

CLINICAL SYNDROMES 313 



Murray states that the sympathetic nervous system theory is not 

 tenable, owing to, first, the absence of a dilatation of the pupil in exoph- 

 thalmic goiter; secondly, the impossibility of a continuance of an irrita- 

 tive lesion for years, and, lastly, the absence of any demonstrated path- 

 ological lesion in the sympathetic ganglia in the majority of the cases. 

 Nevertheless, quite recently L. B. Wilson (/), of the Mayo clinic, from his 

 experimental production of lesions in the cervical sympathetic ganglia of 

 nineteen goats by electrical stimulation and direct bacterial inoculation, 

 concludes that "it would appear that irritation from the presence of certain 

 bacteria within the cervical sympathetic ganglia of the goat, may produce 

 histological pictures within the ganglia and in the thyroid, which parallel 

 those found in the various stages of progressive and regressive exophthal- 

 mic goiter. The evidence supports the suggestion that in exophthalmic 

 goiter the thyroid receives its stimulus to overfunction through its nerve 

 supply and as a result usually of a local infection in the cervical sym- 

 pathetic ganglia. 7 ' 



From the writings of Eppinger, Falta, and Hess it is evident that 

 changes that cause irritation in some portion of the vegetative nervous 

 system are held by many to be the underlying cause of exophthalmic 

 goiter. Some would go further and state that this is a sine qua non for 

 Graves' disease, while a local disease of the thyroid will result in the 

 clinical picture of hyperthyroidism, but without any of the sympa- 

 theticotonic features of Graves' disease. The stimulus, according to L. 

 F. Barker, may be any of the previously mentioned predisposing factors, 

 namely sinus infections, tonsillitis, pulmonary or gastro-intestinal or uro- 

 genital disease. Barker (&), however, states that "my own studies indicate 

 that hyperthyroidism has no unitary origin but may be the result of 

 changes in different parts of the body." 



Biedl has come to the conclusion that the neurogenic theory was based 

 upon inconclusive experiments and isolated, contradictory post-mortem 

 data. Before leaving the neurogenic theories we must briefly refer to Crile's 

 (a) (b) Kinetic theory. The kinetic theory is without doubt the most 

 romantic as yet advanced. Crile points out that a true hypothesis of the 

 pathogenesis of the disease must surely account for the lesions of both the 

 nervous system and of the thyroid gland. In his opinion auto-intoxication 

 and infection, as well as the thyrogenic and neurogenic theories fall short 

 of a true hypothesis, though he admits that in the gross pathology there 

 is a practical agreement between the nervous system and the thyroid. To 

 quote Crile's (6) own words: "Graves' disease is not a disease of a single 

 organ or the result of some fleeting cause, but is a disease of the motor 

 mechanism of man, the same mechanism that causes physical action and 

 that expresses the emotions; its origin is in phylogeny and its excitation 

 is through either some stimulating emotion, intensely or repeatedly given, 

 on some lowering of the threshold of the nerve receptors, thus establish- 



