposogenitalis. Reasoning a priori it is natural to as- 

 sume that the milder manifestations, which depend upon a quantitative 

 functional disturbance, occur relatively much more frequently than the 

 severe manifestations which depend upon an almost completely arrested 

 function. In some of these cases the gland is undersized, being encroached 

 upon by the narrow confines of a pathologically small sella, and roofed 

 in by the enlargement of the clinoid processes. Again others may show 

 a normal sella. In either instance neighborhood symptoms are absent. 

 An example of the latter is Cushing's(6) case of a girl fifteen years of age, 

 weighing 239 pounds (having gained 124 pounds in 14 months), whose 

 chief complaint was headache, obesity, and weakness, with a tendency 

 to amenorrhea and infantile genitalia. There were no neighborhood symp- 

 toms ; the sella was normal, carbohydrate tolerance was increased, thermic 

 reaction was positive, and there were characteristic cutaneous manifesta- 

 tions. 



It is also a well known fact that hypopituitary states frequently occur 

 secondary to functional disorder in the pituitary itself (hyperpituitarism) 

 or are associated with functional insufficiency of other internal secretory 

 glands, especially the thyroid and sex glands, which may be primarily in- 

 volved. Thus, in tracing the cause of hypopituitarism it is necessary 

 to ascertain, if possible, whether the effects were primarily produced on 

 the pituitary or secondarily through the medium of other glands; i.e., 

 thyroid, gonads, thymus, adrenals, etc. This interrelation and inter- 

 action of the glands mentioned led to the designation INSUFFISAXCE PLU- 

 RIGLANDULAIRE by the French authors Claude and Gougerot (1907) ; a 

 clinical condition which has now become generally recognized, and recently 

 much elaborated by Timme(a) and others, 



Predisposing Factors: Heredity. There is unquestionably an in- 

 herited tendency in certain families toward the development of endocrin- 

 opathies, which to some extent follows the Mendelian laws. 



Heredity as a factor has been observed in goiter, myxedema, cretinism, 

 diabetes, gigantism, and Addison's disease. Because of the analogy be- 

 tween the thyroid and pituitar-y it is reasonable to suppose that the same 

 hereditary tendencies obtain in both glands. Definite data on this point 

 are, however, meager. 



It is known that cretins may be born from mild cretinous parents, or 

 from goitrous parents. Paterson reported a family in which the first 

 two children were cretins, the third child born was normal, the mother 

 having taken thyroid from the third month of pregnancy. Moebius might 



