PARATHYROID GLANDS 699 



In 1905, Berkeley asserted that the administration of parathyroid 

 preparations would relieve the symptoms in Parkinson's disease, and since 

 then many clinicians have tested this therapy, some with apparent suc- 

 cess, others with failure. In my own experience with a number of cases, 

 I have not been able to convince myself that any real benefit followed the 

 administration of parathyroid substance, though Berkeley, in later re- 

 ports, assevers that there was striking improvement . in about 65 per cent 

 of his large series of cases from the continuous oral administration of 

 Beebe's parathyronucleoproteid. Koussy and Clunet (a) saw no benefit 

 from parathyroid treatment of Parkinson's disease ; indeed, they assert that 

 their patients were made distinctly worse by it. 



The parathyroid glands in Parkinson's disease have been studied at 

 autopsy by a number of observers. Camp and Berkeley described patho- 

 logical alterations in these glands, though Erdheim and R. L. Thompson, 

 in the glands of their cases, could discover no anatomical lesions. Alguier 

 studied four cases ; in one, he observed changes intermediate between those 

 of hypertrophy with copious colloid formation and those of atrophy; in 

 another, he found vacuolization of the cells and marked eosinophilia ; and, 

 in the two other cases, there was atrophy of, and fatty changes in, the 

 cells. 



Very careful studies of the parathyroid glands in Parkinson's disease 

 have also been made by Roussy and Clunet. In four cases that had been 

 studied exhaustively clinically before death, they found the parathyroid 

 glands definitely enlarged when compared with the glands at 100 autop- 

 sies on non-Parkinsonian cases. In the enlarged glands they demon- 

 strated histologically a simple hyperplasia with increase of colloid, to- 

 gether with large numbe>rs of acidophile cells. These authors interpret 

 these findings as evidence of a hyperfunction of the parathyroid glands in 

 Parkinson's disease, though they admit that the disease may be either a 

 result or a cause of the hyperparathyrosis. They suggest that, possibly, 

 both the Parkinson's disease and the hyperplasia of the parathyroids may 

 be results of some unknown cause of a still larger process. The observa- 

 tions of Roussy and Clunet led Haberfeld and also Mar anon (a) to study 

 the parathyroid glands after death in cases of Parkinson's disease. These 

 investigators assert, however, that they could discover no changes point- 

 ing either to a hyperfunction or a hypofunction of the glands. 



THOMSEN'S DISEASE. In this rare familial and hereditary disease, 

 first clearly described by J. Thomsen (1875-76), and known also as 

 myotonia congenita, the characteristic marks are (1) enlargement of the 

 muscles, and (2) interference with voluntary motion, due to a rigidity 

 that sets in on attempts to make movements. The mechanical excitability 

 of the muscles is increased. On electrical examination, the myotonic re- 

 action of Erb (My R) is met with; there is slight depression of galvanic 

 excitability of the motor nerves ; but the direct galvanic muscular irritabil- 



