The mechanisms of the ocular autonomic dysfunction during the intracarotid amytal suppression test
Abstract
We report the eye findings during selective injections of amytal to the internal carotid artery and to trunk and branches of the middle cerebral artery in three patients. This report comes à propos of our previous observation that fairly dense visual obscuration (probably secondary retinal suppression by the amytal), pupillary dilatation (mydriasis) and impairment of visual accommodation (cycloplegia) are not uncommon during the intracarotid amytal suppression test (AST). Selective injections in these three cases offered additional insight into the mechanisms of the autonomic dysfunction observed in the eye ipsilateral to injection of amytal (EII). Injection of amytal into the trunk and branches of the middle cerebral artery, above the origin of the ophthalmic artery, did not produce ocular autonomic changes in any of the three patients. Injection of amytal in the internal carotid, below the origin of the ophthalmic artery, resulted in pupillary dilatation in the EII in two of the three patients. Based on the anatomy of the vasculature and autonomic innervation of the eye, we postulate that the pupillary dilatation and deficit of visual accommodation observed after intracarotid amytal injection are secondary to parasympathetic suppression in the ciliary ganglion. Amytal reaches the ciliary ganglion via the posterior ciliary arteries, branches of the ophthalmic artery. In summary, injection of amytal in the internal carotid artery below the origin of the ophthalmic artery, but not above it, can impair visual acuity and, in some cases, entirel suppress the vision in the EII secondary to retinal suppression. Dilatation of the pupil due to parasympathetic dysfunction is also common and is likely secondary to suppression of the ciliary ganglion in the orbit.
Keywords: Wada test, Amytal suppression test, Vision, Eye function, Autonomic function, Selective injections, Mydriasis
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PII: S0920-1211(96)00894-7
doi:10.1016/S0920-1211(96)00894-7
© 1997 Elsevier Science B.V. All rights reserved.
