The major interest in the pathology of the exophthalmic goiter syndrome still hinges about the thyroid gland as it has done in an indefinite manner since 1840 and in a specific way since Gauthier and Möbius in 1886 and 1887 advanced the hypothesis that the symptom-complex was dependent on hyperactivity of the thyroid gland with a resultant thyroid intoxication.
But, notwithstanding the large amount of study and experiment that has been directed to this subject during the past twenty-five years, the thyroid hypothesis of the etiology of the exophthalmic goiter syndrome still remains an hypothesis.
In recent years the clinical evidence, especially that of surgical therapy, tends to support the thyroid hypothesis, while at the same time the evidence from pathologic anatomy, chemistry and pathologic physiology rather suggests that the thyroid does not play a primary rôle in the production of the symptom-complex.
I. ANATOMIC CHANGES IN THE THYROID
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