In a previous paper,1 it was demonstrated that the mongoloid appearance is due to a prenatal disturbance affecting the formation of the skull. The small stature of the mongoloid patient is due to lack of proliferation of the cartilage and early closure of the epiphysial lines, so that the growth of the bones is early arrested. It was proved that monglism is neither a racial mutation nor an atavistic regression.
The previous observations were presented to facilitate understanding of the pathologic changes in the endocrine glands associated with this condition. My chief interest in the present investigation was centered in the thyroid, known as one of the most important glands in relation to growth and differentiation of the organism.
The adrenal glands have recently been studied by Hirning and Farber;2 therefore I shall not discuss this material in detail. My observations in 3 new cases of mongolism coincide
BENDA CE. STUDIES IN MONGOLISM: II. THE THYROID GLAND. Arch NeurPsych. 1939;41(2):243–259. doi:10.1001/archneurpsyc.1939.02270140029002
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