EXOPHTHALMOS
- 1 July 1949
- journal article
- review article
- Published by American Physiological Society in Physiological Reviews
- Vol. 29 (3), 260-280
- https://doi.org/10.1152/physrev.1949.29.3.260
Abstract
In lower animals exophthalmos may be produced experimentally by stimulation of the cervical sympathetic nerve trunk, by admn. of thyroxin together with certain sympathomimetic substances or by the use of cyanides. These act by causing contraction of Mailer''s orbital muscle which, in turn, increases the fluid tension behind the eyeball and drives it forward. Almost the whole of the nervous path is known from the hypothalamic region to Muller''s orbital muscle. In apes, stimulation of the cervical sympathetic trunk fails to produce exophthalmos. Exophthalmos may also be produced in the absence of the thyroid gland by anterior pituitary thyrotropic hormone (APTH). It is associated with edema of the orbital contents. The effect of APTH is increased by gonadal substances. True exophthalmos in Graves'' Disease must be distinguished from lid retraction by means of an exophthalmometer. It may exist with a high or with a low BMR. Evidence shows that the form with a high BMR is accompanied by considerable increase of orbital fatty tissue and increase of fat in the extra-ocular muscles. Evidence suggests that this form may be produced by the admn. of thyroxin. It is usually but not always accompanied by lid retraction. It has been produced in a hypothyroid patient by admn. of thyroxin and adrenalin as well as by thyroxin and ephe-drine or ephetonine. Other possible but unproven factors in its causation are smooth muscle in the orbit or disturbances of the orbital circulation. Muller''s orbital muscle is not responsible for exophthalmos in Graves'' Disease. Exophthalmos with a low BMR (hypothyroid, post-thyroidectomy, thyrotropic exophthalmos) is due to the action of an anterior pituitary substance (APTH) which produces edema and round-cell deposits in the loose orbital tissue and in the extrinsic muscles, sometimes increasing their volume to such an extent that not only is the eyeball pushed forward but the circulation in the orbit is obstructed. It is uncertain whether this muscle change is primary or follows changes in the orbital connective tissues as it did in Smelser''s guinea pigs. Brief consideration has been given to the occurrence of exophthalmos due to ophthalmoplegia and myasthenia. Treatment of the condition has not been considered.Keywords
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